Cellular Creativity and the Unselfish Gene

Please read messages 1 and 7 of this thread. They are the foundations of my subsequent postings.Nova

Well, I did, and they don't answer my questions.

Thinking to me is creative and that's why prayer is important to express your creativity!

Why extinctions occur has been a vexing question in Ecology.

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Our knowledge of the proximate causes of background extinctions is surprisingly weak.

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(Cockburn, A. An Introduction to Evolutionary Ecology p.275)The deactivation of the experimenter gene may be one possible route by which extinctions may occur.The first step in this type of extinction is the circulation of a virus carrying a gene that has a side effect of permanently disabling the experimenter gene. The experimenter gene is the primary source of variation upon which Natural Selection operates. Once disabled, the species virtually 'freezes' (ie becomes immutable) in the form it had when the experimenter gene was disabled.The loss of the experimenter gene initially makes the organisms more efficient, since cellular experimentation is both costly and risky. It is costly because any cell that experiences a detrimental effect from its test protein will not be as efficient as it could have been, and it is risky because a test protein could, for example, disable the cell control mechanism and lead to a potential lethal cancer.Being more efficient, those individuals of a species that have lost their experimenter gene out-compete those that have not, and the species stops evolving.Though initially more efficient, the immutable species loses its ability to adapt to the changing biotic and abiotic environment, and it gradually comes under increasing competitive pressures as the biosphere evolves around it. Eventually, the immutable species becomes extinct.The most famous example of a species that has stopped evolving is Latimeria (the coelacanth). Until 1938, when a live specimen was caught, it was thought to have become extinct 70 million years ago. What was most amazing about Latimeria was that it was virtually identical to the fossil coelacanths.

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The characteristics of this large fish were so similar to those of Mesozoic coelacanths that its systematic position was unquestionable.

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The modern and ancient fish are so similar that Latimeria was used to 'confirm' earlier reconstructions of fossil coelacanths.

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A major asset derived from Latimeria's discovery has been the confirmation of the earlier reconstructions based on coelacanth fossils.

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(McFarland, et al, Vertebrate Life p.186)How has Latimeria retained its precise Mesozoic form after of 70 million years of random mutations to its genetic material?According to the system advocated in this thread, Latimeria has not evolved since the Mesozoic because its experimenter gene was disabled in ancient times, causing it to ”stop evolving'. The similarity of Latimeria to the Mesozoic coelacanths is a measure of the relative contributions made by the experimenter gene and random mutations to the evolutionary process: when the experimenter gene is disabled, evolution virtually stops.The large number of relic species would simply not exist if all species were continually evolving into something else.Species can therefore be divided into two general categories. Those transitional species that are still actively experimenting and evolving, and those species that have become immutable but have not yet become extinct.If this is the case, then the large number of extinct and relic species may be understood as a consequence of the ephemeral advantage to a species of having its experimenter gene deactivated.

Sorry, removed my post after reading the rest of this thread.MickThis message has been edited by mick, 11-04-2005 08:56 PM

Hi Nova, All you have to do is point out a single immutable species that has stopped evolving but has not yet become extinct.ThanksMick

Hi MickEr...Latimeria...the coelacanth has not changed (ie has not evolved) in seventy million years. If people have not swept away the last vestige of their population in the Comorro Islands for scientific research, then they have not yet become extinct.

Is that true? I understand there's significant morphological differences between the coelacanth populations we see today and the populations we know from fossils.

Well that's interesting. The Coelocanth is classified as "Critically Endangered" by the IUCN, so, as you admit, they're certainly undergoing an evolutionary process (i.e. extinction). Or is there a non-evolutionary explanation for the coelocanth's extremely low population size?More importantly, can you give an example of a different species for which you can give positive evidence of evolutionary stasis? The coelocanth has never been subject to genetic analysis, so the population genetic processes operating upon it are actually completely unknown (neither in favour of your argument, nor in favour of mine).How about a species which is represented in GenBank (National Center for Biotechnology Information) or something like that?MickAdded in edit: here is what we know about the genetic processes operating upon coelocanth populations: linkAn absence of data is NOT evidence for your point of view.This message has been edited by mick, 11-06-2005 08:32 PM

FROM: Extinction: COELOCANTHS (click) So current Coelacanths are different species from the ones of the fossil record - they have evolved in the intervening time and are NOT in stasis as a species from that time.FROM: Find a Fish, Coelacanth, Latimeria chalumnae Smith, 1939 (click) There may be more to the story of the Coelacanths than we currently know, especially if they have adapted to the deep ocean from a previous shallow sea environment (where the 'protolegs' issue gets its start as evolving into amphibs, why they were of interest originally).Certainly the environmental adaptation has lead to changed behavior and feature modification over time -- again evolution of the modern fish versus the ancestral. {im(s)ao mode}: There is still no possible credible reason for hypothesising that a single specific "experimenter" gene exists. This thread strikes me as a rather mundane mental excercise in semanics for no apparent purpose.

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All we need are genes that are able to change over time in order to find (through selection processes) ones better fit for the next generation. In this regard all genes are "experimenters" and there is no need to make it a single gene. And if all genes fit the description then the concept has null value as a differentiating mechanism.

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In fact the genetic evidence says otherwise: mutations are scattered throughout the genomes of all species and are in different locations in different species. Failure to recognize this fact - and deal with it - makes further discussion on this concept pointless.{/im(s)ao mode}Enjoy.

