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» ISCID Forums   » General   » Brainstorms   » What comes after detecting design? (Page 2)

 
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Author Topic: What comes after detecting design?
Pim van Meurs
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Icon 1 posted 21. June 2003 18:07      Profile for Pim van Meurs     Send New Private Message       Edit/Delete Post 
Mike:

quote:

There is nothing contradictory here, as most regular orthodox scientists don’t employ Darwinian theory in their research. We need to remember that most biological research is carried out with little or no dependency on origin views.

So it was not contradictory but then it was perhaps a non sequitur or strawman. What do you think Mike?

Of cources biologicl research does not deal with origin views but then neither does Darwinism.

But it did seem to be a bit contradictory that on one hand it was suggested that (Darwinian) biology would not have been interested in pseudogenes and yet it was the same (Darwinian) biology (after all little makes sense in biology without the Darwinian theory...) which found these problems. Certainly no need for "intelligent design" for pseudogene research to happen.

I think that was the real lesson to be learned here.

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John Bracht
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Icon 1 posted 21. June 2003 20:58      Profile for John Bracht   Email John Bracht   Send New Private Message       Edit/Delete Post 
RBH said

quote:

One or two remarks on Ryan's posting seem warranted. He suggested that pseudogenes do not warrant much attention in a 'Darwinist' approach, but then notes that there are recent examples of functions found to be associated with pseudogenes. That seems contradictory unless it was ID-based research that found the functions. As far as I know, it was regular orthdox scientists who found those functions.

At least in the case of the Hirostune paper (Nature, 423, May 2003, pp91-96), the pseudogene function was found by accident, when an attempt was made to introduce a transgene which implanted itself into the functional pseudogene, thereby disrupting its function and giving a phenotype.

An intelligent-design based science may well have come across this function much sooner because it would have been much more open to the possibility of pseudogene function and much less likely to dismiss all pseudogenes as evolutionary relics with no function. Indeed, in this case one can cogently argue that Darwinism served as a science-retarder by inhibiting studies of pseudogene function. It took the fotuitous discovery by accidental disruption of the pseudogene before its function came to light. Who knows how much sooner pseudogene function might have been discovered if biologists took a design approach?

John

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Rex Kerr
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Icon 1 posted 22. June 2003 06:35      Profile for Rex Kerr     Send New Private Message       Edit/Delete Post 
My sense is that it is an intuition about design that tells us that pseudogenes are not important. After all, if the purpose of a gene is to make RNA to make a protein to perform some enzymatic or structural function, then a gene that cannot make RNA that yields a functional protein is "broken" and can be neglected.

However, if the apparent design is cause by selection of a bunch of random stuff that just happened to work, then you can't be so sure.

Anyway, it could easily be argued either way in retrospect. I'm not sure we can answer the question of which method is more productive without viewing the results of design-embracing vs. conventional research. Since there is not much design-embracing research going on, apparently, it's pretty hard to judge right now.

However, as a personal note, one of the things that has infuriated me the most about biological research is that things don't work the way they ought to. Biology has overwhelmingly seemed to me to be a huge bunch of stuff, with few crisp guiding principles, and tons of messy details. I'm therefore skeptical that design, even if true, is going to help much at all. It has been my experience that you simply have to go in, in every case, and do the experiments. Weird stuff will happen now and then, and you'll have to deal with results that you never could have anticipated (but perhaps make some sort of sense in hindsight). With design as a principle, you'll still have to do the experiments, and you still won't be able to anticipate things.

So I wouldn't expect there to be a whole lot of difference in how fast we acquire biological knowledge regardless of our point of view--unless we rule out huge classes of experiments because it "couldn't happen that way", and ignore the evidence that it does.

[ 22. June 2003, 06:41: Message edited by: Rex Kerr ]

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Stephen Wright
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Icon 1 posted 22. June 2003 12:12      Profile for Stephen Wright   Email Stephen Wright   Send New Private Message       Edit/Delete Post 
Andy,

The example regarding rock placement is sufficient design to generate a healthy invoice from a landscaper. However, I was intending without being clear, a more restrictive design definition. In this more specific sense a design should be useful as a response to a challenge. It would solve a pressing problem or communicate an important message. Blending-in, while sometimes a desirable plan of behavior, is not new or creative. IC criteria from Dr. Behe, in my limited understanding, would also require an inner cohesion to the design so that removing a single rock would disrupt any emerging functionality.

