Replisome pausing in mutagenesis

Robb Moses, Anne Byford, James A. Hejna

Research output: Contribution to journalArticle

1 Citation (Scopus)

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)
JournalChromosoma
Volume102
Issue number1 Supplement
DOIs
StatePublished - Dec 1992

Fingerprint

Mutagenesis
DNA Polymerase I
Mutation
DNA Polymerase III
Holoenzymes
Temperature
DNA Repair
DNA Damage
Cell Survival
Alleles
Escherichia coli
Genes

ASJC Scopus subject areas

  • Genetics

Cite this

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

Replisome pausing in mutagenesis. / Moses, Robb; Byford, Anne; Hejna, James A.

In: Chromosoma, Vol. 102, No. 1 Supplement, 12.1992.

Research output: Contribution to journalArticle

Moses, R, Byford, A & Hejna, JA 1992, 'Replisome pausing in mutagenesis', Chromosoma, vol. 102, no. 1 Supplement. https://doi.org/10.1007/BF02451801
Moses, Robb ; Byford, Anne ; Hejna, James A. / Replisome pausing in mutagenesis. In: Chromosoma. 1992 ; Vol. 102, No. 1 Supplement.
@article{e1004a1031d94a9c96a4a75a88bba2d5,
title = "Replisome pausing in mutagenesis",
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.",
author = "Robb Moses and Anne Byford and Hejna, {James A.}",
year = "1992",
month = "12",
doi = "10.1007/BF02451801",
language = "English (US)",
volume = "102",
journal = "Chromosoma",
issn = "0009-5915",
publisher = "Springer Science and Business Media Deutschland GmbH",
number = "1 Supplement",

}

TY - JOUR

T1 - Replisome pausing in mutagenesis

AU - Moses, Robb

AU - Byford, Anne

AU - Hejna, James A.

PY - 1992/12

Y1 - 1992/12

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0027074533&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027074533&partnerID=8YFLogxK

U2 - 10.1007/BF02451801

DO - 10.1007/BF02451801

M3 - Article

VL - 102

JO - Chromosoma

JF - Chromosoma

SN - 0009-5915

IS - 1 Supplement

ER -