Genomics 3: Endogenous Clocks & Marathon Mice

Okay there's this gene. Actually there are a number of genes that do the same thing, but the point here is that one seems to be enough. I'll just talk about mPer1, as if I knew what I was talking about. Per, by the way, is short for period. Look at mPer1 when a couple of yellow circles are sitting on top of the promoter segment of the gene labeled C and B. These are inhibitors, and they shut the gene down. When the gene is shut down, changes in the cell eventually result in the inhibitors being stripped off. The gene is activated and begins to change the cell chemistry again. Eventually C and B show up again and bind to the promoter, and the gene is shut down.

Get all that? The whole cycle takes a little more than twenty four hours. That's why it's called a circadian clock. In mammals, these Timex cells are the heart of the suprachiasmatic nuclei, a paired set of nuclei located at the base of the hypothalamus, a brain organ found in most mammals but not in Professor Schaff. The SCN is the central pacemaker for circadian rhythms. It allows mammals to keep a twenty four hour cycle. But it is sensitive to environmental inputs such as daylight cycles. The slightly longer than 24 hour period allows the system to adjust to changes in seasons or sudden changes in location. When a creature with one of these time pieces is kept in long term darkness, it keeps a more than 24 hour day.

This is a case where the gene mechanics can be connected well with the associated behavior. It is also a case where the common ancestry of the species is indicated. When the SNC is disabled in a lab rat, it loses the ability to keep a regular schedule. When the same mechanism is disrupted in fruit flies, you get a very irregular drosophila. But, and here is the punch line, they have transplanted genes from the mammalian SNC into the damaged fruit fly, and the fly is back on the clock.

That's what I got from Martha U. Gillette, a marvelous scientist who spends her time watching other critters keep theirs. Justin Rhodes, a biologist here explained how he and others bred a few lines of super buff mice. They kept several lines of control groups (just let them breed), and bred several lines of really strong wheel runners by selecting the strongest. Some of these mice could do many miles a day on those goofy wheels. By breeding several lines instead of just one, Rhodes and his colleagues could tell what changes in what morphological features and genes were constant across the enhanced lines. That clued them into the changes that were really important and not just random noise.

This is science, and I am entranced by it. This is what we are, at least in part. That, at least in part, is what I have always wanted to know.

DISCLAIMER: This is my very amateur take on all this.  Any mistakes are mine and not those of the expert presenters. 

Comments

[Miranda]

I have a sneaking suspicion that my SCN was destroyed long ago...

[KB]

I dunno. You showed up for most classes on time. Maybe if we put the fruitfly genes in your SCN...