Yes. And in fact… he did just that with Adam and Adam’s Eve … when his pre-Adam population of evolved hominids reached the right stage of development!
Would you agree that the reason species are different from each other is because the DNA sequence of their genomes is different? If so, I don’t understand why it is necessary to know exactly which DNA differences are required for specific differences in phenotype for the types of questions we are asking. If all DNA differences between species are consistent with what we would expect from evolution then it would follow that the DNA differences responsible for physical differences would be among those.
Not completely as I know of a specific instance were gene expression levels are dependent on a small molecule not generated by DNA. Others are claiming more cellular action independent of DNA.
This has not been well established because as mentioned before the signal must be isolated from the noise.
That is actually true of many genes. One of the classic examples if the lac operon in E. coli where gene expression is dependent on the presence of lactose and glucose. However, the ability of organisms to change gene expression in response to molecules found in the environment is dependent on the DNA sequence of their genome. If you mutate the lac operon then you change the pattern of gene expression in response to lactose. In the end, it still boils down to DNA sequence.
But the signal has been isolated from the noise. There is a thread over at BioLogos discussing this very topic:
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This is not true for eukaryotic cells. Small molecules independent of DNA are mission critical for gene expression and also protein action.
This study does not address the signal which is mutations that cause change vs neutral mutations.
If you mutate those genes and proteins then they will respond differently to those small molecules. This is true of both eukaryotes and prokaryotes. It still boils down to DNA sequence.
For example, lipopolysaccharide (LPS) is a molecule found in the cell walls of bacteria, and when it binds to the TLR4 receptors on your immune cells it sets off a whole cascade of gene expression. Mutations in the human gene for TLR4 changes the immune systems reaction to LPS.
This is true throughout the genome. The proteins and small chemicals that interact during embryonic development are just as dependent on DNA sequence.
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If you mutate the genes so the small molecule cannot bind the organism will die.
Lac knock out strains of E. coli do just fine. They don’t die.
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Most likely it would be neutral, than occasionally detrimental or beneficial. Lethality for this would be relatively rare.