My reading of Darwin’s statements seem to draw a line from an organism’s behavior to changes in the physical and neurological systems. Further, the connection to these behavioral patterns and associated physical differences is seen as “an inherited effect”. Maybe you have a more in depth viewpoint on Darwin’s intent.

Speculating only, I would put forward the idea that the information processing systems of an organism’s body have an ability to transmit some small representations of life, as experienced, into the state of its genetic information. It would explain the extreme coordination of behavior, environmental influences and physical form, we observe in nature. I would be curious to know if there is research done to show it "couldn't happen that way". A infinitesimal trickle of information could have a significant effect in the success of a species, especially one in habitat crisis.

I would have no evidence for this

[ 22. June 2003, 12:20: Message edited by: Stephen Wright ]

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Ryan Huxley
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Icon 1 posted 23. June 2003 17:06      Profile for Ryan Huxley   Email Ryan Huxley   Send New Private Message       Edit/Delete Post 
As much as I've enjoyed this thread, work has me swamped right now so this may be my last post for a while (as if I normally post much anyhow - LOL). [Wink]

Andyg:
quote:
I think Ryan's discussion of "Junk" DNA and introns is not really focusing on what I intended, as it seems he's still wonderng whether these could be shown to be consistent with design or evolution.
I don't deny that there may be some pseudogenes that are exactly that - junk. But, there may be others that are not - it's just we've not yet discovered their function. So, your inference that I'm not sure whether pseudogenes are designed are not is correct: it will depend upon what research discovers should pseudogenes be investigated more thoroughly. The main idea I have here is that it may be premature to claim something is junk when we're still in the beginning stages of understanding ALL aspects of how DNA works and functions.

Andyg also brought up another question regarding ID related investigation/research. I've seen this type of question before in other threads. There seems to be the feeling by some that ID is going to "throw out the window" the way we currently do scientific research. I don't think that's the case. The scientific method that allows us to isolate, to the best of our ability, the variables we're interested in will still be the main "nuts and bolts" of research. IMO, what makes ID "revolutionary" (apologies for cliches) is that it will allow us to ask different questions or explore areas we hadn't thought of previously because of our bias against design. So, by and large, I don't imagine the "nuts and bolts" of scientific research will change that much - but the avenues and questions we ask may change drastrically. It's because of new insights in these areas that, potentially, drastic increases in understanding could be made.

(Aside personal note - For those so quick to think I'm making assertions, notice the conditionals I put in there - I did that before on another comment yet was pounced upon, which is fine; but I think that drags the thread as now I'll desire to reply to the mischaracterization of my comments.)

RBH:
quote:
Finally, Ryan commented that it might be helpful to assess how astronomy and cosmology have been changed in light of anthropic considerations. As far as I know (and that's not very far!), the various anthropic proposals have produced no significant or even visible alteration in the ways astronomers and cosmologists actually do research, nor to my knowledge has there been significant effect on the research questions they address. I'd welcome more informed comments, though.
I'll say at the outset that I'm certainly no astronomer - but, I'm at least a bit familiar with this topic. RBH may not be aware of the recent book (not yet published - so, it's no surprise if RBH isn't aware of it) by Guillermo Gonzalez (Astronomer) and Jay Richards - "The Priveleged Planet" - which utilized ID principles to do research. Based on their ID bias, they studied the correlation between habitability and measureability; in other words, it seems that the earth is situated for both allowing survival of life while also being in a great place to make observations of the universe.

