Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-4-23
pubmed:abstractText
Accumulation of non-metabolizable glucose-phosphate in Escherichia coli is growth inhibitory and induces a specific stress response. This is sensed and coordinated by a transcription factor SgrR that in turn activates expression of the primary effector of the stress response, a small regulatory RNA, SgrS. This RNA negatively regulates the translation and stability of the ptsG mRNA, which encodes the major glucose transporter of E. coli. The effect of SgrS on ptsG mRNA occurs through a base-pairing mechanism facilitated by the RNA chaperone Hfq. Other host factors required for the regulation by SgrS include the endonuclease RNase E and components of the RNA degradosome, particularly enolase, a glycolytic enzyme whose role in RNA degradation is currently not understood. There are many unanswered questions regarding the physiology of glucose-phosphate stress, including the cellular signals and targets involved. However, it is clear that the small RNA SgrS is required for adaptation to stress. The current model is that SgrS promotes recovery by stopping the synthesis of glucose transport proteins, which in turn limits the accumulation of toxic sugar-phosphates.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1369-5274
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
146-51
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Physiological consequences of small RNA-mediated regulation of glucose-phosphate stress.
pubmed:affiliation
Department of Microbiology, University of Illinois at Urbana-Champaign B213, Chemical and Life Sciences Laboratories (CLSL), MC-110 Urbana, IL 61801, USA. cvanderp@life.uiuc.edu
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't