Opposing Roles of the Holliday Junction Processing Systems of Escherichia coli in Recombination-Dependent Adaptive Mutation

Aspects of the molecular mechanism of "adaptive" mutation are emerging from one experimental system: reversion of an Escherichia coli lac frameshift mutation carried on a conjugative plasmid. Homologous recombination is required and the mutations resemble polymerase errors. Reports implica...

Full description

Saved in:
Bibliographic Details
Published in:Genetics (Austin) 1996-03, Vol.142 (3), p.681-691
Main Authors: Harris, R. S, Ross, K. J, Rosenberg, S. M
Format: Article
Language:English
Subjects:
Adaptation, Physiological
Bacteria
Bacterial Proteins - genetics
Conjugation, Genetic
DNA Helicases
DNA-Binding Proteins - genetics
Endodeoxyribonucleases - genetics
Escherichia coli
Escherichia coli - genetics
Escherichia coli - growth & development
Escherichia coli Proteins
Genetics
Investigations
Lac Operon
Models, Genetic
Mutation
Recombination, Genetic
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Aspects of the molecular mechanism of "adaptive" mutation are emerging from one experimental system: reversion of an Escherichia coli lac frameshift mutation carried on a conjugative plasmid. Homologous recombination is required and the mutations resemble polymerase errors. Reports implicating a role for conjugal transfer proteins suggested that the mutation mechanism is ordinary replication error occurring during transfer synthesis, followed by conjugation-like recombination, to capture the replicated fragment into an intact replicon. Whereas conjugational recombination uses either of two systems of Holliday junction resolution, we find that the adaptive lac reversions are inhibited by one resolution system and promoted by the other. Moreover, temporary absence of both resolution systems promotes mutation. These results imply that recombination intermediates themselves promote the mutations.
ISSN:0016-6731
1943-2631
1943-2631
DOI:10.1093/genetics/142.3.681