But, probably a better example (and more to the point I was making regarding ID allowing an increase in understanding) would be to go back in time a bit. In the early 1900's, Einstein's equation indicated that the universe had a beginning (we now refer to this as the Big Bang theory). The reigning view of the day (I'm not 100% on this, but fairly certain) was that most thought the universe was eternal. As people became aware of the implications of Einstein's equations regarding a beginning (including Einstein himself), there was much resistance to it - but on philosophical grounds rather than scientific. Consider this quote from Sir Arthur Eddington, an astronomer contemporary with Einstein:

quote:
Philosophically, the notion of a beginning of the present order of Nature is repugnant . . . I should like to find a genuine loophole (Astronomer Sir Arthur Eddington, Nature, 127 [1931], p.450.)
In fact, many theories were proposed (e.g. steady state; etc.) to avoid the Big Bang theory on philosophical grounds. Here’s another more recent example:
quote:
The biggest problem with the Big Bang theory of the origin of the Universe is philosophical - perhaps even theological - what was there before the bang? This problem alone was sufficient to give a great initial impetus to the Steady State theory; but with that theory now sadly in conflict with the observations, the best way round this initial difficulty is provided by a model in which the universe expands from a singularity, collapses back again, and repeats the cycle indefinitely. (Gribbon, John "Oscillating Universe Bounces Back," Nature, 259 pp 15-16, 1976)
It wasn’t until the COBE satellite in the early 1990’s provided overwhelming evidence, and then the more recent WMAP project, that the Big Bang was essentially accepted by most astronomers. (In fact, 1965 was when evidence began to mount for the Big Bang that caused theories like “steady state” to be abandoned.) That’s several decades (at the very least) worth of research that was inhibited for philosophical reasons. The anthropic principle didn’t arise in the literature until the 1960s, but now includes aspects of Big Bang theory (i.e. the “bang” has to be just at this rate or else atomic elements move apart too quickly or too slowly to form the necessary elemental abundances we now have and need for life).

So, we do have examples of how things changed after “design" types of theories became more readily accepted. Notice that the methods used are still essentially the same, but the questions asked and avenues of research have changed. So, to say that the pseudogenes were found using the normal methods of research isn’t going to take away from what I’ve suggested; as John Bracht mentioned, it was by accident that this function was found. While origins are not utilized in the day to day workings of research, they have an impact on what areas or avenues we choose to study in the daily routine.

Additionally, to clarify what I meant regarding studying pseudogenes may not be likely under the Darwinian perspective, here’s what I imagine a scientist would say who held to Darwinian theory: “I’d like to get a research grant to study “junk” ( i.e. pseudogenes), and this “junk,” from my overall understanding and perspective (i.e. Darwinian perspective) serves no purpose in the future but is a relic from the past.” Would that scientist get funded?

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andyg
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Icon 1 posted 23. June 2003 20:47      Profile for andyg         Edit/Delete Post 
Ryan wrote:

quote:
IMO, what makes ID "revolutionary" (apologies for cliches) is that it will allow us to ask different questions or explore areas we hadn't thought of previously because of our bias against design.
That was my purpose in starting this thread in the first place. What are these questions or areas going to be? I am assuming that, in this hypothetical world we develop a reliable way to detect design. We then have in our hands evidence that, say, the E. coli flagellum - or at least part of it - was designed. Where do we go with this information? Do we ask when the design event occurred? Do we ask if there are common themes between the designed objects? Do we try and discern the identity of the designer from the design? Or what?

I am asking these questions because I genuinely do not have any clue myself. Perhaps I'm starting from a wrong assumption in believing that the first breakthrough of the ID field will be to reliably detect design. That seems to me to be where most of the effort in ID is occurring at the moment.

Perhaps a more general way of asking the question is this: What will be the first big breakthrough in ID, and what will come after it?

AndyG

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Ryan Huxley
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Icon 1 posted 07. July 2003 16:07      Profile for Ryan Huxley   Email Ryan Huxley   Send New Private Message       Edit/Delete Post 
Sorry it's taken so long for a reply - work has still had me swamped (including the weekends). This may be my last post again for a while as the fires keep on coming...

AndyG:
quote:
Perhaps a more general way of asking the question is this: What will be the first big breakthrough in ID, and what will come after it?

