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首页> 外文期刊>Eukaryotic cell >Overlapping Functions between SWR1 Deletion and H3K56 Acetylation in Candida albicans
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Overlapping Functions between SWR1 Deletion and H3K56 Acetylation in Candida albicans

机译：白色念珠菌SWR1删除和H3K56乙酰化之间的重叠功能。

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Nucleosome destabilization by histone variants and modifications has been implicated in the epigenetic regulation of gene expression, with the histone variant H2A.Z and acetylation of H3K56 (H3K56ac) being two examples. Here we find that deletion of SWR1, the major subunit of the SWR1 complex depositing H2A.Z into chromatin in exchange for H2A, promotes epigenetic white-opaque switching in Candida albicans. We demonstrate through nucleosome mapping that SWR1 is required for proper nucleosome positioning on the promoter of WOR1, the master regulator of switching, and that its effects differ in white and opaque cells. Furthermore, we find that H2A.Z is enriched adjacent to nucleosome-free regions at the WOR1 promoter in white cells, suggesting a role in the stabilization of a repressive chromatin state. Deletion of YNG2, a subunit of the NuA4 H4 histone acetyltransferase (HAT) that targets SWR1 activity through histone acetylation, produces a switching phenotype similar to that of swr1, and both may act downstream of the GlcNAc signaling pathway. We further uncovered a genetic interaction between swr1 and elevated H3K56ac with the discovery that the swr1 deletion mutant is highly sensitive to nicotinamide. Our results suggest that the interaction of H2A.Z and H3K56ac regulates epigenetic switching at the nucleosome level, as well as having global effects.
机译：组蛋白变体和修饰引起的核小体失稳与基因表达的表观遗传调控有关，其中组蛋白变体H2A.Z和H3K56（H3K56ac）的乙酰化是两个例子。在这里，我们发现删除 SWR1 （SWR1复合体的主要亚基，将H2A.Z沉积到染色质中以换取H2A）促进了白色念珠菌的表观遗传不透明转换。我们通过核小体作图证明SWR1是正确的核小体定位在 WOR1 的启动子（开关的主调节子）上所必需的，并且其作用在白色和不透明细胞中有所不同。此外，我们发现H2A.Z富集在白细胞中 WOR1 启动子处的无核小体区域附近，提示其在稳定染色质状态中的作用。删除 YNG2 ，它是通过组蛋白乙酰化靶向SWR1活性的NuA4 H4组蛋白乙酰基转移酶（HAT）的一个亚基，产生与 swr1 类似的转换表型。在GlcNAc信号传导途径的下游起作用。我们进一步发现 swr1 和升高的H3K56ac之间的遗传相互作用，并发现 swr1 缺失突变体对烟酰胺高度敏感。我们的结果表明，H2A.Z和H3K56ac的相互作用在核小体水平上调节表观遗传转换，并具有整体效应。

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