SGD Paper 
van Welsem T, et al. (2008) Synthetic lethal screens identify gene silencing processes in yeast and implicate the acetylated amino terminus of Sir3 in recognition of the nucleosome core. Mol Cell Biol 28(11):3861-72
Abstract: Dot1 methylates histone H3 lysine 79 (H3K79) on the nucleosome core and is involved in Sir-protein mediated silencing. Previous studies suggested that H3K79 methylation within euchromatin prevents non-specific binding of the Sir proteins, which in turn facilitates binding of the Sir proteins in unmethylated silent chromatin. However, the mechanism by which Sir-protein binding is influenced by this modification is unclear. We performed genome-wide synthetic genetic array (SGA) analysis and identified interactions of DOT1 with SIR1 and POL32. The synthetic growth defects in SGA analysis were attributed to loss of mating type identity caused by a synthetic silencing defect. By epistasis analysis DOT1, SIR1, and POL32 could be placed in different pathways of silencing. Dot1 shared its silencing phenotypes with the NatA N-terminal acetyltransferase complex and the conserved N-terminal Bromo Adjacent Homology (BAH) domain of Sir3 (a substrate of NatA). We classified all of these as affecting a common silencing process, and show that mutations in this process lead to non-specific binding of Sir3 to chromatin. Our results suggest that the BAH domain of Sir3 binds to histone H3K79 and that acetylation of the BAH domain is required for binding specificity of Sir3 for nucleosomes unmethylated at H3K79.
| Status: Published | Type: Journal Article | PubMed ID: 18391024 |
Topics addressed in this paper
Number of different genes curated to this paper: 4
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