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A novel cell response triggered by interphase centromere structural instability
Correspondence to Patrick Lomonte: lomonte{at}cgmc.univ-lyon1.fr
Interphase centromeres are crucial domains for the proper assembly of kinetochores at the onset of mitosis. However, it is not known whether the centromere structure is under tight control during interphase. This study uses the peculiar property of the infected cell protein 0 of herpes simplex virus type 1 to induce centromeric structural damage, revealing a novel cell response triggered by centromere destabilization. It involves centromeric accumulation of the Cajal body–associated coilin and fibrillarin as well as the survival motor neuron proteins. The response, which we have termed interphase centromere damage response (iCDR), was observed in all tested human and mouse cells, indicative of a conserved mechanism. Knockdown cells for several constitutive centromere proteins have shown that the loss of centromeric protein B provokes the centromeric accumulation of coilin. We propose that the iCDR is part of a novel safeguard mechanism that is dedicated to maintaining interphase centromeres compatible with the correct assembly of kinetochores, microtubule binding, and completion of mitosis.
-SAT; -satellite; CB, Cajal body; CENP, centromeric protein; ChIP, chromatin immunoprecipitation; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; HSV-1, herpes simplex virus type 1; iCDR, interphase centromere damage response; ICP0, infected cell protein 0; IF, immunofluorescence; PML, promyelocytic leukaemia; SMN, survival motor neuron; snRNA, small nuclear RNA; WB, Western blotting; wt, wild type.
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