Cell Plans and Evolution

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.

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38 responses to “Cell Plans and Evolution

  1. Mike, as a layperson sitting on the sidelines, I have to say that I’m impressed with the back-and-forth of this discussion. First I read your essays, and I’m persuaded. Then I read Matheson’s response, and I wonder how I could have been so naive to have been swayed by your essays. Finally, I read your reply to Matheson, and it all clicks into place again.

    I am delighted, most of all, with the engagement displayed here. It’s the sort of thing I’ve been seeking since I started following this debate five years ago. Although Matheson occasionally borders on the snarky, you’ve been able to take the high road nevertheless. (I’m dismayed by that, as Matheson claims the label “Christian,” while I’ve never seen you own that. I do claim the label myself.)

    If the discussion on every front in this battlefield could somehow rise to this level, laypersons such as me might actually benefit, and learn something worthwhile!

    (Interesting too, then, that Matheson teaches for a living, while you’ve never claimed to make a living from your teaching…but are merely “fleshing out some ideas in my spare time.”)

  2. Hi Dave,

    Matheson strikes me as a good guy, so I wouldn’t hold any perceived snarkiness against him (believe me, it was very mild compared to the treatment I have received from others). My guess is that he has very little patience for design arguments largely because almost every design proponent out there insists on inserting design, as some form of “obvious best explanation,” on the back of raw anti-evolutionism. Truth be told, I don’t have much patience for that either. I just choose to follow dat wabbit.

  3. Introns, exons, editosomes, spliceosomes, alternative (gene) splicing only make sense from a design perspective.

    Editing and splicing require knowledge- knowledge of what is to be edited and spliced- as well as how to go about that task and when to go about it.

    But anyway- good job Mike and thanks for your information.

  4. Hi Mike,

    I was wondering if you were planning on responding to Art’s comments at Matheson’s blog.

  5. woodchuck64

    Mike:

    “To reach such structural complexity, the cell design had to be radically retooled, partly through endosymbiotic union”

    Endosymbiotic union is believed to result from chance encounters between prokaryotic organisms, so it naturally fits the idea of unguided evolution. Calling it “radical retooling” is a phrase that sounds unnecessarily ID-primed unless you mean prokaryotes were frontloaded with the desire to, once in a great while, form special symbiotic relationships.

  6. Mike,

    Like Dave said, enjoyed the back and forth. There are extremes on both sides. You’re in the gooey middle. Which is fine. S’mores would’nt be S’mores without both crust and goo 😉

    The “editing” that Joe G mentions is why I’m more crust than goo. In order to edit something, how does a purposeless, goaless process create a marker to edit by?

    Finally, offtopic, but important question. I’ve seen so many mention the chimp-human 98% DNA similarity as evidence for evolution. Accepted as fact and espoused as solid.

    What now that DNA is only 70% match at best? Will the unguided evolutionist now use this as evidence, twisting a new story? And how will this new information touch upon your frontloading hypothesis? And what is your reaction in general to the news?

    Thanks

  7. Hi Woodchuckl,

    If you look, you’ll see that Mike linked to a discussion on the possible front-loading of the mechanisms for endosymbiosis.

  8. Oops. Didn’t mean to put the “l” on Woodchuck. Honest

  9. I was wondering if you were planning on responding to Art’s comments at Matheson’s blog.

    I see, so when Sandro J. de Souza, who works in Walter Gilbert’s laboratory at Harvard University (Gilbert is the lead scientist who proposed introns are ancient), writes the following for ScientificAmerican.com, “In general, nuclear introns are widespread in complex eukaryotes, or higher organisms. Simple prokaryotes and eukaryotes (such as fungi and protozoa) lack them,” no problem (the link to de Souza’s comment was in my intron article). But when Mike Gene writes, “First, as a general rule, introns are far more common in multicellular genomes than single-celled genomes,” I’m wrong. LOL. Anytime Art reads something I write, he begins with the conclusion that I am wrong. Haven’t you figured that out yet?

  10. Hi Mike,

    Yes, I figured out Art a long time ago. He is your loyal opposition. But I was referring to his answer to Steve, when he said that he thought that regulatory changes were more important than the size of the proteomes in facilitating the evolution of multicellularity.

  11. Well, you know Bilbo, introns are thought be involved certain aspects of transcriptional
    control. Can’t get more rabbity than that.

  12. Err, introns are thought be involved in certain aspects of transcriptional control. Have to stop using linux text applications to write posts 😛

  13. thought to be, still managed to get that wrong lol

  14. Hi Bilbo,

    I never claimed introns where “the most important” factor behind the evolution of metazoans. In fact, I specifically stated:

    “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.

    To be a significant, even essential, player, does not mean you need to be the lead player. To knock down my position, we need evidence that metazoans could have reached their state of complexity without input from introns. Remember, the hypothesis is that introns facilitated the evolution of metazoan life. They helped it along, as with alternative splicing and other areas to be blogged about later. The hypothesis was not introns were the #1 driving cause behind the evolution of metazoan life.

  15. See? Loyal opponent Art forces Mike to go deeper once again. Or if you were already planning on going deeper, now we all are ready for it.

  16. LOL. Mike’s already diggin deep in that bunnah hole. Anyway, the weather is too beautiful and Easter is almost here.

  17. Cool. Enjoy the weather and the holiday.

  18. Mike,

    Agreed… on your point about resurging interest as teleology gets involved for many and it provides a more robust debate. I didn’t get interested in biology until after changing my mind on design vs undesign. That and turning off TV has done wonders for my curiosity.

