As I noted in the previous entry, Steve Matheson does not see eye-to-eye with me regarding introns and design. In fact, he lists several areas of significant disagreement. Let’s have a look.
Steve focuses on “some mistakes” because he thinks they will illustrate “a particularly serious intellectual danger of design-think.” My first mistake?
Mike asserts that bacteria don’t have introns. This is not quite true. The group II introns are present in many bacteria – in some genes – and are thought to be forebears of the group I introns that are so widespread in animal genomes. The implication is that the intron table was already set long before the eukaryotic (much less multicellular) party had started. The “front-loading” would appear to have occurred in bacteria themselves. (Mike alludes to this in the first post of the series.) And that matters because…
Now this simply makes no sense to me. The first thing I did in starting this series of essays is clarify the term ‘intron’:
First, I will be focusing on introns found in protein-coding genes. In other words, these are the introns that interrupt sequence that code for amino acids and are removed by spliceosomes in order to form the mature mRNA. There are other introns that may have front-loaded the existence of these protein-coding introns, but that is another topic for another day. For now, when I refer to ‘introns,’ I am referring to introns found in protein-coding genes. (emphasis added)
And I even clarified this in the next intron essay:
Bacteria, which lack introns (remember, we’re talking about protein-coding genes) also have not been successful in spawning an organism as complex as a mammal. (emphasis added)
Since I was not talking about all introns, there was no mistake here.
So let’s turn to a more interesting, meaty criticism. I have been asking a simple question in order to provoke thought – “Where are the prokaryotic mice?” Steve thinks the question is bizarre and responds to the basic argument as follows:
Mike asserts that prokaryotes haven’t spawned multicellular life. But that’s not true. In fact, all indications are that prokaryotes spawned all multicellular life. The first eukaryotic cells are thought to have been forged by combinations of prokaryotic cells (this is the well-known endosymbiotic hypothesis) and the presence of group II introns in bacteria is just one of numerous observations that point to common ancestry between eukaryotes and prokaryotes. In other words, unless Mike is disavowing common ancestry (the trunk of the tree of life), then his conclusion doesn’t make any sense. Prokaryotes really did give rise to multicellular life, by giving rise to ever more complex cell types.
Not quite. I am not arguing that “prokaryotes haven’t spawned multicellular life.” Let’s consider an important piece of missed context from “Where are the prokaryotic mice?”:
But what if we moved up the ladder of complexity and considered the two basic cell designs – prokaryotic and eukaryotic….. Yet might the two different cell designs help us further appreciate the manner in which the designer-mimic is constrained by its design material? (emphasis added)
This is not about whether prokaryotes could ultimately spawn eukaryotes, as I accept that. As Steve notes, there is a solid hypothesis about that transition and I have previously explored some of the ways this symbiotic union may have been front-loaded. This is about whether the cell design – the composition and architecture of the prokaryotic cell – is capable of generating something as structurally complex as a mouse (for a mouse, like all animals, is an assembly of cells). Seen from this angle, the endosymbiotic hypothesis supports my position. That is, in order for prokaryotes to ultimately spawn eukaryotes, they first had to go through a radical re-design of cell structure. I thought this point was clear from the conclusion of my essay:
Note that while the vertebrate expression of the eukaryotic cell has been able to spawn 120 different cell types, both eubacteria and archaebacteria have not moved beyond a meager 2, even though these prokaryotes are both more numerous and older than eukaryotes. This suggests that had the eukaryotic cell design failed to emerge, the Earth would contain nothing more complex than any extant bacteria in existence today. And this suggests that the blind watchmaker, working with such an extremely adaptable cell as the prokaryotic cell, could not ever design something like a mouse. In order for the blind watchmaker to craft a mouse, it is reasonable to propose that it needed the basic architecture of the eukaryotic cell plan. (emphasis added).
So here is what we have. Prokaryotic cells can be viewed as the highest expression of mutation and selection, for there is no better cellular candidate for a “self-replicator.” Yet after billions of years, the prokaryotic cell plan has failed to achieve anything near the level of structural complexity as exhibited by the eukaryotic cell plan. To reach such structural complexity, the cell design had to be radically retooled, partly through endosymbiotic union, a one-time event given the widely accepted monophyly of eukaryotes. Once the eukaryotic cell design was established, prior to the radiation of all extant eukaryotes, the basic cell design was now capable of supporting the emergence of complex, metazoan life. The evolution of metazoa did not require further extensive retooling of the eukaryotic cell plan, given that metazoan cells are so similar to protozoan cells; it was more like the natural outflow of the potential inherent in the eukaryotic cell plan.
Let’s next turn to a couple of other areas of disagreement. Steve writes,
Now, maybe you don’t think there’s a big mistake here. Mike is just saying that simple cells can’t make complex multicellular assemblages, right? Well, no, he’s saying something more than that. He’s saying that through vast numbers and vast ages, they should have done so. He thinks it’s notable that prokaryotes, even after almost 4 billion years and countless individual lives, haven’t formed a mouse. I think this is crazy talk.
