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Theory of Intelligent Design, the best explanation of Origins » Molecular biology of the cell » Development biology » Where Do Complex Organisms Come From?

Where Do Complex Organisms Come From?

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1 Where Do Complex Organisms Come From? on Thu Feb 25, 2016 5:59 am

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Where Do Complex Organisms Come From?

http://reasonandscience.heavenforum.org/t2316-where-do-complex-organisms-come-from

Cell and body shape, and organism development depends on following : 

Membrane targets and patterns 
Cytoskeletal arrays

Centrosomes 
Ion channels, and 
Sugar molecules on the exterior of cells (the sugar code)

Gene regulatory networks

Various codes and the encoded epigenetic information is required:

The various codes in the cell
http://reasonandscience.heavenforum.org/t2213-the-various-codes-in-the-cell

The Genetic Code 
The Splicing Codes
The Metabolic Code
The Signal Transduction Codes 
The Signal Integration Codes 
The Histone Code 
The Tubulin Code
The Sugar Code 
The Glycomic Code
The calcium Code
The RNA Code


" Junk DNA "

MicroRNAs--"Once Dismissed as Junk"--Confirmed To Have Important Gene Regulatory Function

In 2008 Scientific American noted that microRNAs were "once dismissed as junk" and said the following:
Tiny snippets of the genome known as microRNA were long thought to be genomic refuse because they were transcribed from so-called "junk DNA," sections of the genome that do not carry information for making proteins responsible for various cellular functions. Evidence has been building since 1993, however, that microRNA is anything but genetic bric-a-brac. Quite the contrary, scientists say that it actually plays a crucial role in switching protein-coding genes on or off and regulating the amount of protein those genes produce.

Transposons and Retrotransposons

striking evidence has accumulated indicating that some proviral sequences and HERV proteins might even serve the needs of the host and are therefore under positive selection. The remarkable progress in the analysis of host genomes has brought to light the significant impact of HERVs and other retroelements on genetic variation, genome evolution, and gene regulation.



Cell and body shape, and organism development does NOT depend exclusively on genetic information.

Stephen C. Meyer, Darwin's doubt:

NEO-DARWINISM AND THE CHALLENGE OF EPIGENETIC INFORMATION
These different sources of epigenetic information in embryonic cells pose an enormous challenge to the sufficiency of the neo-Darwinian mechanism. According to neo-Darwinism, new information, form, and structure arise from natural selection acting on random mutations arising at a very low level within the biological hierarchy—within the genetic text. Yet both body-plan formation during embryological development and major morphological innovation during the history of life depend upon a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. If DNA isn’t wholly responsible for the way an embryo develops— for body-plan morphogenesis—then DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process. Genetic mutations are simply the wrong tool for the job at hand. Even in a best-case scenario—one that ignores the immense improbability of generating new genes by mutation and selection—mutations in DNA sequence would merely produce new genetic information. But building a new body plan requires more than just genetic information. It requires both genetic and epigenetic information—information by definition that is not stored in DNA and thus cannot be generated by mutations to the DNA. It follows that the mechanism of natural selection acting on random mutations in DNA cannot by itself generate novel body plans, such as those that first arose in the Cambrian explosion.

Centrosomes:
Centrosomes play a central role in development: a frog egg can be induced to develop into a frog merely by injecting a sperm centrosome—no sperm DNA is needed. Another non-genetic factor involved in development is the membrane pattern of the egg cell. 

FORM AND INFORMATION
Organismal form and function depend upon the precise arrangement of various constituents as they arise during, or contribute to, embryological development. Thus, the specific arrangement of the other building blocks of biological form—cells, clusters of similar cell types, dGRNs, tissues, and organs—also represent a kind of specified or functional information.

ABOVE AND BEYOND: EPIGENETIC INFORMATION
genes alone do not determine the three-dimensional form and structure of an animal.  Developmental biologists, in particular, are now discovering more and more ways that crucial information for building body plans is imparted by the form and structure of embryonic cells, including information from both the unfertilized and fertilized egg. DNA helps direct protein synthesis. Parts of the DNA molecule also help to regulate the timing and expression of genetic information and the synthesis of various proteins within cells. Yet once proteins are synthesized, they must be arranged into higher-level systems of proteins and structures.
The three-dimensional structure or spatial architecture of embryonic cells plays important roles in determining body-plan formation during embryogenesis. Developmental biologists have identified several sources of epigenetic information in these cells.


CYTOSKELETAL ARRAYS
The precise arrangement of microtubules in the cytoskeleton constitutes a form of critical structural information. neither the tubulin subunits, nor the genes that produce them, account for the differences in the shape of the microtubule arrays that distinguish different kinds of embryos and developmental pathways. Instead, the structure of the microtubule array itself is, once again, determined by the location and arrangement of its subunits, not the properties of the subunits themselves. Jonathan Wells explains it this way: “What matters in [embryological] development is the shape and location of microtubule arrays, and the shape and location of a microtubule array is not determined by its units.” Directed transport involves the cytoskeleton, but it also depends on spatially localized targets in the membrane that are in place before transport occurs. Developmental biologists have shown that these membrane patterns play a crucial role in the embryological development of fruit flies.

Membrane Targets
Preexisting membrane targets, already positioned on the inside surface of the egg cell, determine where these molecules will attach and how they will function. These membrane targets provide crucial information—spatial coordinates—for embryological development.

Ion Channels and Electromagnetic Fields
Experiments have shown that electromagnetic fields have “morphogenetic” effects—in other words, effects that influence the form of a developing organism. In particular, some experiments have shown that the targeted disturbance of these electric fields disrupts normal development in ways that suggest the fields are controlling morphogenesis.2 Artificially applied electric fields can induce and guide cell migration. There is also evidence that direct current can affect gene expression, meaning internally generated electric fields can provide spatial coordinates that guide embryogenesis.3 Although the ion channels that generate the fields consist of proteins that may be encoded by DNA (just as microtubules consist of subunits encoded by DNA), their pattern in the membrane is not. Thus, in addition to the information in DNA that encodes morphogenetic proteins, the spatial arrangement and distribution of these ion channels influences the development of the animal.

The Sugar Code
These sequence-specific information-rich structures influence the arrangement of different cell types during embryological development. Thus, some cell biologists now refer to the arrangements of sugar molecules as the “sugar code” and compare these sequences to the digitally encoded information stored in DNA. As biochemist Hans-Joachim Gabius notes, sugars provide a system with “high-density coding” that is “essential to allow cells to communicate efficiently and swiftly through complex surface interactions.” According to Gabius, “These [sugar] molecules surpass amino acids and nucleotides by far in information-storing capacity.” So the precisely arranged sugar molecules on the surface of cells clearly represent another source of information independent of that stored in DNA base sequences.  These cascades are, along with the cell event itself, associated with the “coding information” on a cell surface, or, using another terminology, are realized due to an instruction for the cell from the morphogenetic field of an organism. The concrete signal transduction pathways connecting the "coding information" on a cell surface and the expression of the given sets of genes need to be elucidated. 


Meyer, Darwins doubt, page 212:

According to neo-Darwinism, new information, form, and structure arise from natural selection acting on random mutations arising at a very low level within the biological hierarchy—within the genetic text. Yet both body-plan formation during embryological development and major morphological innovation during the history of life depend upon a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. If DNA isn’t wholly responsible for the way an embryo develops— for body-plan morphogenesis—then DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process. Genetic mutations are simply the wrong tool for the job at hand.

Even in a best-case scenario—one that ignores the immense improbability of generating new genes by mutation and selection—mutations in DNA sequence would merely produce new genetic information. But building a new body plan requires more than just genetic information. It requires both genetic and epigenetic information—information by definition that is not stored in DNA and thus cannot be generated by mutations to the DNA. It follows that the mechanism of natural selection acting on random mutations in DNA cannot by itself generate novel body plans, such as those that first arose in the Cambrian explosion.



Principal Meanings of Evolution in Biology Textbooks 1

What is fact :
1. Change over time; history of nature; any sequence of events in nature
2. Changes in the frequencies of alleles in the gene pool of a population
3. Limited common descent: the idea that particular groups of organisms have descended from
a common ancestor.
4. The mechanisms responsible for the change required to produce limited descent with modification; chiefly natural selection acting on random variations or mutations

What is not fact: 
5. Universal common descent: the idea that all organisms have descended from a single common ancestor.
6. Blind watchmaker thesis: the idea that all organisms have descended from common ancestors through unguided, unintelligent, purposeless, material processes such as natural
selection acting on random variations or mutations; the idea that the Darwinian mechanism of natural selection acting on random variation, and other similarly naturalistic mechanisms, completely suffice to explain the origin of novel biological forms and the appearance of design in complex organisms.

Macroevolution. Fact, or fantasy ?  2

Micro evolution and secondary speciation is a fact. The macrochange however from one organism into another  in long periods of time, the change of body plans and evolutionary novelties  is not a fact, not even a theory, or even a hypothesis. Its just fantasy without a shred of evidence. Its not possible.  Show me some examples of observed facts;  please provide and give me empirical data of a unorganized undirected unguided Neo-Darwinian accidental random macro-evolutionary event of a change/transition, where  one "kind" can evolve into another beyond the species level (i.e. speciation) ,  like a organism randomly changing/transition into a whole entire different, new fully functioning biological features in an organism, the emergence of new complex functions, a new genus or higher rank in taxonomy, with the arise of new body plans, What is an evolutionary novelty? A list of most-often cited examples include the shell of turtles (Cebra-Thomas et al. 2005), flight (Prum 2005), flowers (Albert, Oppenheimer, and Lindqvist 2002), the ability of great tits to open bottles of milk (Kothbauerhellmann 1990), the transition from the jaw to the ear of some bones during the evolution of mammals from reptiles (Brazeau and Ahlberg 2006), eyes (Fernald 2006), hearts (Olson 2006), bipedalism (Richmond and Strait 2000), and the origin of Hox genes (Wagner, Amemiya, and Ruddle 2003);   Ernst Mayr, a major figure of the MS, defined novelties as “any newly acquired structure or property that permits the performance of a new function, which, in turn, will open a new adaptive zone” (Mayr 1963, 602)something that we merely don't have to just put  blind faith in?

http://www.ncbi.nlm.nih.gov/pubmed/15612191
In the last 25 years, criticism of most theories advanced by Darwin and the neo-Darwinians has increased considerably, and so did their defense. Darwinism has become an ideology, while the most significant theories of Darwin were proven unsupportable. 

Dissecting Darwinism
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246854/
regarding the origin of the species and life (DNA), even Darwin commented, “If it could be shown that complex systems could not arise by small sequential steps, then my theory would completely break down.” Irreducibly complex systems involving thousands of interrelated specifically coded enzymes do exist in every organ of the human body. At an absolute minimum, the inconceivable self-formation of DNA and the inability to explain the incredible information contained in DNA represent fatal defects in the concept of mutation and natural selection to account for the origin of life and the origin of DNA. As new theories emerge that explain the origin of life, the inevitable emotional accusations of heresy and ignorance are not surprising in a period of scientific revolution. It is therefore time to sharpen the minds of students, biologists, and physicians for the possibility of a new paradigm.

