Embryonic development

Since the mid-19th century, improvements in microscopy have enabled an increasingly detailed description of how embryos develop, and an increasing appreciation that it proceeds through differentiation and specialisation of individual cells as the embryo grows. Yet for a long time it was still a mystery as to how the fully-formed organism develops from a ‘simple’ single-celled zygote; to some it seemed too remarkable to be explicable by solely physicochemical mechanisms, and they appealed to ill-defined epigenetic processes [1], or even vitalism.

However, one of the remarkable successes of genetics and biochemistry over the last few decades has been the gradual elucidation of some of the genetic and molecular mechanisms involved in embryonic development. Much has been achieved, and there is much more to find out.

For example, although it has been known since the early 20th century that embryonic processes included induction – where a chemical (the inducer) is released by one developing tissue to affect the development of another (the target) – it is only in the last three or four decades that we have begun to identify some of these inductive signals or ‘chemical messengers’. And we are beginning to understand how they work.

We have also begun to identify and recognise the roles of some of the genes that are involved in controlling embryonic development.

Now, probably for every step in the development of an embryo (at least of vertebrates) there is active research to identify the genes that are responsible, and how they act. It is increasingly clear that there is a constant interplay of genes and their products (e.g. transcription factors), involving a hierarchy of genetic control, some with competing or modulating effects on others, in order to implement overall organisation of development.

And identifying the genes and transcription factors that control development is only the beginning. It is also a question of how their actions are implemented – what molecular processes are activated e.g. to build an organ or a tissue, or even ‘just’ to implement the early stages of embryo development such as cleavage or gastrulation.

Embryonic development and evolution

The complexity of the genetic and molecular mechanisms that implement embryonic development has two important implications so far as the theory of evolution is concerned:

1. The complexity itself defies an evolutionary origin.

Biologists in the 19th century were well aware that organisms are not static or fixed, but vary from generation to generation. At the time they did not know how variations arose, and in effect thought biological tissues to be innately variable or plastic. Although they also knew that the variation that could be achieved by artificial selection was limited, there seemed to be no fundamental reason why, given enough time and the ‘powers of nature’, these limited variations could not be extrapolated to effect large-scale evolution along the lines that Darwin proposed.

However, we now know that biological tissues are not innately plastic. Rather, tissues and organs are constructed in the course of embryonic development in carefully controlled ways by exceedingly complex genetic and molecular mechanisms. These mechanisms are dependent on a large number of genes which must be turned on and off (and sometimes partially) in the right cells and at the right times.

For example, one study not only identified nearly 7000 genes involved in the embryonic development of a teleost fish, but specifically looked at how their patterns of expression changed throughout the different stages of development. For 45% of these genes there was a significant change in their level of expression between temporally adjacent stages. [2]

And a recent study identified at least 347 genes involved in the embryonic development of the eye in mouse. [3] These were identified through phenotypic defects caused by defective genes; so it is likely that there are more genes involved, but not yet characterised.

Once we recognise and give due weight to the prohibitive improbability of obtaining new genes in an opportunistic way and the fact that this improbability increases exponentially when genes are mutually dependent, which is certainly the case in embryonic development, it leaves no doubt whatever that embryonic mechanisms could not have arisen in an evolutionary way.

Unfortunately, evolutionary biologists prefer to ignore these clear genetic and biochemical facts, and continue to believe that the mechanisms of embryonic development must have evolved somehow. Despite the contrary evidence, the view persists that mutations can at least sometimes produce constructive new genes, perhaps appealing to the significant morphological changes that can occur through mutation, not recognising that these arise through the disabling of genes, not the production of new ones.

2. The complexity of embryonic development reinforces the significance of the non-homologous embryonic development of structures (tissues and organs) that appear homologous from an adult morphological perspective: it negates the traditional inference of common ancestry.

For evolution – descent from a common ancestor – to be a credible explanation for homology requires that there are viable routes from the supposed common ancestor to the supposed homologous progeny. That is, routes that can realistically be accounted for in terms of steps that (a) have a reasonable chance of occurring in an undirected manner (e.g. random mutations) and (b) offer an advantage that can be subject to natural selection. But the complexity of embryonic development – involving so many mutually dependent factors – means that it just isn’t credible that random changes will bring about constructive changes. On the contrary, we know all too well that mutations to genes – such as in those involved in the embryonic development of the eye, mentioned above – usually result in pathological conditions, often lethal.

Biologists usually try to explain non-homologous embryonic development by assuming that the developmental mechanisms must have changed, and may propose morphology-based models to indicate how this might have happened; but the genetic and molecular implications of such proposals are usually glossed over or ignored altogether. In other words, just as biologists often try to explain how evolutionary novelties (e.g. legs, wings, flowers) might have arisen in terms of exclusively morphological models – such as Nilsson and Pelger’s model for eye evolution – but with no regard to what would be required at the genetic and molecular level in order to effect such morphological changes; in a similar way, biologists propose exclusively morphological models to try to explain how they think embryonic development might have changed, but without any consideration to what would be required to effect these changes in terms of genetic mechanisms.

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Page created October 2020.