Yes, crazy rabbit that I am, I do think it is notable that the prokaryotic cell design has failed to achieve a level of structural complexity resembling that of a mouse. Consider it the result of a 3.5 billion year old global experiment. So why is this? I proposed that the prokaryotic cell plan is simply not up to the task. That is, since all designers are limited by their design material, and natural selection behaves as a designer-mimic, the prokaryotic cell plan simply can’t be tweaked and tinkered with to generate something like a mouse. To reach that level of complexity, the cell plan itself had to first be radically restructured – a “detected” target for front-loading (in other words, this is not an argument against evolution; it’s a thought process attempting to determine focal points for a front-loading designer).
Steve objects by noting two more problems for my view. First,
Bacteria actually do form very interesting multicellular assemblages. Organisms? Not really. But let’s not ignore the fact that prokaryotes do know how to live in complex and cooperative environments.
Yes, I have already noted that bacteria can form multicellular assemblages. If someone were to ask another crazy question, “Where are the prokaryotic mold?”, I could say, “Over there – check out the actinobacteria.” It’s another remarkable example of convergence.
The fact that bacteria actually do form multicellular assemblages and know how to live in complex and cooperative environments underscores my position. Apparently, it’s not enough for a cell to know how to live in complex and cooperative environments, to communicate with each other, and to have the ability to undergo extensive adaptation. While all these facts apply to bacteria, we are still left with the fact that they remain structurally simple relative to eukaryotes. So my hypothesis is simple – they remain structurally simple because this simple cell plan is inadequate for the task of evolving something akin to a mouse. So let’s make it more interesting and ponder what is the specific problem(s)? That’s where the whole intron discuss came in:
Bacteria, which lack introns (remember, we’re talking about protein-coding genes) also have not been successful in spawning an organism as complex as a mammal. There are probably several reasons for this, and the lack of introns may be one of them.
Next, we can turn to Steve’s last objection to my thesis:
Most importantly, Mike’s thinking here shows a weakness that I believe arises most commonly in design-oriented analyses of evolution. He seems to think that the presence of prokaryotes today, in all their lame simplicity, is notable because they coexist with those majestic miracles of design and performance, the awe-inspiring flora and fauna of metazoan life. But that’s nonsense. Prokaryotes are successful – wildly successful – in countless niches which have never been colonized by multicellular organisms. Why not ask why they are so successful? Why not write a series in which the presence of introns and mobile elements and organelles is put forth as an explanation for the disastrous failure of multicellular life to dislodge the humble archaea and bacteria from these positions of ecological dominance?
This objection does not make sense. Just because I note the bacterial cell plan has not been successful at generating structural complexity does not mean I must be judging bacteria as failures. Bacteria are indeed far more successful in other areas – the ability to colonize just about anywhere on this planet and the ability to generate metabolic complexity, for example. But when Steve asks, “Prokaryotes are successful – wildly successful – in countless niches which have never been colonized by multicellular organisms. Why not ask why they are so successful? “, the simple answer is this – I already have.
For example, such bacterial success is a factor in one of the expectations from front-loading:
4. Front-loading would be linked to terraforming. If we propose that the ancient Earth was seeded with a consortium of single-celled organisms designed in such a way that the evolution of metazoan complexity was rendered more likely, something else is implied.
Organisms complex and sophisticated enough to be composed of different tissue types and to depend on the control mechanisms of a nervous and endocrine system could only exist in a supportive context. For example, if you wanted to front-load something like a mouse, then in order for the mouse-like creature to survive, it would need resources such as food, air, water, a place to live, and a place to reproduce. It would need to be part of an ecosystem. After all, if you dropped the most healthiest of mice on the planet of Mars, they would quickly die. This is because the planet Mars cannot support the life-demands of the mouse.
So if we are to front-load the existence of mice-like creatures into the genomes of single-celled organisms, we also need to ensure the Earth will be prepared, at some point, to receive the mice. And it is the preparation of a receptive Earth that we can call terraforming.
Simply put, that the prokaryotic cell plan has been such a wild success in colonizing is one facet of the front-loading objective – for this impressive ability to colonize is involved in the symbiotic origin of the eukaryotic cell plan and the emergence of metaozoa (more on this latter point another day).
And I have even touched on one key ingredient to the success of bacteria here and here and here. Apparently, Steve thinks I rely on some sort of tunnel vision, obsessed only with metazoan complexity. In reality, I’m just one guy fleshing out some ideas in my spare time. There are more ideas in my head than on this blog. Give it time.
Finally, let’s wrap it up with Steve’s conclusion:
Mike’s right about introns and their likely role in the origins of multicellular organisms. But he’s wrong to associate complexity with success, and I think he’s wrong to assert that introns in particular were necessary for the evolution of multicellularity and its associated complexity. I suspect that there are lots of ways to encourage genetic diversity and modularity, but that introns and splicing, dating to the RNA world, made the contribution because they were there when others weren’t.
I can’t say that introns were necessary for the evolution of multicellularity and its associated complexity. But I can say that introns facilitated the evolution of multicellularity and its associated complexity. To facilitate is to help along, meaning that the transition was more likely to happen because of the introns.
As for Steve’s last sentence, I cannot say he is wrong or unreasonable. After all, this is a popular and respectable position, not to mention a mainstream scientific perspective. But we really have no way of knowing if the suspicion is true and how many ways are “lots of ways.” And we don’t even know if there is a better way. I would simply point out that this position is simply the non-teleological perspective in full view. The Duck sees introns as something that just happened to exist such that they just happened to be of use. The Rabbit sees introns as something that exist in order to help bring about a future state. Duck, rabbit. Rabbit, duck. Take your pick.