Lynn Margulis

Although random mutations influenced the course of evolution, their influence was mainly by loss, alteration, and refinement... Never, however, did that one mutation make a wing, a fruit, a woody stem, or a claw appear. Mutations, in summary, tend to induce sickness, death, or deficiencies. No evidence in the vast literature of heredity changes shows unambiguous evidence that random mutation itself, even with geographical isolation of populations, leads to speciation.

The accumulation of genetic mutations were touted to be enough to change one species to another….No. It wasn’t dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact.

I was taught over and over again that the accumulation of random mutations led to evolutionary change - led to new species. I believed it until I looked for evidence.

biology is opening the black box, and demonstrating how organisms develop. We are slowly getting out of a state of ignorance in regard of what mechanisms determines cell shape, assignment of their planes of division, tendencies to move, directions and rates of movement, modes of differentiation into particular cell types, and cell death (apoptosis).

The process of morphogenesis, which can be defined as an evolution of the form of an organism, is one of the most intriguing mysteries in the life sciences. The discovery and description of the spatial– temporal distribution of the gene expression pattern during morphogenesis, together with its key regulators, is one of the main recent achievements in developmental biology. Nevertheless, gene expression patterns cannot explain the development of the precise geometry of an organism and its parts in space. 1

Stephen C Meyer , Darwin's doubt pg.218: 

Contemporary critics of neo-Darwinism acknowledge, of course, that preexisting forms of life can diversify under the twin influences of natural selection and genetic mutation. Known microevolutionary processes can account for small changes in the coloring of peppered moths, the  acquisition of antibiotic resistance in different strains of bacteria, and cyclical variations in the size of Galápagos finch beaks. Nevertheless, many biologists now argue that neo-Darwinian theory does not provide an adequate explanation for the origin of new body plans or events such as the Cambrian explosion. For example, evolutionary biologist Keith Stewart Thomson, formerly of Yale University, has expressed doubt that large-scale morphological changes could accumulate by minor changes at the genetic level. Geneticist George Miklos, of the Australian National University, has argued that neo- Darwinism fails to provide a mechanism that can produce large-scale innovations in form and structure. Biologists Scott Gilbert, John Opitz, and Rudolf Raff have attempted to develop a new theory of evolution to supplement classical neo-Darwinism, which, they argue, cannot adequately explain large-scale macroevolutionary change. As they note: 

Starting in the 1970s, many biologists began questioning its neo-Darwinism's adequacy in explaining evolution. Genetics might be adequate for explaining microevolution, but  microevolutionary changes in gene frequency were not seen as able to turn a reptile into a mammal or to convert a fish into an amphibian. Microevolution looks at adaptations that concern the survival of the fittest, not the arrival of the fittest. As Goodwin (1995) points out, "the origin of species—Darwin's problem—remains unsolved." 

pg. 204 

Genes alone do not determine the three-dimensional form and structure of an animal. so-called epigenetic information—information stored in cell structures, but not in DNA sequences—plays a crucial role. The Greek prefix epi means "above" or "beyond," so epigenetics refers to a source of information that lies beyond the genes. "Detailed information at the level of the gene does not serve to explain form." "epigenetic" or "contextual information" plays a crucial role in the formation of animal "body  assemblies" during embryological development. 

Recent discoveries about the role of epigenetic information in animal development pose a formidable challenge to the standard neo-Darwinian account of the origin of these body plans—perhaps the most formidable of all. "the neo-Darwinian paradigm still represents the central explanatory framework of evolution," it has "no theory of the generative." neo-Darwinism "completely avoids the question of the origination of phenotypic traits and of organismal form."


Mechanisms known to affect the phenotype.


1. The RNA methylation
2. The DNA dinucleotide methylation
3. The DNA CpG island methylation
4. The histone methylation
5. The chromatin remodeling
6. The DNA coiling
7. The microRNA regulation
8. The alternative splicing

No gene sequence alterations in the list, because
- Deletions, insertions and frameshift mutations are misinterpretations of the alternative splicing mechanism
- Retrogenes and genetic recombinations are misinterpretations of the alternative splicing mechanism
- RNA based gene duplications are misinterpretations of the alternative splicing mechanism
So, what do the evolutionists have left for supporting their idea of random mutations and natural selection?
Point mutations, which don't occur randomly. Methylated cytosine may flip to thymine and this alteration will not be repaired by the repair mechanisms. This is a designed feature. At intensive level it leads to gene inactivation, further it leads to chromatin remodeling and yet further, to chromosome loss. The DNA of every organism gets only degraded, little by little.


Integrins and ion channels in cell migration: implications for neuronal development, wound healing and metastatic spread.
http://www.ncbi.nlm.nih.gov/pubmed/20549944

Morphogenetic fields in embryogenesis, regeneration, and cancer: Non-local control of complex patterning
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413735/

Principles of planar polarity in animal development
http://dev.biologists.org/content/138/10/1877

Morphogenetic Systems as cognitive agents
http://ase.tufts.edu/biology/labs/levin/research/newdirections.htm

Research on the Dynamics of Information Processing in Biological Structures
http://ase.tufts.edu/biology/labs/levin/research/index.htm

Molecular pathways regulating mitotic spindle orientation in animal cells
http://dev.biologists.org/content/140/9/1843

Evolutionary bioscience as regulatory systems biology
http://www.sciencedirect.com/science/article/pii/S0012160611000911?np=y

Global Control Regions and Regulatory Landscapes in Vertebrate Development and Evolution
http://bejerano.stanford.edu/readings/public/80_Function_GCRs.pdf

CONTROL OF TRANSCRIPTION BY SEQUENCESPECIFIC DNA-BINDING PROTEINS
http://www.garlandscience.com/res/pdf/9780815341291_ch08.pdf

The transcription factor code: defining the role of a developmental transcription factor in the adult brain.
For the human brain to develop and function correctly, each of its 100 billion neurons must follow a specific and pre-programmed code of gene expression. This code is driven by key transcription factors that regulate the expression of numerous proteins, moulding the neurons identity to create its unique shape and electrical behaviour.
https://www.findaphd.com/search/projectdetails.aspx?PJID=41943

Unraveling a novel transcription factor code determining the human arterial-specific endothelial cell signature
Our pioneering profiling study on freshly isolated ECs unveiled a combinatorial transcriptional code that induced an arterial fingerprint more proficiently than the current gold standard, HEY2, and this codeconveyed an in vivo arterial-like behavior upon venous ECs.
http://www.bloodjournal.org/content/122/24/3982?sso-checked=true

The transcriptional regulatory code of eukaryotic cells--insights from genome-wide analysis of chromatin organization and transcription factor binding.
The term 'transcriptional regulatory code' has been used to describe the interplay of these events in the complex control of transcription. With the maturation of methods for detecting in vivo protein-DNA interactions on a genome-wide scale, detailed maps of chromatin features and transcription factor localization over entire genomes of eukaryotic cells are enriching our understanding of the properties and nature of this transcriptional regulatory code.
http://www.ncbi.nlm.nih.gov/pubmed/16647254

The Splicing code
rigin and evolution of spliceosomal introns
http://biologydirect.biomedcentral.com/articles/10.1186/1745-6150-7-11

The rna binding protein binding code
A compendium of RNA-binding motifs for decoding gene regulation
http://www.nature.com/nature/journal/v499/n7457/full/nature12311.html

microRNA binding code
The code within the code: microRNAs target coding regions
http://www.ncbi.nlm.nih.gov/pubmed/20372064

The Glycan or Sugar Code
Biological information transfer beyond the genetic code: the sugar code
http://www.ncbi.nlm.nih.gov/pubmed/10798195

Epigenetic Regulation by Heritable RNA
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3990477/




1. http://www.jodkowski.pl/ke/Meanings2000.pdf
2.http://reasonandscience.heavenforum.org/t1390-macroevolution#1982



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2 DEVELOPMENTAL GENE REGULATORY NETWORKS on Sun Mar 06, 2016 8:22 am

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Dembski and J.Wells: The design of life, general notes, page 16:

What Besides DNA Controls Development? If DNA does not control development, what does? Actually, there is good evidence for the involvement of at least two other factors in the developing egg: the cytoskeleton and the membrane. Every animal cell contains a network of microscopic fibers called a cytoskeleton. These fibers include microtubules, which are known to be involved in patterning embryos. For example, one of the gene products involved in head-to-rear patterning of fruit fly embryos is delivered to its proper location by microtubules; if the microtubules are experimentally disrupted, the gene product doesn’t reach its proper destination and the embryo is grossly deformed. Microtubules consist of many identical protein subunits, and each subunit is produced according to a template in the organism’s DNA. What matters in development is the organization of microtubule arrays, and the organization of a microtubule array is not determined by its subunits any more than the layout of a house is determined by its bricks. Instead, microtubule arrays are formed by organelles called centrosomes, which are inherited independently of an organism’s DNA. Centrosomes play a central role in development: a frog egg can be induced to develop into a frog merely by injecting a sperm centrosome—no sperm DNA is needed. Another non-genetic factor involved in development is the membrane pattern of the egg cell. 

Cell membranes are not merely featureless bags, but highly complex structures. For example, a membrane contains specialized channels that pump molecules in and out of the cell, enabling it to control its interactions with the external environment. An egg cell membrane also contains “targets” which ensure that molecules synthesized in the nucleus reach their proper destinations in the embryo. The gene product, which is involved in head-to-rear patterning of fruit fly embryos and which depends on microtubules to deliver it to its proper location, also needs a target molecule to keep it in place after it arrives. The target is already there, embedded in the membrane. Experiments with single-celled animals show that membrane patterns are determined by pre-existing membranes, not by DNA. Like microtubule subunits, the proteins embedded in a membrane are produced according to templates in the organism’s DNA; but like the form and location of microtubule arrays, the patterns of those embedded proteins are inherited independently of the organism’s DNA. So the control exercised by microtubule arrays and membrane patterns over embryonic development is not encoded in DNA sequences. This does not mean that we now understand developmental programs. Far from it! But it is quite clear that they cannot be reduced to genetic programs, written in the language of DNA sequences. It would be more accurate to say that a developmental program is written into the structure of the entire fertilized egg—including its DNA, microtubule arrays, and membrane patterns—in a language of which we are still largely ignorant.