What's really being asked is what does the future hold? Well, if I had the ability to forecast the future, you can bet I wouldn't be doing structural engineering. [Wink] But, joking aside, this is a good question. Since I don't have my finger on ALL the various areas in the ID movement, I can't claim any authority (can anyone?) on what I think would be the first "breakthrough" for ID. Based on my own interests and a few recent findings, maybe it will be in the area of origination of redundancy (I've been involved with a few threads on ISCID on this topic in the past - no time to track down links now) or perhaps in pseudogenes or perhaps in other molecular machines similar to the bacterial flagellum. It could be a more empirical method for detecting design, as you've suggested. I would agree that a fair amount of effort is being put forward in this latter area. Though, I know some people are beginning to already employ design frameworks to look at biological issues (myself included - i.e. redundancy). Time will tell.

I wonder if one were to track what occured with the eventual acceptance of the Big Bang may provide some ideas. I think that with the Anthropic Principle, people began to look more carefully at various parameters (some independent, some not) and their relationships to each other regarding their affect on providing the necessary conditions for life. So, perhaps some areas of biology will begin to consider things from an engineering perspective - because if design is correct in some areas, biologists need to start thinking like engineers (I think John Bracht may have said this at some point).

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Pim van Meurs
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Icon 1 posted 08. July 2003 11:48      Profile for Pim van Meurs     Send New Private Message       Edit/Delete Post 
Ryan: Though, I know some people are beginning to already employ design frameworks to look at biological issues (myself included - i.e. redundancy). Time will tell.

Cool, there is quite a bit of research on the issue of redundancy and more relevant to biology degeneracy. While redundancy seems to be a more common intelligent design concept, degeneracy appaers to be more common a concept found in scale free networks such as proteins, genes etc.

Some useful links

Degeneracy, Redundancy & Complexity in Biological Systems & Their Measures
Qing-jun Wang


Statistical Physics, Biological Information and Complexity

Self organized networks

Systems biology through the back door: function, evolvability, and collaboration in software systems and biochemical networks Chris Myers
Cornell Theory Center


Degeneracy and complexity in biological systems Gerald M. Edelman* and Joseph A. Gally

I believe that the concepts of self organized networks, scale free networks, degeneracy and robustness are intricately related properties. The observations that RNA and perhaps Protein networks are characterized by few very common structures and many uncommon, with the common structures distributed throughout sequence space (neutral evolution) and close neighbors of other structures seems to make for some interesting research.

I am looking forward to your contributions in this area since I am working on some of my own here.

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peter borger
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Icon 1 posted 09. July 2003 02:16      Profile for peter borger   Email peter borger   Send New Private Message       Edit/Delete Post 
Degeneracy of the genetic code may not be genuine, and the term was only coined since we couldn't imagine a function for it. Dr Caporale (and others, including myself) point out that for instance the degeneracy of the genetic code may serve a timely and/or spatial function with respect to expression patterns. Synonymous codons (several codons specify for the same amino acid) may thus not affect the aminoacid sequence in the protein but it may affect the binding of regulatory proteins to the DNA that coordinate gene expression spatially and timely. As Caporale put it: "call me tonight" means contact me by phone at 7 pm, while "phone me tonight" means contact me by phone at 9 pm. So, as long as we don't understand this yet, I'd prefer not refer to the genetic code as degenerate.

PB

[ 09. July 2003, 02:22: Message edited by: peter borger ]

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Rompecabezas
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Icon 1 posted 09. July 2003 10:12      Profile for Rompecabezas   Email Rompecabezas   Send New Private Message       Edit/Delete Post 
quote:
The main idea I have here is that it may be premature to claim something is junk when we're still in the beginning stages of understanding ALL aspects of how DNA works and functions.
That's absolutely true, Ryan. On the other hand, it's just as premature to claim something is designed at this stage.

This Darwinist has always been rankled by the glib notion of 'junk DNA' as well. If most of our genome is junk, I'd expect that natural selection would streamline the system in some way. I'd never expect that billions of completely useless nucleotides would keep being duplicated constantly. I'm encouraged to see that some function can be attributed to non-coding DNA.

However, I don't hear anyone proposing that there is no such thing as junk DNA. There seem to be long stretches of DNA that are of no use to anyone except forensic detectives.

