Abstract：
:Translesion synthesis (TLS) employs low fidelity polymerases to replicate past damaged DNA in a potentially error-prone process. Regulatory mechanisms that prevent TLS-associated mutagenesis are unknown; however, our recent studies suggest that the PCNA-binding protein Spartan plays a role in suppression of damage-induced mutagenesis. Here, we show that Spartan negatively regulates error-prone TLS that is dependent on POLD3, the accessory subunit of the replicative DNA polymerase Pol δ. We demonstrate that the putative zinc metalloprotease domain SprT in Spartan directly interacts with POLD3 and contributes to suppression of damage-induced mutagenesis. Depletion of Spartan induces complex formation of POLD3 with Rev1 and the error-prone TLS polymerase Pol ζ, and elevates mutagenesis that relies on POLD3, Rev1 and Pol ζ. These results suggest that Spartan negatively regulates POLD3 function in Rev1/Pol ζ-dependent TLS, revealing a previously unrecognized regulatory step in error-prone TLS.
journal_name
Nucleic Acids Resjournal_title
Nucleic acids researchauthors
Kim MS,Machida Y,Vashisht AA,Wohlschlegel JA,Pang YP,Machida YJdoi
10.1093/nar/gks1267subject
Has Abstractpub_date
2013-02-01 00:00:00pages
1661-8issue
3eissn
0305-1048issn
1362-4962pii
gks1267journal_volume
41pub_type
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