EVOLUTIONARY BIOSCIENCE AS REGULATORY SYSTEMS BIOLOGY 1
Never in the modern history of evolutionary bioscience have such essentially different ideas about how to understand evolution of the animal body plan been simultaneously current. The first is the classic neo-Darwinian concept that evolution of animal morphology occurs by means of small continuous changes in primary protein sequence which in general require homozygosity to effect phenotype. The second paradigm holds that evolution at all levels can be illuminated by detailed analysis of cis-regulatory changes in genes that are direct targets of sequence level selection, in that they control variation of immediate adaptive significance. An entirely different way of thinking is that the evolution of animal body plans is a system level property of the developmental gene regulatory networks (dGRNs) which control ontogeny of the body plan.


http://reasonandscience.heavenforum.org/t2318-gene-regulatory-networks-controlling-body-plan-development#4804

In the years since, Wells has developed a powerful argument against the adequacy of the neo-Darwinian mechanism as an explanation for the origin of animal body plans. His argument turns on the importance of epigenetic information to animal development. To see why epigenetic information poses an additional challenge to neo-Darwinism and what exactly biologists mean by “epigenetic” information, let’s examine the relationship between biological form and biological information.
Stephen C Meyer , Darwin's doubt pg.11:

FORM AND INFORMATION
 Biologists typically define “form” as a distinctive shape and arrangement of body parts. Organismal forms exist in three spatial dimensions and arise in time—in the case of animals during development from embryo to adult. Animal form arises as material constituents are constrained to establish specific arrangements with an identifiable three-dimensional shape or “topography”—one that we would recognize as the body plan of a particular type of animal. A particular “form,” therefore, represents a highly specific arrangement of material components among a much larger set of possible arrangements. Understanding form in this way suggests a connection to the notion of information in its most theoretically general sense.  Shannon’s mathematical theory of information equated the amount of information transmitted with the amount of uncertainty reduced or eliminated in a series of symbols or characters. Information, in Shannon’s theory, is thus imparted as some options, or possible arrangements, are excluded and others are actualized. The greater the number of arrangements excluded, the greater the amount of information conveyed. Constraining a set of possible material arrangements, by whatever means, involves excluding some options and actualizing others. Such a process generates information in the most general sense of Shannon’s theory. It follows that the constraints that produce biological form also impart information, even if this information is notencoded in digital form.
 
DNA contains not only Shannon information but also functional or specified information. The arrangements of nucleotides in DNA or of amino acids in a protein are highly improbable and thus contain large amounts of Shannon information. But the function of DNA and proteins depends upon extremely specific arrangements of bases and amino acids. Similarly, animal body plans represent, not only highly improbable, but also highly specific
arrangements of matter. Organismal form and function depend upon the precise arrangement of various constituents as they arise during, or contribute to, embryological development. Thus, the specific arrangement of the other building blocks of biological form—cells, clusters of similar cell types, dGRNs, tissues, and organs—also represent a kind of specified or functional information. I noted that the ease with which Shannon’s information theory applies to molecular biology has sometimes led to confusion about the kind of information contained in DNA and proteins. It may have also created confusion about the places that specified information might reside in organisms. Perhaps because the information-carrying capacity of the gene can be so easily measured, biologists have often treated DNA, RNA, and proteins as the sole repositories of biological information. Neo-Darwinists have assumed that genes possess all the information necessary to specify the form of an animal. They have also assumed that mutations in genes will suffice to generate the new information necessary to build a new form of animal life. Yet if biologists understand organismal form as resulting from constraints on the possible arrangements of matter at many levels in the biological hierarchy—from genes and proteins, to cell types and tissues, to organs and body plans —then biological organisms may well exhibit many levels of information-rich structure. Discoveries in developmental biology have confirmed this possibility.


ABOVE AND BEYOND: EPIGENETIC INFORMATION
 In 2003, MIT Press published a groundbreaking collection of scientific essays titled Origination of Organismal Form: Beyond the Gene in Developmental and Evolutionary Biology, edited by two distinguished developmental and evolutionary biologists, Gerd Müller, of the University of Vienna, and Stuart Newman, of New York Medical College. In their volume, Müller and Newman included a number of scientific articles describing recent discoveries in genetics and developmental biology—discoveries suggesting that genes alone do not determine the three-dimensional form and structure of an animal. Instead, many of the scientists in their volume reported that so-called epigenetic information—information stored in cell structures, but not in DNA sequences—plays a crucial role. The Greek prefix epi means “above” or “beyond,” so epigenetics refers to a source of information that lies beyond the genes. As Müller and Newman explain in their introduction, “Detailed information at the level of the gene does not serve to explain form.” Instead, as Newman explains, “epigenetic” or “contextual information” plays a crucial role in the formation of animal “body assemblies” during embryological development. Müller and Newman not only highlighted the importance of epigenetic information to the formation of body plans during development; they also argued that it must have played a similarly important role in the origin and evolution of animal body plans in the first place. They concluded that recent discoveries about the role of epigenetic information in animal development pose a formidable challenge to the standard neo-Darwinian account of the origin of these body plans—perhaps the most formidable of all. In the introductory essay to their volume, Müller and Newman list a number of “open questions” in evolutionary biology, including the question of the origin of Cambrian-era animal body plans and the origin of organismal form generally, the latter being the central topic of their book. They note that though “the neo-Darwinian paradigm still represents the central explanatory framework of evolution,” it has “no theory of the generative.” In their view, neo-Darwinism “completely avoids [the question of] the origination of phenotypic traits and of organismal form.” As they and others in their volume maintain, neo-Darwinism lacks an explanation for the origin of organismal form precisely because it cannot explain the origin of epigenetic information. I first learned about the problem of epigenetic information and the Spemann and Mangold experiment while driving to a private meeting of Darwin-doubting scientists on the central coast of California in 1993. In the car with me was Jonathan Wells , who was then finishing a Ph.D. in developmental biology at the University of California at Berkeley. Like some others in his field, Wells had come to reject the (exclusively) “gene-centric” view of animal development and to recognize the importance of nongenetic sources of information. By that time, I had studied many questions and challenges to standard evolutionary theories arising out of molecular biology. But epigenetics was new to me. On our drive, I asked Wells why developmental biology was so important to evolutionary theory and to assessing neo-Darwinism. I’ll never forget his reply. “Because” he said, “that’s where the whole theory is going to unravel.”


BEYOND GENES
 Many biologists no longer believe that DNA directs virtually everything happening within the cell. Developmental biologists, in particular, are now discovering more and more ways that crucial information for building body plans is imparted by the form and structure of embryonic cells, including information from both the unfertilized and fertilized egg.Biologists now refer to these sources of information as “epigenetic.”10 Spemann and Mangold’s experiment is only one of many to suggest that something beyond DNA may be influencing the development of animal body plans. Since the 1980s, developmental and cell biologists such as Brian Goodwin, Wallace Arthur, Stuart Newman, Fred Nijhout, and Harold Franklin have discovered or analyzed many sources of epigenetic information. Even molecular biologists such as Sidney Brenner, who pioneered the idea that genetic programs direct animal development, now insist that the information needed to code for complex biological systems vastly outstrips the information in DNA. DNA helps direct protein synthesis. Parts of the DNA molecule also help to regulate the timing and expression of genetic information and the synthesis of various proteins within cells. Yet once proteins are synthesized, they must be arranged into higher-level systems of proteins and structures. Genes and proteins are made from simple building blocks—nucleotide bases and amino acids, respectively—arranged in specific ways. Similarly, distinctive cell types are made of, among other things, systems of specialized proteins. Organs are made of specialized arrangements of cell types and tissues. And body plans comprise specific arrangements of specialized organs. Yet the properties of individual proteins do not fully determine the organization of these higher-level structures and patterns. Other sources of information must help arrange individual proteins into systems of proteins, systems of proteins into distinctive cell types, cell types into tissues, and different tissues into organs. And different organs and tissues must be arranged to form body plans.
 
The hierarchical layering or arrangement of different sources of information. Note that the information necessary to build the lower-level electronic components does not determine the arrangement of those components on the circuit board or the arrangement of the circuit board and the other parts necessary to make a computer. That requires additional informational inputs. Two analogies may help clarify the point. At a construction site, builders will make use of many materials: lumber, wires, nails, drywall, piping, and windows. Yet building materials do not determine the floor plan of the house or the arrangement of houses in a neighborhood. Similarly, electronic circuits are composed of many components, such as resistors, capacitors, and transistors. But such lower-level components do not determine their own arrangement in an integrated circuit (see Fig. 14.2). In a similar way, DNA does not by itself direct how individual proteins are assembled into these larger systems or structures—cell types, tissues, organs, and body plans—during animal development.

Harold, “From Morphogenes to Morphogenesis,” 2774; Moss, What Genes Can’t Do. Of course, many proteins bind chemically with each other to form complexes and structures within cells. Nevertheless, these “self-organizational” properties do not fully account for higher levels of organization in cells, organs, or body plans. Or, as Moss has explained “Neither DNA nor any other aperiodic crystal constitutes a unique repository of heritable stability in the cell; in addition, the chemistry of the solid state does not constitute either a unique or even an ontologically or causally privileged basis for explaining the existence and continuity of order in the living world . . .” Moss, What Genes Can’t Do, 76.

Instead, the three-dimensional structure or spatial architecture of embryonic cells plays important roles in determining body-plan formation during embryogenesis. Developmental biologists have identified several sources of epigenetic information in these cells.
 
CYTOSKELETAL ARRAYS
Eukaryotic cells have internal skeletons to give them shape and stability. These “cytoskeletons” are made of several different kinds of filaments including those called the “microtubules.” The structure and location of the microtubules in the cytoskeleton influence the patterning and development of embryos. Microtubule “arrays” within embryonic cells help to distribute essential proteins used during development to specific locations in these cells. Once delivered, these proteins perform functions critical to development, but they can only do so if they are delivered to their correct locations with the help of preexisting, precisely structured microtubule or cytoskeletal arrays (see Figures below).





Thus, the precise arrangement of microtubules in the cytoskeleton constitutes a form of critical structural information. These microtubule arrays are made of proteins called tubulin, which are gene products. Nevertheless, like bricks that can be used to assemble many different structures, the tubulin proteins in the cell’s microtubules are identical to one another. Thus, neither the tubulin subunits, nor the genes that produce them, account for the differences in the shape of the microtubule arrays that distinguish different kinds of embryos and developmental pathways. Instead, the structure of the microtubule array itself is, once again, determined by the location and arrangement of its subunits, not the properties of the subunits themselves. Jonathan Wells explains it this way: “What matters in [embryological] development is the shape and location of microtubule arrays, and the shape and location of a microtubule array is not determined by its units.” For this reason, as University of Colorado cell biologist Franklin Harold notes, it is impossible to predict the structure of the cytoskeleton of the cell from the characteristics of the protein constituents that form that structure.