This brings us back to a point about the 'design perspective': how much truly useless DNA is allowable under your design assumption? There must be some threshold beyond which it is more likely that the design is not the product of intelligence but purposeless mechanisms.

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Argon
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Icon 1 posted 09. July 2003 10:42      Profile for Argon   Email Argon   Send New Private Message       Edit/Delete Post 
peter borger writes:
quote:
Degeneracy of the genetic code may not be genuine, and the term was only coined since we couldn't imagine a function for it.
I wasn't aware that the term "degenerate" as applied to the genetic was coined for that particular reason. I thought it was used to describe the fact that multiple codons could be translated into the same amino acid.

It's been known for several decades that some variations in codon usage affect translational efficiency and even serve in regulatory functions. For example, the relative abundances of different tRNAs for a particular amino acid can affect protein expression. Palindromes which form loop structures in RNA, depend on matches between specific sequences and thus could limit codon substitution. And as Peter mentions, specific sequences are known affect binding of regulatory proteins.

But the fact is, the genetic code is degenerate, in so far as the term "degenerate" is appropriately and commonly defined in this context. That specific codons may have additional roles in gene expression is another issue: The neutrality of codon substitution. And even in this regard, many (most?) codon substitutions have no apparent effect on the organism. Note also that mutations in protein coding sequences typically accumulate more often the third (& most degenerate) base in codons.

[ 09. July 2003, 10:44: Message edited by: Argon ]

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peter borger
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Icon 1 posted 09. July 2003 19:16      Profile for peter borger   Email peter borger   Send New Private Message       Edit/Delete Post 
I can think of several possible functions for alleged junk DNA:

1) structural

2) stabilizing mRNAs (for instance pseudogenes)

3) regulatory

4) damage repair

5) spacers for positioning enhancers

6) to hide identical sequence so they do not recombine out of the genome (for instance DNA flanking tRNA genes)

7) variation induction (mobile elements)

8) ensure 'fractal' properties of DNA (see Ramon-Roldan)

...and probably much more we are not aware of.

PB

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peter borger
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Icon 1 posted 09. July 2003 19:40      Profile for peter borger   Email peter borger   Send New Private Message       Edit/Delete Post 
quote:
But the fact is, the genetic code is degenerate, in so far as the term "degenerate" is appropriately and commonly defined in this context.
Is it degenerate or is is simply the best design for error buffering in protein coding DNA elements? Including the fact that some DNA elements require alternative codons. If we only find one such gene this would invalidiate the general assumption that the code is degenerate. As a matter of fact such genes are around. For instance the calmodulin genes (CALM1-3). Three genes in the genome that code for identical proteins (even in all vertebrates they are identical), but due to the design of the genetic code can spawn several different mRNA's, that specify where and when the protein has to be expressed (for review see: Toutenhoofd & Strehler).

PB

[ 09. July 2003, 19:42: Message edited by: peter borger ]

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Pim van Meurs
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Icon 1 posted 10. July 2003 00:54      Profile for Pim van Meurs     Send New Private Message       Edit/Delete Post 
Peter, I fail to understand your hesitation to accept the observation of degeneracy of the genetic code. Degeneracy is a well defined concept that says nothing directly about the origins of the genetic code, it merely describes a feature.
Ofcourse there are two interesting concepts degeneracy and redundancy and while the latter one is more common found in human designs, degeneracy seems to be prevalent in biology.
As far as the genetic code is concerned, there are some great articles about the evolution of the genetic code. In fact your suggestion that DNA may be the best design for error buffering may have some relevance in that this is what some data may suggest and in fact is not surprising if for instance selection played a role in the evolution of said code.

Your reference to "Toutenhoofd & Strehler" is somewhat ambiguous but I am quite apt at searching the internet. I guess you are refering to the paper

Toutenhoofd SL, and Strehler EE (2000) The calmodulin multigene family as a unique case of genetic redundancy: multiple levels of regulation to provide spatial and temporal control of calmodulin pools? Cell Calcium. 28:83-96.

