Mrc1 transduces signals of DNA replication stress to activate Rad53

被引：420

作者：

Alcasabas, AA

Osborn, AJ

Bachant, J

Hu, FH

Werler, PJH

Bousset, K

Furuya, K

Diffley, JFX

Carr, AM

Elledge, SJ

机构：

[1] Baylor Coll Med, Verna & Marrs McLean Dept Biochem & Mol Biol, Houston, TX 77030 USA

[2] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA

[3] Baylor Coll Med, Howard Hughes Med Inst, Houston, TX 77030 USA

[4] Univ Sussex, Genome Damage & Stabil Ctr, Brighton BN1 9RR, E Sussex, England

[5] Imperial Canc Res Fund, Clare Hall Labs, S Mimms EN6 3LD, Herts, England

来源：

NATURE CELL BIOLOGY | 2001年 / 3卷 / 11期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1038/ncb1101-958

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Cells experiencing DNA replication stress activate a response pathway that delays entry into mitosis and promotes DNA repair and completion of DNA replication. The protein kinases ScRad53 and SpCds1 (in baker's and fission yeast, respectively) are central to this pathway. We describe a conserved protein Mrc1, mediator of the replication checkpoint, required for activation of ScRad53 and SpCds1 during replication stress. mrc1 mutants are sensitive to hydroxyurea and have a checkpoint defect similar to rad53 and cds1 mutants. Mrc1 may be the replicative counterpart of Rad9 and Crb2, which are required for activating ScRad53 and Chk1 in response to DNA damage.

引用

页码：958 / 965

页数：8

共 34 条

[1] THE SAD1/RAD53 PROTEIN-KINASE CONTROLS MULTIPLE CHECKPOINTS AND DNA DAMAGE-INDUCED TRANSCRIPTION IN YEAST [J].