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Taking It Off: Regulation of H3 K56 Acetylation by Hst3 and Hst4
Kyle M Miller, Nancy L Maas and David P Toczyski
volume 5 | issue 22
15 november 2006Pages: 2561 - 2565
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Histone modifications have been implicated in both DNA repair and checkpoint-mediated responses to DNA damage. Recently much attention has focused on the acetylation of H3 K56. Indeed, this modification is cell cycle-regulated, maintained upon replicative damage in a checkpoint-dependent manner, and is essential for surviving DNA damage. We and others have discovered that two members of the HDAC Sirtuin family, Hst3 and Hst4, negatively regulate H3 K56 acetylation in budding yeast. Additionally, we have shown that these two HDACs are targeted for repression by the DNA damage checkpoint, which is vital for DNA damage tolerance. Discovery that two HDACs are negative regulators of the cellular response to DNA damage and that they target the acetylation of H3 K56 reveals a complex relationship between histone modifications, HDACs, and the DNA damage response. Here, we discuss the recent reports of the regulation of H3 K56-Ac by Hst3 and Hst4 and put forth the critical questions that remain for understanding the intimate, though poorly characterized, connection between chromatin states and genomic maintenance.
Authors
Kyle M Miller
University of California, San Francisco, CA
Nancy L Maas
University of California, San Francisco, CA
David P Toczyski
University of California, San Francisco, CA
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.




