Chromatin remodelling at the PHO8 promoter requires SWI-SNF and SAGA at a step subsequent to activator binding
Chromatin remodelling at the PHO8 promoter requires SWI-SNF and SAGA at a step subsequent to activator binding
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DOI：
10.1093/emboj/18.22.6407
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发表时间：
1999-11-15
期刊：
影响因子：
11.4
通讯作者：
Hörz, W
中科院分区：
文献类型：
--
作者：
Gregory, PD;Schmid, A;Hörz, W
SWI-SNF和SAGA复合体分别具有依赖于ATP的核小体重塑活性和组蛋白乙酰转移酶(HAT)活性，这两种突变可以在体内消除SWI-SNF复合体的ATPase活性或SAGA的HAT活性，取消PHO8启动子上适当的染色质重塑。这些影响在机制上是不同的，因为缺乏SWI-SNF使染色质冻结在抑制状态，而缺乏Gcn5允许染色质结构的局部扰动，该结构紧邻上游反式激活物结合位点。然而，这种重塑不会传播到近端的启动子，并且在所有条件下都没有观察到激活。此外，在没有Snf2或Gcn5的情况下，Pho4与PHO8启动子结合，证实了SWI-SNF和SAGA在染色质重塑中的作用，而不依赖于激活剂的结合。这些数据为SWI-SNF和SAGA复合体在体内染色质重塑中的作用提供了新的见解。
The SWI-SNF and SAGA complexes possess ATP-dependent nucleosome remodelling activity and histone acetyltransferase (HAT) activity, respectively, Mutations that eliminate the ATPase activity of the SWI-SNF complex, or the HAT activity of SAGA, abolish proper chromatin remodelling at the PHO8 promoter in vivo. These effects are mechanistically distinct, since the absence of SWI-SNF freezes chromatin in the repressed state, while the absence of Gcn5 permits a localized perturbation of chromatin structure immediately adjacent to the upstream transactivator binding site. However, this remodelling is not propagated to the proximal promoter, and no activation is observed under all conditions. Furthermore, Pho4 is bound to the PHO8 promoter in the absence of Snf2 or Gcn5, confirming a role for SWI-SNF and SAGA in chromatin remodelling independent of activator binding. These data provide new insights into the roles of the SWI-SNF and SAGA complexes in chromatin remodelling in vivo.