Another cell structure influences the arrangement of the microtubule arrays and thus the precise structures they form and the functions they perform. In an animal cell, that structure is called the centrosome (literally, “central body”), a microscopic organelle that sits next to the nucleus between cell divisions in an undividing cell. Emanating from the centrosome is the microtubule array that gives a cell its three-dimensional shape and provides internal tracks for the directed transport of organelles and essential molecules to and from the nucleus. During cell division the centrosome duplicates itself. The two centrosomes form the poles of the cell-division apparatus, and each daughter cell inherits one of the centrosomes; yet the centrosome contains no DNA. Though centrosomes are made of proteins—gene products—the centrosome structure is not determined by genes alone.
Another important source of epigenetic information resides in the two-dimensional patterns of proteins in cell membranes. When messenger RNAs are transcribed, their protein products must be transported to the proper locations in embryonic cells in order to function properly. Directed transport involves the cytoskeleton, but it also depends on spatially localized targets in the membrane that are in place before transport occurs. Developmental biologists have shown that these membrane patterns play a crucial role in the embryological development of fruit flies.

Membrane Targets
For example, early embryo development in the fruit fly Drosophila melanogaster requires the regulatory molecules Bicoid and Nanos (among others). The former is required for anterior (head) development, and the latter is required for posterior (tail) development. In the early stages of embryological development, nurse cells pump Bicoid and Nanos RNAs into the egg. (Nurse cells provide the cell that will become the egg—known as the oocyte—and the embryo with maternally encoded messenger RNAs and proteins.) Cytoskeletal arrays then transport these RNAs through the oocyte, where they become attached to specified targets on the inner surface of the egg. Once in their proper place—but only then—Bicoid and Nanos play critical roles in organizing the head-to-tail axis of the developing fruit fly. They do this by forming two gradients (or differential concentrations), one with Bicoid protein most concentrated at the anterior end and another with Nanos protein most concentrated at the posterior end. Insofar as both of these molecules are RNAs—that is, gene products—genetic information plays an important role in this process. Even so, the information contained in the bicoid and nanos genes does not by itself ensure the proper function of the RNAs and proteins for which the genes code. Instead, preexisting membrane targets, already positioned on the inside surface of the egg cell, determine where these molecules will attach and how they will function. These membrane targets provide crucial information—spatial coordinates—for embryological development.

Ion Channels and Electromagnetic Fields
Membrane patterns can also provide epigenetic information by the precise arrangement of ion channels—openings in the cell wall through which charged electrical particles pass in both directions. For example, one type of channel uses a pump powered by the energy-rich molecule ATP to transport three sodium ions out of the cell for every two potassium ions that enter the cell. Since both ions have a charge of plus one (Na+, K+), the net difference sets up an electromagnetic field across the cell membrane. 1 Experiments have shown that electromagnetic fields have “morphogenetic” effects—in other words, effects that influence the form of a developing organism. In particular, some experiments have shown that the targeted disturbance of these electric fields disrupts normal development in ways that suggest the fields are controlling morphogenesis.2 Artificially applied electric fields can induce and guide cell migration. There is also evidence that direct current can affect gene expression, meaning internally generated electric fields can provide spatial coordinates that guide embryogenesis.3 Although the ion channels that generate the fields consist of proteins that may be encoded by DNA (just as microtubules consist of subunits encoded by DNA), their pattern in the membrane is not. Thus, in addition to the information in DNA that encodes morphogenetic proteins, the spatial arrangement and distribution of these ion channels influences the development of the animal.

The Sugar Code
Biologists know of an additional source of epigenetic information stored in the arrangement of sugar molecules on the exterior surface of the cell membrane. Sugars can be attached to the lipid molecules that make up the membrane itself (in which case they are called “glycolipids”), or they can be attached to the proteins embedded in the membrane (in which case they are called “glycoproteins”). Since simple sugars can be combined in many more ways than amino acids, which make up proteins, the resulting cell surface patterns can be enormously complex. As biologist Ronald Schnaar explains, “Each [sugar] building block can assume several different positions. It is as if an A could serve as four different letters, depending on whether it was standing upright, turned upside down, or laid on either of its sides. In fact, seven simple sugars can be rearranged to form hundreds of thousands of unique words, most of which have no more than five letters.” These sequence-specific information-rich structures influence the arrangement of different cell types during embryological development. Thus, some cell biologists now refer to the arrangements of sugar molecules as the “sugar code” and compare these sequences to the digitally encoded information stored in DNA. As biochemist Hans-Joachim Gabius notes, sugars provide a system with “high-density coding” that is “essential to allow cells to communicate efficiently and swiftly through complex surface interactions.” According to Gabius, “These [sugar] molecules surpass amino acids and nucleotides by far in information-storing capacity.” So the precisely arranged sugar molecules on the surface of cells clearly represent another source of information independent of that stored in DNA base sequences.


First, we suggest that the geometry of the organism and its parts is coded by a molecular code located on the cell surfaces in such a way that, with each cell, there can be associated a corresponding matrix, containing this code. As a particular model, we propose coding by several types of oligosaccharide residues of glycoconjugates. 1 
1. During embryogenesis, each cell undergoes cell divisions, growth, movements (shifts) and expression of specific molecules according to a determinate plan, invariant for each living species. 
2. This determinate plan for development of an organism can be considered as a tree of cell events from the initial state of the first cell (zygote) to a final predetermined state of an organism, where under cell event we understand “developmental events”, such as cell divisions, cell growth (death), cell differentiation and cell shifts. 
3. This determinate plan is coded by a set of specific biological markers, which, most likely, may exist and be transmitted as a set of cell membrane markers. Our main assumption is that such a code may be provided by a pattern of short oligosaccharide residues of glycoproteins (glycoconjugates) on a cell surface, changing in time and space. It is possible that some other cell surface markers, e.g. specific proteins, may play this coding role; however, short oligosaccharide residues of glycoconjugates have several specific features which make them the most plausible substances for such coding.
4. The general laws for cell events (cell motion laws), namely, the dependence of cell events on coded and positional biological information, have to be the same for all living species, leading to different forms and shapes resulting from different sets of species-specific molecular parameters. Our main goal is to describe these cell motion laws. 
5. Cell motion laws can be mathematically formulated using the notion of a morphogenetic field.  It is important to note that, in the framework of our model, the cascades of specific molecular events that correlate with pattern formation (e.g. differential gene expression, directed protein traffic, etc.) appear not to be the reason for a cell event. Rather, these cascades are, along with the cell event itself, associated with the “coding information” on a cell surface, or, using another terminology, are realized due to an instruction for the cell from the morphogenetic field of an organism. The concrete signal transduction pathways connecting the "coding information" on a cell surface and the expression of the given sets of genes need to be elucidated. 

NEO-DARWINISM AND THE CHALLENGE OF EPIGENETIC INFORMATION
These different sources of epigenetic information in embryonic cells pose an enormous challenge to the sufficiency of the neo-Darwinian mechanism. According to neo-Darwinism, new information, form, and structure arise from natural selection acting on random mutations arising at a very low level within the biological hierarchy—within the genetic text. Yet both body-plan formation during embryological development and major morphological innovation during the history of life depend upon a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. If DNA isn’t wholly responsible for the way an embryo develops— for body-plan morphogenesis—then DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process. Genetic mutations are simply the wrong tool for the job at hand. Even in a best-case scenario—one that ignores the immense improbability of generating new genes by mutation and selection—mutations in DNA sequence would merely produce new genetic information. But building a new body plan requires more than just genetic information. It requires both genetic and epigenetic information—information by definition that is not stored in DNA and thus cannot be generated by mutations to the DNA. It follows that the mechanism of natural selection acting on random mutations in DNA cannot by itself generate novel body plans, such as those that first arose in the Cambrian explosion.

GENE-CENTRIC RESPONSES
Many of the biological structures that impart important three-dimensional spatial information—such as cytoskeletal arrays and membrane ion channels—are made of proteins. For this reason, some biologists have insisted that the genetic information in DNA that codes for these proteins does account for the spatial information in these various structures after all. In each case, however, this exclusively “gene-centric” view of the location of biological information—and the origin of biological form—has proven inadequate. First, in at least the case of the sugar molecules on the cell surface, gene products play no direct role. Genetic information produces proteins and RNA molecules, not sugars and carbohydrates. Of course, important glycoproteins and glycolipids (sugar-protein and sugar-fat composite molecules) are modified as the result of biosynthetic pathways involving networks of proteins. Nevertheless, the genetic information that generates the proteins in these pathways only determines the function and structure of the individual proteins; it does not specify the coordinated interaction between the proteins in the pathways that result in the modification of sugars. More important, the location of specific sugar molecules on the exterior surface of embryonic cells plays a critical role in the function that these sugar molecules play in intercellular communication and arrangement. Yet their location is not determined by the genes that code for the proteins to which these sugar molecules might be attached. Instead, research suggests that protein patterns in the cell membrane are transmitted directly from parent membrane to daughter membrane during cell division rather than as a result of gene expression in each new generation of cells. Since the sugar molecules on the exterior of the cell membrane are attached to proteins and lipids, it follows that their position and arrangement probably result from membrane-to-membrane transmission as well. Consider next the membrane targets that play a crucial role in embryological development by attracting morphogenetic molecules to specific places on the inner surface of the cell. These membrane targets consist largely of proteins, most of which are mainly specified by DNA. Even so, many “intrinsically disordered” proteins fold differently depending on the surrounding cellular context. This context thus provides epigenetic information. Further, many membrane targets include more than one protein, and these multiprotein structures do not automatically self-organize to form properly structured targets. Finally, it is not only the molecular structure of these membrane targets, but also their specific location and distribution that determines their function. Yet the location of these targets on the inner surface of the cell is not determined by the gene products out of which they are made any more than, for example, the locations of the bridges across the River Seine in Paris are determined by the properties of the stones out of which they are made.Similarly, the sodium-potassium ion pumps in cell membranes are indeed made of proteins. Nevertheless, it is, again, the location and distribution of those channels and pumps in the cell membrane that establish the contours of the electromagnetic field that, in turn, influence embryological development. The protein constituents of these channels do not determine where the ion channels are located. Like membrane targets and ion channels, microtubules are also made of many protein subunits, themselves undeniably the products of genetic information. In the case of microtubule arrays, defenders of the gene-centric view do not claim that individual tubulin proteins determine the structure of these arrays. Nevertheless, some have suggested that other proteins, or suites of proteins, acting in concert could determine such higher-level form. For example, some biologists have noted that so-called helper proteins—which are gene products—called “microtubule associated proteins” (MAPs) help to assemble the tubulin subunits in the microtubule arrays. Yet MAPs, and indeed many other necessary proteins, are only part of the story. The locations of specified target sites on the interior of the cell membrane also help to determine the shape of the cytoskeleton. And, as noted, the gene products out of which these targets are made do not determine the location of these targets. Similarly, the position and structure of the centrosome—the microtubuleorganizing center—also influences the structure of the cytoskeleton. Although centrosomes are made of proteins, the proteins that form these structures do not entirely determine their location and form. As Mark McNiven, a molecular biologist at the Mayo Clinic, and cell biologist Keith Porter, formerly of the University of Colorado, have shown, centrosome structure and membrane patterns as a whole convey three-dimensional structural information that helps determine the structure of the cytoskeleton and the location of its subunits. Moreover, as several other biologists have shown, the centrioles that compose the centrosomes replicate independently of DNA replication: daughter centrioles receive their form from the overall structure of the mother centriole, not from the individual gene products that constitute them. Additional evidence of this kind comes from ciliates, large single-celled eukaryotic organisms. Biologists have shown that microsurgery on the cell membranes of ciliates can produce heritable changes in membrane patterns without altering the DNA. This suggests that membrane patterns (as opposed to membrane constituents) are impressed directly on daughter cells. In both cases—in membrane patterns and centrosomes—form is transmitted from parent three-dimensional structures to daughter three-dimensional structures directly. It is not entirely contained in DNA sequences or the proteins for which these sequences code. Instead, in each new generation, the form and structure of the cell arises as the result of both gene products and the preexisting three-dimensional structure and organization inherent in cells, cell membranes, and cyto-skeletons. Many cellular structures are built from proteins, but proteins find their way to correct locations in part because of preexisting three-dimensional patterns and organization inherent in cellular structures. Neither structural proteins nor the genes that code for them can alone determine the three-dimensional shape and structure of the entities they build. Gene products provide necessary, but not sufficient, conditions for the development of three-dimensional structure within cells, organs, and body plans. If this is so, then natural selection acting on genetic variation and mutations alone cannot produce the new forms that arise in the history of life.

