QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

Vol. 19, Issue 11, 4993-5005, November 2008

This Article Full Text Full Text (PDF) Supplemental Materials All Versions of this Article: E08-05-0524v1 19/11/4993    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yang, B. Articles by Kirchmaier, A. L. Search for Related Content PubMed PubMed Citation Articles by Yang, B. Articles by Kirchmaier, A. L.

HST3/HST4-dependent Deacetylation of Lysine 56 of Histone H3 in Silent Chromatin

Department of Biochemistry and Purdue Cancer Center, Purdue University, West Lafayette, IN 47907

Submitted May 27, 2008; Revised August 19, 2008; Accepted September 5, 2008
Monitoring Editor: Kerry S. Bloom

The composition of posttranslational modifications on newly synthesized histones must be altered upon their incorporation into chromatin. These changes are necessary to maintain the same gene expression state at individual chromosomal loci before and after DNA replication. We have examined how one modification that occurs on newly synthesized histone H3, acetylation of K56, influences gene expression at epigenetically regulated loci in Saccharomyces cerevisiae. H3 K56 is acetylated by Rtt109p before its incorporation into chromatin during S phase, and this modification is then removed by the NAD⁺-dependent deacetylases Hst3p and Hst4p during G2/M phase. We found silenced loci maintain H3 K56 in a hypoacetylated state, and the absence of this modification in rtt109 mutants was compatible with HM and telomeric silencing. In contrast, loss of HST3 and HST4 resulted in hyperacetylation of H3 K56 within silent loci and telomeric silencing defects, despite the continued presence of Sir2p throughout these loci. These silencing defects in hst3 hst4 mutants could be suppressed by deletion of RTT109. In contrast, overexpression of Sir2p could not restore silencing in hst3 hst4 mutants. Together, our findings argue that HST3 HST4 play critical roles in maintaining the hypoacetylated state of K56 on histone H3 within silent chromatin.

Address correspondence to: Ann L. Kirchmaier (kirchmaier{at}purdue.edu).

Abbreviations used: ChIP, chromatin immunoprecipitation.

This article has been cited by other articles:

				S. Mimura, T. Yamaguchi, S. Ishii, E. Noro, T. Katsura, C. Obuse, and T. Kamura Cul8/Rtt101 Forms a Variety of Protein Complexes That Regulate DNA Damage Response and Transcriptional Silencing J. Biol. Chem., March 26, 2010; 285(13): 9858 - 9867. [Abstract] [Full Text] [PDF]

				S. Varv, K. Kristjuhan, K. Peil, M. Looke, T. Mahlakoiv, K. Paapsi, and A. Kristjuhan Acetylation of H3 K56 Is Required for RNA Polymerase II Transcript Elongation through Heterochromatin in Yeast Mol. Cell. Biol., March 15, 2010; 30(6): 1467 - 1477. [Abstract] [Full Text] [PDF]

				Y. Wan, J.-H. Chiang, C.-H. Lin, C. E. Arens, R. A. Saleem, J. J. Smith, and J. D. Aitchison Histone chaperone Chz1p regulates H2B ubiquitination and subtelomeric anti-silencing Nucleic Acids Res., March 1, 2010; 38(5): 1431 - 1440. [Abstract] [Full Text] [PDF]

				J. Lopes da Rosa, V. L. Boyartchuk, L. J. Zhu, and P. D. Kaufman Histone acetyltransferase Rtt109 is required for Candida albicans pathogenesis PNAS, January 26, 2010; 107(4): 1594 - 1599. [Abstract] [Full Text] [PDF]

				M. R. Koch and L. Pillus From the Cover: The glucanosyltransferase Gas1 functions in transcriptional silencing PNAS, July 7, 2009; 106(27): 11224 - 11229. [Abstract] [Full Text] [PDF]