Plants rely on multiple immune systems to protect themselves from pathogens. When pattern-triggered immunity (PTI)—the first layer of the immune response—is no longer effective as a result of pathogenic effectors, effector-triggered immunity (ETI) often provides resistance. In ETI, host plants directly or indirectly perceive pathogen effectors via resistance proteins and launch a more robust and rapid defense response. Resistance proteins are typically found in the form of nucleotide-binding and leucine-rich-repeat-containing receptors (NLRs). Upon effector recognition, an NLR undergoes structural change and associates with other NLRs. The dimerization or oligomerization of NLRs signals to downstream components, activates “helper” NLRs, and culminates in the ETI response. Originally, PTI was thought to contribute little to ETI. However, most recent studies revealed crosstalk and cooperation between ETI and PTI. Here, we summarize recent advancements in our understanding of the ETI response and its components, as well as how these components cooperate in the innate immune signaling pathways. Based on up-to-date accumulated knowledge, this review provides our current perspective of potential engineering strategies for crop protection.

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 SUPPRESSOR OF rps4-RLD1 (SRFR1), identified in a suppressor screen, reactivated EDS1-dependent ETI to Pseudomonas syringae pv. tomato (Pto) DC3000. Besides, mutations in SRFR1 boosted defense responses to the generalist chewing insect Spodoptera exigua and the sugar beet cyst nematode Heterodera schachtii. Here, we show that mutations in SRFR1 enhance susceptibility to the fungal necrotrophs Fusarium oxysporum f. sp. lycopersici (FOL) and Botrytis cinerea in Arabidopsis. To translate knowledge obtained in AtSRFR1 research to crops, we generated SlSRFR1 alleles in tomato using a CRISPR/Cas9 system. Interestingly, slsrfr1 mutants increased expression of SA-pathway defense genes and enhanced resistance to Pto DC3000. In contrast, slsrfr1 mutants elevated susceptibility to FOL. 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.

Reduced and oxidized glutathione (GSH and GSSG) and buthionine sulfoximine (BSO) were applied to Xanthomonas campestris pv. campestris ( Xcc ) and X. vesicatoria ( Xv ) during liquid cultures, and to Chinese cabbage seedlings to decipher the roles of glutathione in the plant immunity against adapted Xcc and nonadapted Xv . In vitro antibacterial activities of GSH, GSSG, and BSO were evaluated in Xcc and Xv cultures after 24 and 48 h, respectively. GSH and GSSG exhibited in vitro antibacterial activities against Xcc and Xv , but BSO did not. In planta , GSH did not change the Xcc -caused tissue damage, but GSSG reduced leaf damage caused by Xcc infection at 2 and 3 days. BSO accelerated the damage. Neither GSH, GSSG, nor BSO altered gradually increasing Xcc bacterial growth in the mock-treated leaves. GSSG decreased Xv -triggered electrolyte leakage at 24 h and reduced Xv bacterial growth in the leaves at 7 days. In conclusion, exogenous GSH, GSSG, and BSO treatments altered reactive oxygen species and nitric oxide levels in the leaves before bacterial inoculation, and these changes led to differences in tissue damage in inoculated leaves.