Jeffrey Tomkins also provides Monday’s news article: Gene Control Regions Are Protected–Negating Evolution. His premise is that a recent Nature letter, Genetic recombination is directed away from functional genomic elements in mice (figures), rules out an important mechanism for the production of new genetic information for evolution:
The erroneous idea that complex genetic information in the form of genes and regulatory DNA can randomly evolve, has become more untenable with every new discovery in the field of genomics. Just this past week, a discovery published in the prestigious British journal Nature has once again spectacularly confirmed that evolution is nothing but a complete myth. While the discovery was groundbreaking, the research paper received very little publicity or fanfare in the scientific press. I wonder why?
“This past week” of course means “back in late-May.” As for why this study received little publicity it would seem that it lacked a proper press release, the source of most science stories. And Tomkins seems to have been the first to come up with the “spectacularly confirmed that evolution is nothing but a complete myth” angle – even the Intelligent Design lot seem to have missed it. I wonder why?
Tomkins explains his idea fairly well, going back first to basic highschool genetics:
To understand the importance of the discovery, a brief review on some standard biology is in order. When sperm and egg cells are formed in animals, the process of meiosis occurs to create genetic variation. This is why the offspring of two parents are always unique, except for identical twins where the fertilized egg cell splits into two embryos.
Most plant and animal genomes have two sets of chromosomes, one set from the father (paternal) and the other from the mother (maternal). Part of the process to create genetic variation occurs at the beginning of meiosis when the maternal and paternal chromosomes pair up with their similar counterparts and exchange segments of DNA in a process called homologous recombination. This means that only similar (homologous) parts of DNA can be exchanged (recombined) between the sister chromosomes.
Technically only most animal genomes are diploid – polyploidy (when there are more than just the two sets) is so common in plants it may even true for the majority. But then that’s irrelevant here.
Homologous recombination involves the exchanging or shuffling of DNA segments to facilitate genetic variability, only in a highly controlled manner. The DNA segments are typically maintained in the same order on the chromosomes and the process is only allowed to occur in certain parts of the genome. These areas where recombination occurs are called hotspots.
Now, here I have some issues. First, homologous recombination is used to repair double-strand breaks (DSBs) in chromosomes, and may or may not result in the crossing-over of genetic material. The idea that any cell process is “highly controlled” is, frankly, ludicrous. While recombination hotspots do exist (see this PLoS Biology primer, along with figure one of this paper), they do not have a monopoly on recombination. What’s more, some animals (such as Drosophila melanogaster – see, again, that primer) don’t even have such hotspots. Nothing is simple in molecular biology.
The common house mouse (Mus musculus) is one of the primary DNA model systems for animal genomes. Recombination hotspots have recently been mapped all over the mouse genome. Scientists have recently discovered that genetic recombination is directed away from sensitive parts of the genome that contain genetic control elements and features. These key parts of the genome carefully regulate how genes are turned off and on and function in precisely regulated networks.
How this is done – something that Tomkins does not explain – is that a protein (PRDM9) has been found to act to move hotspots in the genome, apparently away from gene-promoting regions. That is to say, the study authors found that mice without the protein still had hotspots (“surprisingly”), but that they were in different locations:
However, in the absence of PRDM9, most recombination is initiated at promoters and at other sites of PRDM9-independent H3K4 trimethylation. Such sites are rarely targeted in wild-type mice, indicating an unexpected role of the PRDM9 protein in sequestering the recombination machinery away from gene-promoter regions and other functional genomic elements.
Once again, Tomkins’ final sentence there (“These key parts of the genome carefully regulate how genes are turned off and on and function in precisely regulated networks.”) is an exaggeration and simplification of what really goes on. The idea that the genome somehow runs like clockwork, rather than the seriously dilapidated FORTRAN program that it really is, is the source of many genetics-related creationist arguments, including this one.
Evolutionists have speculated for years that homologous recombination is one of the key mechanisms associated with the creation of new genes and regulatory DNA sequences. They claim that this operates as some sort of mystical tinkering mechanism that miraculously spits out new genes that somehow become fully and precisely integrated into the genome’s functional networks.
If you remove the “mystical,” “miraculously,” “somehow” etc from that last sentence… he’s getting part of the way there. Large-scale chromosomal movements (large lengths of DNA moving around the place, as opposed to single base substitutions and other more minor mutations)are supposed to have a major role in “the creation of new genes” – duplicating a gene and then mutating it rather gives you a head start, for example. And a part of this does involve the ends of the moving segments of DNA causing different material to come into contact with each other. But that doesn’t make this true:
The emerging concept that homologous recombination is a highly regulated and controlled feature of the genome limited to specific hotspots contradicts the idea of random evolutionary processes being able to produce new genes.
To begin with, the hotspots are only ‘hotspots’ for the actual breakages, and the other parts still get carried along with the recombination. Hence, you can still move and duplicate other parts of the genome perfectly fine (and randomly – even with the hotspots things still are random). Moving the edges away from the regulatory DNA isn’t really problematic. The reason why this ‘protection’ might happen is that these areas may not react very well to being split up by a DSB, but will carry perfectly fine over to the other chromosome if the actual break is nowhere near them. In addition, these hotspots don’t seem to be dodging the genes themselves, so if there is some magic they can work by breaking at that exact spot then they still can.
We also know that the key regulatory parts of the genome that are critical for gene function are protected from recombination processes. This scientific discovery is a virtual death blow to any idea that recombination can serve as a random tinkering tool to create new genes and gene functions.
Only if by ‘virtual’ you mean ‘immaterial.’