#anthropogenesis

“The Kings of Light have departed in wrath. The sins of men have become so black that Earth quivers in her great agony. . . . The azure seats remain empty. Who of the Brown, who of the Red, or yet among the Black (races), can sit in the seats of the Blessed, the Seats of knowledge and mercy! Who can assume the flower of power, the plant of the golden stem and the azure blossom?”

In three generations of the KE family in London, about half of the family members had a severe speech and language defect. The pattern of inheritance suggested that it was caused by a dominant autosomal allele form of a gene... The gene was identified as FOXP2 because of its similarity to a family of the forkhead box transcription factors that are involved in turning on and off the expression of other genes. FOXP2 is expressed in a variety of adult and fetal tissues in addition to the developing brain. The one mutation in that gene found in the KE family essentially prevented that copy of the gene from functioning. Since we each have two copies of every gene... the affected members of the KE family had only half the usual amount of the FOXP2 protein expressed. The link of FOXP2 to vocalization is also found in birds, mice, and echolocating bats.... The expression of FOXP2 is upregulated during the post-hatch learning of birdsong (zebra finch) or during singing season (canary). Ultrasonic vocalization in infant mice is significantly decreased if one copy of FOXP2 is deleted; if both copies are deleted, there is no vocalization and premature death. Echolocating bats... have an unusually high number of non-synonymous mutations in FOXP2. It turns out that FOXP2 is a highly conserved gene with no amino acid changes in the chimpanzee line going back some 90 million years to the common ancestor with the mouse. This resistance to change suggests that FOXP2 is extraordinarily important for vertebrate development and survival. But there are two mutations that change amino acids in FOXP2 in the 6 million years of the human line since the common ancestor with the chimpanzee.... One of the human-specific mutations is shared with wolves tigers, and all members of the order Carnivora. Of the two mutations, this is the one which Enard et al. suggest might make the most difference in protein function by providing a potential site for phosphorylation.

I have a question, if you care to humor me💖

The anthropogenic maintains a fundamental ethical dimension not because environment is a moral issue but because ecology is necessary to the critical ontology of Anthropos in the contemporary.

The SNP density map for chromosome 7 does show a very interesting patern for the area around FOXP2. There is a long stretch of about 4 million bases in which there is a relatively even amount of variation compared with similar stretches in the rest of the chromosome. There are no bins of extra low SNP density and no bins of high SNP density in this section of chromosome 7. The section as a whole has a SNP density somewhat below average, approximately 70% of average. This may be the sign of an unusually strong ancient selective sweep...[The relative SNP density and the rate of the generation of mutations following a selective sweep] brings the date of this selective sweep to about 1.8 or 1.9 million years ago, the time of the Plio-Pleistocene boundary, corresponding to the approximate time when Homo habilis, H. ergaster, and H. erectus emerged in the fossil record. Along with the appearance of the oldest Acheulian tools and the oldest H. erectus fossils outside Africa, it also corresponds to a point in human evolution when the brain size of the early Homo began to expand (eventually to triple) from the 450cc of chimpanzee and australopithecine brains. The beauty of this evidence is its simplicity and transparency. The pattern is so strong that it can be seen by the naked eye. The calculations are so simple that they can be done by hand.... The other beauty of this result [is] if the change in FOXP2 really was involved in an important wayin the evolution of the neuromuscular control of the speech organs, then it is more likely that this change occurred toward the beginning of this evolutionary process rather than at the end. The date of 1.8 or 1.9 million years ago puts the mutations in FOXP2 near the beginnings of adaptive radiation within genus Homo, at the time of explosive evolutionary experimentation.

A plausible hypothesis for the descent of the larynx in other mammals is that it is an adaptation to exaggerate size. Crucially, the same principles apply equally well to early hominids, suggesting that the initial adaptive function of the descended larynx must not have been speech.... Furthermore, we now know that this hypothesis applies to modern humans at puberty, when males (only) undergo a secondary descent of the larynx.... It appears to be a size-exaggerating adaptation, precisely analogous to that found in some other male mammals. Note that... the permanent, primary descent of the larynx in human infants of both sexes... is more likely either an adaptation to speech or a byproduct of some unspecified cranial rearrangements... the strongest evidence that human vocal anatomy reflects a tailoring of the vocal system to speech.

...given the critical role of metaphor in the evolution of language, nominal reference is likely to provide clues as to the domain in which color lexicons arose. The most common analyzable root of any BCT [ie, 'basic color term'] or referent-based simile for hue is 'blood,' probably followed by 'red earth pigment.' Analyzable 'black' and 'white' terms also often refer to things with partible color (e.g. cockatoo feathers, charcoal, cuttlefish ink). Important exceptions to this tendency are 'black' and 'white' terms such as 'night,' 'darkness,' or 'to see,' taking us beyond the labeling of surface color. Such exceptions notwithstanding, ritual display would appear to be deeply implicated in simple forms of color lexicalization.