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RAD53 , DUN1 and PDS1 define two parallel G 2 /M checkpoint pathways in budding yeast
Author(s) -
Gardner Richard,
Putnam Charles W.,
Weinert Ted
Publication year - 1999
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/18.11.3173
Subject(s) - biology , budding yeast , budding , yeast , saccharomyces cerevisiae , g2 m dna damage checkpoint , genetics , microbiology and biotechnology , cell cycle checkpoint , cell cycle , gene
Eukaryotic checkpoint genes regulate multiple cellular responses to DNA damage. In this report, we examine the roles of budding yeast genes involved in G 2 /M arrest and tolerance to UV exposure. A current model posits three gene classes: those encoding proteins acting on damaged DNA (e.g. RAD9 and RAD24 ), those transducing a signal ( MEC1 , RAD53 and DUN1 ) or those participating more directly in arrest ( PDS1 ). Here, we define important features of the pathways subserved by those genes. MEC1 , which we find is required for both establishment and maintenance of G 2 /M arrest, mediates this arrest through two parallel pathways. One pathway requires RAD53 and DUN1 (the ‘ RAD53 pathway’); the other pathway requires PDS1 . Each pathway independently contributes ∼50% to G 2 /M arrest, effects demonstrable after cdc13 ‐induced damage or a double‐stranded break inflicted by the HO endonuclease. Similarly, both pathways contribute independently to tolerance of UV irradiation. How the parallel pathways might interact ultimately to achieve arrest is not yet understood, but we do provide evidence that neither the RAD53 nor the PDS1 pathway appears to maintain arrest by inhibiting adaptation. Instead, we think it likely that both pathways contribute to establishing and maintaining arrest.