Linked Life Data

10708375

Source:http://linkedlifedata.com/resource/pubmed/id/10708375

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2000-5-1
pubmed:abstractText
Changing the growth mode of Saccharomyces cerevisiae by adding fermentable amounts of glucose to cells growing on a non-fermentable carbon source leads to rapid repression of general stress-responsive genes like HSP12. Remarkably, glucose repression of HSP12 appeared to occur even at very low glucose concentrations, down to 0.005%. Although these low levels of glucose do not induce fermentative growth, they do act as a growth signal, since upon addition of glucose to a concentration of 0.02%, growth rate increased and ribosomal protein gene transcription was up-regulated. In an attempt to elucidate how this type of glucose signalling may operate, several signalling mutants were examined. Consistent with the low amounts of glucose that elicit HSP12 repression, neither the main glucose-repression pathway nor cAMP-dependent activation of protein kinase A appeared to play a role in this regulation. Using mutants involved in glucose metabolism, evidence was obtained suggesting that glucose 6-phosphate serves as a signalling molecule. To identify the target for glucose repression on the promoter of the HSP12 gene, a promoter deletion series was used. The major transcription factors governing (stress-induced) transcriptional activation of HSP12 are Msn2p and Msn4p, binding to the general stress-responsive promoter elements (STREs). Surprisingly, glucose repression of HSP12 appeared to be independent of Msn2/4p: HSP12 transcription in glycerol-grown cells was unaffected in a deltamsn2deltamsn4 strain. Nevertheless, evidence was obtained that STRE-mediated transcription is the target of repression by low amounts of glucose. These data suggest that an as yet unidentified factor is involved in STRE-mediated transcriptional regulation of HSP12.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1350-0872
pubmed:author
pubmed:issnType
Print
pubmed:volume
146 ( Pt 2)
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
367-75
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10708375-Culture Media, pubmed-meshheading:10708375-Cyclic AMP, pubmed-meshheading:10708375-Cyclic AMP-Dependent Protein Kinases, pubmed-meshheading:10708375-Enzyme Activation, pubmed-meshheading:10708375-Gene Expression Regulation, Fungal, pubmed-meshheading:10708375-Glucose, pubmed-meshheading:10708375-Glucose-6-Phosphate, pubmed-meshheading:10708375-Heat-Shock Proteins, pubmed-meshheading:10708375-Phosphorylation, pubmed-meshheading:10708375-Promoter Regions, Genetic, pubmed-meshheading:10708375-RNA, Messenger, pubmed-meshheading:10708375-Repressor Proteins, pubmed-meshheading:10708375-Saccharomyces cerevisiae, pubmed-meshheading:10708375-Saccharomyces cerevisiae Proteins, pubmed-meshheading:10708375-Signal Transduction, pubmed-meshheading:10708375-Trans-Activators, pubmed-meshheading:10708375-Transcription, Genetic
pubmed:year
2000
pubmed:articleTitle
Very low amounts of glucose cause repression of the stress-responsive gene HSP12 in Saccharomyces cerevisiae.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, IMBW, BioCentrum Amsterdam, Vrije Universiteit, The Netherlands.
pubmed:publicationType
Journal Article