Category Archives: eukarya

Ancestral Eukaryote with modern-like complexity

Recall that the eukaryotic cell plan is needlessly complex.

Recall the evidence suggests this needless complexity was essential for the emergence of metazoan-type existence.

And it looks like the key feature that facilitated the emergence of metazoan-type complexity is the nucleus (see here and here).

Of course, the nucleus, even without the chromosomes within, is a very complex and sophisticated structure.  Yet just how old is this complexity?

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Eukaryotes and Prokaryotes

I’ve long found it fascinating that every living thing on this planet can be cleanly split into two categories – prokaryotes and eukaryotes.  The prokaryotes consist of all the bacteria while the eukaryotes include animals, plants, fungi, and various protozoa.  The core life processes of the two cells are much the same, being built around the triad of proteins, RNA, and DNA, relying on the ribosome to build the proteins that synthesize everything else, including RNA and DNA, using ATP as the primary energy currency, and using lipid bilayer membranes to compartmentalize.  So what makes the two cell plans so different?

Below is a nice figure that helps you answer this question.

 

As you can see, there are two primary differences: size and level of compartmentalization.  Typical eukaryotic cells are much larger than bacteria and show a much more extensive level of compartmentalization given the numerous membrane-bound organelles and membranous folds.

Yet a question to ponder is why there are two cell types and only two cell types?  The non-telic perspective would explain this (away?) as simply an artifact of a contingent past.  There is no reason to ponder the question “why?”  It just happened that way.  But the telic perspective allows us to think of these two cell plans at a level that runs deeper.

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Nudging Mitochondria Along

It the previous posting, we saw there was good reason to think mitochondria were a necessary prerequisite for the evolutionary emergence of metazoan-type complexity.  Again, as Lane and Martin clearly point out:

Our considerations reveal why the exploration of protein sequence space en route to eukaryotic complexity required mitochondria. Without mitochondria, prokaryotes—even giant polyploids—cannot pay the energetic price of complexity; the lack of true intermediates in the prokaryote-to-eukaryote transition has a bioenergetic cause.

So we can see that natural selection, functioning as a designer-mimic, is, like other designers, constrained (and thus guided) by the materials used to express the design.  Just as there is no reason to think natural selection could craft something as complex and sophisticated as the prokaryotic cell without proteins, natural selection apparently cannot craft something as complex as a mouse or squid without the eukaryotic cell plan.  That’s why cells had to be first re-tooled through an endosymbiotic relation.

But why haven’t bacteria, after billions of years, ever been able to discover a method of evolving something mitochondrial-like without relying on endosymbiosis?   At first, it might seem to be simply an issue of scale, as the typical mitochondrion is roughly the same size as the typical bacteria.  But there are bacteria that are as large as some eukaryotic cells and it looks like they try to mimic mitochondria, but never quite make it.  One such bacterium is Thiomargarita.  

Lane and Martin discuss this bacterium and Myers summarizes their argument as follows:

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More Explanation for the Missing Prokaryotic Mouse

A few months back, I used the hypothesis of front-loading evolution to outline a subtle, but very important, shift in our perspective of evolution.  Instead of viewing evolution as all about selection picking from a pool of variants, consider the possibility that some variants are more special than others.  In this case, let’s pick a variation that is very special – the complete redesign of the cell plan, as it is this change that was necessary for setting the stage for the emergence of metazoan life.  I explained this as follows:

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.

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.

It turns out there is now more scientific evidence to support the contention that the emergence of the eukaryotic cell plan was a necessary prerequisite for the emergence of something as complex as a mouse:

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Fulfilling Future Needs

[I’ve combined all the previous RNAP entries together to make it easier to read.  However, I did not have the time to thoroughly edit, so some parts might seem a little repetitive.]

It is well known that eukaryotic cells are more complex than prokaryotic cells. For example, while the typical eukaryotic cell is 10-100 micrometers in diameter, contains numerous membranous organelles, has an elaborate cytoskeleton, and reproduces through mitosis, the typical bacterial cell is only 0.2-2.0 micrometers in diameter, lacks organelles, and reproduces through binary fission. Clearly, the cytological complexity of the eukaryotic cell is not needed in order to be alive.

Yet the theme of needless complexity repeats itself at increasingly smaller scales like a fractal image.

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Nudging Multicellularity into Existence

As we have seen, the bacterial and archaeal RNA polyermase (RNAP) differ in complexity. Despite the fact that the cell plan of both life forms is small, relatively simple, and streamlined, the RNAPs differ remarkably in terms of complexity, where the bacterial version is built from four parts, while the archaeal version is built from 11 parts. The archaeal version has homologs of the four bacterial components needed to carry out the core process of transcription, meaning the remaining parts are “bells and whistles”

As far as I have been able to determine, no one has thought to ask why the archaeal RNAP is so much more needlessly complex than the bacterial version. I would expect the non-teleological perspective would “explain” this disparity by insisting that there are many ways to transcribe DNA into RNA and these two RNAPs would merely reflect the many roads to Rome. But that is not a very satisfying speculation. So let me be the first to ask the question and the first to propose an answer.

From the hypothesis of front-loading, allow me to formulate a testable hypothesis – the “bells and whistles” of the archaeal RNAP – Rbp 4, 5, 7, 10, 11, and 12 – will play crucial roles in the emergence of a) the eukaryotic cell and/or b) complex, metazoan life

If we begin our analysis by focusing on Rbp4 and 7, which function together as a dimer, we have already seen some clues to support this hypothesis. First, Rnp4 and probably 7 are not needed in order for archaebacteria or single-celled yeast cells to survive, but are essential for the survival of multicellular fungi. Second, Rnp4/7 appear to be preadapted to facilitate the emergence of the complex eukaryotic cell plan given they not only function in transcription, but also moonlight to control RNA decay outside of the nucleus. Let’s now add some more clues.

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Linking Opposites

With the emergence of the nucleus as part of the eukaryotic cell plan comes the decoupling of transcription and translation. But something else is decoupled – the two processes that control the levels of messenger RNA in the cell.  These two processes are mRNA synthesis, which occurs within the nucleus, and mRNA decay, which occurs in the cytoplasm.  By physically separating the two processes, you run into a potential control problem where an increase in the synthesis of mRNA, for example, might not translate as an increase in mRNA levels because elevated mRNA decay rates in the cytoplasm might cancel out any increase in synthesis rates.  And given that mRNA levels play important roles in embryological development, this could pose a serious problem for the evolutionary emergence of metazoa.

So is there a way to keep mRNA synthesis and decay rates coupled while allowing for the enhanced compartmentalization of the eukaryotic cells?  Consider some recent research findings.

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