What Is The "Clock" Driving DNA Gene Expression?

I’m puzzled- all life changes over time, and humans have periods when the DNA activates different genes. What (in the DNA) acts as the clock? Is there some genes that in effect, keep time? And, can this clock mechanism be interupted?
Take the example of human puberty-at a certain age, the DNA in us activates a set of genes, that cause us to develop sexual organs-this happens betweem roughly 12 and 16 years after birth. Has anyone isolated the mechanism as to how this is timed to occur?

Short answer: it’s not known yet, but people are working on it.

There is a relatively well-described set of “clock” genes that control the differences in day/night gene activity, but that’s a different thing.

Some of the longer-term timing mechanisms you’re talking about have been partially decribed in embryos, and they vary considerably. Sometimes, when one tissue is formed it signals for the next “step” to occur - so one thing leads to another. Sometimes, a tissue has to grow large enough to trigger a change to become something new. Sometimes, cells count how many times they divide, and when they have divided the appropriate number of times, they turn on a new set of genes. There are many more options. Which, if any of these, functions to control puberty is not currently known, and how that hypothetical mechanism interacts with things like overall nutrition, stress, etc., that all affect the timing of puberty is also not known.

On the other hand, some timing issues are very clear - menopause, for instance, happens when you run out of eggs to ovulate. Aging doesn’t seem to be “timed” so much as a general breakdown in lots of different processes - although it is characterised by typical changes in gene activation pattens.

Does that give you a rough answer to your question? Did you want to post this in GQ?


I recall hearing about the end of the genes contain some sort of clock, when the gene divides this end part does not divide but halves, each split it gets shorter, when it’s down to the end the death of the cell, instead of division, is going to happen.

I think that what you’re thinking of is telomeres, which form the ends of chromosomes. Cells can’t replicate DNA all the way out to the end, so each time they divide, the telomeres get a little shorter. When people have forced cells to divide many, many times, the telomere length gets used up, chromosomes break and fuse, and the cell usually dies. Cells in old people have shorter telomeres, because their cells have divided more times. However, during the early stages of embryonic development, cells add new telomere length so that each generation “starts fresh” with long telomeres.

Unfortunately, this doesn’t appear to be relevant to changes during your lifespan. (The following is my analysis of a controversial field, so don’t take it as set in stone.) As far as anyone can tell, cells don’t appear to run out of telomeres in a normal lifespan. Noone has been albe to show that any human cell type ever runs out of telomeres, and mice that have been engineered to be unable to “start fresh” with long telomeres don’t have any problems at all for many generations, so there seems to be excess length built in. Also, many of the tissues which change as we grow older are composed of cells which divide only very rarely (glandular tissue, heart) or not at all (brain), so it doesn’t make any sense that these cells would have problems with their telomeres.