An essential ingredient of Darwin's theory is that " Individuals possessing traits well suited for the struggle for local resources will contribute more offspring to the next generation ". This means that individuals with a certain genotype for a given locus or gene have more reproductive success than individuals within the same population that have other genotypes for that same gene. What determines whether a gene variant spreads or not depends on an incredibly complex web of factors - the species' ecology, its physical and social environment and sexual behavior. A further factor adding complexity is the fact that high social rank is associated with high levels of both copulatory behavior and the production of offspring which is widespread in the study of animal social behavior
As alpha males have on average higher reproductive success than other males, since they outcompete weaker individuals, and get preference to copulate, if other ( weaker ) males gain beneficial mutations (or the alphas negative mutations) as the alphas can outperform and win the battle for reproduction, thus selection has an additional hurdle to overcome and spread the new variant in the population. This does not say anything about the fact that it would have to be determined what gene loci are responsible for sexual selection and behavior, and only mutations that influence sexual behavior would have influence in fitness and the struggle to contribute more offspring to the next generation. Science would need furthermore to have the knowledge what traits are favored in which environment. adaptation rates and mutational diversity and other spatiotemporal parameters, including population density, mutation rate, and the relative expansion speed and spatial dimensions. It is in praxis impossible to isolate these factors and see which is of selective importance, quantify them, plug them in (usually in this context) to a mixed multivariate model, and see what's statistically significant, and get meaningful, real life results. The varying factors are too many and nonpredictive.
Is there evidence for natural selection?
What we observe is gene entropy.
1. Random mutations deteriorate the genome.
In a new paper in Science,3Khan et al, working with Richard Lenski [Michigan State], leader of the longest-running experiment on the evolution of E. coli, found a law of diminishing returns with beneficial mutations due to negative epistasis. The abstract said:
Epistatic interactions between mutations play a prominent role in evolutionary theories. Many studies have found that epistasis is widespread, but they have rarely considered beneficial mutations. We analyzed the effects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations—the larger the expected benefit, the more negative the epistatic effect. Epistasis thus tended to produce diminishing returns with genotype fitness, although interactions involving one particular mutation had the opposite effect. These data support models in which negative epistasis contributes to declining rates of adaptation over time.
2. Mechanisms that affect the phenotype
Non random mutations: How life changes itself: the Read-Write (RW) genome 2 3
And all available scientific evidence also indicates that evolution is an engineered process. In engineering and computer science, evolution never happens by accident. It’s always the result of a deliberate act. A program that can self-evolve is always considered an engineering marvel.
The genome has traditionally been treated as a Read-Only Memory (ROM) subject to change by copying errors and accidents. 7 I propose that we need to change that perspective and understand the genome as an intricately formatted Read-Write (RW) data storage system constantly subject to cellular modifications and inscriptions. Cells operate under changing conditions and are continually modifying themselves by genome inscriptions. These inscriptions occur over three distinct time-scales (cell reproduction, multicellular development, and evolutionary change) and involve a variety of different processes at each time scale (forming nucleoprotein complexes, epigenetic formatting and changes in DNA sequence structure). Research dating back to the 1930s has shown that genetic change is the result of cell-mediated processes, not simply accidents or damage to the DNA. This cell-active view of genome change applies to all scales of DNA sequence variation, from point mutations to large-scale genome rearrangements and whole genome duplications (WGDs). This conceptual change to active cell inscriptions controlling RW genome functions has profound implications for all areas of the life sciences.
Ever since the formulation of the neo-Darwinist Modern Synthesis evolutionary theoryin the 1930s and 1940s, it has been an article of faith that hereditary variation results from stochastic copying errors and unavoidable damage to the genome
In the past 60 years, since the structure of DNA was elucidated, molecular biologists have studied the basic mechanisms of long-term genome change. They have discovered a wide array of proofreading and damage repair biochemical systems that remove copying errors and correct DNA damage. At the same time, they have revealed an amazing and wholly unanticipated array of cellular and molecular systems that operate to generate genome variability, both temporary and structural. As we begin the second decade of the 21st century, accumulating empirical evidence has thus shifted the perspective on genome variation to that of an active inscription process changing the information passed on to future generations.
WHAT DARWIN GOT WRONG JERRY FODOR and MASSIMO PIATTELLI-PALMARINI
Additional phenomena, such as developmental modules, entrenchment, and robustness, further separate random mutations at the DNA level from expressed phenotypes at the level of organisms.
