Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-3-7
pubmed:abstractText
High-pressure treatment (>100 MPa) is known to induce several heat shock proteins as well as an SOS response in Escherichia coli. In the current work, we have investigated properties with respect to high-pressure treatment of mutants-deficient in Lon, a pressure-induced ATP-dependent protease that belongs to the heat shock regulon but that also has a link to the SOS regulon. We report that lon mutants show increased pressure sensitivity and exhibit hyperfilamentation during growth after high-pressure treatment. Both phenotypes could be entirely attributed to the action of the SOS protein SulA, a potent inhibitor of the cell division ring protein FtsZ and a specific target of the Lon protease, since they were suppressed by knock-out of SulA. Introduction of the lexA1 allele, which effectively blocks the entire SOS response, also suppressed the high pressure hypersensitivity of lon mutants, but not their UV hypersensitivity. These results indicate the existence of a SulA-dependent pathway of high-pressure-induced cell filamentation, and suggest involvement of the SOS response, and particularly of SulA, in high-pressure-mediated cell death in E. coli strains which are compromised in Lon function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0923-2508
pubmed:author
pubmed:issnType
Print
pubmed:volume
156
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
233-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
SulA-dependent hypersensitivity to high pressure and hyperfilamentation after high-pressure treatment of Escherichia coli lon mutants.
pubmed:affiliation
Laboratory of Food Microbiology, Katholieke Universiteit Leuven, Kasteelpark Arenberg 22, 3001 Heverlee, Belgium. abram.aertsen@agr.kuleuven.ac.be
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't