Circadian clock regulation of innate immunity in plants

RA Ingle1, C Muchapirei1, R Joseph1, C Stoker2, KJ Denby2,3 and LC Roden1

  1. Department of Molecular and Cell Biology, University of Cape Town, South Africa
  2. School of Life Sciences, University of Warwick, United Kingdom
  3. Department of Biology, University of York, United Kingdom

The circadian clock is an endogenous time-keeping mechanism that synchronises biological processes with the external environment, such that they occur at optimal times of the day While the clock has long been known to allow plants to anticipate predictable daily changes in abiotic stimuli, only recently has it become apparent that it also allows them to anticipate interactions with other organisms. We have demonstrated that the clock modulates the strength of the plant immune response against both the biotrophic bacterial pathogen Pseudomonas syringae and the necrotrophic fungus Botrytis cinerea; Arabidopsis displays differential susceptibility to these pathogens that is dependent on the time of infection, persists under constant light conditions, and is lost in arrhythmic clock mutants. As a first step towards understanding the molecular mechanisms by which the clock regulates plant innate immunity, we carried out transcriptome profiling of Arabidopsis following inoculation with B. cinerea spores at subjective dawn or night. We observed that decreased susceptibility to B. cinerea following inoculation at subjective dawn was associated with a more rapid and robust transcriptional regulation of the defence response, suggesting that the clock gates the expression of infection-responsive genes. Direct target genes of core clock regulators were also enriched among the transcription factors that responded more rapidly to infection at subjective dawn than subjective night, suggesting a direct influence of the clock on the defence regulatory network. Finally, jasmonate signalling plays a crucial role in the rhythmic susceptibility of Arabidopsis to B. cinerea as demonstrated by the loss of temporal variation in susceptibility in mutants defective in key transcriptional and post-transcriptional regulators in this hormone signalling pathway.