Friday, January 14, 2011

Guest Speaker: Dr. Max Robinson Part II

Today Dr. Robinson continued his talk about atherosclerosis.  The focus was on how the gene, ABCA1, is regulated.  He also discussed some of the techniques used to discover which proteins act as transcription factors of this gene. 

There is no specific homework due on Tuesday, but if you haven't looked at the epigenetics resources from Wednesday I advise you to take a look at them.

Enjoy your three days!

1 comment:

  1. One of the students asked me, at the end of class, whether there are any human genes that are related to the firefly luciferase gene we discussed in class.

    I'm very happy to say that there are! Firefly luciferase is related to a kind of enzyme, "long-chain fatty acyl CoA synthetases". These enzymes don't make light; they cause a chemical reaction that is the first step in the body's use of fatty acids from our diet. Some of the fatty acids we eat are used to make lipids, which as you know are mostly found in lipid bilayers in our cells. Other fatty acids are burned to produce energy. The first step in either of these uses of fatty acids is considered "activation", and this is what the luciferase-like enzymes do in our body.

    You might find it interesting that firefly luciferase doesn't generate light itself, either! Instead, what it does is catalyze the same kind of "activation" reaction on a different kind of molecule, luciferin. After activation, the luciferin is in an unstable, high-energy state, but due to the exact nature of the high-energy state, the only way it can transition to a lower-energy state is by emitting light.

    Unfortunately, the activation of long-chain fatty acids doesn't leave them in such a weird high-energy state, and they can release their energy in a way that doesn't produce light. Too bad for us...if it did, we'd probably be able to tell how much fat we were burning while we were exercising by how much we glowed!!!

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