Poster
Fay Bennett
University of Warwick
Coventry, England, United Kingdom
Erin Stroud
University of Warwick
COVENTRY, England, United Kingdom
Emily Breeze
University of Warwick
Coventry, England, United Kingdom
Murray Grant
University of Warwick
Coventry, England, United Kingdom
Gram-negative bacterial pathogens secrete Type III effector proteins which collectively act to suppress plant immunity and reconfigure host metabolism. Plants deploy resistance (R) genes to recognise effectors and activate effector-triggered immunity (ETI), manifested by a localised hypersensitive (HR) response and Systemic Acquired Resistance (SAR). The SAR signalling cascade primes uninfected tissue to enhance defence against a broad spectrum of pathogens, however, the mechanism of propagation and establishment remains unclear. Here, we utilise the model Arabidopsis-Pseudomonas syringae pv. tomato DC3000 system to study a transmembrane ER-localised SAR reporter gene, JASMONATE-INDUCED SYSTEMIC SIGNAL 1 (JISS1), to investigate the temporal and spatial dynamics of SAR. Rapidly induced in adaxial epidermal cells and vasculature during ETI, JISS1 signalling has been found to be altered in abscisic acid (ABA) signalling and biosynthetic mutants, with exogenous pre-treatment abolishing JISS1 activation. Interestingly, the stress-induced phytohormone ABA appears to impact SAR signal generation, with further studies revealing an antagonistic role at the local HR level. Additionally, while JISS1 is unaffected in SA mutants, it is lost in JA mutants, indicating a complex role for phytohormones in SAR propagation.