The different components of a genome and/or of a developmental structure usually have different effects 'downstream', that is, on the characteristics of the fully developed adult, through the entire lifetime. The magnitude of these effects is measured by the 'entrenchment' of that structure. The entrenchment of a gene or a gene complex changes by degrees - it's not an all-or-none property. From an evolutionary point of view, the entrenchment of a unit has multiple and deep consequences for its role in different groups of organisms and different species, notably affecting other units that depend on its functioning. Generative entrenchment is seen both as an 'engine' of development and evolutionary change and as a constraint. This amounts to saying that crucial developmental factors ('pivots' in Wimsatt's terms) may be highly conserved and be buffered against change, or may undergo minor heritable changes with major evolutionary consequences. Generative entrenchment, as the expression aptly suggests, is very probably linked to spontaneous and quite general collective form-generating processes, but it is (of course) also under the control of genes, gene complexes, and developmental pathways. How these different sources of order and change (some generically Physico-chemical and some specifically genetic) interact is still largely unknown.
A trait is said to be robust with respect to a genetic or environmental variable if variation of the one is only weakly correlated with variations in the other. In other words, robustness is the persistence of a trait of an organism under perturbations, be they random developmental noise, environmental change or genetic change. In recent years, robustness has been shown to be of paramount importance in understanding evolution, because robustness permits hidden genetic variation to accumulate. Such hidden variation may serve as a source of new adaptations and evolutionary innovations. It is an open, empirical and highly substantive question how narrowly such endogenous effects constrain the phenotypic variations on which external selection operates. It will take a while to find out. But, until that question gets answered, it is unadvisable to take a neo-Darwinist account of evolution for granted.
Master genes are 'masters'
Many different traits are indissociably genetically controlled by the same 'master gene'. Any mutation affecting one master gene, if viable, has an impact on many traits at once. A well studied gene family, called Otx, masterminds the development of kidneys, cranio-facial structures (Suda et al., 2009), guts, gonads and the cerebral cortex (segmentation and cortical organization).
Let's start with a definition. A module is a unit that is highly integrated internally and relatively insensitive to context externally. Developmental modules exist at different levels of the organization, from gene regulation to networks of interacting genes to organ primordia. They are relatively insensitive to the surrounding context and can thus behave invariantly, even when they are multiply realized in different tissues and in different developmental phases. Different combinations of developmental modules in each context, however, produce a difference in their functions in development. There is evidence of the integration of several interacting elements into a module when perturbation of one element results in perturbations of the other elements in that module, or in gene-gene interaction (epistasis) within the module, in such a way that the overall developmental input-output relation is altered. This is another signal case in which the conservation of genetic and developmental building blocks, together with their multiple recombinations in different tissues and organisms, explains the diversity of life forms as well as the invariance of basic body plans. The reverberation of the effects of gene mutations is usually multiple and only the viable overall result is then accessible to selection. This complex system of master signals regulates tissues as different as the central nervous system, pharynx, hair cells, odontoblasts, kidney, feathers, gut, lung, pancreas, hair and ciliated epidermal cells across many different vertebrate and invertebrate species. Every mutation in any one of the genes involved will alter many organs and their functions - a far cry from 'beanbag genetics'. The lesson here is that modularity gives a new complex picture of evolution, one in which internal constraints and internal dynamics filter what selection can act upon, and to what extent it can do so. Precisely because so much cannot change, other things can change at the (so to speak) genetic periphery of organisms. It is often (although not always) the case that when we witness gene duplications, a ubiquitous kind of genetic modification, the 'original' gene continues acting as it did in earlier forms of life, while the 'copy' can 'explore' new functions over evolutionary time (these metaphors are commonplace in the professional literature) .
The Russian zoologist and evolutionist Ivan Ivanovich Schmalhausen (1884-1963) had rightly stressed that living organisms are not the mere atomic 'a position' of separate parts, but rather highly 'coordinated' systems (for a historical and critical review, see Levit et al., 2006). Today justice is done to Schmalhausen by experimental evidence that some mutations in genes specifically affecting one part of the body carry with them suitable modifications in other related parts. When limbs are induced ectopically (that is, where they don't belong), often sensory neurons, receptor organs, cartilage and blood vessels also develop as a consequence around them (see Kirschner and Gerhart, 2005 for stunning examples). A laboratory-induced and quantitatively controllable modification in two key proteins in chick and finch embryos early in development produces as the main result variable elongation
1. RNA methylation
2. DNA dinucleotide methylation
3. DNA CpG island methylation
4. Histone methylation
5. Chromatin remodeling
6. DNA coiling
7. MicroRNA regulation
8. Alternative splicing
9. Flanking binding sites of the DNA
No gene sequence alterations in the list, because
- Deletions, insertions and frameshift mutations during protein synthesis are misinterpretations of the alternative splicing mechanism
- Retrogenes and genetic recombinations are misinterpretations of microRNAs and the alternative splicing mechanism
- RNA based gene duplications are misinterpretations of the alternative splicing mechanism
So, what do the evolutionists have 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. Hydroxymethylated cytosine turns to Guanine and this seems to be another epigenetic-based mechanism. The immune system is a dynamic part of the genome and some genes may be altered due to defense mechanism against pathogens.
