Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-2-15
pubmed:abstractText
Stress-induced mutagenesis describes the accumulation of mutations that occur in nongrowing cells, in contrast to mutagenesis that occurs in actively dividing populations, and has been referred to as stationary-phase or adaptive mutagenesis. The most widely studied system for stress-induced mutagenesis involves monitoring the appearance of Lac(+) revertants of the strain FC40 under starvation conditions in Escherichia coli. The SOS-inducible translesion DNA polymerase DinB plays an important role in this phenomenon. Loss of DinB (DNA pol IV) function results in a severe reduction of Lac(+) revertants. We previously reported that NusA, an essential component of elongating RNA polymerases, interacts with DinB. Here we report our unexpected observation that wild-type NusA function is required for stress-induced mutagenesis. We present evidence that this effect is unlikely to be due to defects in transcription of lac genes but rather is due to an inability to adapt and mutate in response to environmental stress. Furthermore, we extended our analysis to the formation of stress-induced mutants in response to antibiotic treatment, observing the same striking abolition of mutagenesis under entirely different conditions. Our results are the first to implicate NusA as a crucial participant in the phenomenon of stress-induced mutagenesis.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-10628968, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-11006276, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-11433357, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-11463382, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-11515498, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-11683261, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-11830643, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-12760017, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-14617178, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-15020458, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-15262920, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-15629916, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-15869329, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-16045619, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-16168374, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-16761951, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-17082307, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-17917873, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-17917874, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-18996995, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-1916241, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-19270270, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-20152136, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-3023618, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-6154941, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-6302271, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-6337627, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-6771759, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-7826010, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-8023163, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-8023164, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-8146657, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-8770582, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-8849879, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-8978023, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-9045812, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-9303418, http://linkedlifedata.com/resource/pubmed/commentcorrection/20036541-9804552
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1879-0445
pubmed:author
pubmed:copyrightInfo
Copyright 2010 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
12
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
80-5
pubmed:dateRevised
2011-7-20
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
The transcription elongation factor NusA is required for stress-induced mutagenesis in Escherichia coli.
pubmed:affiliation
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural