由α2/Mcm1定位的核小体在体内阻止Hap1激活剂结合。
A nucleosome positioned by alpha2/Mcm1 prevents Hap1 activator binding in vivo.
作者信息
Morohashi Nobuyuki, Nakajima Kumiko, Kurihara Daichi, Mukai Yukio, Mitchell Aaron P, Shimizu Mitsuhiro
机构信息
Department of Chemistry, Meisei University, 2-1-1 Hodokubo, Hino, Tokyo 191-8506, Japan.
出版信息
Biochem Biophys Res Commun. 2007 Dec 21;364(3):583-8. doi: 10.1016/j.bbrc.2007.10.037. Epub 2007 Oct 16.
Nucleosome positioning has been proposed as a mechanism of transcriptional repression. Here, we examined whether nucleosome positioning affects activator binding in living yeast cells. We introduced the cognate Hap1 binding site (UAS1) at a location 24-43 bp, 29-48 bp, or 61-80 bp interior to the edge of a nucleosome positioned by alpha2/Mcm1 in yeast minichromosomes. Hap1 binding to the UAS1 was severely inhibited, not only at the pseudo-dyad but also in the peripheral region of the positioned nucleosome in alpha cells, while it was detectable in a cells, in which the nucleosomes were not positioned. Hap1 binding was restored in alpha cells with tup1 or isw2 mutations, which caused the loss of nucleosome positioning. These results support the mechanism in which alpha2/Mcm1-dependent nucleosome positioning has a regulatory function to limit the access of transcription factors.
核小体定位已被提出作为一种转录抑制机制。在此，我们研究了核小体定位是否会影响活酵母细胞中激活剂的结合。我们将同源的Hap1结合位点（UAS1）引入到酵母微型染色体中由alpha2/Mcm1定位的核小体边缘内侧24 - 43 bp、29 - 48 bp或61 - 80 bp的位置。在α细胞中，Hap1与UAS1的结合受到严重抑制，不仅在假二分体处，而且在定位核小体的周边区域也是如此，而在未定位核小体的a细胞中则可检测到Hap1结合。在tup1或isw2突变的α细胞中，Hap1结合得以恢复，这两种突变导致了核小体定位的丧失。这些结果支持了这样一种机制，即α2/Mcm1依赖性核小体定位具有限制转录因子 access 的调节功能。 （注：原文中“access”可能有误，推测可能是“accessibility”，“限制转录因子的可及性”更符合语境）
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