Why would a sudden gusher of cAMP in a wound be significant? That means that we already have some ability to limit damage and plug leaks in a primitive, low-pressure system. The vertebrate fibrinogen gene, just like genes for the other proteins of the clotting sequence, was formed by the duplication and modification of pre-existing genes. But just as soon as the occasional clot becomes large enough to present health risks, natural selection would favor the evolution of systems to keep clot formation in check. This would leave us with system in which circulating plasma contains both an inactive serine protease and its fibrinogen target.
Now, "beauty" is a word that most people wouldn't think to put in the same sentence with "biochemistry," but the biochemistry of this pathway is beautiful indeed. Works for them, and therefore there is no reason why it wouldn't have worked for the ancestors of today vertebrates, either! The key to understanding the evolution of this intricate system, as Russell Doolittle has pointed out, is the fact that the clotting factors share an exquisite and revealing similarity. This would leave us with system in which circulating plasma contains both an inactive serine protease and its fibrinogen target. That it wouldn't be sufficient to seal breaks? So, both of these ultimate stimuli lead to the same set of clot-forming proteins Factor X, thrombin, and fibrin , but neither does it directly. Now, what organ produces lots of serine proteases? That means that we already have some ability to limit damage and plug leaks in a primitive, low-pressure system. Like all biochemical systems, it evolved from genes and proteins that originally served different purposes. As you look up, you can trace this process to one of two different external stimuli, both of which make good sense. The result is that clumps of newly-insoluble protein fragments begin to assumulate at the tissue-plasma interface, helping to seal the break and forming a very primitive clot. Imitating Rube Does the human clotting system lend itself to the same kind of analysis? But just as soon as the occasional clot becomes large enough to present health risks, natural selection would favor the evolution of systems to keep clot formation in check. But one day, through a well-understood process called "exon shuffling," a DNA sequence known as an "EGF domain" is spliced into one end of the protease gene. And where would these systems come from? OK, so what activates Factor X? Now, let's suppose that a gene duplication occurs in the gene for our protease, producing a new B version of the gene: Because the selective value of the plasma protease is pretty low it doesn't help clotting all that much , most of these changes make very little difference. Look closely, and you'll see that our 1-step clotting system required a direct interaction with TF to activate each protease. Remember the lobster system as an example. Gene duplications happen all the time, and they are generally of such little importance that they are known as "neutral" mutations, having no effect on an organism's fittness. Our next step is to consider the nature of blood itself. So the tissues of our ancestral vertebrate would be laden with protein-cutting enzymes for reasons completely unrelated to clotting. For example, most of the enzymes involved in clotting are serine proteases, protein-cutting enzymes so-named because of the presence of a highly reactive serine in their active sites, the business ends of the protein. So, just as soon as clotting systems became strong enough, gene duplication would have presented natural selection with a working protease inhibitor that could then evolve into antithrombin, a similar inhibitor that today blocks the action of the primary fibrinogen-cleaving protease, thrombin. The fortuitious combination of a EGF sequence with the plasma protease changes everything.
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