Poster: Plant-pathogen interactions

Abs # 516: High humidity suppresses ssi4-mediated cell death and disease resistance upstream of MAP kinase activation, H₂O₂ production and defense gene expression

Presenter:	Zhou, Fasong , fz25@cornell.edu
Authors	Zhou, Fasong  (A)   Frank, Menke  (A)   Keiko, Yoshioka  (A)   Wolfgang, Moder  (A)   Yumiko, Shirano  (A)   Daniel, Klessig  (A)
Affiliations:	(A): Boyce Thompson Institute for Plant Research

Arabidopsis ssi4 is a gain-of-function mutation in a TIR-NBS-LRR type disease resistance (R) gene. In this study and our previous report, we demonstrated that ssi4 mutant exhibits characteristics of R gene-mediated defense responses, including activation of defense responsive MAP kinases, accumulation of H₂O₂ and SA, induction of defense-related gene expression, triggering HR-like cell death and enhancing disease resistance to virulent pathogens. EDS1 and SA are required for ssi4-mediated signaling that is NPR1 and NDR1 independent. Interestingly, high relative humidity (HRH) suppresses all the ssi4-triggered defense responses investigated so far. By comparing the suppression effects of HRH with those of eds1 and nahG, we postulate that a high sensitive factor functions upstream of AtMPK3/AtMPK6, EDS1, H₂O₂, SA, WRKY6/WRKY29 and PR1/PR5. HRH also suppresses ssi4-induced expression of RPW8.1 and RPW8.2, powdery mildew resistance genes with distinguished features, whose over-expression triggers humidity-sensitive HR-like cell death. This suggests that ssi4 initiates defense responses likely via activation of RPW8.