Excision Repair Cross Complementing Rodent Repair Deficiency Complementation 6 Like Protein (ERCC6L)

PICH was phosphorylated on thr1063 by CDK1 (CDC2) during mitosis, resulting in recruitment of PLK1. Starting in prometaphase, PICH accumulated at kinetochores and inner centromeres. It decorated threads that formed during metaphase before increasing in length and progressively diminishing during anaphase. PICH-positive threads connected sister kinetochores and were dependent on tension, sensitive to DNase, and exacerbated in response to premature loss of cohesins or inhibition of topoisomerase II , suggesting that the threads represented stretched centromeric chromatin. Depletion of PICH caused selective loss of MAD2 (MAD2L1) from kinetochores and completely abrogated the spindle checkpoint, resulting in massive chromosome missegregation.