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Theory of Intelligent Design, the best explanation of Origins » Molecular biology of the cell » Development biology » Ontogeny , evidence of design

Ontogeny , evidence of design

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1 Ontogeny , evidence of design on Tue Oct 06, 2015 10:12 am


The Evolution of Early Animal Complexity 1

The argument of the development of an embryo
1a. During the development of an embryo, everything happens at a specific moment. In about 48 hours, it will grow from the top to the bottom, one slice at a time – scientists call this the embryo’s segmentation. “We’re made up of thirty-odd horizontal slices,” explains Denis Duboule, a professor at EPFL and Unige. “These slices correspond more or less to the number of vertebrae we have.”
1b. Every hour and a half, a new segment is built. The genes corresponding to the cervical vertebrae, the thoracic vertebrae, the lumbar vertebrae and the tailbone become activated at exactly the right moment one after another.”
1c. The process is astonishingly simple. In the embryo’s first moments, the Hox genes are dormant, packaged like a spool of wound yarn on the DNA. When the time is right, the strand begins to unwind. When the embryo begins to form the upper levels, the genes encoding the formation of cervical vertebrae come off the spool and become activated. Then it is the thoracic vertebrae’s turn, and so on down to the tailbone. The DNA strand acts a bit like an old-fashioned computer punchcard, delivering specific instructions as it progressively goes through the machine.
1d. “A new gene comes out of the spool every ninety minutes, which corresponds to the time needed for a new layer of the embryo to be built,” explains Duboule. “It takes two days for the strand to completely unwind; this is the same time that’s needed for all the layers of the embryo to be completed.” This system is the first “mechanical” clock ever discovered in genetics; it is so remarkably precise.
1e. The Hox clock is a demonstration of the extraordinary complexity of the species.
2. The scientists don’t offer any evolutionary explanations. By discovering more and more complexities, the God arguments are increasing; we can only explain the complexities as being by God’s creation and control.
3. God exists.

Review: General Pattern of Development

1. Fertilization - In all animals, germ cells produce by meiosis eggs or sperm. The fusion of an egg or sperm to form a zygote is called fertilization. This is the starting point for development.
2. Cleavage - The division of the zygote into smaller and smaller cells.
3. Blastulation - cleavage eventually gives rise to a hollow ball of tiny cells called a blastula.
4. Gastrulation - The sorting out of cells of the blastula into layers (ectoderm, mesoderm, endoderm) that become committed to the formation of future body organs.
5. Differentiation - the formation of body tissues and organs. The basic body plan of the animal is established.
6. Growth - increased size of the animal.

Differentiation is a key feature of multicellular life:

An embryo is a multicellular diploid eukaryote in its earliest stage of development, from the time of fertilization through sexual reproduction until birth, hatching, or germination.

In embryology, cleavage is the division of cells in the early embryo. The zygotes of many species undergo rapid cell cycles with no significant growth, producing a cluster of cells the same size as the original zygote. The different cells derived from cleavage are called blastomeres and form a compact mass called the morula. Cleavage ends with the formation of the blastula.

A morula is distinct from a blastocyst in that a morula (3-4 days post fertilization) is an 8 cell mass in a spherical shape whereas a blastocyst (4-5 days post fertilization) has a cavity inside the zona pellucida along with an inner cell mass. A morula, if untouched and allowed to remain implanted, will eventually develop into a blastocyst.[3]
The morula is produced by a series of cleavage divisions of the early embryo, starting with the single-celled zygote. Once the embryo has divided into 16 cells, it begins to resemble a mulberry, hence the name morula (Latin, morus: mulberry).[4] Within a few days after fertilization, cells on the outer part of the morula become bound tightly together with the formation of desmosomes and gap junctions, becoming nearly indistinguishable. This process is known as compaction.