EPIGENETIC MUTATIONS
When I explain this in public talks, I can count on getting the same question. Someone in the audience will ask whether mutations could alter the structures in which epigenetic information resides. The questioner wonders if changes in epigenetic information could supply the variation and innovation that natural selection needs to generate new form, in much the same way that neo-Darwinists envision genetic mutations doing so. It’s a reasonable thing to ask, but it turns out that mutating epigenetic information doesn’t offer a realistic way of generating new forms of life. First, the structures in which epigenetic information inheres—cytoskeletal arrays and membrane patterns, for example—are much larger than individual nucleotide bases or even stretches of DNA. For this reason, these structures are not vulnerable to alteration by many of the typical sources of mutation that affect genes such as radiation and chemical agent. Second, to the extent that cell structures can be altered, these alterations are overwhelmingly likely to have harmful or catastrophic consequences. The original Spemann and Mangold experiment did, of course, involve forcibly altering an important repository of epigenetic information in a developing embryo. Yet the resulting embryo, though interesting and illustrative of the importance of epigenetic information, did not stand a chance of surviving in the wild, let alone reproducing. Altering the cell structures in which epigenetic information inheres will likely result in embryo death or sterile offspring—for much the same reason that mutating regulatory genes or developmental gene regulatory networks also produces evolutionary dead ends. The epigenetic information provided by various cell structures is critical to body-plan development, and many aspects of embryological development depend upon the precise three-dimensional placement and location of these informationrich cell structures. For example, the specific function of morphogenetic proteins, the regulatory proteins produced by master regulatory (Hox) genes, and developmental gene regulatory networks (dGRNs) all depend upon the location of specific, information-rich, and preexisting cell structures. For this reason, altering these cell structures will in all likelihood damage something else crucial during the developmental trajectory of the organism. Too many different entities involved in development depend for their proper function upon epigenetic information for such changes to have a beneficial or even neutral effect.

DARWIN’S GROWING ANOMALY
With the publication of On the Origin of Species in 1859, Darwin advanced, first and foremost, an explanation for the origin of biological form. At the time, he acknowledged that the pattern of appearance of the Cambrian animals did not conform to his gradualist picture of the history of life. Thus, he regarded the Cambrian explosion as primarily a problem of incompleteness in the fossil record.
 Yet clearly a more fundamental problem now afflicts the whole edifice of modern neo-Darwinian theory. The neo-Darwinian mechanism does not account for either the origin of the genetic or the epigenetic information necessary to produce new forms of life. Consequently, the problems posed to the theory by the Cambrian explosion remain unsolved. But further, the central problem that Darwin set out to answer in 1859, namely the origin of animal form in general, remains unanswered—as Müller and Newman in particular have noted. Contemporary critics of neo-Darwinism acknowledge, of course, that preexisting forms of life can diversify under the twin influences of natural selection and genetic mutation. Known microevolutionary processes can account for small changes in the coloring of peppered moths, the acquisition of antibiotic resistance in different strains of bacteria, and cyclical variations in the size of Galápagos finch beaks. Nevertheless, many biologists now argue that neo-Darwinian theory does not provide an adequate explanation for the origin of new body plans or events such as the Cambrian explosion. For example, evolutionary biologist Keith Stewart Thomson, formerly of Yale University, has expressed doubt that large-scale morphological changes could accumulate by minor changes at the genetic level.38 Geneticist George Miklos, of the Australian National University, has argued that neo-Darwinism fails to provide a mechanism that can produce large-scale innovations in form and structure. Biologists Scott Gilbert, John Opitz, and Rudolf Raff have attempted to develop a new theory of evolution to supplement classical neo-Darwinism, which, they argue, cannot adequately explain large-scale macroevolutionary change. As they note:

Starting in the 1970s, many biologists began questioning its [neo-Darwinism’s] adequacy in explaining evolution. Genetics might be adequate for explaining microevolution, but microevolutionary changes in gene frequency were not seen as able to turn a reptile into a mammal or to convert a fish into an amphibian. Microevolution looks at adaptations that concern the survival of the fittest, not the arrival of the fittest. As Goodwin (1995) points out, “the origin of species—Darwin’s problem—remains unsolved.” Gilbert and his colleagues have tried to solve the problem of the origin of form by invoking mutations in genes called Hox genes, which regulate the expression of other genes involved in animal development. Notwithstanding, many leading biologists and paleontologists—Gerry Webster and Brian Goodwin, Günter Theissen, Marc Kirschner, and John Gerhart, Jeffrey Schwartz, Douglas Erwin, Eric Davidson, Eugene Koonin, Simon Conway Morris, Robert Carroll, Gunter Wagner, Heinz-Albert Becker and Wolf-Eckhart Lönnig, Stuart Newman and Gerd Müller, Stuart Kauffman, Peter Stadler, Heinz Saedler, James Valentine, Giuseppe Sermonti, James Shapiro and Michael Lynch, to name several—have raised questions about the adequacy of the standard neo-Darwinian mechanism, and/or the problem of evolutionary novelty in particular. 

The perspective of Eugene Koonin, a biologist at the National Center for Biotechnology Information at the National Institutes of Health, provides just one good example of this skepticism. Koonin, “The Origin at 150,” He argues: 
“The edifice of the modern synthesis has crumbled, apparently, beyond repair . . . The summary of the state of affairs on the 150th anniversary of the Origin is somewhat shocking. In the postgenomic era, all major tenets of the modern synthesis have been, if not outright overturned, replaced by a new and incomparably more complex vision of the key aspects of evolution. So, not to mince words, the modern synthesis is gone. What comes next? The answer suggested by the Darwinian discourse of 2009 is a postmodern state, not so far a postmodern synthesis. Above all, such a state is characterized by the pluralism of processes and patterns in evolution that defies any straightforward generalization.”



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3 Re: Where Do Complex Organisms Come From? on Mon Mar 21, 2016 10:27 pm

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Stephen C Meyer , Darwin's doubt pg.268:
THE HIERARCHICAL ORGANIZATION OF GENETIC AND EPIGENETIC  INFORMATION
In addition to the information stored in individual genes and the information present in the integrated  networks of genes and proteins in dGRNs, animal forms exemplify hierarchical arrangements or layers of information-rich molecules, systems, and structures. For example, developing embryos require epigenetic information in the form of specifically arranged
 
(a) membrane targets and patterns, 
(b) cytoskeletal arrays, 
(c) ion channels, and 
(d) sugar molecules on the exterior of cells (the sugar code).

 
Much of this epigenetic information resides in the structure of the maternal egg and is inherited directly from membrane to membrane independently of DNA.  This three-dimensional structural information interacts with other information-rich molecules and systems of molecules to ensure the proper development of an animal. In particular, epigenetic information influences the proper positioning and thus the function of regulatory proteins (including  DNA-binding proteins), messenger RNAs, and various membrane components. Epigenetic information also influences the function of developmental gene regulatory networks. Thus, information at a higher structural level in the maternal egg helps to determine the function of both whole networks of genes and proteins (dGRNs) and individual molecules (gene products) at a lower level within a developing animal. Genetic information is necessary to specify the arrangement of amino acids in a protein or bases in an RNA molecule. Similarly, dGRNs are necessary to specify the location and/or function of many gene products. And, in a similar way, epigenetic information is necessary to specify the location and determine the function of lower-level molecules and systems of molecules, including the dGRNs themselves.  Furthermore, the role of epigenetic information provides just one of many examples of the hierarchical arrangement (or layering) of information-rich structures, systems, and molecules within animals. Indeed, at every level of the biological hierarchy, organisms require specified and highly improbable (information-rich) arrangements of lower-level constituents in order to maintain their form and function. Genes require specified arrangements of nucleotide bases; proteins require specified arrangements of amino acids; cell structures and cell types require specified arrangements of proteins or systems of proteins; tissues and organs require specific arrangements of specific cell types; and body plans require specialized arrangements of tissues and organs. Animal forms contain information-rich lower-level components (such as proteins and genes). But they also contain information-rich arrangements of those components (such as the arrangement of genes and gene products in dGRNs or proteins in cytoskeletal arrays or membrane targets). Finally, animals also exhibit information-rich arrangements of higher-level systems and structures (such as the arrangements of specific cell types, tissues, and organs that form specific body plans).
 
The highly specified, tightly integrated, hierarchical arrangements of molecular components and systems within animal body plans also suggest intelligent design. This is, again, because of our experience with the features and systems that intelligent agents—and only intelligent agents— produce. Indeed, based on our experience, we know that intelligent human agents have the capacity to generate complex and functionally specified arrangements of matter—that is, to generate specified complexity or specified information. Further, human agents often design information-rich hierarchies, in which both individual modules and the arrangement of those modules exhibit complexity and specificity—specified information. Individual transistors, resistors, and capacitors in an integrated circuit exhibit considerable complexity and specificity of design. Yet at a higher level of organization, the specific arrangement and connection of these components within an integrated circuit requires additional information and reflects further design (see Fig.below).
 

 
Figure 14.2.

