Discussion in 'General Science & Technology' started by S.A.M., Jul 10, 2009.
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In the gene centered theory as expounded by the selfish gene we are.
But why does it matter if the gene for say, glucose oxidation is in a kangaroo, an emu or an outback settler? Why should an extinction of any one of the three be relevant if only number of copies are important? Are we measuring fitness of the gene or fitness of the genome package?
And there doesn't seem to be any "we" here. Nobody other than you is on board with your misinterpretations.
Explain how the gene centered view as expounded by the selfish gene theory is not at the level of the gene.
Explain how it is "contained" at the level of the gene as you content is relevant.
Dawkins differentiates between replicators and vehicles [the organism being the vehicle and genes the replicators]. He does admit that genes are selected by proxy [ie the vehicle] but then maintains that natural selection at the level of the gene overrides natural selection at the level of the organism.
To me, that is nonsense, the genes are not the target of the selection process. The organisms are. Its not the best gene that survives, its the best package that is produced by a combination of genes. I also think his model ignores stuff like random gene deletion [which in one memorable instance, he describes as "a replicating entity"].
What do you mean "overrides?" The selections are one and the same.
The selection process is not "targetted." It has no mind, no will.
How are those contradictory? Doesn't the latter survival necessarily imply the survival of the gene?
And when did any proponent of the selfish gene ever contend that the fitness of a particular gene can be evaluated outside the context of its environment (including the rest of the genome)?
I don't think so. Its not the genes that die, its the organisms.
Not really. If a species goes extinct, do the genes not survive in other species?
Or "it's not the species that die, it's the organisms" Or a hundred other ways to wreck a discussion with bullshit.
The copies, versions, alleles, varieties, complexifications, and so forth, in any given organism die with it. If all the organisms that have copies etc fail to reproduce them, the gene is gone.
Genes, alleles, variations, etc, that live in more than one species often have better odds, yes. Most do. Some don't.
Nothing in there about evaluating a gene's odds of reproduction and spread outside of its environment. There are many levels of environment, some directly affecting the physical gene inside the genome within the cell, some operating at the level of solar system asteroid statistics.
I blame dogmatic theistic upbringing for that kind of "thinking". Are there other explanations available, taht fit this situation?
So how do biologists estimate the fitness of the gene?
For the genes. The organism, no matter how successful, will not survive. It's genes will.
Usually those proposing an organism-centred version of genetics tend to be closet theists operating on some variant of the moral imperative, or have difficulty attributing proportional advantage to selective systems, preferring to operate mentally on the simplistic binary survival/fail impression.
Again, how would you estimate fitness trends for a gene? e.g. the gene for glucose oxidation?
It certainly is not. Which package of genes survives? Is it transmitted intact? If so, then it operates no differently to single-gene transmission, and so falls into Dawkins' thesis. If these packages are broken up, then it has no survival except as Mendelian reconstructions.
If you want to say that a particular type needs to persist as that type to survive its environment, that would be reasonable. But novel mutations will cause variance within such systems, and some of these mutations will be beneficial, providing a mutation advantage.
Correlate increases in its frequency with the efficiency with which it oxidizes glucose.
Increases in its frequency? How would you measure its frequency baseline? Or increase thereof?
?? Yes, increases in gene frequency. Historical sampling of phenotype and/or genotype and monitoring. Experimental comparison.
Give an example of historical sampling of phenotype and or genotyoe monitoring for the glucose oxidation gene. Could you link me to a published paper that shows such instances where the gene's fitness is independent of the organism? You can show me a paper on some other gene if the glucose oxidation gene is not available. I'm interested in the methodology used.
For the future? They don't - not very well, anyway.
That's a pretty big topic, and a young science. Probably a uniquely mutated variation whose expressions directly kill its harboring organism during juvenile development is less fit than a member of the homeobox complex common planetwide in bilaterally symmetric organisms, but it's just a guess.
Well, maybe more than "just" a guess.
But if you want to do some pondering along those lines, ask yourself about the genes involved in symbiosis and parasitism and the like. Which organism is their fitness dependent upon?
This is Geoffp's area of expertise, perhaps he can help us to see how its done.
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