Modulation of DNA repair by mutations flanking the DNA channel through RNA polymerase
AUTOR(ES)
Trautinger, Brigitte W.
FONTE
Oxford University Press
RESUMO
The RuvABC and RecBCD proteins promote rescue of stalled or broken DNA replication forks in Escherichia coli. Strains lacking these proteins cope poorly with DNA damage and have problems with chromosome segregation and cell division. We show how these difficulties are overcome to varying degrees by a sub-class of RNA polymerase mutations selected for their stringent phenotype. Thirty-five mutations were sequenced. All but one change single amino acids in RpoB or RpoC that lie on or near the path taken by DNA through the enzyme, indicating they may affect the stability of transcription complexes. Four mutant enzymes are shown to form unstable open complexes at the λcro promoter. At least one may also release stalled complexes or limit their formation, as it re duces the need for reactivation of transcription by GreA or GreB, and for transcription-coupled DNA repair of UV damage by Mfd. The results shed light on the interplay between DNA replication and transcription and suggest ways in which conflicts between these two vital cellular processes are avoided or resolved.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=139083Documentos Relacionados
- RNA polymerase mutants defective in the initiation of transcription-coupled DNA repair
- RNA polymerase II transcription inhibits DNA repair by photolyase in the transcribed strand of active yeast genes.
- In vivo modulation of yeast tRNA gene expression by 5'-flanking sequences.
- Introduction of specific point mutations into RNA polymerase II by gene targeting in mouse embryonic stem cells: evidence for a DNA mismatch repair mechanism.
- Initiation by the DNA-dependent RNA polymerase.