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Mol Cell. 2007 Dec 28;28(6):1058-70.

UmuD and RecA directly modulate the mutagenic potential of the Y family DNA polymerase DinB.

Author information

1
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

Abstract

DinB is the only translesion Y family DNA polymerase conserved among bacteria, archaea, and eukaryotes. DinB and its orthologs possess a specialized lesion bypass function but also display potentially deleterious -1 frameshift mutagenic phenotypes when overproduced. We show that the DNA damage-inducible proteins UmuD(2) and RecA act in concert to modulate this mutagenic activity. Structural modeling suggests that the relatively open active site of DinB is enclosed by interaction with these proteins, thereby preventing the template bulging responsible for -1 frameshift mutagenesis. Intriguingly, residues that define the UmuD(2)-interacting surface on DinB statistically covary throughout evolution, suggesting a driving force for the maintenance of a regulatory protein-protein interaction at this site. Together, these observations indicate that proteins like RecA and UmuD(2) may be responsible for managing the mutagenic potential of DinB orthologs throughout evolution.

PMID:
18158902
PMCID:
PMC2265384
DOI:
10.1016/j.molcel.2007.10.025
[Indexed for MEDLINE]
Free PMC Article

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