Scientists: Genetic mutation prompted human evolution
The provocative discovery suggests that this genetic twist - toward smaller, weaker jaws - unleashed a cascade of profound biological changes. The smaller jaws would allow for dramatic brain growth necessary for tool- making, language and other hallmarks of human evolution on the plains of East Africa.
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The mutation is reported in the latest issue of the journal Nature, not by anthropologists, but by a team of biologists and plastic surgeons at the University of Pennsylvania and the Children's Hospital of Philadelphia.
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The report provoked strong reactions throughout the hotly contested field of human origins with one scientist declaring it "counter to the fundamentals of evolution" and another pronouncing it "super."
I read some texts on paleoanthropology a few years ago. The "strong reactions" are consistant with an observation of one of the authors - that there is so much specialization and competition in the sciences that there exist few who have a depth of knowledge, or even an appreciation of the validity of other specialties - and that this often results in faulty conclusions and outright dismissiveness.
Here's an example;
Critics said the study wrongly assumes that evolution works so neatly.
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The first early humans with the mutation probably would have had weaker mouths, but still had large teeth and jaws. Many additional mutations would have been needed.
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"The mutation would have reduced the Darwinian fitness of those individuals," said anthropologist Bernard Wood of George Washington University. "It only would've become fixed if it coincided with mutations that reduced tooth size, jaw size and increased brain size. What are the chances of that?"
Anthropologists aren't geneticists. The chances are actually not that bad. A single gene mutation can influence an array of seamingly unrelated features - it's called pleiotropy. An example :
Alaskan Malamute's dwarfism is a pleiotropic genetic defect that shows up as both dwarfism of their particular type and a blood disorder. It has been fairly extensively studied, and while one dog may vary in appearance considerably from the other, the disorder is a simple autosomal (not sex-linked) recessive trait with complete penetrance. Asynchronous growth of the radius and ulna (one at a different rate or completion than the other, remember) is part of the deformity in this breed. The chondrodysplasia in this breed has at times been mistaken for the Vitamin D deficiency called rickets, but only the tubular bones are affected, other than retarded ossification of the lateral tarsal (cuboid) bone. The head, spine, and other bones are not stunted or changed, and body length is normal. The gene that causes this chondrodysplasia also creates a macrocytic hypochromic anemia; the discovery of this being indicative of the way carriers may be found. A third effect of this one gene, by the way, is a different ability to bind certain trace minerals in the liver.
And certainly, pleitropy may not be a factor here, but it's entertaining to see the reactions when academic toes have been stepped on.
Bump!
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