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Antagonistic Gcn5-Hda1 interactions revealed by mutations to the Anaphase Promoting Complex in yeast

机译：酵母后期促进复合物突变揭示了拮抗Gcn5-Hda1相互作用。

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Background Histone post-translational modifications are critical for gene expression and cell viability. A broad spectrum of histone lysine residues have been identified in yeast that are targeted by a variety of modifying enzymes. However, the regulation and interaction of these enzymes remains relatively uncharacterized. Previously we demonstrated that deletion of either the histone acetyltransferase (HAT) GCN5 or the histone deacetylase (HDAC) HDA1 exacerbated the temperature sensitive (ts) mutant phenotype of the Anaphase Promoting Complex (APC) apc5CA allele. Here, the apc5CA mutant background is used to study a previously uncharacterized functional antagonistic genetic interaction between Gcn5 and Hda1 that is not detected in APC5 cells. Results Using Northerns, Westerns, reverse transcriptase PCR (rtPCR), chromatin immunoprecipitation (ChIP), and mutant phenotype suppression analysis, we observed that Hda1 and Gcn5 appear to compete for recruitment to promoters. We observed that the presence of Hda1 can partially occlude the binding of Gcn5 to the same promoter. Occlusion of Gcn5 recruitment to these promoters involved Hda1 and Tup1. Using sequential ChIP we show that Hda1 and Tup1 likely form complexes at these promoters, and that complex formation can be increased by deleting GCN5. Conclusions Our data suggests large Gcn5 and Hda1 containing complexes may compete for space on promoters that utilize the Ssn6/Tup1 repressor complex. We predict that in apc5CA cells the accumulation of an APC target may compensate for the loss of both GCN5 and HDA1.
机译：背景组蛋白翻译后修饰对于基因表达和细胞生存力至关重要。已经在酵母中鉴定了广谱的组蛋白赖氨酸残基，其被多种修饰酶靶向。然而，这些酶的调节和相互作用仍然没有被表征。以前我们证明了组蛋白乙酰转移酶（HAT）GCN5或组蛋白脱乙酰基酶（HDAC）HDA1的缺失加剧了后期促进复合体（APC）apc5 CA CA等位基因的温度敏感性（ts）突变表型。在这里，apc5 CA 突变背景用于研究在APC5细胞中未检测到的Gcn5和Hda1之间以前未表征的功能性拮抗遗传相互作用。结果使用Northerns，Westerns，逆转录酶PCR（rtPCR），染色质免疫沉淀（ChIP）和突变表型抑制分析，我们观察到Hda1和Gcn5似乎竞争募集启动子。我们观察到Hda1的存在可以部分遮盖Gcn5与同一启动子的结合。这些启动子的Gcn5募集涉及Hda1和Tup1。使用顺序ChIP，我们显示Hda1和Tup1可能在这些启动子上形成复合物，并且可以通过删除GCN5来增加复合物的形成。结论我们的数据表明，含有大量Gcn5和Hda1的复合物可能在利用Ssn6 / Tup1阻遏物复合物的启动子上竞争空间。我们预测，在apc5 CA 细胞中，APC目标的积累可能补偿GCN5和HDA1的损失。

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