Statistical/probability issues in speciation

[Biochemist]

....It would be interesting to find an organism that LACK either insulin or glucagon, but not both, as that would put a nail in your hypothesis, as far as I can see...

Thanks for the synopsis of insulin receptor biochemistry. I suspect this kind of post will winnow down the population of discussants to the biochemists and the insomniacs.

 

Remember, the enzyme system that manages insulin synthesis and release in the pancreas is required as well. We can defer the detail on that side, but the statistical problems are exagerated by the complexity of enzyme systems on both ends of the homeostatic mechanism.

 

One more point: when we find genomic precursors that have nothing to do with glucose metabolism (as I suspect we will) we will still need to address the probabilistic issue of how these proteins were able to arise through independent "mutation", and then aggregate at a single receptor site, a site that replicates in enough quantity to modulate energy response.

[MortenS]

I'll use this post as a repository for some of the articles and website I found during my research of this question. You might read some of them for amusement, as they contain a few ideas that might reduce your probabilities a bit.

 

 

Evolution of alternative splicing

http://www.fdhope.org/FamilialDysautonomia/Articles/alternativesplicing.pdf

 

Evolution of protein kinases from yeast to man

http://kinase.com/evolution/TiBS_Kinase_Evolution.pdf

 

Protein and proteome evolution

http://www.la-press.com/EBO-1-Gabaldon(Pr).pdf

 

Evolution of the protein repertoire

http://supfam.org/gough/chothia_science_repertoire.pdf

 

The Evolution of Controlled Multitasked Gene Networks: The Role of Introns and Other Noncoding RNAs in the Development of Complex Organisms

http://mbe.oxfordjournals.org/cgi/content/full/18/9/1611

 

Identification of Intron and Exon Sequences Involved in Alternative Splicing of Insulin Receptor Pre-mRNA

http://www.jbc.org/cgi/content/full/273/17/10331

 

Treefam database:

http://www.treefam.org/

 

This post will be updated...

[Biochemist]

I'll use this post as a repository for some of the articles and website I found during my research of this question. You might read some of them for amusement, as they contain a few ideas that might reduce your probabilities a bit...

This is a great reference list, Mort.

 

I have only gotten through the first two, but these are great review articles.

 

I think I ought to clarify the question on the table give a little more specificity to my question.

 

My hypothesis is really twofold:

 

1) It appears unlikely the many evolutionary developments occurred randomly, and

 

2) It appears in many instances that serial genomic changes did not have enough calendar time to express themselves pheotypically, and result in natural selection.

 

You are essentially agreeing with the first element, and have offered a number of genomic mechanisms that reduce the randomness of genomic behavior and thus expedite genomic change. Further, you have listed a number of credible connections between higher and lower phyla (or commonalities between higher phyla) that indeed strongly suggest common genetic history.

 

On the second question, you have suggested that the fossil record is incomplete (since there are areas where we have reason to believe that it is) and that that lack of "randomness" in the serial genomic changes would allow for a compressed time requirement for the creation of the diverse phylogeny that we see.

 

My core question is this: If the genomic alterations are as complex as they seem, including known genomic machinery (off the top of my head) such as:

 

1) Alternative splicing of gene exons by multiple alternative splicing mechanisms

2) Transposons

3) Retrotransposons

4) Multiple mechanisms for gene duplication

5) Chromosome crossover

 

Why do we assume that genomic alterations are mutations? Wouldn't it be reasonable to leave open the possibility that there are drivers in the parent species that make specific genomic changes highly likely? If the genomic cellular machinery is as complex as we believe it to be, why not allow for the existence of "protogenes" in the genome of the parent species, that will actually proscribe the speciation of the daughter species? In this model, the speciation of the daughter species would not have to be selected.

 

Further, biological machinery, particularly protein machinery, has very highly specific actions. The greater the reuse of parent species genomic material to generate future biological mechanisms unrelated to their original use, the more likely it is that the daughter species usage was proscribed in the parent. If a highly specific building block can be used in two very different ways, this is only evidence of genetic heritage. It argues against mutation or natural selection as a speciation mechanism.