Sorry Mark, when you said evidence, I assumed you'd provide more than a bunch of unevidenced assertions. Just to clarify, could you provide actual evidence please.
Would actual peer reviewed scientific evidence suffice or do you require a chase around the mulberry bush?
They have discovered at least two dramatic giant leaps that would have had to occur in order of the human brain to have emerged from ape like ancestors SRGAP2, HAR1F. In addition genes involved with the development of language (FOXP2), changes in the musculature of the jaw (MYH16) , and limb and digit specializations (HACNS1).
The ancestral SRGAP2 protein sequence is highly constrained based on our analysis of 10 mammalian lineages. We find only a single amino-acid change between human and mouse and no changes among nonhuman primates within the first nine exons of the SRGAP2 orthologs. This is in stark contrast to the duplicate copies, which diverged from ancestral SRGAP2A less than 4 mya, but have accumulated as many as seven amino-acid replacements compared to one synonymous change. (Human-specific evolution of novel SRGAP2 genes by incomplete segmental duplication Cell May 2012)
What is the problem with 7 amino acid replacements in a highly conserved brain related gene? The only observed effects of changes in this gene in humans is disease and disorder:
- 15,767 individuals reported by Cooper et al. (2011)] for potential copy-number variation. We identified six large (>1 Mbp) copy-number variants (CNVs), including three deletions of the ancestral 1q32.1 region…
- A ten year old child with a history of seizures, attention deficit disorder, and learning disabilities. An MRI of this patient also indicates several brain malformations, including hypoplasia of the posterior body of the corpus callosum…
- Translocation breaking within intron 6 of SRGAP2A was reported in a five-year-old girl diagnosed with West syndrome and exhibiting epileptic seizures, intellectual disability, cortical atrophy, and a thin corpus callosum. (Human-specific evolution of novel SRGAP2 genes by incomplete segmental duplication Cell May 2012)
The search for variation with regard to this vital gene yielded no beneficial effect upon which selection could have acted. The only conceivable way the changes happen is relaxed functional constraint which, unless it emerged from the initial mutation perfectly functional it surly would have killed the host. Mutations are found in children with 'developmental delay and brain malformations, including West Syndrome, agenesis of the corpus callosum, and epileptic encephalopathies'.(cited above)
Of course Creationists have their opinions about this gene:
SRGAP2A, SRGAP2B, SRGAP2C, and SRGAP2D, which are located in three completely separate regions on chromosome number 1.1 They appear to play an important role in brain development.2 Perhaps the most striking discovery is that three of the four genes (SRGAP2B, SRGAP2C, and SRGAP2D) are completely unique to humans and found in no other mammal species, not even apes…Unique in their protein coding arrangement and structure. The genes do not look duplicated at all… (
Newly Discovered Human Brain Genes Are Bad News for Evolution by Jeffrey P. Tomkins, Ph.D)
In one of the areas of the human genome that would have had to change the most, Human Accelerated Region (HAR), we find a gene that has changed the least over just under 400 million years HAR1F. Just after the Cambrian is would have had to emerge de novo, fully formed, fully functional and permanently fixed along broad taxonomic categories. In all the time since it would allow only two substitutions, then, while the DNA around it is being completely overhauled it allows 18 substitutions in a regulatory gene only 118 nucleotides long. The vital function of this gene cannot be overstated:
The most dramatic of these ‘human accelerated regions’, HAR1, is part of a novel RNA gene (HAR1F) that is expressed specifically in Cajal– Retzius neurons in the developing human neocortex from 7 to 19 gestational weeks, a crucial period for cortical neuron specification and migration. HAR1F is co-expressed with reelin, a product of Cajal–Retzius neurons that is of fundamental importance in specifying the six-layer structure of the human cortex. (An RNA gene expressed during cortical development evolved rapidly in humans, Nature 16 August 2006)
This all has to occur after the chimpanzee human split, while our ancestors were contemporaries in equatorial Africa, with none of the selective pressures effecting our ancestral cousins. This is in addition to no less then 60 de novo (brand new) brain related genes with no known molecular mechanism to produce them. Selection can explain the survival of the fittest but the arrival of the fittest requires a cause:
The de novo origin of a new protein-coding gene from non-coding DNA is considered to be a very rare occurrence in genomes. Here we identify 60 new protein-coding genes that originated de novo on the human lineage since divergence from the chimpanzee. The functionality of these genes is supported by both transcriptional and proteomic evidence. RNA– seq data indicate that these genes have their highest expression levels in the cerebral cortex and testes, which might suggest that these genes contribute to phenotypic traits that are unique to humans, such as improved cognitive ability. Our results are inconsistent with the traditional view that the de novo origin of new genes is very rare, thus there should be greater appreciation of the importance of the de novo origination of genes…(De Novo Origin of Human Protein-Coding Genes PLoS 2011)
Whatever you think happened one thing is for sure, random mutations are the worst explanation possible. They cannot produce de novo genes and invariably disrupt functional genes. You can forget about gradual accumulation of, 'slow and gradual accumulation of numerous, slight, yet profitable, variations' (
Darwin). That would require virtually no cost and extreme benefit with the molecular cause fabricated from vain imagination and suspended by pure faith.
