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Qri2/Nse4, a component of the essential Smc5/6 DNA repair complex
Author(s) -
Hu Bin,
Liao Chunyan,
Millson Stefan H.,
Mollapour Mehdi,
Prodromou Chrisostomos,
Pearl Laurence H.,
Piper Peter W.,
Panaretou Barry
Publication year - 2005
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2005.04531.x
Subject(s) - biology , cell cycle checkpoint , dna damage , microbiology and biotechnology , checkpoint kinase 2 , g2 m dna damage checkpoint , dna repair , mitosis , mutant , saccharomyces cerevisiae , effector , chromosome segregation , chek1 , genome instability , cell cycle , dna , genetics , chromosome , cell , gene
Summary We demonstrate a role for Qri2 in the essential DNA repair function of the Smc5/6 complex in Saccharomyces cerevisiae . We generated temperature‐sensitive ( ts ) mutants in QRI2 and characterized their properties. The mutants arrest after S phase and prior to mitosis. Furthermore, the arrest is dependant on the Rad24 checkpoint, and is also accompanied by phosphorylation of the Rad53 checkpoint effector kinase. The mutants also display genome instability and are sensitive to agents that damage DNA. Two‐hybrid screens reveal a physical interaction between Qri2 and proteins that are n on‐ S mc e lements of the Smc5/6 DNA repair complex, which is why we propose the name NSE4 for the open reading frame previously known as QRI2 . A key role for Nse4 in Smc5/6 function is likely, as overexpressing known subunits of the Smc5/6 complex suppresses nse4 ts cell cycle arrest. The nse4 ts growth arrest is non‐lethal and unlike the catastrophic nuclear fragmentation phenotype of smc6 ts mutants, the nucleus remains intact; replicative intermediates and sheared DNA are not detected. This could imply a role for Nse4 in maintenance of higher order chromosome structure.