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J. Biol. Chem., Vol. 278, Issue 27, 25247-25255, July 4, 2003

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Properties of Bacteriophage T4 Proteins Deficient in Replication Repair^*

Farid A. Kadyrov and John W. Drake 

From the Laboratory of Molecular Genetics, NIEHS, National Institutes of Health/Department of Health and Human Services, Research Triangle Park, North Carolina 27709-2233

An epistasis group of mutations engendering increased sensitivity to diverse DNA-damaging agents was described previously in bacteriophage T4. These mutations are alleles of genes 32 and 41, which, respectively, encode a single-stranded DNA-binding protein (gp32) and the replicative DNA helicase (gp41). The mechanism by which the lethality of DNA damage is mitigated is unknown but seems not to involve the direct reversal of damage, excision repair, conventional recombination repair, or translesion synthesis. Here we explore the hypothesis that the mechanism involves a switch in DNA primer extension from the cognate template to an alternative template, the just-synthesized daughter strand of the other parental strand. The activities of the mutant proteins are reduced about 2-fold (for gp32) or 4-fold (for gp41) in replication complexes catalyzing coordinated synthesis of leading and lagging strands, in binding single-stranded DNA, promoting DNA annealing, and promoting branch migration. In striking contrast, the mutant proteins are strongly impaired in promoting template switching, thus supporting the hypothesis of survival by template switching.

Received for publication, March 13, 2003 , and in revised form, April 9, 2003.

This report is dedicated to the memory of Gisela Mosig, whose passion and skill in unraveling the complexities of T4 DNA transactions were unparalleled.

^* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Laboratory of Molecular Genetics E3–01, NIEHS, National Institutes Health, Research Triangle Park, NC 27709-2233. Tel.: 919-541-3361; Fax: 919-541-7613; E-mail: drake{at}niehs.nih.gov.

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