National Laboratory of Plant Molecular Genetics, CAS Center for Excellence in Molecular Plant Sciences, Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200032, China.
University of the Chinese Academy of Sciences, Beijing, 100049, China.
Plant J. 2019 Jan;97(2):368-377. doi: 10.1111/tpj.14125. Epub 2018 Nov 28.
The phytohormone abscisic acid (ABA)-induced leaf senescence facilitates nutrient reuse and potentially contributes to enhancing plant stress tolerance. However, excessive senescence causes serious reductions in crop yield, and the mechanism by which senescence is finely tuned at different levels is still insufficiently understood. Here, we found that the double mutant of core enzymes of the polycomb repressive complex 2 (PRC2) is hypersensitive to ABA in Arabidopsis thaliana. To elucidate the interplay between ABA and PRC2 at the genome level, we extensively profiled the transcriptomic and epigenomic changes triggered by ABA. We observed that H3K27me3 preferentially targets ABA-induced senescence-associated genes (SAGs). In the double, but not single, mutant of PRC2 enzymes, these SAGs were derepressed and could be more highly induced by ABA compared with the wild-type, suggesting a redundant role for the PRC2 enzymes in negatively regulating ABA-induced senescence. Contrary to the rapid transcriptomic changes triggered by ABA, the reduction of H3K27me3 at these SAGs falls far behind the induction of their expression, indicating that PRC2-mediated H3K27me3 contributed to long-term damping of ABA-induced senescence to prevent an oversensitive response. The findings of this study may serve as a paradigm for a global understanding of the interplay between the rapid effects of a phytohormone such as ABA and the long-term effects of the epigenetic machinery in regulating plant senescence processes and environmental responses.
植物激素脱落酸（ABA）诱导的叶片衰老促进了养分的再利用，并可能有助于提高植物的抗胁迫能力。然而，过度衰老会导致作物产量严重下降，而衰老在不同水平上如何被精细调控的机制仍了解不足。在这里，我们发现拟南芥多梳抑制复合物 2（PRC2）核心酶的双突变体对 ABA 敏感。为了阐明 ABA 和 PRC2 在基因组水平上的相互作用，我们广泛分析了 ABA 触发的转录组和表观基因组变化。我们观察到 H3K27me3 优先靶向 ABA 诱导的衰老相关基因（SAGs）。在 PRC2 酶的双突变体中，但不在单突变体中，这些 SAGs被去阻遏，并且可以比野生型更容易被 ABA 诱导，这表明 PRC2 酶在负调控 ABA 诱导的衰老中具有冗余作用。与 ABA 触发的快速转录组变化相反，这些 SAG 上 H3K27me3 的减少远远落后于其表达的诱导，这表明 PRC2 介导的 H3K27me3 有助于长期抑制 ABA 诱导的衰老，以防止过度敏感的反应。本研究的发现可能为全面理解植物衰老过程和环境响应中激素如 ABA 的快速作用与表观遗传机制的长期作用之间的相互作用提供一个范例。
