> Pax6 is only one of thousands of genes encoding transcription factors
Last time I checked humans only had ~1800 TFs. I don’t know about “thousands”. Maybe if we count all TFs in all organisms excluding homologs...
> While geneticists have made leaps in understanding how genes with relatively simple, direct functions could have evolved, explanations for transcription factors have largely eluded scientists.
Is it that much different though? TFs bind short DNA sequences throughout the genome. These sequences don’t have to be exact, some variation is allowed. Now, random mutations can change the DNA and enable TF binding, thus increasing the fitness(since TF increasing or decreasing expression of a gene can give some advantage).
A transcription factor gene regulatory network is much more likely to arise through gene duplication and upstream transposon insertions than by random mutation - especially in plants and animals, which have long generation times, low population sizes, and proofreading processes to suppress point mutations, while also facilitating gene duplication via sexual recombination. Eukaryotes have also evolved chromatin accessibility restrictions to control not just expression but evolvability of DNA regions. Point mutations on their own don't seem like a plausible mechanism for the level of plasticity exhibited in plant and animal genomes.
Last time I checked humans only had ~1800 TFs. I don’t know about “thousands”. Maybe if we count all TFs in all organisms excluding homologs...
> While geneticists have made leaps in understanding how genes with relatively simple, direct functions could have evolved, explanations for transcription factors have largely eluded scientists.
Is it that much different though? TFs bind short DNA sequences throughout the genome. These sequences don’t have to be exact, some variation is allowed. Now, random mutations can change the DNA and enable TF binding, thus increasing the fitness(since TF increasing or decreasing expression of a gene can give some advantage).