Annoying Creationists
If you think that the ancestor gene for hemoglobin was not formed by random point mutations and natural selection, how was this gene formed? If you think that ancestor protein for hemoglobin formed first, how was this protein formed? Then how was the gene for this protein that now exists formed from this protein?
Paul, are you ever going to post your data that shows the generations for convergence increases linearly with genome length when you use a mutation rate fixed to a given number of bases?
Would somebody give that whimpering crybaby Adequate a bottle, maybe that will calm him down? (Not you Delphi)
If the mutation does confer an immediate advantage it should select for that organism and will increase the likelihood that this mutation will be passed to future generations whether it improves function of the gene or improves control of the gene. The frequency of occurrence of a helpful mutation should increase in the population. If the mutation doesn’t offer an immediate selective advantage and neither helps nor harms the reproduction of that organism, the frequency of occurrence of that mutation should not be increasing in the population. If the mutation is harmful to the organism, the organism will be selected out of the population and the frequency of that mutation will decrease in the population. Neutral mutations by their very nature can not be acted on by natural selection. You don’t have selective pressure to increase their frequency in the population in order to make more complex genetic structures. Wasn’t it Richard Dawkins who said natural selection doesn’t have any long term plans?Kleinman said:So how does complex chemistry select for a particular random point mutation that doesn’t offer an immediate selective advantage?Paul said:Perhaps it does offer an immediate advantage, if the binding controls some gene expression in a more optimal fashion. Or supresses some other molecule that in turn controls a function. Or, maybe it doesn't offer an immediate advantage, but doesn't cause any harm either.
Paul, this is one of the reasons why I think the theory of evolution is nonsense. Living things have a tightly bound interaction between DNA and proteins. Both forms of molecules are required to form one another. Evolutionists are forced to take contorted positions like saying that RNA was the initial molecular form that formed the DNA and proteins.Kleinman said:Dr Schneider has demonstrated how binding sites can be formed, albeit it occurs at a profoundly slow rate, how do you form the ancestral single-function molecule that gives rise to the descending molecule? What is the selection process that would allow random point mutations to generate such a gene? What form can natural selection take that would allow bases to be assembled to form this ancestral single-function molecule? In the early stages of the formation of this ancestral gene, what would select for the first 200 bases of this gene without there being a selective advantage for this sequence of bases?Paul said:Why do random point mutations have to create the gene? How do you even know whether the gene or molecule came first? And why did you skip this part:
If you think that the ancestor gene for hemoglobin was not formed by random point mutations and natural selection, how was this gene formed? If you think that ancestor protein for hemoglobin formed first, how was this protein formed? Then how was the gene for this protein that now exists formed from this protein?
Bolding was added by Paul. Ross Hardison is speculating on the function of Hemoglobin. Hemoglobin does much more than bind oxygen, it also binds carbon dioxide and carbon monoxide and perhaps other molecules as well. The binding of theses molecules is dependent on their respective partial pressures. If Hardison’s speculations have any reasonable basis, then how many amino acids are required in the primitive protein that caged the metal atom? And how do you select for the bases to form this first gene to make this primitive protein?Ross Hardison said:The compromise was a chemical one. It appears that the apparatus that sequesters oxygen in cells, possibly to protect them, is almost identical to the one that, in different contexts, exploits oxygen for its energy-generating potential. At first this apparatus was quite primitive, probably limited to a caged metal atom capable of binding oxygen or tearing away its electrons, which are used in metabolism. But this basic chemical apparatus grew increasingly complex through time and evolution. At some point the metal atom was fixed inside a kind of flat molecular cage called a porphyrin ring, and later that porphyrin ring became embedded in larger organic compounds called proteins.
Paul, are you ever going to post your data that shows the generations for convergence increases linearly with genome length when you use a mutation rate fixed to a given number of bases?
Would somebody give that whimpering crybaby Adequate a bottle, maybe that will calm him down? (Not you Delphi)
