S2.4: Unravelling SA-independent processes during systemic acquired resistance (SAR)
Christiane Gatz & Xin Li & Yuelin Zhang
PhD student: Isha Goyal
Pathogen attack does not only elicit local defense responses at the site of infection, but it also activates immune responses in uninfected parts of the plant (systemic acquired resistance, SAR, see also M2.1). According to the current model, a mobile signal is generated in the locally infected leaf that primes systemic leaves to respond in a more efficient way to further pathogen attack. SAR requires two regulatory metabolites: salicylic acid (SA) and N-hydroxy-pipecolic acid (NHP). A subgroup of SAR genes can be activated by NHP in mutant plants that cannot synthesize SA. In SAR leaves, these genes respond faster to NHP than in naïve leaves. We are interested in understanding how NHP activates these gene and how priming of NHP perception is mediated. The work will be performed using Arabidopsis thaliana as a model plant.
The project is done in close collaboration with Prof. Yuelin Zhang at UBC Vancouver who is an expert in the elucidation of transcriptional control mechanisms in plant defense responses.
Hartmann M, Zeier T, Bernsdorff F, Reichel-Deland V, Kim D, Hohmann M, Scholten N, Schuck S, Brautigam A, Holzel T, et al. 2018. Flavin monooxygenase-generated N-hydroxypipecolic acid is a critical element of plant systemic immunity. Cell 173, 456-469.