oh_noes wrote on Dec 26th, 2009 at 5:27pm:Oooh some interesting reading there, but thats not quite what I meant. I was referring particularly to the high incidence of carriers of the gene that codes for cystic fibrosis. There must be some heterozygote advantage to enable it to spread so we are looking for what the advantage conferred might be.
Yeah. My apology. I've managed to missed, that the topic was about the cystic fibrosis. But let me make it up for it, since I've found something quote interesting from the genetic and evolutionary perspective;
How this happens:
http://ghr.nlm.nih.gov/condition=cysticfibrosis and the description of the gene, that causes CF, called appropriately CFTR located here: http://ghr.nlm.nih.gov/gene=cftr
And I've also found a possible evolutionary treat for this, quoting:
Quote:Cystic Fibrosis
Balanced polymorphism may explain why cystic fibrosis is so common- the anatomical defect that underlies CF protects against diarrheal illnesses, such as cholera.
Cholera epidemics have left their mark on human populations, causing widespread death in just days. In the summer of 1831, an epidemic killed 10 percent of the population of St. Louis, and in 1991, an epidemic swept Peru. Cholera bacteria causes diarrhea, which rapidly dehydrates the body and can lead to shock and kidney and heart failure. The bacterium produces a toxin that opens chloride channels in the small intestine. As salt (NaCl) leaves the cells, water follows, in a natural chemical tendency to dilute the salt. Water rushing out of intestinal cells leaves the body as diarrhea.
In 1989, when geneticists identified the CF gene and described its protein product as a regulator of a chloride channel in certain secretory cells, a possible explanation for the prevalence of the inherited disorder emerged. Cholera opens chloride channels, letting chloride and water leave cells. The CFTR protein does just the opposite, closing chloride channels and trapping salt and water in cells, which dries out mucus and other secretions. A person with CF cannot contract cholera, because the toxin cannot open the chloride channels in the small intestine.
Carriers of CF enjoy the mixed blessing of a balanced polymorphism. They do not have enough abnormal chloride channels to cause the labored breathing and clogged pancreas of cystic fibrosis, but they do have enough of a defect to prevent the cholera from taking hold. During the devastating cholera epidemics that have peppered history, individuals carrying mutant CF alleles had a selective advantage, and they disproportionately transmitted those alleles to future generations. However, because CF arose in Western Europe and cholera in Africa, perhaps an initial increase in CF herterozygosity was a response to a different diarrheal infection.
(quoted from http://www.pbs.org/wgbh/evolution/educators/course/session7/explain_b_pop1.html ), which references
Human Genetics: Concepts and Applications (Second edition, 1997) pp. 247-248 by Ricki Lewis Quote:However, I'm now intrigued about the kid with the instance of double anti-myostatin genes. Do you have a reference I can go and take a peak at, I'm envisaging some kind of Arnie Kid.
Sure do. The best is found here: http://www.sciencentral.com/articles/view.php3?article_id=218392292&cat=1_2 and the reference about the myostatin (the protein, that breaks the development of muscle) can be found here: http://en.wikipedia.org/wiki/Myostatin
Quote:Actually, is this the kid who was all over the news as the worlds strongest child?
Yep. That was him. But it's not human-only mutation. Also, the cow called "The Belgian Blue" has this exact mutation. ( http://en.wikipedia.org/wiki/Belgian_Blue )