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首页> 外文期刊>Epigenetics & Chromatin >An H4K16 histone acetyltransferase mediates decondensation of the X chromosome in C. elegans males
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An H4K16 histone acetyltransferase mediates decondensation of the X chromosome in C. elegans males

机译：H4K16组蛋白乙酰基转移酶介导秀丽隐杆线虫男性X染色体的解聚

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Background In C. elegans , in order to equalize gene expression between the sexes and balance X and autosomal expression, two steps are believed to be required. First, an unknown mechanism is hypothesized to upregulate the X chromosome in both sexes. This mechanism balances the X to autosomal expression in males, but creates X overexpression in hermaphrodites. Therefore, to restore the balance, hermaphrodites downregulate gene expression twofold on both X chromosomes. While many studies have focused on X chromosome downregulation, the mechanism of X upregulation is not known. Results To gain more insight into X upregulation, we studied the effects of chromatin condensation and histone acetylation on gene expression levels in male C. elegans . We have found that the H4K16 histone acetyltransferase MYS-1/Tip60 mediates dramatic decondensation of the male X chromosome as measured by FISH. However, RNA-seq analysis revealed that MYS-1 contributes only slightly to upregulation of gene expression on the X chromosome. These results suggest that the level of chromosome decondensation does not necessarily correlate with the degree of gene expression change in vivo. Furthermore, the X chromosome is more sensitive to MYS-1-mediated decondensation than the autosomes, despite similar levels of H4K16ac on all chromosomes, as measured by ChIP-seq. H4K16ac levels weakly correlate with gene expression levels on both the X and the autosomes, but highly expressed genes on the X chromosome do not contain exceptionally high levels of H4K16ac. Conclusion These results indicate that H4K16ac and chromosome decondensation influence regulation of the male X chromosome; however, they do not fully account for the high levels of gene expression observed on the X chromosomes.
机译：背景技术在秀丽隐杆线虫中，为了平衡两性之间的基因表达并平衡X和常染色体表达，需要两个步骤。首先，假设存在未知的机制来上调男女的X染色体。这种机制使X与雄性中的常染色体表达保持平衡，但在雌雄同体中导致X过度表达。因此，为了恢复平衡，雌雄同体下调了两个X染色体上基因表达的两倍。虽然许多研究集中在X染色体下调，但X上调的机制尚不清楚。结果为了深入了解X上调，我们研究了染色质浓缩和组蛋白乙酰化对雄性秀丽隐杆线虫基因表达水平的影响。我们已经发现，H4K16组蛋白乙酰基转移酶MYS-1 / Tip60通过FISH介导了雄性X染色体的剧烈缩合。但是，RNA-seq分析显示MYS-1仅对X染色体上的基因表达上调有轻微贡献。这些结果表明，染色体解聚的水平不一定与体内基因表达变化的程度相关。此外，尽管通过ChIP-seq测定，尽管所有染色体上H4K16ac的水平相似，但X染色体比常染色体对MYS-1介导的缩合更为敏感。 H4K16ac水平与X和常染色体上的基因表达水平均弱相关，但X染色体上高表达的基因不包含异常高水平的H4K16ac。结论H4K16ac和染色体的缩合影响了雄性X染色体的调控。但是，它们并不能完全解释X染色体上观察到的高水平基因表达。

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