Within the field of developmental biology one goal is to understand how a particular cell (or embryo) develops into the final cell type (or organism), essentially how a cell’s fate is determined. Within an embryo, 4 processes play out at the cellular and tissue level to essentially create the final organism. These processes are cell proliferation, cell specialization, cell interaction and cell movement. Each cell in the embryo receives and gives cues to its neighboring cells and retains a cell memory of its own cell proliferation history. Almost all animals undergo a similar sequence of events duringembryogenesis and have, at least at this developmental stage, the three germ layers and undergo gastrulation. While embryogenesis has been studied for more than a century, it was only recently (the past 15 years or so) that scientists discovered that a basic set of the same proteins and mRNAs are involved in all of embryogenesis. This is one of the reasons that model systems such as the fly (Drosophila melanogaster), the mouse (Muridae), and the leech (Helobdella), can all be used to study embryogenesis and developmental biology relevant to other animals, including humans. What continues to be discovered and investigated is how the basic set of proteins (and mRNAs) are expressed differentially between cells types, temporally and spatially; and whether this is responsible for the vast diversity of organisms produced. This leads to one of the key questions of developmental biology of how is cell fate determined.


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Deciphering Complexity in Biology: Induction of Embryonic Cell Differentiation by Morphogen Gradients  1

One of the most complex and mysterious processes in nature is the development of a vertebrate animal from a single cell into an organism consisting of hundreds of differentiated cell types that are reproducibly arranged in specific spatial patterns.Understanding developmental mechanisms is essential because it is during development that the information contained in the DNA (the genotype) is interpreted into morphological phenotypes. Historically, developmental biology has attempted to study the embryo as a complete system that develops seamlessly into a perfectly shaped organism. For example, embryologists were fascinated by the fact that when an embryo is divided into two halves perfectly patterned twins can form. Fortunately,this vocation of embryology towards studying the whole is now paying off and we are beginning to understand how cells can communicate with each other over long distances spanning hundreds of cells.

we are still very far from understanding the principles by which the genotype is converted into phenotype.We know the sequence of nucleotides, but do not understand how the genetic program is interpreted to produce a perfect organism generation after generation


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3 Re: Ontogeny , evidence of design on Sat Oct 10, 2015 6:44 pm


Transcriptional regulators can determine cell types. 1


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4 Re: Ontogeny , evidence of design on Mon Dec 07, 2015 12:56 pm


Clocks and Hox 1

Segmentation is a key feature of many animals. New molecular studies add to our understanding of how vertebrate segments form and how this process is linked to the genes that make each segment unique.

In vertebrates, the spine, ribcage and breastbone are derived from repeated blocks of tissue that begin as identical units in early development and are then modified into unique shapes with different purposes. Some segments, for example, allow the head to move; some are sites of attachment for the muscles involved in breathing; and some protect the organs in the chest. To produce such a body plan, there must be mechanisms both for generating the segments and for giving each its distinct identity. For vertebrates, the task of producing repeated units seems to be controlled partly by a molecular clock in the unsegmented paraxial mesoderm — the tissue from which the units arise. The identity of the units is controlled by the differential expression of genes known as Hox genes in a nested pattern from the head to the tail1. Writing in Cell, Dubrulle et al.2 and Zákány et al.3 suggest that these processes are causally connected. Simply put, segmentation in vertebrate embryos occurs as follows. On each side of the neural tube (which forms the spinal cord) is a strip of unsegmented (‘presomitic’) mesoderm. Cells from this tissue progressively bud off, contributing to somites — the units of cells that will later develop into vertebrae and associated muscles. This differentiation process occurs in a wave that moves gradually from the head to the tail (that is, down the anterior–posterior axis), with presomitic mesoderm in front of the wave and somites in its wake. The molecular and genetic mechanisms that control vertebrate segmentation are not yet understood, but emerging evidence supports a long-standing theory known as the ‘clock-and-wavefront’ model4 (Fig. 1).