1.The alternative role of DNA methylation in splicing regulation
2. Co-regulation of miRNA biogenesis and alternative pre-mRNA splicing of host gene
3. Histone methylation, alternative splicing, and neuronal differentiation.
Seven things Darwin didn't tell you because he didn't know.
1. Alterations in diet, climate, stress and other environmental factors cause mechanism based inheritable changes in organisms, not random mutations and selection.
An example: Italian wall lizards experienced radical changes in morphology and behavior after changing their diet from insects to plants. This occurred very rapidly, just in three decades. They even had a 'new' structure in their gut, so called Cecal Valve. Genes that control the growth of the Cecal Valve were differently expressed due to the changed diet.
2. Random mutations don't enhance the genomic information. Random mutations are genetic errors and they destroy biological information and disrupt genetic integrity.
An example: There are about 200,000 disease-causing genetic mutations in the human DNA pointing out that evolution is not happening and that so called natural selection is not able to weed those mutations out.
3. Most of so-called mutations are not random changes. Genetic changes occur due to oxidative stress, changing diet, exposure to toxins, disrupted methylation patterns, viruses etc. However, most of them still disrupt genetic integrity.
- A lack of methyl groups in gene body may develop cancer and trigger genetic mutations.
- Viruses play a potential role in causing aberrant methylation patterns. According to a fresh study, more than 1 in 5 adults has cancer-causing HPV infection.
4. Biological information is multi-layered. There are at least three forms of biological information in the cell:
1. Gene sequences - Digital information layer
2. Epigenetic markers, 3D genome, flanking binding sites - Analog information layer
3. Gene regulatory networks, genomic integrity and stability - Meta data
- The cell uses cytokines as knobs instead of switches.
- DNA methylation influences continuous variation in ant worker size
5. Biological information is extremely complex. The 'grammar' of the human genetic code is more complex than that of even the most intricately constructed spoken languages in the world.
6. Organisms can experience rapid variation due to epigenetic mechanisms.
7. Life is not driven by gene sequences. Genes are driven by lifestyle.
The industrial melanism mutation in British peppered moths is a transposable element. 5
Discovering the mutational events that fuel adaptation to environmental change remains an important challenge for evolutionary biology. The classroom example of a visible evolutionary response is industrial melanism in the peppered moth (Biston betularia): the replacement, during the Industrial Revolution, of the common pale typica form by a previously unknown black (carbonaria) form, driven by the interaction between bird predation and coal pollution. The carbonaria locus has been coarsely localized to a 200-kilobase region, but the specific identity and nature of the sequence difference controlling the carbonaria-typica polymorphism, and the gene it influences, are unknown. Here we show that the mutation event giving rise to industrial melanism in Britain was the insertion of a large, tandemly repeated, transposable element into the first intron of the gene cortex. Statistical inference based on the distribution of recombined carbonaria haplotypes indicates that this transposition event occurred around 1819, consistent with the historical record. We have begun to dissect the mode of action of the carbonaria transposable element by showing that it increases the abundance of a cortex transcript, the protein product of which plays an important role in cell-cycle regulation, during early wing disc development. Our findings fill a substantial knowledge gap in the iconic example of microevolutionary change, adding a further layer of insight into the mechanism of adaptation in response to natural selection. The discovery that the mutation itself is a transposable element will stimulate further debate about the importance of 'jumping genes' as a source of major phenotypic novelty.
