Chitosan primes plant defence mechanisms against Botrytis cinerea, including expression of Avr9/Cf-9 rapidly elicited genes.

Current crop protection strategies against the fungal pathogen Botrytis cinerea rely on a combination of conventional fungicides and host genetic resistance. However, due to pathogen evolution and legislation in the use of fungicides, these strategies are not sufficient to protect plants against this pathogen. Defence elicitors can stimulate plant defence mechanisms through a phenomenon known as defence priming. Priming results in a faster and/or stronger expression of resistance upon pathogen recognition by the host. This work aims to study defence priming by a commercial formulation of the elicitor chitosan. Treatments with chitosan result in induced resistance (IR) in solanaceous and brassicaceous plants. In tomato plants, enhanced resistance has been linked with priming of callose deposition and accumulation of the plant hormone jasmonic acid (JA). Large-scale transcriptomic analysis revealed that chitosan primes gene expression at early time-points after infection. In addition, two novel tomato genes with a characteristic priming profile were identified, Avr9/Cf-9 rapidly elicited protein 75 (ACRE75) and 180 (ACRE180). Transient and stable over-expression of ACRE75, ACRE180 and their Nicotiana benthamiana homologs, revealed that they are positive regulators of plant resistance against B. cinerea. This provides valuable information in the search for strategies to protect Solanaceae plants against B. cinerea.

SUMO conjugation to the pattern recognition receptor FLS2 triggers intracellular signalling in plant innate immunity.

Detection of conserved microbial patterns by host cell surface pattern recognition receptors (PRRs) activates innate immunity. The FLAGELLIN-SENSITIVE 2 (FLS2) receptor perceives bacterial flagellin and recruits another PRR, BAK1 and the cytoplasmic-kinase BIK1 to form an active co-receptor complex that initiates antibacterial immunity in Arabidopsis. Molecular mechanisms that transmit flagellin perception from the plasma-membrane FLS2-associated receptor complex to intracellular events are less well understood. Here, we show that flagellin induces the conjugation of the SMALL UBIQUITIN-LIKE MODIFIER (SUMO) protein to FLS2 to trigger release of BIK1. Disruption of FLS2 SUMOylation can abolish immune responses, resulting in susceptibility to bacterial pathogens in Arabidopsis. We also identify the molecular machinery that regulates FLS2 SUMOylation and demonstrate a role for the deSUMOylating enzyme, Desi3a in innate immunity. Flagellin induces the degradation of Desi3a and enhances FLS2 SUMOylation to promote BIK1 dissociation and trigger intracellular immune signalling.

Post-translational modifications in priming the plant immune system: ripe for exploitation?

Microbes constantly challenge plants, and some can successfully infect their host and cause disease. Basal immunity against plant pathogens in many cases is not enough for survival and leads to disease and, ultimately, a premature death of the host plant. However, the plant immune system can be temporarily and even transgenerationally primed; this 'primed state' leads to changes in the plant involving transcriptional, post-translational, metabolic, physiological and epigenetic reprogramming, which enables fine-tuning defence mechanisms for a rapid and/or more robust response after abiotic and/or biotic stress. This can ultimately affect pathogen infection speed and, hence, decrease its ability to overcome host resistance and the final outcome of the host-pathogen interaction. The role of the three major post-translational modifications (PTMs) (protein ubiquitination, phosphorylation and SUMOylation) in plant immunity has been well established. However, the role of PTMs on defence priming, and how the PTM machinery is affected in primed plants and its connection to plant resistance against biotic/abiotic stress is not well understood. This Review highlights the current state of play of priming-mediated post-translational reprogramming and explores new areas for future research.