Human fragile site FRA16B DNA excludes nucleosomes in the presence of distamycin
Human fragile site FRA16B DNA excludes nucleosomes in the presence of distamycin
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DOI：
10.1074/jbc.m200901200
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发表时间：
2002-05-10
影响因子：
4.8
通讯作者：
Wang, YH
中科院分区：
文献类型：
--
作者：
Hsu, YY;Wang, YH
人类脆性位点是由特定培养条件产生的染色体中的弱染色缺口。来自叶酸敏感脆性位点的短CGG重复DNA已被证明排除单个核小体。为了测试这种核小体排除模型是否提供了一个通用的分子机制，形成脆性位点，一个不同类别的脆性位点，33个碱基对AT丰富的重复DNA来自罕见的偏端霉素诱导位点，FRA 16 B，检查其组装单个核小体和核小体阵列的能力，使用体外核小体重建方法。FRA 16 B DNA片段强烈排除核小体组装只有在偏端霉素的存在下，和增加的33-bp的重复序列的数量增加的影响偏端霉素的不稳定的核小体形成，这表明一个共同的机制，形成脆性位点。
Human fragile sites are weak staining gaps in chromosomes generated by specific culture conditions. The short CGG repeating DNA derived from folate-sensitive fragile sites has been shown to exclude single nucleosomes. To test whether this nucleosome exclusion model provides a general molecular mechanism for the formation of fragile sites, a different class of fragile site, the 33-base pair AT-rich repeating DNAs derived from the rare distamycin-inducible site, FRA16B, was examined for its ability to assemble single nucleosomes and nucleosome arrays using in vitro nucleosome reconstitution methods. The FRA16B DNA fragments strongly exclude nucleosome assembly only in the presence of distamycin, and increasing the number of 33-bp repeats increases the effect of distamycin in the destabilization of the nucleosome formation, suggesting a common mechanism for the formation of fragile sites.