Moving through the Stressed Genome: Emerging Regulatory Roles for Transposons in Plant Stress Response 6
The recognition of a positive correlation between organism genome size with its transposable element (TE) content, represents a key discovery of the field of genome biology. Considerable evidence accumulated since then suggests the involvement of TEs in genome structure, evolution and function. The global genome reorganization brought about by transposon activity might play an adaptive/regulatory role in the host response to environmental challenges, reminiscent of McClintock's original ‘Controlling Element’ hypothesis. This regulatory aspect of TEs is also garnering support in light of the recent evidences, which project TEs as “distributed genomic control modules.” According to this view, TEs are capable of actively reprogramming host genes circuits and ultimately fine-tuning the host response to specific environmental stimuli. Moreover, the stress-induced changes in epigenetic status of TE activity may allow TEs to propagate their stress responsive elements to host genes; the resulting genome fluidity can permit phenotypic plasticity and adaptation to stress. Given their predominating presence in the plant genomes, nested organization in the genic regions and potential regulatory role in stress response, TEs hold unexplored potential for crop improvement programs. This review intends to present the current information about the roles played by TEs in plant genome organization, evolution, and function and highlight the regulatory mechanisms in plant stress responses. We will also briefly discuss the connection between TE activity, host epigenetic response and phenotypic plasticity as a critical link for traversing the translational bridge from a purely basic study of TEs, to the applied field of stress adaptation and crop improvement. TEs not only rewire host transcriptional circuits in times of stress, but the extensive genomic rearrangements mediated by such TE bursts shapes genome architecture, ultimately leading to speciation and evolution of plant genomes.
Profuse evolutionary diversification and speciation on volcanic islands: transposon instability and amplification bursts explain the genetic paradox 1
Eukaryotic genomes harbor many families of transposable elements (TEs) that are mobilized by genome shock; these elements may be the primary drivers of genetic reorganization and speciation on volcanic islands. TEs are a key factor, even a prerequisite, in the evolution of species-rich lineages. Thus evolutionarily constrained lineages may be unable to undergo the rapid genome remodeling that leads to an adaptive radiation primarily because of a severe lack of TEs in their ancestral genomes. On the other hand, lineages with abundant TEs in their genomes are equipped to respond to the stress of founder events and the harsh conditions of active volcanic habitats by generating a host of new genetic combinations as a result of bursts of TE amplification, setting the stage for profuse speciation and adaptive radiation. TEs may therefore play a critical role in the survival, rampant speciation and adaptation of plants and animals in volcanic environments, and may underlie many of the evolutionary innovations frequently associated with adaptive radiations.
Fungal evolutionary genomics provides insight into the mechanisms of adaptive divergence in eukaryotes 2
Many predictions have been validated, such as the role of gene duplication in novel functions, the positive impact of TEs on evolvability, the importance of changes in gene regulation, the clustering of some adaptive changes in particular genomic regions and the occurrence of BDM incompatibilities 3. Other processes, previously considered anecdotal, have been shown to feature prominently among the drivers of adaptive divergence. These processes include gene deletions, introgressions, changes in genomic architecture and HGTs. The strength and nature of ecologically based divergent selection or life cycle characteristics have also been shown to be important. The genomic heterogeneity in rates of evolution in some fungi, with regions differing in their susceptibility to mutations, may facilitate the resolution of an apparent ‘conflict of interest’ between different classes of genes. Isochore-like structures, for instance, make it possible to cope with trade-offs in which there is a need to maintain some functions under strong constraints, with others evolving rapidly in response to positive selection. This trade-off may also be resolved by gene regulation, with promoters differing in evolvability according to the type of function.
Adaptation to Global Change: A Transposable Element–Epigenetics Perspective 4
Understanding how organisms cope with global change is a major scientific challenge. The molecular pathways underlying rapid adaptive phenotypic responses to global change remain poorly understood. Here, we highlight the relevance of two environment-sensitive molecular elements: transposable elements (TEs) and epigenetic components (ECs).
Transposable element islands facilitate adaptation to novel environments in an invasive species 4
Adaptation requires genetic variation, but founder populations are generally genetically depleted. Here we sequence two populations of an inbred ant that diverge in phenotype to determine how variability is generated. Cardiocondyla obscurior has the smallest of the sequenced ant genomes and its structure suggests a fundamental role of transposable elements (TEs) in adaptive evolution. Accumulations of TEs (TE islands) comprising 7.18% of the genome evolve faster than other regions with regard to single-nucleotide variants, gene/exon duplications and deletions and gene homology. A non-random distribution of gene families, larvae/adult specific gene expression and signs of differential methylation in TE islands indicate intragenomic differences in regulation, evolutionary rates and coalescent effective population size. Our study reveals a tripartite interplay between TEs, life history and adaptation in an invasive species. Mechanisms controlling TEs are as old as prokaryotes9 and in fact most TEs are epigenetically silenced through either methylation, histone modifications or RNAi The current understanding of TE activity dynamics in genomes is that periods of relative dormancy are followed by bursts of activity, often induced by biotic and abiotic stress, such as exposure to novel habitats. Frequent TE transposition during bursts leads to genomic rearrangements, thus producing new genetic variants and eventually even promoting speciation TEs represent a major force in evolution, contributing to the generation of genetic variation especially in species confronted with hurdles like inbreeding or repeated bottlenecks.
