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介体亚基 17 整合茉莉酸和生长素信号通路来调控热形态发生。

MEDIATOR SUBUNIT17 integrates jasmonate and auxin signaling pathways to regulate thermomorphogenesis.

机构信息

Plant Mediator Lab, National Institute of Plant Genome Research, New Delhi 110067, India.

Signalling Lab, National Institute of Plant Genome Research, New Delhi 110067, India.

出版信息

Plant Physiol. 2022 Aug 1;189(4):2259-2280. doi: 10.1093/plphys/kiac220.

Abstract

Plant adjustment to environmental changes involves complex crosstalk between extrinsic and intrinsic cues. In the past two decades, extensive research has elucidated the key roles of PHYTOCHROME-INTERACTING FACTOR4 (PIF4) and the phytohormone auxin in thermomorphogenesis. In this study, we identified a previously unexplored role of jasmonate (JA) signaling components, the Mediator complex, and their integration with auxin signaling during thermomorphogenesis in Arabidopsis (Arabidopsis thaliana). Warm temperature induces expression of JA signaling genes including MYC2, but, surprisingly, this transcriptional activation is not JA dependent. Warm temperature also promotes accumulation of the JA signaling receptor CORONATINE INSENSITIVE1 (COI1) and degradation of the JA signaling repressor JASMONATE-ZIM-DOMAIN PROTEIN9, which probably leads to de-repression of MYC2, enabling it to contribute to the expression of MEDIATOR SUBUNIT17 (MED17). In response to warm temperature, MED17 occupies the promoters of thermosensory genes including PIF4, YUCCA8 (YUC8), INDOLE-3-ACETIC ACID INDUCIBLE19 (IAA19), and IAA29. Moreover, MED17 facilitates enrichment of H3K4me3 on the promoters of PIF4, YUC8, IAA19, and IAA29 genes. Interestingly, both occupancy of MED17 and enrichment of H3K4me3 on these thermomorphogenesis-related promoters are dependent on PIF4 (or PIFs). Altered accumulation of COI1 under warm temperature in the med17 mutant suggests the possibility of a feedback mechanism. Overall, this study reveals the role of the Mediator complex as an integrator of JA and auxin signaling pathways during thermomorphogenesis.

摘要

植物对环境变化的适应涉及外在和内在信号之间的复杂串扰。在过去的二十年中,广泛的研究阐明了 PHYTOCHROME-INTERACTING FACTOR4(PIF4)和植物激素生长素在热形态发生中的关键作用。在这项研究中,我们鉴定了茉莉酸(JA)信号成分、中介复合物以及它们在拟南芥(Arabidopsis thaliana)热形态发生中与生长素信号整合的一个以前未被探索的作用。温暖的温度诱导包括 MYC2 在内的 JA 信号基因的表达,但令人惊讶的是,这种转录激活不是 JA 依赖性的。温暖的温度还促进了 JA 信号受体 CORONATINE INSENSITIVE1(COI1)的积累和 JA 信号抑制剂 JASMONATE-ZIM-DOMAIN PROTEIN9 的降解,这可能导致 MYC2 的去抑制,使其能够为 MEDIATOR SUBUNIT17(MED17)的表达做出贡献。响应温暖的温度,MED17 占据了包括 PIF4、YUCCA8(YUC8)、INDOLE-3-ACETIC ACID INDUCIBLE19(IAA19)和 IAA29 在内的热感觉基因的启动子。此外,MED17 促进了 H3K4me3 在 PIF4、YUC8、IAA19 和 IAA29 基因启动子上的富集。有趣的是,MED17 的占据和 H3K4me3 在这些热形态发生相关启动子上的富集都依赖于 PIF4(或 PIFs)。在 med17 突变体中,温暖温度下 COI1 的积累改变表明存在反馈机制的可能性。总的来说,这项研究揭示了中介复合物作为 JA 和生长素信号通路在热形态发生过程中的整合者的作用。

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