Protein evolution

Tazimus Maximus suggested adding the evolution of protein structural domains to the thread on gross structural mutations. Since this is a huge topic I think it deserves a thread of its own.So just what is so special about the homoeobox? What use is half a zinc finger motif?Should we just go the whole hog and start a thread about the evolution of regulatory elements to run in parallel as well?

Hi WK
You could try to separate regulatory sequences into their own thread but I think the threads would end up getting mixed anyway. Some changes in Hox related phenotypes are due to regulatory element changes but this also tells you something about the protein..or at least timing or amount of expression. I would lump them together until it seems like the thread is off topic.

I do not have a great deal of time but maybe this can get the ball rolling. The co-opting of structures for different, new of novel purposes with subsequent selection and selective pressure on the structure to fit the new use is a well defined aspect of evolution. The same apparently happens to proteins and metabolic pathways, for example the relationships between blood clotting and the primative defense mechanisms in horseshoe crabs and other arthropods. The relevance to Wounded Kings topic is in teh evolution of new protein families.For quite some time Tranquility Base has made claims that protein families arrise with no real evolutionary mechanism to support their arrival. My comment was that new families arose form novel re-arrangements of more elemental protein domains. As an introduction here are two sites that provide information on the movement of protein domain containing exons with the potential for rearrangement and the generation of new protein families.
The first is a general overview by Lynn Caporalle concerning potential molecular strategies for evolution. THe second is more specific to the evolution of protein domains and the potential for recombinantion of exons and domains for the genreation of new protein families as well as the use of these domains to try to generate relationships and learn more about the earliest life forms.That should be enough to kick-start this discussion.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

This, too, hot off the press: abstract of Lev-Maor, et al., Science, 300, pp 1288-1291 (23 May 2003)And from the companion news article in the same issue:

An important point associated with this issue is the complexity of specific genes. A recent review paper highlights the fact that it is not neccessary to evolve a novel gene for every aspect of a cellular network. The incorporation of a specific interaction domain into an already existing protein may be sufficient to introduce novelty into a signalling network.This has a significant impact on the popular conception that more genes are required for more complexity. Obviously an increase in the complexity of a gene and subsequent interconnectedness of the gene network is also sufficient to increase the complexity of a system.
Pawson T, Nash P.
Assembly of cell regulatory systems through protein interaction domains.
Science. 2003 Apr 18;300(5618):445-52.[This message has been edited by Wounded King, 06-06-2003]

Notice however you noted "signalling" (network). The change of a gene or its modification or "evolution" is a material thing not only a photon or its logically equivalent for the purposes of information transfer. If the notion of phenotype and genotype is only a German prediliction then the dilligent could think as per any genetic (DIVISION) (the DNA equivalent (also chemical and not mere light)that the orthogonality of that domian testing may not but form the network and NOT provided evidence of transmission itself) particularly if the gene flow produces no individual variation that was but a radom flucutation but the ossilation between the interpretation of the NUMBER of genes and the sign vs symbol nature of the interaction perhaps WITH light could support your reasoning.It is true however that one finds indeed that there is a need to stress the componentability of sequences and not the division only of the "gene" as a linear construct chromosmally. Still the "transduction" materiality may have been unspeicifed by this bare logic of a process you called good attention to.

I wasnt specifically thinking of signalling as in intercellular signals and signal transduction, ie for photoreception. I was also thinking of intracellular networks where downstream effects of differential gene expression can be considered a signal being introduced to the gene network.

quote:

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I wasnt specifically thinking of signalling as in intercellular signals and signal transduction, ie for photoreception. I was also thinking of intracellular networks where downstream effects of differential gene expression can be considered a signal being introduced to the gene network.

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You are correct, I did think that I had left out the case of the electron vs the photon and indeed in that case as well I comment in the same artery...When 'we' speak of "downstream" one EITHER has to have a known or unknown committment to a Waddingtion kind of relation of language and development or esle some kind of post IT mentality to which I do not deny that you neither both which to disposses nor find undue assocation linguistically with but i now preety much think that divisions of differentiation and expression concepts that this kind of post-operon cell biology finds accessible cardinally is not not sufficent to EXPLORE the possibility in the same sense for electrons as I noted for photons previously.What I meant was that there is NOT a problem, and I agree entirely with you on the MATERIALITY REQUIREMENT for transmission of any signal across generations and in this case you are highlighting the temporal involvement of this strigency on the affordance of any transparency that may remain. That is all to the good and I agree with you in the writing you have produced to that effect but introduceing a substance, in this case the downstream expressed gene product, and that being actually "a signal" are differnt things even if there is not a probelm if they are not. In pre-mole bio one had to think of mutations that are beneficial or not etc... But I would agree indeed that it may be signal to "the gene network" and yet I can concieve a hypothetical possiblity such that NO distinction in the transduction of thIS signal is necessary across the archteture of the network as nodally attached to the cell's collected in the process of the research.Specifically,let me take the case of capsases and endonucleases as proximality essences involved in cell death and note that perhaps a quantum mechanical investigation will show the same affordance for both sturctures with differnt degrees of opacity (that is the lingo I would have used in the document)due merely to differnt electrotonic functions such that merely changeing from capsase 1 to 11 or 3 to 9 or Ca vs Mg dependent DNA clevers DOES not change the node the "signal" materially moves about and yet this position could create a testable genetic hypothesis. For instance, there are TWO synergid cells that pollen must pass the graped wrath of enroute to a egg of which 3/4 may have already died from cell death. If there is a correlation between meiotic cell death position and the PLACE of cell death on entry of the pollen towards the zygote then indeed as you said a mutated new downstream gene product could enhance fitness assocaited with the kinetic activity of the pollen perhaps transported dynamically by insects such that not only could co-evolution change but if the it is only a matter of different electrotonic functions of the participating up and down stream endo nucleasus and capsates then the DIRECTION of the torque on the dielectrics involved should Maxwell's displacment current be constinutive as well is remanded when not other more simple consequences. Also of course there would be likely benefits for medical research when not also medecine.no, I did not misunderstand you I just thought you might try to think about what an orthogonal participation of parrallel computation may have to the notion of the signal within the peptide and not without it. Of course the THEORY may be wrong but the hypothesis is testable. Thanks again.

