It's raining. =(August wrote:Don't cancel golf, that just isn't right....
I'm going to go to the museums.
But first lets continue the discussion.
Last time we duplicated a protein analogous to hiring Josh's twin.
Now in the organic world the company can be duplicated over and over again each one being slightly different. With two genes encoding for Josh they both get expressed. Lets get back to the analogy.
Josh and Josh's twin are both responsible for the same things. What is most likely to happen? Well at first they would both do their assigned job. But if one day Josh decides to go play a game of golf there isn't any harm done to the company because his twin is effectively doing the job. After days and days of truancy Josh is fired!
But this might not always happen. Josh may be given a promotion. That is being so similar to his twin; identical in fact, he may be given a supervisory role given his experience.
Now in the biological world it doesn't quite happen this way. No genes get promoted or fired. But duplicated genes allow one of the genes the freedom to degrade. As Kmart pointed out earlier both genes are not necessary for the mechanism to continue functioning. However both genes continue to be expressed.
If for instance a mutation occurs in one of the genes, it is less likely to be harmful because the other gene is still there. Now in most cases the duplicated gene mutates to the point of becoming detrimental. However sometimes the resulting protein from mutated the gene can have a novel function. Neither is the case here.
If we go back to out original discussions an added step allows an initial condition like tissue factor to be amplified. The duplicate gene is beneficial from the get-go. While maintaining the flexibility provided by being a duplicate gene.
So how do the blood clotting factors interact?
A simplistic view was diagrammed in the pages which Kmart has had earlier scanned for us. But there are some details which were left out. First the extrinsic cascade is usually too late. When a cut causes tissue factor to be released into the blood the intrinsic pathway set off and clotting begins. Platelets in the blood complete the clotting after initial fibrinogen clumping. Yet the extrinsic cascade continues? Well if you remember earlier the extrinsic pathway also creates anti-thrombin. It's a breaking system.
How does it all work?
As discussed earlier the function of a protein depends on its shape. Many of the factors are shaped the same and work the same.
Factors can cleave themselves and Prothrombin. When an organism is cut the extrinsic pathway is not taken exactly as described. Many of the factors act on each other, themselves and prothrombine outside of the sequence previously described. Not only that, Thrombine acts on some of the clotting factors as well activating them.
Next I will continue with the analogy and answer the question, “What happens if I add an additional step to the cascade”?
Also if there is any pont here you with to dispute, please do so.
