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UV irradiation stimulates histone acetylation and chromatin remodeling at a repressed yeast locus

机译:紫外线照射可在抑制的酵母基因座上刺激组蛋白乙酰化和染色质重塑

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摘要

Chromatin immunoprecipitation with anti-acetyl histone H3 (K9 and K14) and anti-acetyl histone H4 (K5, K8, K12, and K16) antibodies shows that Lys-9 and/or Lys-14 of histone H3, but not the relevant sites of histone H4 in nucleosomes at the repressed MFA2 promoter, are hyperacetylated after UV irradiation. This level of histone hyperacetylation diminishes gradually as repair proceeds. Accompanying this, chromatin in the promoter becomes more accessible to restriction enzymes after UV irradiation and returns to the pre-UV state gradually. UV-related histone hyperacetylation and chromatin remodeling in the MFA2 promoter depend on Gcn5p and partially on Swi2p, respectively. Deletion of GCN5, but not of SWI2 impairs repair of DNA damage in the MFA2 promoter. The post-UV histone modifications and chromatin remodeling at the repressed MFA2 promoter do not activate MFA2 transcriptionally, nor do they require damage recognition by Rad4p or Rad14p. Furthermore, we show that UV irradiation triggers genome-wide histone hyperacetylation at both histone H3 and H4. These experiments indicate that chromatin at a yeast repressed locus undergoes active change after UV radiation treatment and that failure to achieve histone H3 hyperacetylation impairs the repair of DNA damage.
机译:用抗乙酰基组蛋白H3(K9和K14)和抗乙酰基组蛋白H4(K5,K8,K12和K16)抗体染色质免疫沉淀显示组蛋白H3的Lys-9和/或Lys-14,但没有相关位点紫外线照射后,被抑制的MFA2启动子上核小体中组蛋白H4的高乙酰化。随着修复的进行,组蛋白高乙酰化的水平逐渐降低。随之,启动子中的染色质在紫外线照射后变得更容易被限制性内切酶吸收,并逐渐返回到紫外线前状态。 MFA2启动子中与紫外线相关的组蛋白超乙酰化和染色质重塑分别取决于Gcn5p和部分取决于Swi2p。 GCN5而不是SWI2的缺失会削弱MFA2启动子中DNA损伤的修复。 UVA后的组蛋白修饰和被抑制的MFA2启动子上的染色质重塑不会转录激活MFA2,也不需要Rad4p或Rad14p识别损伤。此外,我们显示紫外线照射在组蛋白H3和H4处触发全基因组组蛋白超乙酰化。这些实验表明,在紫外线辐射处理后,酵母抑制的基因座处的染色质发生了主动变化,而无法实现组蛋白H3超乙酰化会损害DNA损伤的修复。

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