Transcription increases multiple spontaneous point mutations in Salmonella enterica

The spontaneous rate of G·C→A·T mutations and a hotspot T·A→G·C transversion are known to increase with the frequency of transcription—increases that have been ascribed primarily to processes that affect only these specific mutations. To investigate how transcription induces other spontaneous point...

Full description

Saved in:
Bibliographic Details
Published inNucleic acids research Vol. 31; no. 15; pp. 4517 - 4522
Main Authors Hudson, Richard Ellis, Bergthorsson, Ulfar, Ochman, Howard
Format Journal Article
LanguageEnglish
Published England Oxford University Press 01.08.2003
Oxford Publishing Limited (England)
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:The spontaneous rate of G·C→A·T mutations and a hotspot T·A→G·C transversion are known to increase with the frequency of transcription—increases that have been ascribed primarily to processes that affect only these specific mutations. To investigate how transcription induces other spontaneous point mutations, we tested for its effects in repair‐proficient Salmonella enterica using reversion assays of chromosomally inserted alleles. Our results indicate that transcription increases rates of all tested point mutations in the induced gene: induction significantly increased the individual rates of an A·T→T·A transversion, an A·T→G·C transition and the pooled rates of the three other point mutations assayed. Although the S.enterica genome is thought to have a mutational bias towards G·C base pairs, transitions creating A·T pairs were approximately 10 times more frequent than the reverse mutation, resulting in an overall mutation pressure to lower G+C contents. Transitions occurred at roughly twice the rate of transversions, similar to results from sequence comparisons; however, several individual transversions are more frequent than the least common transition.
Bibliography:local:gkg651
To whom correspondence should be addressed. Tel: +1 520 626 8355; Fax: +1 520 621 3709; Email: hochman@email.arizona.edu
Received April 2, 2003; Revised May 31, 2003; Accepted June 10, 2003
ark:/67375/HXZ-45JRQNFB-M
istex:D29275C6461D6318F5C68D6ACCC859AEBE2ED8A9
ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
ISSN:0305-1048
1362-4962
1362-4962
DOI:10.1093/nar/gkg651