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Mutat. Res. Dec (2007); 625(1):164-76
Pol32 is required for Pol zeta-dependent translesion synthesis and prevents double-strand breaks at the replication fork-
Hanna M, Ball LG, Tong AH, Boone C, Xiao W
Department of Microbiology and Immunology, University of Saskatchewan, 107 Wiggins Road, Saskatoon, Sask-, Canada-
Abstract: POL32 encodes a non-essential subunit of Poldelta and plays a role in Poldelta processivity and DNA repair- In order to understand how Pol32 is involved in these processes, we performed extensive genetic analysis and demonstrated that POL32 is required for Polzeta-mediated translesion synthesis, but not for Poleta-mediated activity- Unlike Polzeta, inactivation of Pol32 does not result in decreased spontaneous mutagenesis, nor does it limit genome instability in the absence of the error-free postreplication repair pathway- In contrast, inactivation of Pol32 results in an increased rate of replication slippage and recombination- A genome-wide synthetic lethal screen revealed that in the absence of Pol32, homologous recombination repair and cell cycle checkpoints play crucial roles in maintaining cell survival and growth- These results are consistent with a model in which Pol32 functions as a coupling factor to facilitate a switch from replication to translesion synthesis when Poldelta encounters replication-blocking lesions- When Pol32 is absent, the S-phase checkpoint complex Mrc1-Tof1 becomes crucial to stabilize the stalled replication fork and recruit Top3 and Sgs1- Lack of any of the above activities will cause double strand breaks at or near the replication fork that require recombination as well as Rad9 for cell survival-
[PUBMED: 17681555] Download Biogrid Interactions in a variety of formats including PSI FormatPUBMED
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Chris Stark, Bobby-Joe Breitkreutz, Teresa Reguly, Lorrie Boucher, Ashton Breitkreutz, Mike Tyers.
Nucleic Acids Res. Jan 1;34:D535-9.