期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2001
卷号：98
期号：23
页码：13213-13218
DOI：10.1073/pnas.181486098
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：The inactivity of Ure2p, caused by either a ure2 mutation or the presence of the [URE3] prion, increases DAL5 transcription and thus enables Saccharomyces cerevisiae to take up ureidosuccinate (USA+). Rtg2p regulates transcription of glutamate-repressible genes by facilitation of the nuclear entry of the Rtg1 and Rtg3 proteins. We find that rtg2{Delta} cells take up USA even without the presence of [URE3]. Thus, the USA+ phenotype of rtg2{Delta} strains is not the result generation of the [URE3] prion but is a regulatory effect. Because rtg1{Delta} or rtg3{Delta} mutations or the presence of glutamate do not produce the USA+ phenotype, this is a novel function of Rtg2p. The USA+ phenotype of rtg2{Delta} strains depends on GLN3, is caused by overexpression of DAL5, and is blocked by mks1{Delta