In this model, an autonomous developmental timer (the segmentation clock) interacts with a molecular wavefront of differentiation, which converts information from the clock into spatial information. The model has received support from the discovery of several genes whose expression patterns oscillate in the presomitic mesoderm with the same periodicity as that of somite formation (reviewed in ref. 5). Dubrulle et al.2now provide evidence that the wavefront may correspond to a sharp gradient of fibroblast growth factor-8 (FGF- 8 ) protein within the presomitic mesoderm. Grafting experiments in chick embryos2 showed that presumptive somites –I to –V (see Fig. 1) are fixed with respect to their anterior–posterior polarity and boundaries. But the tissue posterior to somite –V is not yet fixed in this way. Dubrulle et al. show that this ‘undetermined’ zone of the presomitic mesoderm corresponds to a posterior domain of high FGF-8 expression. Dubrulle et al. also found that widespread, forced expression of FGF-8 is sufficient to keep the cells of the presomitic mesoderm in an immature, undifferentiated state. Moreover, when FGF-8 protein was applied locally to one part of the presomitic mesoderm, a series of small somites formed. However, the total number of somites remained the same, because a larger-than normal somite developed posterior to the smaller ones. Conversely, when signalling from FGF-8 was blocked, larger somites formed. How can these results be explained? The authors’ detailed observations2 of oscillating gene expression show that forced FGF-8 signalling does not affect the segmentation clock itself. Rather, their data suggest that an interaction between FGF-8 signalling and the clock controls somite size, possibly by specifying the location of boundaries between presumptive somites. So, the clock determines when the boundaries form, and the gradient of FGF-8 determines where. When more FGF-8 is applied to the embryo, the FGF-8 gradient continues further than normal in the anterior direction, and more presomitic mesodermal cells are prevented from contributing to somites. But each somite is programmed to develop at the same time as usual, so each somite ends up containing fewer cells and is therefore smaller. Conversely, blocking FGF signalling shifts the determination front in the posterior direction, and so more cells are allocated to each somite behind the front. This interpretation is consistent with a role for FGF signalling in mediating the wavefront component of the clock-andwavefront model (Fig. 1). Once somites have formed, they must express the appropriate complement of Hox genes, which determine the nature of the somites. The ability to manipulate somite size, and hence the number of somites in a given region, allowed Dubrulle et al. to investigate whether the boundaries of Hox-gene expression follow somite number or absolute anterior–posterior position. The answer is that the embryo seems to count somites to set the boundaries of Hox expression. Zákány et al.3 suggest that the coordination of Hox-gene expression with segmentation requires the molecules of the segmentation clock. They found that several Hox genes are activated in the presomitic mesoderm in mice at the location where the next somite will form. This region coincides both spatially and temporally with a wave of expression of lunatic-fringe, a gene that is cyclically expressed in presomitic mesoderm and is controlled by signalling from Notch — a component of the segmentation clock. So it seemed that Hox expression might likewise be regulated by the clock. The authors confirmed this by showing that mice with a mutation in a protein downstream of Notch fail to activate significant levels of Hox expression in the presomitic mesoderm. At minimum, this provides a mechanism for aligning the levels of Hox expression with the segments, as Hox-gene expression is triggered up to the sharp boundary formed by the action of the clock and wavefront. Once a particular Hox gene is activated by the clock, its anterior boundary of expression is maintained at the level of the somite that was formed at the time the gene was switched on. These studies2,3 provide convincing evidence of a link between activation of Hox genes and segmentation. It seems that once Hox genes are activated by the clock in the presomitic mesoderm, they maintain their expression boundaries in somites and their derivatives. So the time at which a Hox gene is activated establishes its boundary of expression in the embryo. But it is not clear why one Hox gene is activated rather than another in a given clock cycle. As there are more somites than Hox genes, the mechanism must be more complicated than ‘one somite, one Hox gene’. The activation of Hox genes follows the physical order of the genes on the relevant chromosome, and this ‘temporal co-linearity’ depends on the release of the DNA containing the Hox genes from a repressive configuration6. The data discussed here suggest that Notch signalling is involved in periodic activation of the expression of unrepressed Hox genes. The details of how the release from repression is coordinated with the segmentation clock will be the next piece of the puzzle


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