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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Mice develop normally without the H1(0) linker histone.
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Mice develop normally without the H1(0) linker histone.

机译：没有H1（0）接头组蛋白的小鼠正常发育。

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摘要

H1 histones bind to the linker DNA between nucleosome core particles and facilitate the folding of chromatin into a 30-nm fiber. Mice contain at least seven nonallelic subtypes of H1, including the somatic variants H1a through H1e, the testis-specific variant H1t, and the replacement linker histone H1(0). H1(0) accumulates in terminally differentiating cells from many lineages, at about the time when the cells cease dividing. To investigate the role of H1(0) in development, we have disrupted the single-copy H1(0) gene by homologous recombination in mouse embryonic stem cells. Mice homozygous for the mutation and completely lacking H1(0) mRNA and protein grew and reproduced normally and exhibited no anatomic or histologic abnormalities. Examination of tissues in which H1(0) is normally present at high levels also failed to reveal any abnormality in cell division patterns. Chromatin from H1(0)-deficient animals showed no significant change in the relative proportions of the other H1 subtypes or in the stoichiometry between linker histones and nucleosomes, suggesting that the other H1 histones can compensate for the deficiency in H1(0) by occupying sites that normally contain H1(0). Our results indicate that despite the unique properties and expression pattern of H1(0), its function is dispensable for normal mouse development.
机译：H1组蛋白与核小体核心颗粒之间的接头DNA结合，并促进染色质折叠成30 nm纤维。小鼠至少含有H1的七个非等位基因亚型，包括体细胞变体H1a至H1e，睾丸特异性变体H1t和替代接头组蛋白H1（0）。 H1（0）大约在细胞停止分裂的时候从许多谱系中最终分化出的细胞中积累。若要调查H1（0）在发展中的作用，我们已经通过小鼠胚胎干细胞中的同源重组破坏了单拷贝H1（0）基因。纯合子突变和完全缺乏H1（0）mRNA和蛋白质的小鼠正常生长和繁殖，没有解剖或组织学异常。通常高水平存在H1（0）的组织的检查也未能显示出细胞分裂模式的任何异常。来自H1（0）缺陷动物的染色质在其他H1亚型的相对比例或接头组蛋白和核小体之间的化学计量上没有显示任何显着变化，这表明其他H1组蛋白可以通过占据而弥补H1（0）的不足通常包含H1（0）的站点。我们的结果表明，尽管H1（0）具有独特的属性和表达模式，但其功能对于正常的小鼠发育是必不可少的。

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