ArticleGenetics1996
Isolation and identification of genes activating UAS2-dependent ADH2 expression in Saccharomyces cerevisiae.
Article in Genetics, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Natural promoters and promoter engineering strategies for metabolic regulation in Saccharomyces cerevisiae.Journal of industrial microbiology & biotechnology · 2023Review
- Expression of MTAP inhibits tumor-related phenotypes in HT1080 cells via a mechanism unrelated to its enzymatic function.G3 (Bethesda, Md.) · 2014Article
- Carbon source dependent promoters in yeasts.Microbial cell factories · 2014Review
- Chemical genetic screening for compounds that preferentially inhibit growth of methylthioadenosine phosphorylase (MTAP)-deficient Saccharomyces cerevisiae.Journal of biomolecular screening · 2011Article
- Yeast carbon catabolite repression.Microbiology and molecular biology reviews : MMBR · 1998Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Two cis-acting elements have been identified that act synergistically to regulate expression of the glucose-repressed alcohol dehydrogenase 2 (ADH2) gene. UAS1 is bound by the trans-activator Adr1p. UAS2 is thought to be the binding site for an unidentified regulatory protein. A genetic selection based on a UAS2-dependent ADH2 reporter was devised to isolate genes capable of activating UAS2-dependent transcription. One set of UAS2-dependent genes contained SPT6/CRE2/SSN20. Multicopy SPT6 caused improper expression of chromosomal ADH2. A second set of UAS2-dependent clones contained a previously uncharacterized open reading frame designated MEU1 (Multicopy Enhancer of UAS2). A frame shift mutation in MEU1 abolished its ability to activate UAS2-dependent gene expression. Multicopy MEU1 expression suppressed the constitutive ADH2 expression caused by cre2-1. Disruption of MEU1 reduced endogenous ADH2 expression about twofold but had no effect on cell viability or growth. No homologues of MEU1 were identified by low-stringency Southern hybridization of yeast genomic DNA, and no significant homologues were found in the sequence data bases. A MEU1/beta-gal fusion protein was not localized to a particular region of the cell. MEU1 is linked to PPR1 on chromosome XII.
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Registered trials
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