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| Cdc2-cyclin B kinase activity links Crb2 and Rqh1-topoisomerase III |
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| Author(s): Caspari T, Murray JM, Carr AM |
| Source: GENES & DEVELOPMENT Volume: 16 Issue: 10 Pages: 1195-1208 Published: MAY 15 2002 |
| Times Cited: 95 References: 59 |
| Abstract: The availability of a sister chromatid, and thus the cell cycle phase in which DNA double-strand breaks (DSBs) occur, influences the choice between homologous recombination (HR) or nonhomologous end joining (NHEJ). The sequential activation and destruction of CDK-cyclin activities controls progression through the cell cycle. Here we provide evidence that the major Schizosaccharomyces pombe CDK, Cdc2-cyclin B, influences recombinational repair of radiation-induced DSBs during the G, phase at two distinct stages. At an early stage in HR, a defect in Cdc2 kinase activity, which is caused by a single amino acid change in cyclin B, affects the formation of Rhp51 (Rad51(sp)) foci in response to ionizing radiation in a process that is redundant with the function of Rad50. At a late stage in HR, low Cdc2-cyclin B activity prevents the proper regulation of topoisomerase III (Top3) function, disrupting a recombination step that occurs after the assembly of Rhp51 foci. This effect of Cdc2-cyclin B kinase on Top3 function is mediated by the BRCT-domain-containing checkpoint protein Crb2, thus linking checkpoint proteins directly with recombinational repair in G(2). Our data suggest a model in which CDK activity links processing of recombination intermediates to cell cycle progression via checkpoint proteins. |
| Document Type: Article |
| Language: English |
| Reprint Address: Carr, AM (reprint author), Univ Sussex, Genome Damage & Stabil Ctr, Brighton BN1 9RQ, E Sussex England |
Addresses:
1. Univ Sussex, Genome Damage & Stabil Ctr, Brighton BN1 9RQ, E Sussex England |
| Publisher: COLD SPRING HARBOR LAB PRESS, 1 BUNGTOWN RD, PLAINVIEW, NY 11724 USA |
| Subject Category: Cell Biology; Developmental Biology; Genetics & Heredity |
| IDS Number: 555UJ |
| ISSN: 0890-9369 |
| DOI: 10.1101/gad.221402 |
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