Ehrentraut, Stefan; Weber, Jan; Dybowski, Jan Nikolaj; Hoffmann, Daniel; Ehrenhofer-Murray, Ann:
Rpd3-dependent boundary formation at telomeres by removal of Sir2 substrate.
2010
In: Proceedings of the National Academy of Sciences of the United States of America : PNAS, Jg. 107 (2010), Heft 12, S. 5522 - 5527
Artikel/Aufsatz in Zeitschrift / Fach: Medizin; Biologie; Informatik
Fakultät für Biologie » Genetik
Titel:
Rpd3-dependent boundary formation at telomeres by removal of Sir2 substrate.
Autor(in):
Ehrentraut, Stefan; Weber, Jan im Online-Personal- und -Vorlesungsverzeichnis LSF anzeigen; Dybowski, Jan Nikolaj im Online-Personal- und -Vorlesungsverzeichnis LSF anzeigen; Hoffmann, Daniel im Online-Personal- und -Vorlesungsverzeichnis LSF anzeigen; Ehrenhofer-Murray, Ann im Online-Personal- und -Vorlesungsverzeichnis LSF anzeigen
Erscheinungsjahr
2010
Erschienen in:
Proceedings of the National Academy of Sciences of the United States of America : PNAS, Jg. 107 (2010), Heft 12, S. 5522 - 5527
ISSN
WWW URL

Abstract:

Boundaries between euchromatic and heterochromatic regions until now have been associated with chromatin-opening activities. Here, we identified an unexpected role for histone deacetylation in this process. Significantly, the histone deacetylase (HDAC) Rpd3 was necessary for boundary formation in Saccharomyces cerevisiae. rpd3Delta led to silent information regulator (SIR) spreading and repression of subtelomeric genes. In the absence of a known boundary factor, the histone acetyltransferase complex SAS-I, rpd3Delta caused inappropriate SIR spreading that was lethal to yeast cells. Notably, Rpd3 was capable of creating a boundary when targeted to heterochromatin. Our data suggest a mechanism for boundary formation whereby histone deacetylation by Rpd3 removes the substrate for the HDAC Sir2, so that Sir2 no longer can produce O-acetyl-ADP ribose (OAADPR) by consumption of NAD(+) in the deacetylation reaction. In essence, OAADPR therefore is unavailable for binding to Sir3, preventing SIR propagation.