Last year I discussed a study of how transcription factor binding is not conserved between mice and men. Evolutionists were surprised to find that similar transcription factors in human and mouse embryonic stem cells bind in very different DNA locations. In fact, the binding sites are often so-called “lineage-specific,” meaning that the transcription factor binds to a section of DNA that is unique to that species. As one writer explained:
Remarkably, many of these RABS [repeat-associated binding sites] were found in lineage-specific repeat elements that are absent in the comparison species, suggesting that large numbers of binding sites arose more recently in evolution and may have rewired the regulatory architecture in embryonic stem cells on a substantial scale.
Rewired the regulatory architecture on a substantial scale? In other words, evolutionists must believe that although evolution had provided, in a common ancestor to mice and men, perfectly good transcription factors and perfectly good binding sites for those transcription factors to attach to, nonetheless this was all “rewired.”
They call this species-specific or lineage-specific biology, which simply means that evolution’s predictions don’t work. Evolution doesn’t help explain the findings, it is a gratuitous, unparsimonious layer added to the science. Rather then the theory guiding the science and elucidating the findings, it is the science that is contradicting the theory.
Such divergence between transcription factor binding sites even shows up in very similar species, such as different species of yeast. As one paper explains, “most of these sites have diverged across these species, far exceeding the interspecies variation in orthologous genes.” And as usual the evolutionists did not miss a step in reinventing their theory to accommodate the contradictory findings:
Transcription factor binding sites have therefore diverged substantially faster than ortholog content. Thus, gene regulation resulting from transcription factor binding is likely to be a major cause of divergence between related species.
In other words, the unexpected findings between different species become a causal mechanism for the evolutionists. The right mutations just happened to occur in both the genes that code for the transcription factors, and in the DNA to create new binding sites which just happened to drive evolutionary change to fantastic new designs. Saying this is unlikely is putting it kindly.
Another study found “large interspecies differences in transcriptional regulation” between different vertebrates which the evolutionists claimed “provide insight into regulatory evolution” and reveal “the evolutionary dynamics of transcription factor binding.” But of course the findings reveal no such thing. There were no “evolutionary dynamics” revealed by the transcription factor binding differences. That is a multiplied entity based on the dogma that evolution is a fact. Here is how one writer described the findings:
Researchers from Cambridge, Glasgow and Greece have discovered a remarkable amount of plasticity in how transcription factors, the proteins that bind to DNA to control the activation of genes, maintain their function over large evolutionary distances.
The text books tell us that transcription factors recognise the genes that they regulate by binding to short, sequence-specific lengths of DNA upstream or downstream of their target genes. It was widely assumed that, like the sequences of the genes themselves, these transcription factor binding sites would be highly conserved throughout evolution. However, this turns out not to be the case in mammals.
In all tested species, the transcription factors CEBPA and HNF4A are master regulators of liver-specific genes. By mapping the binding of CEBPA and HNF4A in the genomes of each species and comparing those maps, they found that in most cases neither the site nor the sequence of the transcription factor binding sites is conserved, yet despite this, these transcription factors still manage to regulate the largely conserved gene expression and function of liver tissue.
"By studying changes in transcription factor binding, we can understand the evolution of gene regulation," said Duncan Odom from Cancer Research UK Cambridge Research Institute and coauthor on the paper.
Once again the evolutionary textbooks are wrong, but no matter, evolution is a fact. Religion drives science and it matters.