You did that all on your own.
Hogwash, you guys troll these boards for creationists. I know a lot of fundamentalists and evangelicals that believe wholeheartedly in a literal Genesis and they care nothing about these debates. On the other hand the professional scientists care deeply about them, they feel threatened in some way.
Actually by and large yes, yes I do. Not you however. You I think are intelligent, which is why it is so frustrating watching you turn your intellect off.
Who needs it to field one insult after another and have everything you say twisted? You never call the evolutionists on blatant errors made repeatedly but you just lunge for whatever you can find in a Creationists post.
Once more, with feeling. Its an RNA gene. It does not code for any amino acids, it doesn't get translated. The RNA folds and has its own enzymatic/metabolic activity purely based on its structure and completely independent of any translational mechanism.
I know the difference between a protein coding gene and a regulatory gene. I know why you keep pushing this, you are hoping the real issue will go away. So for the Nth time, how does a regulatory gene that has allowed only 2 substitutions in 400 million years suddenly, 2 million years ago get 18 substitutions?
The obvious answer is you don't have a clue since this is what happens in reality:
Other genes regulating neuronal migration
The putative relationship between mDab1 and Abl suggests a possible link between scrambler and human mutations affecting neuronal migration in the cortex... Lissencephaly is a severe migrational disturbance in which the majority of cortical neurons migrate successfully out of the ventricular zone, but then arrest along the migratory route to the cortex. Complete absence of cortical gyri (giving rise to the smooth-surfaced brain described by the term lissencephaly) is thought to be a secondary result. Similarities between lissencephaly and the reeler and scrambler phenotype include the fact that neurons in the lissencephalic cortex do migrate, because they are not arrested in the germinal zone as is seen in other migrational disturbances. As in reeler and scrambler mutant mice, neurons migrate most of the way to the cortex, but arrest short of the appropriate location.
Another gene causing human lissencephaly presents a histological phenotype indistinguishable from DC/XLIS . This gene, called LIS1, is located on chromosome 17, and has been identified as encoding a regulatory subunit of platelet-activating factor acetylhydrolase containing eight WD40 repeats with homology to beta -subunits of heterotrimeric G-proteins. Nonreceptor tyrosine kinases such as Abl have been shown to phosphorylate the alpha -subunit of several different heterotrimeric G-proteins. Although the relationship between LIS1, Doublin, and mDab1 is completely unknown, an interaction between LIS1 and Abl via a Galpha subunit is an intriguing possibility.
Recently, two engineered mutations in mice have generated phenotypes that resemble reeler and scrambler to a certain degree. Cdk5 expression in the nervous system is limited to postmitotic neurons of the PNS and CNS (Nikolic et al., 1996). Mice homozygous for mutations in the cdk5 gene die on the day of birth and show many neurological abnormalities (Ohshima et al., 1996). The cerebral cortex of the cdk5 -/- mutants shows a lack of obvious lamination and an excess of neurons in the marginal zone, highly reminiscent of the reeler/scrambler phenotype. It should be noted, however, that birthdating studies have not been performed to confirm the similarity. Engineered mutations in p35, which was identified on the basis of the binding of p35 to Cdk5 (Tsai et al., 1994), also result in brain abnormalities reminiscent of reeler and scrambler (Chae et al., 1997). As in reeler and scrambler, cortical plate neurons appear to retain their normal birthdate patterns but fail to migrate normally, resulting in a somewhat inverted and disorganized cortical layering. In contrast to the reeler and scrambler phenotype, the marginal zone in the p35 mutants is strikingly well formed. The exact relationship of Cdk5 and p35 to other genes involved in neuronal migration is not clear. (
Birthdate and Cell Marker Analysis of Scrambler: A Novel Mutation Affecting Cortical Development with a Reeler-Like Phenotype)
Its an RNA gene. It doesn't code for anything.
I don't care, it doesn't matter and you keep repeating this as if there was a point. You can keep running in circles but there is no where to hide. It's a novel non-coding RNA gene...so what?
HAR1 lies in a pair of novel non-coding RNA genes
The 118-bp HAR1 region showed the most dramatically accelerated change (FDR-adjusted P , 0.0005), with an estimated 18 substitutions in the human lineage since the human–chimpanzee ancestor, compared with the expected 0.27 substitutions on the basis of the slow rate of change in this region in other amniotes. Only two bases (out of 118) are changed between chimpanzee and chicken, indicating that the region was present and functional in our ancestor at least 310 million years (Myr) ago. No orthologue of HAR1 was detected in the frog (Xenopus tropicalis), any of the available fish genomes (zebrafish, Takifugu and Tetraodon), or in any invertebrate lineage, indicating that it originated no more than about 400Myr ago. ( An RNA gene expressed during cortical development evolved rapidly in humans, Nature 2006)
And by the way, your simplistic view of how translation wors, with its "all three types of RNA", might suit primary school kids, it is woefully inadequate in this discussion. Have a look at ncRNA, siRNA, miRNA, snoRNA some time, assuming you ever actually want to learn anything.
Then what? By the way, I have researched a couple of those and I am actually looking for ways things adapt. Instead what I get is one insult hurled at me after another so I keep beating you guys up with this topic because I know you are completely clueless.
Of course it is asked, you just want the answers RIGHT NOW. THe work is competely novel and only 1 year old. THis kind of research takes time.
For well over 50 years evolutionists are telling us that we are 99% chimpanzee in our DNA. Then fairly recently it is realized that we are actually 95%. Then they say it was a few changes in a few genes and that was found to be false. You guys didn't predict the level of divergence nor where you expecting to find this regulatory gene dramatically different when it has not changed nearly half a billion years. Then when asked about it you want to play this semantical shell came designed to cloud the mind and rattle the confidence. The problem is you guys have done this too many times to be convincing, I guess whatever makes you a good scientist makes you a lousy actor.
Now you don't want to talk about it...typical. When the DNA is 99% the same that is the first thing that comes out of your mouth. When that is found to be false you want to change the subject.
Do let me know if you ever do read it, rather than skimming to a sentence you like and stopping.
You too
When does anyone on here show the slightest interest? You certainly haven't. It doesn't matter what I read or don't read the arguments on here have never changed.
Let me just break down a couple of points:
- The genetic basis for the adaptation of the human brain from apes is unknown.
- Questioning any aspect of the single common ancestry is never allowed.
- The known genetic divergence is at least five times what would be expected with known mutation rates.
- There are no chimpanzee ancestor fossils represented in the fossil record for well over 5 million years while hominid fossils have thousands.
Is this what a Creationist can expect to encounter if they decide to study the life sciences? Do you think that Fundamentalist/evangelical theology is just going to go away because the academic status quo does not like it?
Ever hear of the Scientific Revolution? It was made possible by the Protestant Reformation that wrestled science and religion away from the academic status quo. I think that is probably what you guys are afraid of, Christianity has overthrown the status quo before and could again. Don't be afraid, we only want to help you.
Arguments from Incredulity are sooo 4 years ago.
It doesn't code for a protein because it codes for RNA that's functional in its own right. Being a regulatory gene doesn't imply that there's no protein product. The sonic hedgehog gene is regulatory, too, and codes for a protein with the same name (involved, among others, in vertebrate limb development).
