Regulation of RAD53 by the ATM-like kinases MEC1 and TEL1 in yeast cell cycle checkpoint pathways

被引：547

作者：

Sanchez, Y ^{[1
]}

Desany, BA ^{[1
]}

Jones, WJ ^{[1
]}

Liu, QH ^{[1
]}

Wang, B ^{[1
]}

Elledge, SJ ^{[1
]}

机构：

[1] BAYLOR COLL MED, HOWARD HUGHES MED INST, DEPT MOLEC & HUMAN GENET, DEPT BIOCHEM, HOUSTON, TX 77030 USA

来源：

SCIENCE | 1996年 / 271卷 / 5247期

关键词：

D O I：

10.1126/science.271.5247.357

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Mutants of the Saccharomyces cerevisiae ataxia telangiectasia mutated (ATM) homolog MEC1/SAD3/ESR1 were identified that could live only if the RAD53/SAD1 checkpoint kinase was overproduced. MEC1 and a structurally related gene, TEL1, have overlapping functions in response to DNA damage and replication blocks that in mutants can be provided by overproduction of RAD53. Both MEC1 and TEL1 were found to control phosphorylation of Rad53p in response to DNA damage. These results indicate that RAD53 is a signal transducer in the DNA damage and replication checkpoint pathways and functions downstream of two members of the ATM lipid kinase family. Because several members of this pathway are conserved among eukaryotes, it is likely that a RAD53-related kinase will function downstream of the human ATM gene product and play an important role in the mammalian response to DNA damage.

引用

页码：357 / 360

页数：4

共 36 条

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