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dc.contributor.authorPina, Benjamin
dc.contributor.authorBerger, Shelley L.
dc.contributor.authorMarcus, Gregory A.
dc.contributor.authorSilverman, Neal S.
dc.contributor.authorAgapite, Julie
dc.contributor.authorGuarente, Leonard
dc.date2022-08-11T08:09:09.000
dc.date.accessioned2022-08-23T16:19:31Z
dc.date.available2022-08-23T16:19:31Z
dc.date.issued1993-10-01
dc.date.submitted2009-12-15
dc.identifier.citationMol Cell Biol. 1993 Oct;13(10):5981-9. <a href="http://mcb.asm.org/cgi/reprint/13/10/5981">Link to article on publisher's site</a>
dc.identifier.issn0270-7306 (Print)
dc.identifier.pmid8413201
dc.identifier.urihttp://hdl.handle.net/20.500.14038/35067
dc.description.abstractWe describe the isolation of a yeast gene, ADA3, mutations in which prevent the toxicity of GAL4-VP16 in vivo. Toxicity was previously proposed to be due to the trapping of general transcription factors required at RNA polymerase II promoters (S. L. Berger, B. Pina, N. Silverman, G. A. Marcus, J. Agapite, J. L. Regier, S. J. Triezenberg, and L. Guarente, Cell 70:251-265, 1992). trans activation by VP16 as well as the acidic activation domain of GCN4 is reduced in the mutant. Other activation domains, such as those of GAL4 and HAP4, are only slightly affected in the mutant. This spectrum is similar to that observed for mutants with lesions in ADA2, a gene proposed to encode a transcriptional adaptor. The ADA3 gene is not absolutely essential for cell growth, but gene disruption mutants grow slowly and are temperature sensitive. Strains doubly disrupted for ada2 and ada3 grow no more slowly than single mutants, providing further evidence that these genes function in the same pathway. Selection of initiation sites by the general transcriptional machinery in vitro is altered in the ada3 mutant, providing a clue that ADA3 could be a novel general transcription factor involved in the response to acidic activators.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=8413201&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://mcb.asm.org/cgi/reprint/13/10/5981
dc.subjectAmino Acid Sequence
dc.subjectBase Sequence
dc.subjectCloning, Molecular
dc.subjectDNA, Fungal
dc.subjectDrug Resistance, Microbial
dc.subjectFungal Proteins
dc.subject*Genes, Fungal
dc.subjectMolecular Sequence Data
dc.subjectMutation
dc.subjectPromoter Regions, Genetic
dc.subjectSaccharomyces cerevisiae
dc.subject*Saccharomyces cerevisiae Proteins
dc.subjectTrans-Activators
dc.subjectTranscription Factors
dc.subjectTranscription, Genetic
dc.subjectTranscriptional Activation
dc.subjectImmunology and Infectious Disease
dc.titleADA3: a gene, identified by resistance to GAL4-VP16, with properties similar to and different from those of ADA2
dc.typeJournal Article
dc.source.journaltitleMolecular and cellular biology
dc.source.volume13
dc.source.issue10
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/infdis_pp/28
dc.identifier.contextkey1088925
html.description.abstract<p>We describe the isolation of a yeast gene, ADA3, mutations in which prevent the toxicity of GAL4-VP16 in vivo. Toxicity was previously proposed to be due to the trapping of general transcription factors required at RNA polymerase II promoters (S. L. Berger, B. Pina, N. Silverman, G. A. Marcus, J. Agapite, J. L. Regier, S. J. Triezenberg, and L. Guarente, Cell 70:251-265, 1992). trans activation by VP16 as well as the acidic activation domain of GCN4 is reduced in the mutant. Other activation domains, such as those of GAL4 and HAP4, are only slightly affected in the mutant. This spectrum is similar to that observed for mutants with lesions in ADA2, a gene proposed to encode a transcriptional adaptor. The ADA3 gene is not absolutely essential for cell growth, but gene disruption mutants grow slowly and are temperature sensitive. Strains doubly disrupted for ada2 and ada3 grow no more slowly than single mutants, providing further evidence that these genes function in the same pathway. Selection of initiation sites by the general transcriptional machinery in vitro is altered in the ada3 mutant, providing a clue that ADA3 could be a novel general transcription factor involved in the response to acidic activators.</p>
dc.identifier.submissionpathinfdis_pp/28
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pages5981-9


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