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I'm currently reading this article by Ken Miller on a plausible account of how the blood clotting mechanism in vertebrates might have evolved. There's some things I don't understand but which I hope someone here will explain to me:
Here's the article:
http://www.millerandlevine.com/km/evol/DI/clot/Clotting.html
All quotes are from the hyperlinked article.
Here's the article:
http://www.millerandlevine.com/km/evol/DI/clot/Clotting.html
All quotes are from the hyperlinked article.
What does it mean for the gene to be "switched on" only in the pancreas? And more importantly, why does the fact that it being switched on in both the pancreas and liver causes the enzyme to be released into the bloodstream?However, the original gene had a control region that switched it on only in the pancreas. During the duplication, the control region of the duplicate is damaged so that the new gene is switched on in both the pancreas and the liver. As a result, the inactive form of the enzyme, a zymogen, is relesased into the bloodstream.
If serine proteases are, as the article states able to self-activate (by mere presence of amino acids in the bloodstream), and if, by the first quoted paragraph, where the serine protease is released into the bloodstream, then wouldn't it be possible for blood to clot itself even when no blood vessels are broken? If so, wouldn't this be disruptive to normal functioning?Most serine proteases, including trypsin and thrombin, are auto-catalytic. That means that some extent they can activate themselves, in many cases by cleaving a few amino acids to switch on their active sites.