Here is an interview with cell and developmental biologist Stuart Newman. I would encourage you to read the entire interview, but for now, I want to focus on one aspect where Newman explains the significance in finding deep homology in developmental processes and how it would tie into nudging/front-loading evolution.
Two ancient organismal forms that were hollow, for example, did not need to have to have a common ancestor that was hollow. They could have developed their interior body cavities completely independently by the physical consequences of localization of similar (or even different) proteins products on the surfaces of cells.
Consider segmented organisms. Worms are segmented. Our backbones are segmented. Insects are segmented. Some scientists at one point wanted to say that if you have segmentation, all of the segmented forms had to have a common ancestor. But, in fact, it’s generally acknowledged now that animal segmentation probably arose independently in several different lineages, maybe half a dozen times. If that’s the case, then you can’t trace segmentation as a morphological motif back to a common ancestor.
And this raises an interesting question. Is it possible that evolutionary events currently envisioned to occur once (monophyly) actually happened several times over, but the signal for multiple origins is blurred by convergence as a result of front-loading? This is a point that I teased with in my discussion of Tom20: “So how did this occur? We can think of this example of convergent evolution as the unfolding of the preadapted state. This original preadapted state channeled the blind watchmaker, much as a seeing eye dog can lead a blind man. And if it wasn’t for the lucky fact that the proteins are in reverse, an example of convergent evolution would be scored by everyone as an example of common descent.”
But let’s move on.
But what threw people for a loop is that organisms in lineages that didn’t seem to have a common ancestor nonetheless use evolutionarily very related (“homologous”) genes to generate those functionally similar (“analogous”) motifs. Flies, for example, have legs, and so do humans. Paleontology tells us that the worm-like common ancestor of the fly and the human did not have legs. So arthropod and tetrapod legs are analogous, rather than homologous, structures.
But if you look at the genes used to make a fly’s leg and those used to make a human leg, many of the same genes are used–which is a big puzzle.
This should help people see why the discovery of deep homology was a blow to the non-teleological perspective. Newman is saying the same thing as evolutionary biologist Sean Carroll, who noted, “When you think about all of the diversity of forms out there, we first believed this would involve all sorts of novel creations, starting from scratch, again and again and again.” From the non-telic perspective, this was the expectation/prediction – the legs of flies and mice evolved independently simply because the environment would provide a strong selection pressure to build some type of leg. It would not matter what it was made of and it would not matter how it was constructed. All that would matter is that it functioned as a “leg.”
Ernst Mayr, who played a significant role in shaping the Modern Synthesis (the synthesis of Darwinian evolution and Mendelian genetics), explained the logic: “Much that has been learned about gene physiology makes it evident that the search for homologous genes is quite futile except in very close relatives. If there is only one efficient solution for a certain functional demand, very different gene complexes will come up with the same solution, no matter how different the pathway by which it is achieved. The saying “Many roads lead to Rome” is as true in evolution as in daily affairs.”
The genes are homologous, but the structures are not. They’re analogous. I call this the “molecular homology-analogy paradox.” The only way to understand that is to think that the very same genes have been mobilized in completely different lineages to make structures similar to each other even though those structures can’t be traced back to a common ancestor.
Let that last sentence sink in: The only way to understand that is to think that the very same genes have been mobilized in completely different lineages to make structures similar to each other even though those structures can’t be traced back to a common ancestor. Feel the telic echoes?
The resolution of this apparent paradox can be found in the concept of DPMs (dynamical patterning modules), in which there are molecules that are predisposed to mobilizing certain processes of the physical world. When this mobilization occurs in a tissue mass structures get made. For example, if a certain kind of protein on the surface of a cell – a “cadherin”–tends to get sticky under certain microenvironmental conditions, and when this happens cadherin-bearing cells will clump together.
And molecules that are predisposed to mobilize certain processes of the physical world would be excellent candidates for nudges. For a predisposition (preadaptation) is, if you think about it, a nudge.
This is the basis of the most fundamental DPM, cell adhesion, which is the sine-qua-non of multicellularity. The single-celled ancestors of the modern animals are known to have had cadherins on their surfaces, even though those cells didn’t use the cadherins to stick to each other.
Because the function of a cadherin as a sticky protein is environmentally dependent, you can imagine that somewhere in Australia and somewhere in North America the environment might have changed and these single-celled organisms turned into clumps rather than single cells. But this obviously does not imply that clumpiness was a character that appeared in a common ancestor from which all multicellular forms descended. Rather, all cells that had this protein on their surface had the tendency, upon slight changes in the environment, to mobilize the physical force of adhesion. Without having a common clumpy ancestor, you got individual clumped forms at very distant places. And so on with other things like the genes whose products are involved in forming appendages–the limb of a human and the limb of a fly.
There’s a propensity of some of those gene products to cause a sheet of cells they are associated with to bend and protrude in certain ways. So when the context changes in a way that favors that, you’ll get an appendage forming and you’ll have two different evolutionary lineages–insects and vertebrates–that have appendages and use the same genes for appendages, but had a common ancestor that didn’t have appendages.
So we can see how to nudge evolution. Think of a cadherin in a unicellular organism doing its function for the unicellular organism as a nudge-in-waiting. When the right environment condition arises – just a matter of time – the nudge will occur. And if it occurs enough times in enough places, the nudge will eventually push evolution into a new trajectory. In other words, guiding evolution.