Cells respond to broken or damaged DNA by arresting their cell cycle while the damage is repaired. If the tips of chromosomes were recognised as broken DNA, cells would be constantly trying to repair the ends of chromosomes, leading to cell death and possible mutations in the DNA. Telomeres, caps made up of protein and DNA at the tips of chromosomes, stop this from happening. Yet, telomeres attract and bind several of the proteins involved in DNA repair. Why then, does DNA repair not happen at these sites?
The award-winning paper describes painstakingly detailed experiments, carried out in fission yeast, that shed light on this long-standing paradox. One of the histones (a protein bound to DNA) neighbouring the telomeres lacks a chemical signal, thus making the DNA repair complex assembled at the telomere effectively inactive. This single change helps the cell distinguish a chromosome end from a break in the DNA.
The SPGH prize is sponsored by Applied Biosystems, and was awarded during the Society's annual meeting, held from 10-12 November, in Lisbon.
(*) Tiago Carneiro, Lyne Khair, Clara C. Reis, Vanessa Borges, Bettina A. Moser, Toru M. Nakamura & Miguel Godinho Ferreira; ‘Telomeres avoid end detection by severing the checkpoint signal transduction pathway’; Nature, volume 467, issue 7312, pp 228-232. DOI: 10.1038/nature09353
The Telomere and Genome Stability Laboratory. Tiago Carneiro is first on the right.