Wang Y H, Gellibolian R, Shimizu M, Wells R D, Griffith J
Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill 27599-7295, USA.
J Mol Biol. 1996 Nov 8;263(4):511-6. doi: 10.1006/jmbi.1996.0593.
The rare folate-sensitive, fragile sites on chromsomes X, 11, and 16 contain blocks of CCG triplet repeats and large expansions of the CCG block at the FRAXA site produce the fragile X syndrome (FraX). The fragile, poorly staining nature of these sites suggested an altered chromatin structure. Here, repeating CCG DNAs from FraX patients were tested for their ability to assemble into nucleosomes, the basic subunits of chromatin, using in vitro nucleosome reconstitution, electron microscopy and competitive assembly gel retardation assays. CCG blocks of >50 repeats displayed strong nucleosome exclusion, providing a possible explanation for the nature of these sites.
X、11和16号染色体上罕见的对叶酸敏感的脆性位点含有CCG三联体重复序列,FRAXA位点处CCG序列的大量扩增会导致脆性X综合征(FraX)。这些位点的脆性、染色不佳的特性表明染色质结构发生了改变。在这里,使用体外核小体重组、电子显微镜和竞争性组装凝胶阻滞试验,检测了脆性X综合征患者的重复CCG DNA组装成核小体(染色质的基本亚基)的能力。超过50个重复的CCG序列表现出强烈的核小体排斥,这为这些位点的特性提供了一种可能的解释。