In the past, I have raised the hypothesis that introns have a function – to facilitate the evolution of metazoan organisms. I raised the hypothesis here and defended it from criticism here.
A recent paper adds more support to this hypothesis:
Origin and evolution of spliceosomal introns.
Rogozin IB, Carmel L, Csuros M, Koonin EV.
Biol Direct. 2012 Apr 16;7(1):11.
Let’s go through the abstract.
As readers of this blog know, I have proposed that introns have facilitated metazoan evolution. For example, after discussing alternative splicing, I noted:
It should now become clear to you why introns are so useful in a multicellular state and, conversely, why the cell design of a prokaryote could never have evolved something like a mouse. Introns impart extreme flexibility that would facilitate the emergence of different cell types under the constraint of the same genome.
Recent research has shown how one splicing network that is important in the development of the brain may have evolved. What’s interesting to me is not simply more data that supports my hypothesis about the role of introns in metazoan evolution, but that this gene network was pieced together prior to the emergence of the brain.
Recall that I hypothesized that introns have played a key role in facilitating metaozoan evolution. Here’s some more support support for that hypothesis:
Previously, I took issue with John Avise’s abrupt description of alternative splicing as having “some advantage,” as alternative splicing may play a crucial role in the evolution of metazoans by shielding sequence from selection, allowing minor variants to emerge and grow before being put to the full test of selection. It’s such shielding that might be required to expand a more complex state. One way to think of alternative splicing is as an evolutionary capacitor. I’ll let the Masel group describe what that means:
Let me add one more comment concerning Avise’s PNAS paper. In the last entry, I focused on his argument that introns counts as evidence against intelligent design. We saw the whole argument fails if we envision design working through evolution. But I want to you to notice something else. In the paragraph preceding the discussion of introns, Avise wrote:
Approximately 1% of all known genes in the human genome encode molecular products that our cells employ to build spliceosomes and conduct splicing operations on premRNA. All this rigmarole has some advantages (e.g., opportunities for alternative splicing during ontogeny and exon shuffling during evolution, both of which can generate functional protein diversity), but such benefits do not come without major fitness costs.
Note that Avise describes alternative splicing as something that confers “some advantage.” Some advantage. As if alternative splicing is just a minor factor in evolution.
Now let’s contrast this to the abstract from a paper by Stephanie Boue, Ivica Letunic, and Peer Bork (Alternative splicing and evolution. BioEssays 2003 25:1031–1034):
Alternative splicing is a critical post-transcriptional event leading to an increase in the transcriptome diversity. Recent bioinformatics studies revealed a high frequency of alternative splicing. Although the extent of AS conservation among mammals is still being discussed, it has been argued that major forms of alternatively spliced transcripts are much better conserved than minor forms.(1) It suggests that alternative splicing plays a major role in genome evolution allowing new exons to evolve with less constraint.
“A major role in genome evolution” sounds a tad more than “some advantage “ to me. In fact, consider the conclusion of Boue et al.:
Posted in design, evolution, introns, rationality
Tagged design, evolution, introns, rationality
I have not forgotten the Tetrahymena quiz, but I wanted to throw out one more juicy tidbt about introns first. As I have suggested, introns may have facilitated the evolution of metazoan-like complexity and one possible mechanism is by making alternative splicing possible. Recall that alternative splicing enables a single genome to spawn immensely diverse set of gene products, something that would come in very handy when it comes to spawning multiple cell types. But we might get even more radical, as introns, along with alternative splicing may very well have facilitated the emergence of the brain. In fact, we could even make a reasonable case that without introns, there would be no brains to discover introns. Consider just three examples:
We have seen that that last common ancestor of all eukaryotes had a genome that contained as many, if not more, introns as complex, metazoan life forms. So how did these ancient organisms process all these introns? Did they have a simple mechanism for doing so or did they rely on something like a modern-day spliceosome?
Recently, a study was published that addressed just this issue [1]. It began by listing three possible hypotheses:
Investigating the distribution of splicing mechanisms and spliceosome components among eukaryotic lineages can reveal how splicing and the spliceosome evolved within eukaryotes. In this study, we investigate three hypotheses of spliceosome evolution.
The first is that the spliceosome appeared in eukaryotes shortly after the eukaryotic ancestor, possibly by invasion by self-splicing introns. It is possible under this hypothesis that some eukaryotic lineages do not contain introns or spliceosomal components.
The second hypothesis is that the eukaryotic ancestor had a basic spliceosome that increased in complexity in multicellular eukaryotes. This complexity increase through time would be similar to intron length which appears to have increased in multicellular eukaryotes. Under this scenario, we could expect to find some, but not many, highly conserved splicing proteins present throughout extant eukaryotes.
These first two hypotheses are not mutually exclusive in that an invading self-splicing intron could lead to a spliceosome that increased in complexity over time.
The third hypothesis is that the eukaryotic ancestor contained a spliceosome that is similar in complexity to the spliceosome present in today’s eukaryotes, with the expectation that we could find many spliceosomal proteins throughout eukaryotic lineages.
So which hypothesis is best supported by the evidence?
I recently tried to show you a pattern that speaks to foresight. Specifically, one way to infer foresight is if we detect a) a past cost that is b) linked to a future benefit. Given the growing list of evidence that the last common ancestor of all eukaryotes had as many or more introns than current metazoans*, we are now in a position to infer a past cost if many/most of the lineages that evolved from this state showed a net loss of introns (costly enough to be removed by selection) and a future benefit if introns play a significant role in multicellular development and/or physiology.
We have seen a hint of future benefit through the manner in which alternative splicing may play a key role in the emergence tissues and organs. This, and other possibilities, need more exploration.
We have also seen a hint of past cost, where the evolution of chromalveolates was dominated by intron loss. Well, it turns out that another lineage appears to show the same pattern.
As I noted earlier, one of the clues to support the hypothesis that introns facilitated the evolution of multicellular life was that as a general rule, introns are far more common in multicellular genomes than single-celled genomes. I then pointed to a few specific examples to illustrate this point. Let me help you better visualize this by considering intron counts in 29 different eukaryotic species, including metazoans, plants, fungi, and protozoans. If you go here, you will find a table from a research paper that provides the count.
There’s another paper that supports my front-loading hypothesis that envisions introns as part of the mechanism to facilitate the emergence of metazoan-like complexity. The paper is: Extremely intron-rich genes in the alveolate ancestors inferred with a flexible maximum-likelihood approach, by Csurös M, Rogozin IB, and Koonin EV (Mol Biol Evol. 2008 May;25(5):903-11).
Let’s walk through the abstract.
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