SWI/SNF complex: dissection of a chromatin remodeling cycle.

SWI/SNF complex: dissection of a chromatin remodeling cycle.
复制标题

SWI/SNF 复合体:染色质重塑周期的剖析。

DOI:
10.1101/sqb.1998.63.545
复制
发表时间:
1998
期刊:
Cold Spring Harbor symposia on quantitative biology
影响因子:
--
通讯作者:
Peterson,CL
Peterson,CL
中科院分区:
--
文献类型:
--
作者:
Peterson,CL

文献摘要

被引文献

相似文献

图1.SWI/SNF重塑周期循环(1-4)中的步骤在正文中详细描述。星号用于表示数组的重塑状态。在两种不同的纯化方案中从全酶中分离出CALY(Côtéet al.1994年;凯恩斯等人。1996年)。这种目标模式仍然存在争议。或者,将SWI/SNF活性靶向到特定的染色体位点可能涉及与上游激活蛋白的相互作用。哺乳动物的SWI/SNF和糖皮质激素受体(GR)在体内(Fryer和Archer,1998)以及酵母提取物(Yoshinaga等人)的酵母提取物(Yoshinaga et al.)中已被证明存在这种相互作用。SWI/SNF也可能通过特定染色体位点的特殊染色质结构而被靶向。例如,SWI/SNF可以识别含有不同类型的组蛋白翻译后修饰的核小体阵列,例如位点特异性乙酰化或磷酸化(有关讨论,参见Pollard和Peterson 1998)。组蛋白乙酰转移酶GCN5是表达许多需要SWI/SNF活性的相同基因所必需的,GCN5和SWI/SNF显示出与染色质成分相似的遗传相互作用(Pollard和Peterson 1997)。一种可能性是SWI/SNF靶向于被GCN5 HAT复合物乙酰化的核小体阵列,或者SWI/SNF的重塑活性可能受到组蛋白乙酰化的调节(见下文)。
Figure 1. The SWI/SNF remodeling cycle. Steps in the cycle (1–4) are described in detail in the text. Asterisks are used to denote the remodeled state of the array. cally separated from the holoenzyme in two different purification schemes (Côté et al. 1994; Cairns et al. 1996). This targeting model remains controversial. Alternatively, targeting of SWI/SNF activity to specific chromosomal loci may involve interactions with upstream activator proteins. Such an interaction has been demonstrated for mammalian SWI/SNF and the glucocorticoid receptor (GR) in vivo (Fryer and Archer 1998) and yeast SWI/SNF and the rat GR in vitro in yeast extracts (Yoshinaga et al. 1992).SWI/SNF might also be targeted to specific chromosomal loci by a special chromatin structure of the locus. For instance, SWI/SNF may recognize nucleosome arrays that harbor a distinct type of histone posttranslational modification, such as site-specific acetylation or phosphorylation (for discussion, see Pollard and Peterson 1998). The histone acetyltransferase, GCN5, is required for expression of many of the same genes that require SWI/SNF activity, and GCN5 and SWI/SNF show similar genetic interactions with chromatin components (Pollard and Peterson 1997). One possibility is that SWI/SNF is targeted to nucleosome arrays that have been acetylated by GCN5 HAT complexes, or alternatively, the remodeling activity of SWI/SNF might be modulated by histone acetylation (see below).