    I was hoping you might take a moment to comment on my question about DNA… chimp vs human. It was a serious inquiry. How evolutionist see it and how you might diverge in opinion or see advantages/disadvantages for your guided hypothesis.

    From AP…
    “A new study comparing the Y chromosomes from humans and chimpanzees, our nearest living relatives, show that they are about 30 percent different. That is far greater than the 2 percent difference between the rest of the human genetic code and that of the chimp’s, according to a study appearing online Wednesday in the journal Nature.”

    “”Wow,” said R. Scott Hawley, a genetics researcher at the Stowers Institute in Kansas City. “That result is astounding.””

    The nature link:
    http://www.nature.com/nature/journal/v463/n7280/full/nature08700.html

    “Indeed, at 6 million years of separation, the difference in MSY gene content in chimpanzee and human is more comparable to the difference in autosomal gene content in chicken and human, at 310 million years of separation.”

    Is this a surprise to most seasoned geneticist? It seems so. And this last quote makes an excellent point regarding evolution. It seems to be whatever unguided evolutionist allow.

    The rules seem to change over time 😉

  19. In conclusion, this is the first report of introns in protein-coding genes in Archaea.

    Source:

    Introns in protein-coding genes in Archaea

    De Souza was commenting in 1999. The cited paper was published in 2002.

  20. woodchuck64

    Bilbo:

    If you look, you’ll see that Mike linked to a discussion on the possible front-loading of the mechanisms for endosymbiosis.

    Oops! Thanks, and my apologies for hasty reading.

  21. De Souza was commenting in 1999. The cited paper was published in 2002.

    We have known that bakers yeast have introns long before 1999, Alan. You should note that he qualified his entire claim with “In general.” Nevertheless, I think my wording is more accurate.

    Are you under the impression this study somehow refutes my position?

  22. DATCG,

    For future reference, I prefer to keep the comments close to the topic of the blog entry. You can always use Rabbit postings for off topic material.

    As for the Y chromosome, it does not have many genes on it and certainly no genes essential for human life (females don’t have it). So I’m not terribly surprised it would behave differently from the autosomes.

  23. Are you under the impression this study somehow refutes my position?

    No, as I freely admit, I have no real idea what your position is. Is the issue of introns central to your position?

  24. Though it does occur to me that if Archaea are a monophyletic group and Eucaryotes are more closely related to Archaea than Bacteria, wouldn’t one expect to see introns in Archaea rather than in Bacteria?

  25. And aren’t yeasts about the simplest Eucaryotes? Is there a pattern forming?

  26. Nope, the introns in bacteria are the ones thought to be ancestral to the introns in Eukaryotes.

  27. Hi, Nelson

    Nope, the introns in bacteria are the ones thought to be ancestral to the introns in Eukaryotes.

    On what evidence, and by whom?

    Hi, Nelson

  28. “It is generally accepted that group II introns originated in bacteria before spreading to mitochondria and chloroplasts. ”
    Environ Microbiol. 2003 Mar;5(3):143-51.

    Here’s a recent paper about it:

    http://www.ncbi.nlm.nih.gov/pubmed/20351053

  29. From the abstract of the paper:

    However, the ability of group II introns to function outside of the bacteria-derived organelles is debatable, since they are not found in the nuclear genomes of eukaryotes.

  30. lol, try reading the entire abstract, that’s what they addressed:

    “Here, we show that the Lactococcus lactis Ll.LtrB group II intron splices accurately and efficiently from different pre-mRNAs in a eukaryote…Thus, a group II intron can splice from a nuclear transcript…consistent with the bacterial group II intron ancestry hypothesis.

  31. Alan,

    No, the issue of introns is not central to my position. I raised the issue after reading Steve’s review of Meyer’s book, as I thought some people might be interested in a different approach than the usual evolution vs. design template. The intron issue is just one facet of my front-loading thesis and I once again demonstrated that a teleological perspective can a) generate testable hypotheses that are b) supported by some evidence.

  32. Michael, thanks for response. I’ll keep in mind the wabbit postings from now on.

  33. try reading the entire abstract

    Perhaps the full text is available without suscription. Do you have access? I see Koonin has written on this and there has been some discussion.

    This all may be moot as Mike says introns are not central to his position, anyway.

  34. I don’t get your last response Alan. You clearly misunderstood the abstract (or didn’t even bother to read it).

  35. I don’t get your last response Alan. You clearly misunderstood the abstract (or didn’t even bother to read it).

    I’ll try and enlighten you! I can’t access the full paper unless I pay 15 dollars for a 24hr view. On looking at the literature on group II introns, there seems a lively discussion on the issue and Koonin’s paper, available without subscription with annotated referee comments seems to demonstrate this. So does Chalamcharia et al’s paper settle the matter? I suspect not.

  36. Hi Alan,

    Actually I was referring to how you stopped reading the abstract after read this part:

    “However, the ability of group II introns to function outside of the bacteria-derived organelles is debatable, since they are not found in the nuclear genomes of eukaryotes.”

    You failed to understand that that is exactly what the paper addressed! You don’t need to have read the entire paper to understand it, just had to keep reading the abstract.

  37. Alan wrote:

    On looking at the literature on group II introns, there seems a lively discussion on the issue

    Nope, Koonin’s hypothesis is that a bacterium spread group II introns into an archaeal genome through symbiosis. So the basic idea is still there, that group II introns originated in bacteria. The comments you reference simply disagree that an archeon entered the picture at any point on the endosymbiosis that lead to eukarya.

  38. Pingback: Origin of Eukarya: Follow the Clues «

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