Open AccessDirect Role for the Rpd3 Complex in Transcriptional Induction of the Anaerobic DAN/TIR Genes in Yeast
Author(s) -
Odeniel Sertil,
Arvind Vemula,
Sharon L. Salmon,
Randall H. Morse,
Charles V. Lowry
Publication year - 2007
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.02297-06
Subject(s) - biology , repressor , chromatin immunoprecipitation , histone deacetylase , chromatin , psychological repression , activator (genetics) , chromatin remodeling , histone h4 , histone , nucleosome , swi/snf , genetics , transcription factor , saccharomyces cerevisiae , histone code , coactivator , promoter , microbiology and biotechnology , gene , gene expression
Saccharomyces cerevisiae adapts to hypoxia by expressing a large group of “anaerobic” genes. Among these, the eightDAN/TIR genes are regulated by the repressors Rox1 and Mot3 and the activator Upc2/Mox4. In attempting to identify factors recruited by the DNA binding repressor Mot3 to enhance repression of theDAN/TIR genes, we found that the histone deacetylase and global repressor complex, Rpd3-Sin3-Sap30, was not required for repression. Strikingly, the complex was instead required for activation. In addition, the histone H3 and H4 amino termini, which are targets of Rpd3, were also required forDAN1 expression. Epistasis tests demonstrated that the Rpd3 complex is not required in the absence of the repressor Mot3. Furthermore, the Rpd3 complex was required for normal function and stable binding of the activator Upc2 at theDAN1 promoter. Moreover, the Swi/Snf chromatin remodeling complex was strongly required for activation ofDAN1 , and chromatin immunoprecipitation analysis showed an Rpd3-dependent reduction inDAN1 promoter-associated nucleosomes upon induction. Taken together, these data provide evidence that during anaerobiosis, the Rpd3 complex acts at theDAN1 promoter to antagonize the chromatin-mediated repression caused by Mot3 and Rox1 and that chromatin remodeling by Swi/Snf is necessary for normal expression.