• Heat‐stressed Arabidopsis plants release heterochromatin‐associated transposable element (TE) silencing, yet it is not accompanied by major reductions of epigenetic repressive modifications. In this study, we explored the functional role of histone H1 in repressing heterochromatic TEs in response to heat stress.
• We generated and analyzed RNA and bisulfite‐sequencing data of wild‐type and h1 mutant seedlings before and after heat stress.
• Loss of H1 caused activation of pericentromeric Gypsy elements upon heat treatment, despite these elements remaining highly methylated. By contrast, nonpericentromeric Copia elements became activated concomitantly with loss of DNA methylation. The same Copia elements became activated in heat‐treated chromomethylase 2 (cmt2) mutants, indicating that H1 represses Copia elements through maintaining DNA methylation under heat.
• We discovered that H1 is required for TE repression in response to heat stress, but its functional role differs depending on TE location. Strikingly, H1‐deficient plants treated with the DNA methyltransferase inhibitor zebularine were highly tolerant to heat stress, suggesting that both H1 and DNA methylation redundantly suppress the plant response to heat stress.

中文翻译：

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H1和DNA甲基化在热应激期间转座因子选择性调控中的作用

• 热应激拟南芥植物释放异染色质相关转座因子 (TE) 沉默，但并未伴随表观遗传抑制修饰的大幅减少。在这项研究中，我们探讨了组蛋白 H1 在抑制异色 TE 以响应热应激的功能作用。
• 我们生成并分析了热应激前后野生型和h1突变体幼苗的 RNA 和亚硫酸氢盐测序数据。
• 尽管这些元素保持高度甲基化，但H1 的缺失导致在热处理后激活着丝粒周围的吉普赛元素。相比之下，非着丝粒周围的Copia元件随着 DNA 甲基化的丧失而被激活。相同的Copia元件在热处理的铬甲基化酶2 ( cmt2 ) 突变体中被激活，表明 H1通过在加热下维持 DNA 甲基化来抑制Copia元件。
• 我们发现 H1 是 TE 抑制热应激所必需的，但其功能作用因 TE 位置而异。引人注目的是，用 DNA 甲基转移酶抑制剂 zebularine 处理的 H1 缺陷植物对热胁迫具有高度耐受性，这表明 H1 和 DNA 甲基化都过度抑制了植物对热胁迫的反应。