4.8 Article

The Arabidopsis mediator complex subunit 8 regulates oxidative stress responses

期刊

PLANT CELL
卷 33, 期 6, 页码 2032-2057

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OXFORD UNIV PRESS INC
DOI: 10.1093/plcell/koab079

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资金

  1. Research Foundation-Flanders [30829584]
  2. Agency for Innovation by Science and Technology [100555, 070347]
  3. Ghent University [01J11311]
  4. China Scholarship Council (CSC) [201406350070]

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Our study reveals that MED8, a subunit of the Mediator complex, regulates H2O2 responses and influences salicylic acid pathway and cell death in Arabidopsis. Additionally, MED8 acts as a negative regulator in oxidative stress, which is crucial for plant defense responses.
Signaling events triggered by hydrogen peroxide (H2O2) regulate plant growth and defense by orchestrating a genome-wide transcriptional reprogramming. However, the specific mechanisms that govern H2O2-dependent gene expression are still poorly understood. Here, we identify the Arabidopsis Mediator complex subunit MED8 as a regulator of H2O2 responses. The introduction of the med8 mutation in a constitutive oxidative stress genetic background (catalase-deficient, cat2) was associated with enhanced activation of the salicylic acid pathway and accelerated cell death. Interestingly, med8 seedlings were more tolerant to oxidative stress generated by the herbicide methyl viologen (MV) and exhibited transcriptional hyperactivation of defense signaling, in particular salicylic acid- and jasmonic acid-related pathways. The med8-triggered tolerance to MV was manipulated by the introduction of secondary mutations in salicylic acid and jasmonic acid pathways. In addition, analysis of the Mediator interactome revealed interactions with components involved in mRNA processing and microRNA biogenesis, hence expanding the role of Mediator beyond transcription. Notably, MED8 interacted with the transcriptional regulator NEGATIVE ON TATA-LESS, NOT2, to control the expression of H2O2-inducible genes and stress responses. Our work establishes MED8 as a component regulating oxidative stress responses and demonstrates that it acts as a negative regulator of H2O2-driven activation of defense gene expression.

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