Replisome pausing in mutagenesis

Robb E. Moses, Anne Byford, James A. Hejna

Research output: Contribution to journalArticle

1 Scopus citations

Abstract

E. coli cells containing a temperature-sensitive dnaE mutation, in the α-subunit of holoenzyme DNA polymerase III, do not survive at the restrictive temperature. Such cells may survive in the presence of the pcbA1 mutation, an allele of the gyrB gene. Such survival is dependent on an active DNA polymerase I. Evidence indicates that DNA polymerase I interacts directly in the replisome (REP·A). Despite normal survival for cells using the pcbA replication pathway after some type of DNA damage, we have noted a failure of damage-induced mutagenesis. Here we present evidence supporting a model of replisome pausing in cells dependent upon the pcbA replication pathway. The model argues that the (REP·A) complex pauses longer at the site of the lesion, allowing excision repair to occur completely. In the normal replication pathway (REP·E) bypass of the lesion occurs, fixing the mutation.

Original languageEnglish (US)
Pages (from-to)S157-S160
JournalChromosoma
Volume102
Issue number1 Supplement
DOIs
StatePublished - Dec 1 1992

ASJC Scopus subject areas

  • Genetics
  • Genetics(clinical)

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    Moses, R. E., Byford, A., & Hejna, J. A. (1992). Replisome pausing in mutagenesis. Chromosoma, 102(1 Supplement), S157-S160. https://doi.org/10.1007/BF02451801