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首页> 外文期刊>Nucleus >The linker histone H1C contributes to the SCA7 nuclear phenotype
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The linker histone H1C contributes to the SCA7 nuclear phenotype

机译：接头组蛋白H1C促进SCA7核表型

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Spinocerebellar ataxia type 7 (SCA7) is a neurodegenerative disease caused by a polyglutamine expansion in ataxin-7, a subunit of the SAGA coactivator, which leads to progressive neuronal dysfunction and cell death in cerebellum, brainstem and retina. Increased nuclear volume, chromatin decondensation and deregulated gene expression were reported in a SCA7 mouse model expressing mutant ataxin-7 in rod photoreceptors. We analyzed the SCA7-induced chromatin reorganization by immunogold labeling, stereology, electron tomography and showed that in SCA7 rods the most external heterochromatin ring, corresponding to facultative heterochromatin, becomes fragmented and decondensed. The amounts of acetylated histone H3 and H4 tails were found to be unchanged in nuclear extracts of SCA7 retinas and their cellular distribution appeared similar in wild-type and SCA7 mice in so far that in both cases acetylated histones are positioned at the interface between eu- and hetero-chromatin. We found that the amount of the linker histone H1c is strongly reduced in nuclear extracts of SCA7 retinas and that the cellular distribution of H1c is particularly altered in the facultative heterochromatin compartment. The decreased histone H1c content thus provides a coherent explanation for the chromatin decondensation observed in SCA7 rod photoreceptor nuclei.
机译：脊髓小脑性共济失调7型（SCA7）是一种神经退行性疾病，由SAGA共激活子的一个亚基ataxin-7中的聚谷氨酰胺扩展引起，导致小脑，脑干和视网膜的进行性神经元功能障碍和细胞死亡。据报道，在杆状光感受器中表达突变型共青素7的SCA7小鼠模型中，核体积增加，染色质解聚和基因表达失控。我们通过免疫金标记，立体学，电子断层扫描分析了SCA7诱导的染色质重组，并显示在SCA7棒中，最外部的异染色质环（对应于兼性异染色质）变得碎片化和缩聚。迄今为止，在迄今为止的两种情况下，乙酰化组蛋白都位于eu-之间的界面上，发现在SCA7视网膜的核提取物中乙酰化组蛋白H3和H4尾巴的数量没有变化，并且它们的细胞分布在野生型和SCA7小鼠中似乎相似。和异染色质。我们发现，在SCA7视网膜的核提取物中，接头组蛋白H1c的含量大大降低，并且H1c的细胞分布在兼性异染色质区室中特别改变。因此，降低的组蛋白H1c含量为在SCA7杆感光细胞核中观察到的染色质缩聚提供了连贯的解释。

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