作者: Mithilesh Mishra , Jim Karagiannis , Susanne Trautmann , Hongyan Wang , Dannel McCollum
DOI: 10.1242/JCS.01244
关键词:
摘要: Fission yeast mutants defective in actomyosin ring formation and function exhibit a prolonged G2 delay following cytokinesis failure. This depends on the SIN, signaling network essential for cytokinesis, non-essential Cdc14p family phosphatase, Clp1p/Flp1p has been proposed to signify checkpoint mechanism. However, physiological relevance of this Clp1p/Flp1p-dependent is unclear because all previous studies were carried out using mutations components under fully restrictive conditions thus these cells would have died regardless presence checkpoint. Here we show that delays caused by minor perturbations different cytokinetic machinery, which normally cause only mild defects, become lethal when inactivated. In addition, does not simply inhibit further rounds nuclear division, but also allows damaged rings be maintained facilitate completion cell division. Ectopic activation SIN significantly bypasses requirement as well cytokinesis. We conclude provides previously unrecognized survival advantage division apparatus mildly perturbed.