Friend or Foe: Epigenetic Regulation of Retrotransposons in Mammalian Oogenesis and Early Development 7
TEs bridge genetic and epigenetic landscapes because TEs are genetic elements whose silencing and de-repression are regulated by epigenetic mechanisms that are sensitive to environmental factors. Ultimately, transposition events can change size, content, and function of mammalian genomes. Thus, TEs act beyond mutagenic agents reshuffling the genomes, and epigenetic regulation of TEs may act as a proximate mechanism by which evolutionary forces increase a species’ hidden reserve of epigenetic and phenotypic variability facilitating the adaptation of genomes to their environment. If we put aside the mechanistic details of precise molecular interactions, it seems that epigenetic regulation of TEs may act as a proximate mechanism by which evolutionary forces, and selection pressure, utilize TEs to increase the species’ “hidden reserve of variability”
Plants’ Epigenetic Secrets
While the mechanisms that determine biodiversity , bodyshape, phenotype and primary speciation were pretty clear to me after my investigations, and the evidence that came to light provided good reasons to refute darwinian macro-evolution as possible mechanism,
Where Do Complex Organisms Come From?
it was not really elucidated what mechanisms determine adaptation to the environment, and microevolution. I knew it was a pre-programmed process, based on the work of Shapiro, McClintock et al, and proponents of the third way
Only who has no grasp whatsoever about how evolution works, can believe, that microevolution can lead to macroevolution and biodiversity. I have not found any scientific paper that provided conclusive proof and evidence that mutations , natural selection or genetic drift provide organismal adaptation to stress , ecological niches and separation, and microevolution, or even macro-evolution. But papers that refute the claim :
The frailty of adaptive hypotheses for the origins of organismal complexity
There is no evidence at any level of biological organization that natural selection is a directional force encouraging complexity.
The evidence also refutes the hypothesis of macroevolution
Macroevolution. Fact, or fantasy ?
I read already about Transposons and their various essential functions :
Transposons and Retrotransposons
but today came the aha! breakthrough moment. After googling, i found the papers that made it clear that transposable elements (TE's) , which were called junk , play a major if not the main role in microevolution, and so do epigenetic gene regulatory networks that orchestrate TE's responsible for the adaptation of organisms, and their species restricted physical change.
Stephen C. Meyer, Darwin's doubt, page 167:
Evolutionary scenarios envisioning other mutational mechanisms also presuppose important sources of preexistent genetic information. Gene duplication, as the name implies, involves the production of a duplicate copy of a preexisting gene, already rich in functionally specified information. Retropositioning of messenger RNA transcripts occurs when an enzyme called reverse transcriptase takes a preexisting strand of messenger RNA and inserts its corresponding DNA sequence into a genome, also producing a duplicate of the coding portion of a preexisting gene. Lateral gene transfer involves transferring a preexisting gene from one organism (usually a bacterium) into the genome of another. The transfer of mobile genetic elements likewise occurs when preexisting genes enclosed in circular strands of DNA called plasmids enter one organism from another and eventually find themselves incorporated into a new genome. This process also mainly occurs in single-celled organisms. A similar process can occur in eukaryotes, where mobile genetic elements called transposons—often called “jumping genes”—can hop from place to place in the genome. Gene fusion occurs when two adjacent preexisting genes, each rich with specified genetic information, link together after the deletion of intervening genetic material.” Each of these six mutational mechanisms presupposes preexisting modules of specified genetic information. Some of these mutational mechanisms also depend upon sophisticated preexistent molecular machines such as the reverse transcriptase enzyme used in retropositioning or other complex cellular machinery involved in DNA replication. Since building these machines requires other sources of genetic information, scenarios that presuppose the availability of such molecular machines to assist in the cutting, splicing, or positioning of modular sections of genetic information clearly beg the question.
Further readings :
How Junk DNA confirms intelligent design predictions
But, But, But … We’re 98% Similar to the Chimp!
Last edited by Admin on Sat Apr 22, 2017 4:28 pm; edited 7 times in total