eh?

Don't worry about it - this isn't the first time Brad's posts have managed to totally escape the clutches of clarity.I wonder if perhaps Brad has a kind of aphasia or something.

There is an online pre print version available of an absoloutely mammoth review of the evolution of regulatory sequences in Molecular Biology and Evolution. At 150 pages I havent quite managed to wade throught the whole thing thing yet but it looks fascinating.
Wray GA, Hahn MW, Abouheif E, Balhoff JP, Pizer M, Rockman MV, Romano L.
The Evolution of Transcriptional Regulation in Eukaryotes.
Mol Biol Evol. 2003 May 30

If you understand the TRANSITION between 1 and 2 Corinthians then you are aware that there may indeed be a difference of spirtual and physical death PREcisely as Paul suggested (or not). Regardless of the theology, its potential mere existence is a BROADER frame from which to think about the issue of cell death whether or not the comptuer analogy/metaphor of "programmed" CONTINUES to hold up as Wolfram's "intution" (Sic!) is technisized in InternetII etc, so that when it comes to evaluating if perhaps the Maxwell IDLE WHEEL (which if true would be the cause of confusion about the Demon asleep at the switch, you can not switch BACK the moleuclar motion of gas but the probabilties my be SEQUENCED differently in prior time if..) IS a MITOCHONDRIA (hence Margulis may be shown possibly genetically to be mistaken endosymbiotically for another arms race that did not exist...)the DEATH FROM WITHIN that correctly criticized the transmission of information IN LIFE across the gap of generations may depend on a language construct closer to theology than the competition of bacteria but FIRST a PRIOR NATURAL SELECTION OF DEATH would have to be shown IN NATURE (for sufficency but this is more stringent than necessity)short of a discontinuacne of Wolframs explanation of lack of optimality in biology. That is a large project and even formulating it logically correct is difficult. I hope that worked. Instead I may need to explain how I am using Topobiology to create the first empirical approximation rather than leaving the cusp in the fold. But REGULATION need not be operative category of thought here for programmed cell death only an arthemetically increased geometric overlap that is not supported topologically in any incidence THAT IS FORCED. Crashfrog please try to learn to only say things that are nice"". I was annyoed when I read and heard pretty much Mayr tell me the same. But indeed I am trying to solve the whole problem and not just the part about why I do not have a job solving it.

Another interesting paper, this one shows the previously noted relationship between substitution rates and the number of protein protein interactions a protein can take part in. The relationship appears to be a fairly linear one with more protein protein interactions corresponding to less substitutions.Fraser HB, Wall DP, Hirsh AE.
A simple dependence between protein evolution rate and the number of protein-protein interactions.
BMC Evol Biol. 2003 May 23A simple dependence between protein evolution rate and the number of protein-protein interactions | BMC Ecology and Evolution | Full Text

An interesting but short review, in contrast to the last one, in 'Science' on the evolution of proteins. The review discusses why early evolution of protein classes ab initio has been replaced by a prevalence of duplication and divergence or recombination as major mechanisms of protein evolution.Chothia C, Gough J, Vogel C, Teichmann SA.
Evolution of the protein repertoire.
Science. 2003 Jun 13;300(5626):1701-3.

This one is very interesting. Hybrid inviability, and therefore reproductive isolation, between D. melanogaster and D. simulans, is attributable to variations in one gene encoding a nucleoporin protein. The mutations leading to the hybrid inviability appear to have been positively selected for. I wasn't sure if this was better suited for the protein evolution or the speciation topics, but I am very sad and want to get the protein evolution thread up to 15 messages.Presgraves DC, Balagopalan L, Abmayr SM, Orr HA.
Adaptive evolution drives divergence of a hybrid inviability gene between two species of Drosophila.
Nature. 2003 Jun 12;423(6941):715-9.