PDF(Pubmed)
Abstract：
At the molecular scale, adaptive advantages during plant growth and development rely on modulation of gene expression, primarily provided by epigenetic machinery. One crucial part of this machinery is histone posttranslational modifications, which form a flexible system, driving transient changes in chromatin, and defining particular epigenetic states. Posttranslational modifications work in concert with replication-independent histone variants further adapted for transcriptional regulation and chromatin repair. However, little is known about how such complex regulatory pathways are orchestrated and interconnected in cells. In this work, we demonstrate the utility of mass spectrometry-based approaches to explore how different epigenetic layers interact in Arabidopsis mutants lacking certain histone chaperones. We show that defects in histone chaperone function (e.g., chromatin assembly factor-1 or nucleosome assembly protein 1 mutations) translate into an altered epigenetic landscape, which aids the plant in mitigating internal instability. We observe changes in both the levels and distribution of H2A.W.7, altogether with partial repurposing of H3.3 and changes in the key repressive (H3K27me1/2) or euchromatic marks (H3K36me1/2). These shifts in the epigenetic profile serve as a compensatory mechanism in response to impaired integration of the H3.1 histone in the fas1 mutants. Altogether, our findings suggest that maintaining genome stability involves a two-tiered approach. The first relies on flexible adjustments in histone marks, while the second level requires the assistance of chaperones for histone variant replacement.
摘要：
在分子尺度上,植物生长和发育过程中的适应性优势依赖于基因表达的调节，主要由表观遗传机制提供。这种机制的一个关键部分是组蛋白翻译后修饰（PTM），形成一个灵活的系统，驱动染色质的瞬时变化和定义特定的表观遗传状态。PTM与进一步适用于转录调节和染色质修复的复制非依赖性组蛋白变体协同工作。然而,对于这种复杂的调节途径在细胞中如何协调和相互联系，人们知之甚少。在这项工作中,我们证明了基于质谱的方法的实用性，以探索不同的表观遗传层如何在缺乏某些组蛋白伴侣的拟南芥突变体中相互作用。我们证明了组蛋白伴侣功能的缺陷(例如，CAF-1或NAP1突变)转化为改变的表观遗传景观，这有助于植物减轻内部不稳定。我们观察到H2A水平和分布的变化。W.7，与H3.3的部分再利用和关键压抑（H3K27me1/2）或常色差标记（H3K36me1/2）的变化。表观遗传谱中的这些变化作为对fas1突变体中H3.1组蛋白整合受损的反应的补偿机制。总之,我们的研究结果表明,保持基因组稳定性涉及一个双层方法.第一个依赖于组蛋白标记的灵活调整，而第二个水平需要伴侣的协助进行组蛋白变体替换。
