Long DNA molecules almost miraculously cram into cell nuclei that are almost a million times smaller than they are. They do so by wrapping around proteins called histones, which array themselves along the length of the DNA molecule like beads on a string. These DNA-wrapped histones then form larger arrays. The densely packed mass is then modified chemically by other proteins to form heterochromatin.
The dense packing of heterochromatin hides the DNA sequence from the cellular machinery that reads its genetic information, so the DNA in heterochromatin is silenced. The genes it contains are effectively turned off.
Surprisingly, the clumping persists even after cells divide, although, says Dr. Martienssen, its always been a mystery how modifications of histones could be inherited. A few years ago, however, his group and others solved this mystery. They found that histone modification is controlled by complicated cellular mechanisms broadly known as RNA interference, or RNAi.
In RNAi, RNA that is copied from particular regions of DNA interacts with various proteins to modify histones in the same regions. Because the RNA matches only the section of DNA that produced it, it provides the specificity that you need to make sure that only that part of the chromosome gets these histone modifications, Dr. Martienssen says. If the whole chromosome were to get those histone modifications, youd be dead.
All in the Timing
These results raised a new puzzle, though: Since genes contained within heterochromatin are silenced, how can they give rise to the RNA molecules that help to modify histones? In new research, Martienssens team has now solved this puzzle by tracking the cells through their cycle of growth and division.
They found that the interfering RNA molecules appear only during the brie
|Contact: Jim Bono|
Cold Spring Harbor Laboratory