4.8 Article

MEDIATOR SUBUNIT17 integrates jasmonate and auxin signaling pathways to regulate thermomorphogenesis

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PLANT PHYSIOLOGY
卷 189, 期 4, 页码 2259-2280

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OXFORD UNIV PRESS INC
DOI: 10.1093/plphys/kiac220

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资金

  1. Department of Biotechnology, Government of India [BT/PR13009/BPA/118/71/2015]
  2. Council of Scientific and Industrial Research, Government of India
  3. Department of Biotechnology, Government of India
  4. Short Term Fellowship from National Institute of Plant Genome Research
  5. National Post-Doctoral Fellowship from Science and Engineering Research Board, Government of India
  6. INTER-COST [LTC 20003]
  7. European Regional Development Fund Project SINGING PLANT [CZ.02.01/0.0/0.0/16_026/0008446]

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This study reveals the role of the Mediator complex as an integrator of jasmonate (JA) and auxin signaling pathways during thermomorphogenesis in Arabidopsis. Warm temperature induces the expression of JA signaling genes and promotes the accumulation of the JA signaling receptor COI1 and degradation of the JA signaling repressor JASMONATE-ZIM-DOMAIN PROTEIN9. The Mediator complex, specifically the mediator subunit MED17, occupies the promoters of thermosensory genes and facilitates enrichment of H3K4me3, which is dependent on the bHLH transcription factor PIF4.
Jasmonate signaling components, the Mediator complex, and their integration with auxin signaling play a role during thermomorphogenesis in Arabidopsis. 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.

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