Linked Life Data

16556229

Source:http://linkedlifedata.com/resource/pubmed/id/16556229

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-3-24
pubmed:abstractText
Bacteria rapidly adapt to changes in growth conditions through control of transcription and specific mRNA degradation. Interplay of both mechanisms must exist in order to achieve fine-tuned regulation of gene expression. Transcription of the Escherichia coli bolA gene is mediated by the RpoS/sigmaS transcription factor in response to environmental signals. In this report it is shown that the mechanisms of bolA1p mRNA transcription and degradation are tightly connected at the onset of stationary phase and in response to sudden carbon starvation. In stationary phase, bolA1p mRNA levels were reduced 2.5-fold in a poly(A)-polymerase I (PAPI) mutant, explained by the significant threefold reduction in sigmaS protein levels in the same strain. Furthermore, fusions with the rpoS gene, analysis of the stability of sigmaS and the levels of RssB indicate that the absence of PAPI enhances RssB-mediated sigmaS proteolysis specifically in starved cells. The fact that PAPI induces higher cellular levels of a global regulator is a novel finding of wide biological significance. PAPI could work as a linker between transcription and mRNA degradation with the ultimate goal of adapting and surviving to growth-limiting conditions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0950-382X
pubmed:author
pubmed:issnType
Print
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
177-88
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Poly(A)-polymerase I links transcription with mRNA degradation via sigmaS proteolysis.
pubmed:affiliation
Instituto de Tecnologia Química e Biológica (ITQB), Universidade Nova de Lisboa, Apt 127, 2781-901 Oeiras, Portugal.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't