Of course redundancy is quite different from degeneracy but may likely be a somewhat common inaccurate usage of the term

quote:

Calmodulin (CaM) is a ubiquitous, highly conserved calcium sensor protein involved in the regulation of a wide variety of cellular events. In vertebrates, an identical CaM protein is encoded by a family of non-allelic genes, raising questions concerning the evolutionary pressure responsible for the maintenance of this apparently redundant family. Here we review the evidence that the control of the spatial and temporal availability of CaM may require multiple regulatory levels to ensure the proper localization, maintenance and size of intracellular CaM pools. Differential transcription of the CaM genes provides one level of regulation to meet tissue-specific, developmental and cell-specific needs for altered CaM levels. Post-transcriptional regulation occurs at the level of mRNA stability, perhaps dependent on alternative polyadenylation and differences in the untranslated sequences of the multiple gene transcripts. Recent evidence indicates that trafficking of specific CaM mRNAs may occur to specialized cellular locales such as the dendrites of neurons. This could allow local CaM synthesis and thereby help generate local pools of CaM. Local CaM activity may be further regulated by post-translational mechanisms such as phosphorylation or storage of CaM in a 'masked' form. The spatial resolution of CaM activity is enhanced by the limited free diffusion of CaM combined with differential affinity for and availability of target proteins. Preserving multiple CaM genes with divergent noncoding sequences may be necessary in complex organisms to ensure that the many CaM-dependent processes occur with the requisite spatial and temporal resolution. Transgenic mouse models and studies on mice carrying single and double gene 'knockouts' promise to shed further light on the role of specificity versus redundancy in the evolutionary maintenance of the vertebrate CaM multigene family.

What the abstract suggests to me is redundancy in the form of three distinct cDNAs all encoding Calmodulin.

in 'Three synonymous genes encode calmodulin in a reptile, the Japanese tortoise, Clemmys japonica' it is reported that

quote:

The amino acid (aa) sequence of CaM protein is well conserved in organisms whose evolution diverged millions of years ago. Three non-allelic CaM genes encoding exactly the same 148 aa protein (17,000 daltons) were identified in the rat (Nojima, 1989 ), mouse (Bender et al., 1988;
Danchin et al., 1989), and humans (Fischer et al., 1988);

A well conserved sequence indeed

I found your article on redundant genes

I find your statement "On the contrary, the mutation-selection hypothesis would rather predict that super-conserved redundant gene families do not exist!" to be in need of some supporting arguments. Would you care to explain?

As far as gene duplication is concerned

quote:

Centrin (= caltractin) is a ubiquitous, cytoskeletal protein which is a member of the EF-hand superfamily of calcium-binding proteins. A centrin-coding cDNA was isolated and characterized from the prasinophyte green alga Scherffelia dubia. Centrin PCR amplification primers were used to isolate partial, homologous cDNA sequences from the green algae Tetraselmis striata and Spermatozopsis similis. Annealing analyses suggested that centrin is a single-copy-coding region in T. striata and S. similis and other green algae studied. Centrin-coding regions from S. dubia, S. similis and T. striata encode four colinear EF-hand domains which putatively bind calcium. Phylogenetic analyses, including homologous sequences from Chlamydomonas reinhardtii and the land plant Atriplex nummularia, demonstrate that the domains of centrins are congruent and arose from the two-fold duplication of an ancestral EF hand with Domains 1+3 and Domains 2+4 clustering. The domains of centrins are also congruent with those of calmodulins demonstrating that, like calmodulin, centrin is an ancient protein which arose within the ancestor of all eukaryotes via gene duplication. Phylogenetic relationships inferred from centrin-coding region comparisons mirror results of small subunit ribosomal RNA sequence analyses suggesting that centrin-coding regions are useful evolutionary markers within the green algae.