Conscious and rational agents have, as part of their powers of purposive intelligence, the capacity to design information-rich parts and to organize those parts into functional information-rich systems and hierarchies. We know of no other causal entity or process that has this capacity. Clearly, we have good reason to doubt that mutation and selection, self-organizational processes, or any of the other undirected processes cited by other materialistic evolutionary theories, can do so. Thus, based upon our present experience of the causal powers of various entities and a careful assessment of the efficacy of various evolutionary mechanisms, we can infer intelligent design as the best explanation for the origin of the hierarchically organized layers of information needed to build the animal forms that arose in the Cambrian period.
 
There is another remarkable aspect of the hierarchical organization of information in animal forms.  Many of the same genes and proteins play very different roles, depending upon the larger organismal  and informational context in which they find themselves in different animal groups. For example, the  same gene (Pax-6 or its homolog, called eyeless), helps to regulate the development of the eyes of fruit flies (arthropods) and those of squid and mice (cephalopods and vertebrates, respectively). Yet arthropod eyes exemplify a completely different structure from vertebrate or cephalopod eyes. The fruit fly possesses a compound eye with hundreds of separate lenses (ommatidia), whereas both mice and squid employ a camera-type eye with a single lens and retinal surface. In addition, although the eyes of squid and mice resemble each other optically (single lens, large internal chamber, single retinal surface), they focus differently. They undergo completely different patterns of development and utilize different internal structures and nerve connections to the visual centers of the brain. Yet the Pax-6 gene and its homologs play a key role in regulating the construction of all three of these different adult sensory structures. Moreover, evolutionary and developmental biologists have found that this pattern of "same genes, different anatomy" recurs throughout the bilaterian phyla, for features  as fundamental as appendages, segmentation, the gut, heart, and sense organs
 

 
This pattern contradicts the expectations of textbook evolutionary theory. Neo-Darwinism predicts that disparate adult structures should be produced by different genes. This prediction follows directly from the neo-Darwinian assumption that all evolutionary (including anatomical) transformations begin with mutations in DNA sequences—mutations that are fixed in populations by natural selection, genetic drift, or other evolutionary processes. The arrow of causality flows one way from genes (DNA) to development to adult anatomy. Thus, if biologists observe different animal forms, it follows that they should expect that different genes will specify those forms during animal development. Given the profound differences between the fruit-fly compound eye and the vertebrate camera eye, neo-Darwinian theory would not predict that the "same" genes would be involved in building different eyes in arthropods and chordates.

DEVELOPMENTAL GENE REGULATORY NETWORKS

Darwins doubt, page 199

Another line of research in developmental biology has revealed a related challenge to the creative power of the neo-Darwinian mechanism. Developmental biologists have discovered that many gene products (proteins and RNAs) needed for the development of specific animal body plans transmit signals that influence the way individual cells develop and differentiate themselves. Additionally, these signals affect how cells are organized and interact with each other during embryological development. These signaling molecules influence each other to form circuits or networks of coordinated interaction, much like integrated circuits on a circuitboard. For example, exactly when a signaling molecule gets transmitted often depends upon when a signal from another molecule is received, which in turn affects the transmission of still others—all of which are coordinated and integrated to perform specific time-critical functions. The coordination and integration of these signaling molecules in cells ensures the proper differentiation and organization of distinct cell types during the development of an animal body plan. Consequently, just as mutating an individual regulatory gene early in the development of an animal will inevitably shut down development, so too will mutations or alterations in the whole network of interacting signaling molecules destroy a developing embryo. No biologist has explored the regulatory logic of animal development more deeply than Eric Davidson, at the California Institute of Technology. Early in his career, collaborating with molecular biologist Roy Britten, Davidson formulated a theory of “gene regulation for higher cells.”1 By “higher cells” Davidson and Britten meant the differentiated, or specialized, cells found in any animal after the earliest stages of embryological development. Davidson observed that the cells of an individual animal, no matter how varied in form or function, “generally contain identical genomes.” During the life cycle of an organism, the genomes of these specialized cells express only a small fraction of their DNA at any given time and produce different RNAs as a result. These facts strongly suggest that some animal-wide system of genetic control functions to turn specific genes on and off as needed throughout the life of the organism—and that such a system functions during the development of an animal from egg to adult as different cell types are being constructed.

When they proposed their theory in 1969, Britten and Davidson acknowledged that “little is known. . . of the molecular mechanisms by which gene expression is controlled in differentiated cells.” Nevertheless, they deduced that such a system must be at work. Given:

(1) that tens or hundreds of specialized cell types arise during the development of animals, and
(2) that each cell contains the same genome, they reasoned
(3) that some control system must determine which genes are expressed in different cells at different times to ensure the differentiation of different cell types from each other—some system-wide regulatory logic must oversee and coordinate the expression of the genome.

Davidson has dedicated his career to discovering and describing the mechanisms by which these systems of gene regulation and control work during embryological development. During the last two decades, research in genomics has revealed that nonprotein-coding regions of the genome control and regulate the timing of the expression of the protein-coding regions of the genome. Davidson has shown that the nonprotein-coding regions of DNA that regulate and control gene expression and the protein-coding regions of the genome together function as circuits. These circuits, which Davidson calls “developmental gene regulatory networks” (or dGRNs) control the embryological development of animals.



On arriving at Caltech in 1971, Davidson chose the purple sea urchin, Strongylocentrotus purpuratus, as his experimental model system. The biology of S. purpuratus makes it an attractive laboratory subject: the species occurs abundantly along the Pacific coast, produces enormous quantities of easily fertilized eggs in the lab, and lives for many years. Davidson and his coworkers pioneered the technology and experimental protocols required to dissect the sea urchin’s genetic regulatory system. The remarkable complexity of what they found needs to be depicted visually. Figure 13.4a shows the urchin embryo as it appears six hours after development has begun (top left of diagram). This is the 16-cell stage, meaning that four rounds of cell division have already occurred (1 → 2 → 4 → 8 → 16). As development proceeds in the next four stages, both the number of cells and the degree of cellular specialization increases, until, at 55 hours, elements of the urchin skeleton come into focus. Figure 13.4b shows, corresponding to these drawings of embryo development, a schematic diagram with the major classes of genes (for cell and tissue types) represented as boxes, linked by control arrows. Last, Figure 13.4c shows what Davidson calls “the genetic circuitry” that turns on the specific biomineralization genes that produce the structural proteins needed to build the urchin skeleton. 2

This last diagram represents a developmental gene regulatory network (or dGRN), an integrated network of protein and RNA-signaling molecules responsible for the differentiation and arrangement of the specialized cells that establish the rigid skeleton of the sea urchin. Notice that, to express the biomineralization genes that produce structural proteins that make the skeleton, genes far upstream, activated many hours earlier in development, must first play their role. This process does not happen fortuitously in the sea urchin but via highly regulated and precise control systems, as it does in all animals. Indeed, even one of the simplest animals, the worm C. elegans, possessing just over 1,000 cells as an adult, is constructed during development by dGRNs of remarkable precision and complexity. In all animals, the various dGRNs direct what Davidson describes as the embryo’s “progressive increase in complexity”—an increase, he writes, that can be measured in “informational terms.” Davidson notes that, once established, the complexity of the dGRNs as integrated circuits makes them stubbornly resistant to mutational change—a point he has stressed in nearly every publication on the topic over the past fifteen years. “In the sea urchin embryo,” he points out, “disarming any one of
these subcircuits produces some abnormality in expression.” Developmental gene regulatory networks resist mutational change because they are organized hierarchically. This means that some developmental gene regulatory networks control other gene regulatory networks, while some influence only the individual genes and proteins under their control. At the center of this regulatory hierarchy are the regulatory networks that specify the axis and global form of the animal body plan during development. These dGRNs cannot vary without causing catastrophic effects to the organism. Indeed, there are no examples of these deeply entrenched, functionally critical circuits varying at all. At the periphery of the hierarchy are gene regulatory networks that specify the arrangements for smaller-scale features that can sometimes vary. Yet, to produce a new body plan requires altering the axis and global form of the animal. This requires mutating the very circuits that do not vary without catastrophic effects. As Davidson emphasizes, mutations affecting the dGRNs that regulate body-plan development lead to “catastrophic loss of the body part or loss of viability altogether.”3  He explains in more detail:

There is always an observable consequence if a dGRN subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.

ENGINEERING CONSTRAINTS


Davidson’s findings present a profound challenge to the adequacy of the neo-Darwinian mechanism. Building a new animal body plan requires not just new genes and proteins, but new dGRNs. But to build a new dGRN from a preexisting dGRN by mutation and selection necessarily requires altering the preexisting developmental gene regulatory network. (the very kind of change that  cannot arise without multiple coordinated mutations). In any case, Davidson’s work has also shown that such alterations inevitably have catastrophic consequences. Davidson’s work highlights a profound contradiction between the neo-Darwinian account of how
new animal body plans are built and one of the most basic principles of engineering—the principle of constraints. Engineers have long understood that the more functionally integrated a system is, the more difficult it is to change any part of it without damaging or destroying the system as a whole. Davidson’s work confirms that this principle applies to developing organisms in spades. The system of gene regulation that controls animal-body-plan development is exquisitely integrated, so that significant alterations in these gene regulatory networks inevitably damage or destroy the developing animal.

As Davidson explains, “Interference with expression of any [multiply linked dGRNs] by mutation or experimental manipulation has severe effects on the phase of development that they initiate. This accentuates the selective conservation of the whole subcircuit, on pain of developmental catastrophe” (Davidson and Erwin, “An Integrated View of Precambrian Eumetazoan Evolution”

But given this, how could a new animal body plan, and the new dGRNs necessary to produce it, ever evolve gradually via mutation and selection from a preexisting body plan and set of dGRNs? Davidson makes clear that no one really knows: “contrary to classical evolution theory, the processes that drive the small changes observed as species diverge cannot be taken as models for the evolution of the body plans of animals.” He elaborates:

Neo-Darwinian evolution . . . assumes that all process works the same way, so that evolution of enzymes or flower colors can be used as current proxies for study of evolution of the body plan. It erroneously assumes that change in protein-coding sequence is the basic cause of change in developmental program; and it erroneously assumes that evolutionary change in body-plan morphology occurs by a continuous process. All of these assumptions are basically counterfactual. This cannot be surprising, since the neo-Darwinian synthesis from which these ideas stem was a premolecular biology concoction focused on population genetics and . . . natural history, neither of which have any direct mechanistic import for the genomic regulatory systems that drive embryonic development of the body plan.

NOW AND THEN

Eric Davidson’s work, like that of Nüsslein-Volhard and Wieschaus, highlights a difficulty of obvious relevance to the Cambrian explosion. Typically, paleontologists understand the Cambrian explosion as the geologically sudden appearance of new forms of animal life. Building these forms requires new developmental programs—including both new early-acting regulatory genes and new developmental gene regulatory networks. Yet if neither early-acting regulatory genes nor dGRNs can be altered by mutation without destroying existing developmental programs (and thus animal form), then mutating these entities will leave natural selection with nothing favorable to select and the evolution of animal form will, at that point, terminate. Darwin’s doubt about the Cambrian explosion centered on the problem of missing fossil intermediates. Not only have those forms not been found, but the Cambrian explosion itself illustrates a profound engineering problem that fossil evidence does not address—the problem of building a new form of animal life by gradually transforming one tightly integrated system of genetic components and their products into another. 

