<p>The plant circadian clock drives temporal differences in susceptibility to pathogens. We investigated the role of TIMING OF CAB EXPRESSION 1 (TOC1) in the regulation of defence against <i>Botrytis cinerea</i> in Arabidopsis. The temporal variation in susceptibility to <i>B. cinerea</i> observed in wild-type Arabidopsis was abolished in <i>TOC1-ox</i> and <i>toc1-2</i> plants under both diurnal and constant light conditions. In addition, <i>TOC1-ox</i> plants were more susceptible than Col-0 following inoculation at dawn, while inoculation at night led to enhanced resistance in <i>toc1-2</i> plants versus C24 plants, suggesting that TOC1 is a negative regulator of immunity. RNA-seq analysis showed that the genes mis-regulated in <i>toc1-2</i> plants had significant enrichment for terms related to biotic stress, an overrepresentation of G-box elements in their promoters and included genes encoding key transcription factors (TFs) involved in defence against necrotrophic pathogens. Chromatin immunoprecipitation-qPCR showed that TOC1 occupies G-box containing regions of the defence TFs <i>ERF4</i>, <i>ORA47</i>, <i>ORA59</i> and <i>WRKY33</i> in a pathogen-responsive and MYC2-dependent manner. We suggest that the phased TOC1 occupancy of defence gene promoters contributes to the gating of plant immunity against necrotrophic pathogens, while the MYC2-dependent release of TOC1 in response to pathogen detection allows plants to mount an acute immune response.</p>

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The core clock transcription factor TOC1 binds directly to defence gene promoters regulating immunity in Arabidopsis

  • Shannon-Leigh Sparks,
  • Laura C. Roden,
  • Robert A. Ingle

摘要

The plant circadian clock drives temporal differences in susceptibility to pathogens. We investigated the role of TIMING OF CAB EXPRESSION 1 (TOC1) in the regulation of defence against Botrytis cinerea in Arabidopsis. The temporal variation in susceptibility to B. cinerea observed in wild-type Arabidopsis was abolished in TOC1-ox and toc1-2 plants under both diurnal and constant light conditions. In addition, TOC1-ox plants were more susceptible than Col-0 following inoculation at dawn, while inoculation at night led to enhanced resistance in toc1-2 plants versus C24 plants, suggesting that TOC1 is a negative regulator of immunity. RNA-seq analysis showed that the genes mis-regulated in toc1-2 plants had significant enrichment for terms related to biotic stress, an overrepresentation of G-box elements in their promoters and included genes encoding key transcription factors (TFs) involved in defence against necrotrophic pathogens. Chromatin immunoprecipitation-qPCR showed that TOC1 occupies G-box containing regions of the defence TFs ERF4, ORA47, ORA59 and WRKY33 in a pathogen-responsive and MYC2-dependent manner. We suggest that the phased TOC1 occupancy of defence gene promoters contributes to the gating of plant immunity against necrotrophic pathogens, while the MYC2-dependent release of TOC1 in response to pathogen detection allows plants to mount an acute immune response.