"Molecular cloning and evolutionary analysis of the calcium-modulated contractile protein, centrin, in green algae and land plants."
Bhattacharya D, Steinkotter J, Melkonian M. Plant Mol Biol. 1993 Dec;23(6):1243-54.

or

Hardy D.O., Bender P.K., Kretsinger R.H.;
"Two calmodulin genes are expressed in Arbacia punctulata. An ancient gene duplication is indicated."; J. Mol. Biol. 199:223-227(1988).

quote:

Calmodulin is highly conserved, and only in the sea urchin Arbacia punctulata have two distinct isotypes been reported. We have isolated and sequenced two cDNAs from a lambda gt 11 library constructed from RNA from ovary tissue of A. punctulata. One clone, designated alpha, encodes a calmodulin isotype previously designated A. It encodes an amino acid sequence that is identical with calmodulin of most vertebrates in positions 1 through 141; however, it does not encode the last seven amino acids. The other clone, designated beta, starts with an open reading frame and encodes the B form of calmodulin from position 11 through the C-terminal position 148. It has only four differences from vertebrate calmodulin, occurring at positions 78 (Asp, beta Glu), 99 (Tyr, beta Phe), 143 (Gln, beta Ala) and 147 (Ala, beta Ser). The nucleic acid sequences of the alpha and beta cDNAs differ at 46 nucleotide positions that are distributed throughout their coding sequences. We conclude that the corresponding mRNAs are not derived from post-transcriptional processing of a single gene, and we infer that they are transcribed from two non-allelic genes. The gene duplication is inferred to have occurred prior to the divergence of the vertebrates and the echinoderms. The expression of these calmodulin mRNAs in ovary tissue and eggs of a single animal differs as judged by hybridization of probes to RNA immobilized to filters.

quote:

Calmodulin (CaM), an important intracellular calcium sensor, modulates the activity of many target proteins and is one of the most highly conserved proteins in eucaryotic cells. CaM has four binding sites for calcium and arose by gene duplication and fusion. CaM proteins are encoded by three nonallelic mammalian genes that differ in the promoter region and in the 5'and 3'- untranslated regions ( UTRs ). To ascertain whether this multi-gene one protein system exhibited in mammals extends to all vertebrates, a bioinformatic study of the expressed sequence tags (ESTs) of the available DNA sequences of fish was done. At least three genes for CaM were identified and were designated alpha, beta and gamma. Probes to the unique sequences of the 5'- and 3'-UTR of the three genes of Paralichthys olivaceus, Perca favensces and Calamaichthys calabaricus were also prepared and used with gel electrophoresis and sequencing to ascertain the presence of these genes in the different species. The beta gene was identified for the first time in Paralichthys olivaceus, and the presence of the alpha and beta enes was confirmed for Paralichthys olivaceus & Perca favensces, respectively. Genomic DNA was isolated from Calamaichthys calabaricus & examined for the occurrence of each of the genes. Probes of the three genes in fish will be useful in future studies of the role of CaM in development and differentiation.

IDENTIFICATION OF CALMODULIN GENES IN TELEOSTAIN FISH SPECIES Tamika Tyson and Grisel Muniz

and the interesting article

The early adaptive evolution of calmodulin by ML Baba, M Goodman, J Berger-Cohn, JG Demaille, G Matsuda Molecular Biology and evolution Volume 1, Issue 6, November 1984

quote:

interaction between gene duplication and natural selection in molecular evolution was investigated utilizing a phylogenetic tree constructed by the parsimony procedure from amino acid sequences of 50 calmodulin family protein members



[ 10. July 2003, 01:15: Message edited by: Pim van Meurs ]

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Argon
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Icon 1 posted 10. July 2003 10:51      Profile for Argon   Email Argon   Send New Private Message       Edit/Delete Post 
peter borger writes:
quote:
Is it [the triplet code for amino acids - Argon] degenerate or is is simply the best design for error buffering in protein coding DNA elements?
As I said, it really is degenerate - by definition. Multiple codons can translate into identical amino acids. That's the definition of "degenerate" within the context of the triplet code.

What you are talking about is the neutrality of codon substitutions, and now, the error-handling capability of the triplet code. Interesting subjects, but distinct from what the simple definition of codon degeneracy entails.

Further:
quote:
If we only find one such gene this would invalidiate the general assumption that the code is degenerate.
It has been known for decades that some genes can be regulated by specific codon preferences.

[ 10. July 2003, 10:59: Message edited by: Argon ]

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