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Evolution of blood clotting mechanism

  1. Dec 28, 2007 #1


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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:


    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?

    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?
  2. jcsd
  3. Dec 28, 2007 #2


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    Experiments have shown that genes randomly switch between an activated state (on) and an inactive state (off). Only in the active state, is the gene capable of transcription (producing mRNA).
  4. Dec 28, 2007 #3


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    But how does this imply that it being switched on in the pancreas only causes the enzyme to be released into the bloodstream?
  5. Dec 29, 2007 #4

    jim mcnamara

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    This thread is confusing.

    Bare bones clotting works by having part of the fibrinogen molecule removed by an enzyme. This creates fibrin. Fibrin is sticky and forms little nets or piles of straw-like fibers which are the glue that holds a clot together. Notice I did not use names of enzymes or any real particulars, on purpose.

    Now strictly in terms of the overly simplified model above, do you see the clotting mechanism and how it works?

    Let's try another tack. There is a cell type (tissue) in the pancreas, Islets of Langerhans, that manufactures insulin. This is the only place in the body where insulin is made. So, the gene for making insulin exists in every cell in the body, but it "works" only in these little blobs of tissue. It is turned on there. It is not turned on anywhere else. The turning-on is a result of the location in the embryo of the cells that later make up the pancreas, a positional effect.

    So, we can have genes turned on or turned off by dint of where the cell lives.
    This all makes sense, right? Next, there are other kinds of switches to turn genes off/on. There is no one single switch type.
    Last edited: Dec 29, 2007
  6. Dec 29, 2007 #5


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    It's not the thread that is confusing, everything I have written here is based on the hyperlinked article.

    The only question I have, since I think I can understand the 2nd part, is why does the gene being switched on in both the liver and pancreas cause the enzyme to be released in the bloodstream.
  7. Dec 30, 2007 #6
    I think you have two pieces of confusion. One is about gene regulation. As others have said, every cell in the human body (and most living things) contains a full set of genes. It is the differring regulation of these genes that makes an eye cell different from a liver cell. Gene regulation is what determines how much mRNA is transcribed from a gene and consequently how much of its protein is made. Gene regulation in humans is extremely complicated but you don't need to really understand it to get this article.

    As to the question above: The pancrease produces digestive enzymes that empty into the intestine. So even if it were producing great clotting proteins we'd never get any benefit from that.

    The liver, on the other hand, can produce products that are released into the blood stream. If the gene is switched on (ie transcribed) in liver cells than its protein product could potentially be useful in clotting blood.
  8. Dec 30, 2007 #7
    My interpretation after reading the second half of the article. This part is providing a hypothesis for how the complex multi-step process of clotting evolved:

    What the article doesn't say (but I assume to be true) is that this self activation occurs at a very low level. It's significance comes into play only once the gene duplication occurs. At this point the duplicate gene is able to tolerate mutations which ultimately lead to the evolution of a new protease specialized for cleaving the protein which binds tissue factor.
  9. Dec 31, 2007 #8


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    Ah, I see, I get the first part now.

    The article explains the second part here:

    The only question I believe that remains is how natural selection and the evolutionary process manages to fine-tune the blood-clotting mechanism such that it would trigger only when substantial blood vessels are broken, as opposed to small stimuli triggering. The article seems only to gloss over this question in the above 2 paragraphs without explaining how.
  10. Jan 2, 2008 #9
    I'm still recovering from new years but when my brain is working I'll try to read the beginning of the article again and figure out your question.
  11. Jan 3, 2008 #10
    That part is true, but earlier it's also explained that gene duplication first gave rise to specialized proteins involved in clotting, not clot dissolving. Preexisting self-cleavage ability for these serine proteases was important in encouraging specialization after gene duplication. This is an example of how evolution often works by fine tuning pre-existing traits.

    The article does gloss over exactly how the body knows how to use the "tools" its developed to strike a balance between clotting and blood flow. I looked it up in my physiology text (marieb). Anybody who understands this better than I feel free to add any clarification:

    Plasminogen (active form plasmin) is incorporated into the clot complex and becomes a time activated clot dissolver, triggered by tissue plasminogen activator released from endothelial cells. Thrombin itself also activates plasminogen. Damaged endothelial cells inevitably heal, while at the same time plasmin is dissolving the clot.
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