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EMBO reports 9, 1, 97–102 (2008)
doi:10.1038/sj.embor.7401112
AOP Published online: 9 November 2007
Saccharomyces cerevisiae Rad16 mediates ultraviolet-dependent histone H3 acetylation required for efficient global genome nucleotide-excision repair
Yumin Teng, Hairong Liu, Hefin W Gill, Yachuan Yu, Raymond Waters & Simon H Reed
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Department of Pathology, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK
To whom correspondence should be addressed
Yumin Teng Tel: +44 29 20745576; Fax: +44 29 20742579; E-mail: reedsh1@cardiff.ac.uk
Received 23 April 2007; Accepted 28 September 2007; Published online 9 November 2007.
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Abstract
In yeast, global genome nucleotide-excision repair (GG-NER) requires a protein complex containing Rad7 and Rad16. Rad16 is a member of the switch/sucrose nonfermentable superfamily, and it is presumed that chromatin remodelling is its primary function during repair. We show that RAD16 is required for ultraviolet-dependent hyperacetylation of histone H3 (Lys 9 and Lys 14) at the MFA2 promoter and throughout the genome. The yeast repressor complex Ssn6–Tup1 represses many genes including MFA2. TUP1 deletion results in constitutive hyperacetylation of histone H3, nucleosome disruption and derepression of gene transcription in Tup1-regulated genes. GG-NER in the MFA2 promoter proceeds more rapidly in tup1  -cells compared with wild type, even when transcription is inhibited. We show that elevated histone H3 acetylation levels in the MFA2 promoter in tup1 -cells result in Rad7- and Rad16-independent GG-NER, and that Rad16 mediates the ultraviolet-induced acetylation of histone H3, necessary for efficient GG-NER.
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