Although evidence is all around us of a deep geological past, and of multifarious genealogical relationships among ourselves and the organisms we currently share the planet with, scientists still have only sketchy ideas about how complex living forms arose in the course of evolution. As James Shapiro described in a recent Huffington Post blog entry, there has been good progress in understanding how complex cells arose from simpler ones by cell mergers, or "symbiogenesis." But even "simple" cells are quite complex, and the origins of cellular life (aka "chemical evolution"; read more here), are far from settled.

What about the complex bodies and organs of animals and plants? This is what primarily concerned the nineteenth century naturalists Alfred Russel Wallace and Charles Darwin (neither of whom knew anything about the internal intricacies of cells, including the nature of their genes), as they pondered the transformations of life throughout its history. Their solution was "natural selection," the acquisition of new forms and functions in populations of organisms by small increments, over long times, with each gradual change being subject to the sieve of "adaptation." Was each heritable variation better suited to some pre-existing task? If so, its exemplars increased and multiplied. If not, their kind faded away.

While it may be an adequate scenario for the refinement of some already-existing characters -- the beaks of finches, color intensity of moths -- the "microevolutionary" process envisioned by Darwin and his successors does not account in any plausible way for "macroevolutionary" patterns such as the differences between oysters and grasshoppers, fish and birds. In fact, adaptationist gradualism, though still popular in some scientific circles, is increasingly questioned and found wanting by evolutionary biologists working in an expanded set of disciplines.

By incorporating embryonic development and its underlying physico-genetic processes into evolutionary theory, investigators are learning that abrupt alterations in body plan and other aspects of organismal form can occur in response to environmental change or gene mutation in ways that affect multiple members of a population and exhibit consistent patterns of inheritance. Furthermore, there is increasing emphasis on the resourcefulness of organisms and their ability to construct their own niches. Having a "phenotype" (the outward manifestation of biological identity), very different from that of one's progenitors is no longer considered disqualifying for survival.

Although the writings of Wallace and Darwin's predecessor Jean-Baptiste Lamarck anticipated some current ideas about the morphologically prolific processes of embryo generation ("Le pouvoir de la vie") and the active strivings of organisms for survival in their environmental settings ("L'influence des circonstances"), Darwin's less speculative approach encouraged readier acceptance of his ideas by other scientists and the educated public. (The playwright George Bernard Shaw, in the preface to Back to Methuselah, put it more sharply as "Why Darwin converted the crowd.") By specifying that the variations in organismal form and function sorted out by natural selection were entirely incremental, Darwin's theory could side-step any questions about how the altered forms actually arose. It also created an incentive to deny the relevance of the more profound changes (Darwin called them "sports") that were well known to arise in natural populations. This may have been the best that could be done circa 1850, but its retention in the so-called modern evolutionary synthesis a century later was a scandalous legacy of the banishment of developmental biology (embryology) from the synthesis, and the indifferent attitude of biological education regarding the physical sciences.

The physical science of Darwin's time, which provided a backdrop to his thinking, was dominated by Newton's concept that material bodies only change course in proportion to external forces that act on them. It also included the often more pertinent notion (e.g., for the molding of pliable materials) from Aristotle of matter changing position or shape only to the extent that it continues to be pushed. These ideas, however, did not pretend to account for the sudden reorganizational changes (freezing, melting, phase separation, compositional change) seen in complex chemically and mechanically active materials. We now recognize that the tissues of a developing embryo are indeed such non-Newtonian, non-Aristotelian materials. By the end of Darwin's life new physical theories were being put forward to explain abrupt and large-scale changes in such materials, and by extension, the character and transformations of organisms and their organs.

Here is a partial list of late nineteenth and early twentieth-century physical concepts that have proved relevant to developmental processes (with the phenomenon they explain, at least partly, in parentheses): dynamical systems (ability of cells having the same genome to switch between different "types"), phase separation of liquids (capacity of embryonic tissues to form several non-mixing layers), chemical oscillations (propensity of embryonic tissues to organize into tandem segments), "Turing-type" reaction-diffusion systems (the formation in tissues of regularly spaced structures like feather and hair buds, pigment stripes, or the bones of the limb skeleton). All or most of these processes (termed "mesoscale," being most relevant to objects the size and texture of cell clusters), along with several others, are harnessed and mobilized by the secreted products of specific genes during embryogenesis in every one of the animal phyla (e.g., arthropods, mollusks, nematodes, chordates and so forth).

What can the existence and action of such protean generative processes tell us about the origin of organismal complexity? First, let's look at some of the expectations of the natural selection-based modern synthesis: (i) the largest differences within given categories of multicellular organisms, the animals or plants, for example, should have appeared gradually, only after exceptionally long periods of evolution; (ii) the extensive genetic changes required to generate such large differences over such vast times would have virtually erased any similarity between the sets of genes coordinating development in the different types of organism; and (iii) evolution of body types and organs should continue indefinitely. Since genetic mutation never ceases, novel organismal forms should constantly be appearing.


All these predictions of the standard model have proved to be incorrect. The actual state of affairs however, are expected outcomes of the "physico-genetic" picture outlined above. Briefly, we now know that complex multicellular organisms appeared rapidly (on a geological time scale, i.e., two episodes of no more than 10-20 million years each), employing for developmental patterning not newly evolved genes, but genes that had evolved for entirely different functions in single-celled ancestors. Generation of novel complex forms was able to happen so rapidly because the genetic ingredients were already at hand, but in addition because the mesoscale physical processes described above also did not require an incremental sequence of steps to come into existence. Everything was in place for an organismal "big bang" once simple multicellular clusters had appeared.

Unlike the presumption of the standard model, however, the physico-genetic scenario for the origination of complex multicellular forms is not open-ended and limitless. As with any material organizational process (think waves and eddies in liquid water), the relevant physics can only elicit those structural motifs inherent to the material in question. Thus we should not expect to see, and indeed don't, the "endless forms" that Darwin invoked in The Origin of Species.

With a 19th century notion of incremental material transformations no longer relevant to comprehending the range of organismal variation that has appeared throughout the history of life on Earth, the other pillar of the standard model can be discarded along with it. Specifically, if, as affirmed by niche construction theory, phenotypically novel animals or plants can invent new modes of existence in novel settings, rather than succumbing to a struggle for survival in the niches of their origin, there is no need for cycles of selection for marginal adaptive advantage to be the default explanation for macroevolutionary change.

Additional reading

Newman, S.A. (2012). Physico-genetic determinants in the evolution of development. Science 338, 217-219.

Müller, G.B. (2007). Evo-devo: extending the evolutionary synthesis. Nature Reviews Genetic 8, 943-949.

Forgacs, G., and Newman, S.A. (2005). Biological physics of the developing embryo (Cambridge, Cambridge Univ. Press).

Odling-Smee, F.J., Laland, K.N., and Feldman, M.W. (2003). Niche construction: the neglected process in evolution (Princeton, N.J., Princeton University Press).
Follow Stuart A. Newman on Twitter: www.twitter.com/sanewman1

1) http://www.huffingtonpost.com/stuart-a-newman/complex-organisms_b_2240232.html
1) https://embryo.asu.edu/pages/gene-regulation-higher-cells-theory-1969-roy-j-britten-and-eric-h-davidson
2) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2329687/
3) http://www.sciencedirect.com/science/article/pii/S0012160611000911?np=y
4) https://arxiv.org/ftp/arxiv/papers/1205/1205.1158.pdf

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4 Re: Where Do Complex Organisms Come From? on Sun Sep 11, 2016 8:05 am

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"The fact of evolution is widely acknowledged and has been a central pillar of modern biology since prominent natural historians (i.e., paleontologists, systematists, and evolutionary theorists) and Mendelian geneticists began to reconcile findings from their respective fields in the mid-1930s and forged what came to be known as the Modern Evolutionary Synthesis little more than a decade later (Bowler, 2003 and Mayr, 1983; for a pre-Modern Synthesis perspective, see Patten, 1920). However, despite broad acceptance of this framework, the tempo and mode of evolution (see Simpson, 1984) have remained persistent points of controversy and debate among contemporary biologists (Gould and Eldredge, 1977, Gould and Lewontin, 1979, Coyne, 2008, Noble, 2015 and Shapiro, 2011). Indeed, Laland et al. (2015) recently suggested that evolutionary theory is now at a major crossroads, due largely to the fact that the Modern Evolutionary Synthesis has not satisfactorily incorporated progress in developmental biology, genomics, and ecology—findings that could otherwise greatly illuminate the pace, nature, and mechanisms of evolutionary change. They propose a new framework, the extended evolutionary synthesis (EES), which underlines a prominent role for constructive developmental processes in evolution and champions a reciprocal causal picture of organismal change, i.e., the idea that “… organisms shape, and are shaped by, selective and developmental environments” ( Laland et al., 2015, p. 2). 

Origin of the vertebrate body plan via mechanically biased conservation of regular geometrical patterns in the structure of the blastula

We present a plausible account of the origin of the archetypal vertebrate bauplan. We offer a theoretical reconstruction of the geometrically regular structure of the blastula resulting from the sequential subdivision of the egg, followed by mechanical deformations of the blastula in subsequent stages of gastrulation. We suggest that the formation of the vertebrate bauplan during development, as well as fixation of its variants over the course of evolution, have been constrained and guided by global mechanical biases. Arguably, the role of such biases in directing morphology—though all but neglected in previous accounts of both development and macroevolution—is critical to any substantive explanation for the origin of the archetypal vertebrate bauplan. We surmise that the blastula inherently preserves the underlying geometry of the cuboidal array of eight cells produced by the first three cleavages that ultimately define the medial-lateral, dorsal-ventral, and anterior-posterior axes of the future body plan. Through graphical depictions, we demonstrate the formation of principal structures of the vertebrate body via mechanical deformation of predictable geometrical patterns during gastrulation. The descriptive rigor of our model is supported through comparisons with previous characterizations of the embryonic and adult vertebrate bauplane. Though speculative, the model addresses the poignant absence in the literature of any plausible account of the origin of vertebrate morphology. A robust solution to the problem of morphogenesis—currently an elusive goal—will only emerge from consideration of both top-down (e.g., the mechanical constraints and geometric properties considered here) and bottom-up (e.g., molecular and mechano-chemical) influences.

http://www.sciencedirect.com/science/article/pii/S0079610716300542

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5 Re: Where Do Complex Organisms Come From? on Tue Dec 13, 2016 3:26 pm

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Transgenerational inheritance: Models and mechanisms of non–DNA sequence–based inheritance 1

Advances in molecular biology in the second half of the 20th century firmly established DNA sequence as the molecular substrate of inheritance. It appears that biology is much richer: Many phenomena and mechanisms of nongenetic and/or non–DNA sequence–based inheritance have been described in a range of model organisms, challenging our perception of the well-established relationship between transmitted genotype and phenotype. How can we learn more about the mechanism and effects of this extended type of inheritance? A useful distinction is often made between intergenerational and transgenerational inheritance. In the former, the environment of the parent can directly affect germ cells of the offspring.

