Coilin (green) gloms onto damaged centromeres (red).

Before they advance through mitosis, cells carefully check for damage to their DNA and to the spindle that helps divvy up the chromosomes. During interphase, cells also monitor the centromeres that will be necessary for chromosomes to separate, as Morency et al. show on page 757. The researchers identify a crew of proteins that hurries to marred centromeres.

Centromeres provide anchorage for kinetochores, which latch onto the spindle fibers that pull the chromosomes apart. Cells halt mitosis if kinetochores are defective. But scientists didn't know whether cells also kept track of centromere integrity.

Morency et al. had previously observed that centromeres are subject to attack by the herpes simplex virus, which spurs cells to demolish the centromere proteins CENP-A, CENP-B, and CENP-C. The researchers have now identified a novel cell response to this destruction during interphase. Three proteins—coilin, fibrillarin, and SMN—clustered at the battered centromeres. Depleting any of the three CENP proteins with siRNA lured coilin to the centromeres. But fibrillarin and SMN remained aloof. That difference suggests that these two proteins respond to more severe damage than does coilin.

Coilin, fibrillarin, and SMN don't appear to replace the missing CENPs, and their function at the centromeres remains a mystery. The proteins are also found in bodies where small RNAs mature, so perhaps they deliver these RNAs to centrosomes to trigger repair. Whether centromere damage naturally occurs often enough to hamper cells is uncertain, but it could result from any stress that injures the DNA or chromatin.