Conserved Opposite Functions in Plant Resistance to Biotrophic and Necrotrophic Pathogens of the Immune Regulator SRFR1.

Plant immunity is mediated in large part by specific interactions between a host resistance protein and a pathogen effector protein, named effector-triggered immunity (ETI). ETI needs to be tightly controlled both positively and negatively to enable normal plant growth because constitutively activated defense responses are detrimental to the host. In previous work, we reported that mutations in (), identified in a suppressor screen, reactivated EDS1-dependent ETI to pv. () DC3000. Besides, mutations in boosted defense responses to the generalist chewing insect and the sugar beet cyst nematode . Here, we show that mutations in enhance susceptibility to the fungal necrotrophs f. sp. and in Arabidopsis. To translate knowledge obtained in research to crops, we generated alleles in tomato using a CRISPR/Cas9 system. Interestingly, mutants increased expression of SA-pathway defense genes and enhanced resistance to DC3000. In contrast, mutants elevated susceptibility to . Together, these data suggest that SRFR1 is functionally conserved in both Arabidopsis and tomato and functions antagonistically as a negative regulator to (hemi-) biotrophic pathogens and a positive regulator to necrotrophic pathogens.