A number of  heritable effects  can be modulated by environmental influences. When considering environmentally induced effects, a particular emphasis has been put on nutrition and stress as inducers of nongenetic effects. For example, parental diet can affect the phenotype of the offspring.  As shown in one recent study exploring metabolic outcomes in both male and female mice born to parents that consumed a high-fat diet (33). Early life stress is another example for which several rodent models have been reported (35–37). An emphasis on nutritional models in mice might be the consequence of evocative epidemiological studies in humans that suggest maternal and paternal inheritance of nutritional states (38, 39). Although in most of the examples mentioned above the mechanisms of inheritance are unlikely to be DNA sequence–based, with varying strength of evidence, the mode(s) of transmission of nongenetic effects remain to be discovered.

“…a complete understanding of non–DNA sequence–based heritable effects requires a number of components, and we do not currently have the complete picture for any natural example.”

“Many phenomena and mechanisms of nongenetic and/or non–DNA sequence–based inheritance have been described in a range of model organisms, challenging our perception of the well-established relationship between transmitted genotype and phenotype.”

The semiconservative mechanism of DNA replication (40) provides a clear paradigm of how genetic information is faithfully transmitted during each cell division in mitosis and meiosis. This paradigm is so powerful that great emphasis has been placed on replicative inheritance of other information. Due to the well-understood mechanisms associated with the propagation of epigenetic states such as DNA methylation, experiments analyzing epigenetic modifications to DNA and chromatin have proved popular in attempts to explain the heritable memory of environmental experience. In both cases, enzymes have been identified that can “read” a modification and replicate it locally on the newly synthesized strand (in the case of DNA) or can propagate it on newly assembled histones on chromatin (41).

1. http://science.sciencemag.org/content/354/6308/59.full
http://iose-gen.blogspot.com.br/2010/06/origin-of-body-plan-level-biodiversity.html

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It's hard to believe that the zygote can contain all the information needed to build/grow the adult organism. In fact, it's about as contrary to common sense as neo-Darwininst evolution.

I see that Jonathan Wells now believes that extra information must come in - from 'above', as it were, in his diagram - at each stage in the development process. See youtube 'Design beyond DNA: a Conversation' at 44.00 and following.

If mind - or in my Christian viewpoint, probably first spirit then soul - are prior to matter then this is possible.

Andrew

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7 Re: Where Do Complex Organisms Come From? on Thu Sep 14, 2017 10:25 am

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Andrew Chapman wrote:It's hard to believe that the zygote can contain all the information needed to build/grow the adult organism. In fact, it's about as contrary to common sense as neo-Darwininst evolution.

I see that Jonathan Wells now believes that extra information must come in - from 'above', as it were, in his diagram - at each stage in the development process. See youtube 'Design beyond DNA: a Conversation' at 44.00 and following.

If mind - or in my Christian viewpoint, probably first spirit then soul - are prior to matter then this is possible.

Andrew

Andrew, i don't think there is a continual input of information from above. What i believe is, that at each conception, God puts its spirit into the cell. But the information to make a new human, is all stored in the sperm and egg.

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8 Re: Where Do Complex Organisms Come From? on Thu Sep 14, 2017 11:37 am

So, how do you think - to take something relatively easy - the zygote stores the shape of the ear, for example?

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9 Re: Where Do Complex Organisms Come From? on Thu Sep 14, 2017 2:35 pm

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Andrew Chapman wrote:So, how do you think - to take something relatively easy - the zygote stores the shape of the ear, for example?

throuh genetic, and epigenetic information

How the various informational codes in the cell point to design

http://reasonandscience.heavenforum.org/t2213-the-various-codes-in-the-cell

The deeper science digs, the more we discover, how complex and ingenious life is. The ones that argue that the more science moves forward, the less God is necessary, have it just backward. It's exactly the opposite: The more science discovers, the more intelligent design becomes evident.  Would Darwin ever imagine how complex cell factories are? And the fact, that life is permeated by information? So far, we know about at least 12 different code systems in the cell, of which the glycan code of glycoproteins exceeds DNA complexity by far, and science is just in the beginning to unravel its complexity. 

The various codes in the cell

http://reasonandscience.heavenforum.org/t2213-the-various-codes-in-the-cell

The Genetic Code 
The Splicing Codes
The Metabolic Code
The Signal Transduction Codes 
The Signal Integration Codes 
The Histone Code 
The Tubulin Code
The Sugar Code 
The Glycomic Code
The non-ribosomal code
The Calcium Code
The RNA code

and at least 19 different gene codes ( below i am listing 26! ):

The different genetic codes

the National Center for Biotechnology Information (NCBI), currently acknowledges nineteen different coding languages for DNA

http://reasonandscience.heavenforum.org/t2277-the-different-genetic-codes

1. The Standard Code
2. The Vertebrate Mitochondrial Code
3. The Yeast Mitochondrial Code
4. The Mold, Protozoan, and Coelenterate Mitochondrial Code and the Mycoplasma/Spiroplasma Code
5. The Invertebrate Mitochondrial Code
6. The Ciliate, Dasycladacean and Hexamita Nuclear Code
9. The Echinoderm and Flatworm Mitochondrial Code
10. The Euplotid Nuclear Code
11. The Bacterial, Archaeal and Plant Plastid Code
12. The Alternative Yeast Nuclear Code
13. The Ascidian Mitochondrial Code
14. The Alternative Flatworm Mitochondrial Code
16. Chlorophycean Mitochondrial Code
21. Trematode Mitochondrial Code
22. Scenedesmus obliquus Mitochondrial Code
23. Thraustochytrium Mitochondrial Code
24. Pterobranchia Mitochondrial Code
25. Candidate Division SR1 and Gracilibacteria Code
26. Pachysolen tannophilus Nuclear Code
27. Karyorelict Nuclear
28. Condylostoma Nuclear
29. Mesodinium Nuclear
30. Peritrich Nuclear
31. Blastocrithidia Nuclear

they had to emerge independently. One could not have evolved from another.

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Thanks for this. Is there anything here other than templates to generate complex molecules? Even if you get the right proteins for the right cell, you are still a long way from building the cell - these are just the raw materials, so to say.

You say that codes convey meaning, but I am not sure that is true for the genetic code. It's a template to map one set of molecules to another. It's different from the Morse Code say. ... _ _ _ ... maps to SOS, but this then has a meaning. A protein is just a molecule.

I realise that other sections of DNA are involved in gene regulation, but these also just map to proteins or RNA, and are also just molecules. How do they know what to do and when?

Can one even conceive of a code that would tell a cell twenty divisions down the line to differentiate from ectoderm to neural cells or skin cells or whatever? And how is that cell meant to know what a skin cell looks like?

Or looking at it another way, how much information is needed to specify the adult? There's a hundred trillion cells, and I think thousands of different types, each of which would have to be specified. How? With a 'blueprint', as some call DNA? But molecules can't read, they haven't been to college to learn how to read a 3-D drawing or whatever.

Andrew

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11 Re: Where Do Complex Organisms Come From? on Sat Sep 16, 2017 9:31 pm

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Andrew Chapman wrote:

Thanks for this. Is there anything here other than templates to generate complex molecules? Even if you get the right proteins for the right cell, you are still a long way from building the cell - these are just the raw materials, so to say.

You say that codes convey meaning, but I am not sure that is true for the genetic code. It's a template to map one set of molecules to another. It's different from the Morse Code say. ... _ _ _ ... maps to SOS, but this then has a meaning. A protein is just a molecule.

I realise that other sections of DNA are involved in gene regulation, but these also just map to proteins or RNA, and are also just molecules. How do they know what to do and when?

Can one even conceive of a code that would tell a cell twenty divisions down the line to differentiate from ectoderm to neural cells or skin cells or whatever? And how is that cell meant to know what a skin cell looks like?

Or looking at it another way, how much information is needed to specify the adult? There's a hundred trillion cells, and I think thousands of different types, each of which would have to be specified. How? With a 'blueprint', as some call DNA? But molecules can't read, they haven't been to college to learn how to read a 3-D drawing or whatever.

Andrew

That precisely what i outline here :

The amazing task of evolution

http://reasonandscience.heavenforum.org/t2010-unicellular-and-multicellular-organisms-are-best-explained-through-design#5651

The progression of biological systems: from a supposed prebiotic soup to the first self-replicating cell. From there, to the 3 domains of life: eukaryotic, archaea, and prokaryotes. From unicellular to multicellular life. From one kind of cell to specialized cells, and pluripotent cells. From there to tissues, organs, and whole bodies. From " simple " sponges to humans. EACH of these leaps of complexity is a QUANTUM step. Each node in Darwin's tree of split is the change compared to a mousetrap to a spaceship in terms of complexity. Must not EACH new cell be precisely specified through a master program which, coordinates, instructs, specifies each Cell in regard of its

1. Kind or type of cell ( Histology),
2. Cell size
3. It's specific function,
4. Position and place in the body. This is crucial. Limbs like legs, fins, eyes etc. must all be placed at the right place.  
5. How it is interconnected with other cells,
6. What communication it requires to communicate with other cells, and the setup of the communication channels
7. What specific sensory and stimuli functions are required and does it have to acquire in regard to its environment and surroundings?
8. What specific new regulatory functions it acquires
9. When will the development program of the organism express the genes to grow the new cells during development?
11. Precisely how many new cell types must be produced for each tissue and organ?
10. Specification of the cell - cell adhesion and which ones will be used in each cell to adhere to the neighbor cells ( there are 4 classes )
11. Programming of  time period the cell keeps alive in the body, and when is it time to self-destruct and be replaced by newly produced cells of the same kind
12. Set up its specific nutrition demands

I don't know how many mutations would be required in the genome to instruct all these things for one Cell. Now imagine the requirement to grow two or four legs, mutations had to generate NEW information for EACH cell, and for each new organ and body part, according to Axe's paper, 10^64 ( that's a one with 64 zeroes ) mutations for ONE positive mutation. And the information would be required in regard of body plan architecture  IN ADVANCE.  That mutation must be fixed in the genome and spread in the population. How many would be required for millions, billions of mutations to grow NEW cells, tissues, organs, and body plans? Nope, not millions, not billions, or trillions of years would be enough......

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