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we are limited in our ability to understand
by our ability to understand

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RebelAAmerican.Zen[Deist
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No it is not true...there is substantial (4.1%) differences in the characterized DNA sequences...there goes Nova's assertion of stasis, genetic or morphological...note, these are just living species..not even dealing with extinct latemeria groups.Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12616-20. Related Articles, LinksTwo living species of coelacanths?Holder MT, Erdmann MV, Wilcox TP, Caldwell RL, Hillis DM.Section of Integrative Biology, Institute of Cellular and Molecular Biology, University of Texas, Austin, TX 78712, USA. mtholder@mail.utexas.eduDuring the period of September 1997 through July 1998, two coelacanth fishes were captured off Manado Tua Island, Sulawesi, Indonesia. These specimens were caught almost 10,000 km from the only other known population of living coelacanths, Latimeria chalumnae, near the Comores. The Indonesian fish was described recently as a new species, Latimeria menadoensis, based on morphological differentiation and DNA sequence divergence in fragments of the cytochrome b and 12S rRNA genes. We have obtained the sequence of 4,823 bp of mitochondrial DNA from the same specimen, including the entire genes for cytochrome b, 12S rRNA, 16S rRNA, four tRNAs, and the control region. The sequence is 4.1% different from the published sequence of an animal captured from the Comores, indicating substantial divergence between the Indonesian and Comorean populations. Nine morphological and meristic differences are purported to distinguish L. menadoensis and L. chalumnae, based on comparison of a single specimen of L. menadoensis to a description of five individuals of L. chalumnae from the Comores. A survey of the literature provided data on 4 of the characters used to distinguish L. menadoensis from L. chalumnae from an additional 16 African coelacanths; for all 4 characters, the Indonesian sample was within the range of variation reported for the African specimens. Nonetheless, L. chalumnae and L. menadoensis appear to be separate species based on divergence of mitochondrial DNA.

I'm still waiting for you to answer my questions. A review of the posts you mentioned shows nothing in them that would answer them.

Sorry to keep you waiting crashfrog...what are your questions?(ps one at a time if possible )

You quoted them in your message 31, at the top of this page.

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Your model is wrong simply because it would be too successful.
  —"crashfrog"

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Your comments and further consideration on my part have induced me to modify the original postulate for the Eureka Hypothesis:Instead of postulating that ”each cell expresses its experimenter gene when formed’, it will be postulated that ”each cell inherits the latent ability to activate its experimenter gene under particular chemical circumstances’.As I pointed out in my previous essay, cellular experimentation is both costly and risky, so it would be in the interest of a species to reduce cellular experimentation to a minimum, especially if the species had already achieved a high degree of integration with its environment. If a species has discovered a niche where it functions with extremely high efficiency, then further cellular experimentation could be more detrimental than beneficial.Also, if all cells automatically experimented on formation, a cell might yell "Eureka!!" falsely, being surrounded by cells that have been rendered relatively less efficient by the detrimental effects of their own test proteins. For the experimental process to be most accurate, (ie the minimum selection of false positives), it would be required that each actively experimenting cell be surrounded by cells expressing the standard genome so that the efficiency of the experimenting cell can be accurately gauged against cells expressing the standard basal metabolic rate.Limiting experimentation to a proportion of the cell population decreases the creative potential of the species, but ensures that the process is accurate in selecting only genes that are beneficial at the cellular level. For example, if we assume that only one in a hundred thousand cells actively experiments, then the probability would be high that each experimenting cell was surrounded by non-experimenting cells. Since "the human body is believed to contain at least 10exp 14 cells" (Lehninger p.15), then there would still be 10exp9 cells experimenting in every human being. Multiplying this by the number of people on Earth (6.2exp9) gives a total of 6.2exp18 experimenting human cells on Earth. This means that even if there is only one chance in a thousand million billion that any particular test protein will decrease cellular inefficiency, then six such new proteins will occur in today's human cellular population. This shows that restricting cellular experimentation to one in a hundred thousand cells does not impede life's ability to evolve against extreme improbability gradients.But my assumption of one in a hundred thousand experimenting cells was merely to illustrate my example. What is the proportion of experimenter cells in reality? Or is the proportion variable?If random mutations were the source of variation that Natural Selection operates on, then no control could be exerted on the rate of production of variation (and thus on the species evolutionary rate), since random mutations are unpredictable in time and space. But if, as these essays contend, the source of new genes is the experimenter gene, then the degree of expression of the gene could be directly and automatically regulated by hormonal influences generated at the level of the organism, (at least in species with a well developed endocrine system, such as vertebrates).It is reasonable to postulate that one of the stress-induced hormones (call it stress-induced hormone X) would be responsible for activating the experimenter gene, since stress hormones directly measure the integrated 'ease of living' (ie degree of adaptiveness) of the current phenotype.If an animal is in balance with its environment and is satisfying its needs and wants with a minimum amount of 'struggle', then the concentration of stress-induced hormone X will be low, the level of cellular experimentation will be low, and the species will 'stabilize' somewhat in its well adjusted form.If, however, a species is maladjusted, and experiencing stress trying to survive, then the high concentration of stress hormone X in its system will trigger a higher proportion of cells to experiment, thus giving the organism (and the species) a greater chance to evolve a somatic solution to its problems.The biosphere may thus be a mosaic of an accumulation of slowly evolving ”satisfied’ species, rapidly evolving ”dissatisfied’ species, and species that have lost their experimenter gene altogether and have become virtually immutable.Humans subjectively interpret a lack of stress and the easy satisfaction of needs and wants as ”happiness’. It has been noted in many studies that happy people are less prone to diseases than unhappy people. This may be because ”unhappy’ people are induced to perform more cellular experimentation, and thus take the risks and pay the costs involved. Unhappy people may thus be unconsciously martyring themselves for the benefit of our species.