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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
9
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pubmed:dateCreated |
1994-9-19
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pubmed:abstractText |
Changes in gene dosage of the YAP1 gene, encoding the yAP-1 transcriptional regulatory protein, cause profound alterations in cellular drug and metal resistance. Previous studies on yAP-1 action in yeast cells have used the AP-1 response element (ARE) from simian virus 40 as an artificial site for yAP-1-mediated transcriptional activation. No authentic yeast target sites for control of gene expression by yAP-1 are known. Here we show that the GSH1 gene, encoding gamma-glutamylcysteine synthetase, is transcriptionally responsive to the yAP-1 protein. GSH1 encodes the rate-limiting step in yeast glutathione biosynthesis and contains within its promoter region a DNA element that matches the ARE in 11 of 12 positions. The GSH1 yAP-1 response element (YRE) was recognized by yAP-1 protein in vitro. Northern (RNA) blot analysis showed that GSH1 mRNA levels were responsive to YAP1 gene dosage. A site-directed mutation in the YRE that blocked yAP-1 binding in vitro prevented the mutant GSH1 promoter from responding to elevation in YAP1 gene dosage. A delta gsh1 mutant strain was constructed and unable to grow in the absence of exogenous glutathione. A mutant GSH1 gene lacking the YRE was unable to confer normal cadmium tolerance, although other yAP-1-mediated phenotypes remained normal. Thus, GSH1 is one of several genes that are transcriptionally controlled by yAP-1 and influence drug resistance.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-1448080,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-1525853,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-1687097,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-1878996,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-1889413,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-1899230,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-2005793,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-2160400,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-2190191,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-2659436,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-2834068,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-2836064,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-2838470,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-2868014,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-3053703,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-3289117,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-3305158,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-3319781,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-3346245,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-3532321,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-3815519,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-3883197,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-4388022,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-6310321,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-6323449,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-6336730,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-6387704,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-6394957,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-8182076,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-8226890,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-8313910,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7915005-8360174
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0270-7306
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
14
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pubmed:geneSymbol |
GSH1,
yAP-1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5832-9
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:7915005-Base Sequence,
pubmed-meshheading:7915005-DNA, Fungal,
pubmed-meshheading:7915005-DNA Primers,
pubmed-meshheading:7915005-Gene Expression Regulation, Fungal,
pubmed-meshheading:7915005-Glutamate-Cysteine Ligase,
pubmed-meshheading:7915005-Molecular Sequence Data,
pubmed-meshheading:7915005-Promoter Regions, Genetic,
pubmed-meshheading:7915005-Proto-Oncogene Proteins c-jun,
pubmed-meshheading:7915005-RNA, Fungal,
pubmed-meshheading:7915005-RNA, Messenger,
pubmed-meshheading:7915005-Saccharomyces cerevisiae,
pubmed-meshheading:7915005-Transcription, Genetic,
pubmed-meshheading:7915005-Transcriptional Activation
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pubmed:year |
1994
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pubmed:articleTitle |
GSH1, which encodes gamma-glutamylcysteine synthetase, is a target gene for yAP-1 transcriptional regulation.
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pubmed:affiliation |
Program in Molecular Biology, University of Iowa, Iowa City 52242.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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