DNA is under constant attack, from internal factors like free radicals and external ones like ionizing radiation. About 10 double-strand breaks – the kind that snap both backbones of the double helix – occur every time a human cell divides. To prevent not only gene mutations but broken chromosomes and chromosomal abnormalities known to cause cancer, infertility, and other diseases in humans, prompt, precise DNA repair is essential.
Scientists at the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab), working with cell lines of the fruit fly Drosophila melanogaster, have discovered an unsuspected and dramatic process by which double-strand breaks in heterochromatin – one of the two major kinds of chromatin that make up chromosomes, which accounts for a third of the chromatin in both humans and fruit flies – are repaired in a series of steps. The repair starts where the break occurs, but stalls until the repair site physically moves away from the original heterochromatin region, before continuing to completion.
Unlike euchromatin, where most of an organism’s genes reside and where most DNA consists of long, unrepetitive sequences of base pairs, DNA in heterochromatin consists mostly of short repeated sequences that don’t code for proteins; indeed, heterochromatin was long regarded as containing mostly “junk” DNA.
Heterochromatin is now known to be anything but junk, playing a crucial role in organizing chromosomes and maintaining their integrity during cell division. It is concentrated near centromeres, where chromatids are in closest contact, which are required to transmit chromosomes from one generation to the next. Maintaining heterochromatin structure is necessary to the normal growth and functions of cells and organisms.
Read more hear Safeguarding genome integrity through extraordinary DNA repair.