Extended Data Fig. 4: HR development is not affected in mutants with impaired JA biosynthesis (aos) or perception (coi1-16) but coi1-16 has reduced disease susceptibility.

(A) RT-PCR verification loss of JISS1 expression in the aos T-DNA insertion line. Actin2 expression was used as a loading control (B) Phenotyping of Col-0 and aos and coi1-16 mutants showing that loss of JA biosynthesis and signalling does not affect HR development. (C) SAR growth curve of Psm4 following DCavrRpm1 or mock pre-treatment on Col-0 (**** p = <0.0001, t = 15.36, df=10 [unpaired t test]) and the coi1-16 mutant (p = 0.9421, t = 0.07450, df=10). coi1-16 is more resistant to Psm4 than wild-type Col-0 (*** p = 0.0004, t = 5.154, df=10) (n = 6 biological replicates). Col-0 mock: min=7.88, max=7.96, median=7.92, Q1 = 7.91, Q3 = 7.94; Col-0 DCavrRpm1: min=7.15, max=7.42, median=7.22, Q1 = 7.19, Q3 = 7.31; coi1-16 mock: min=7.03, max=7.71, median=7.28, Q1 = 7.07, Q3 = 7.53; coi1-16 DCavrRpm1: min=7.19, max=7.36, median=7.33, Q1 = 7.31, Q3 = 7.35.