Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-6-18
pubmed:abstractText
An Escherichia coli pgsA null mutant deficient in acidic phospholipids shows a thermosensitive cell lysis phenotype because of activation of the Rcs phosphorelay signal transduction system. We conducted a DNA microarray analysis with special attention to the genes affected by growth temperature in the mutant deficient in acidic phospholipids. Among the genes identified as highly expressed at high temperature in the pgsA null mutant, the osmB gene was shown to be dependent on the Rcs system for the high expression by dot blot hybridization. Induction of the cloned osmB in the pgsA null mutant caused the thermosensitive defect even in the absence of the Rcs system. Although the deletion of osmB did not suppress the thermosensitivity in the presence of the Rcs system, indicating a multifactorial nature of the deleterious effect of the Rcs activation, we suggest that the osmB hyperexpression is one of the causes of the Rcs-dependent lysis phenotype of the pgsA null mutant.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1260
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
143-51
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Hyperexpression of the osmB gene in an acidic phospholipid-deficient Escherichia coli mutant.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, Course in Life Science, Graduate School of Science and Engineering, Saitama University, Saitama 338-8570, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't