Canonical ETI-Dependent and -Independent Pathways Mediate Autoimmunity Caused by Loss of CBP60b Clade Function

Calmodulin-Binding Protein 60 (CBP60), a plant-specific atypical transcription factor family, plays pivotal roles in reprogramming plant immunity. Loss of function of the CBP60b and CBP60b/c/d/e/f subfamily constitutively activates immune responses (autoimmunity). However, the specific mechanisms and pathways underlying this autoimmunity remain elusive. Here, through EMS mutagenesis of the cbp60b mutant, we isolated a dominant suppressor mutant that suppresses the cbp60b autoimmune phenotype. Sequencing identified a point mutation in CBP60g (designated cbp60g-3) that causes an aspartate-to-asparagine substitution at position 252 and reduces its transcriptional activity. Increasing the expression of CBP60g^D252N restored the pathogen response defect of the cbp60g;sard1 mutant. Strikingly, while wild-type CBP60g failed to suppress the autoimmunity of cbp60b, the transcriptionally compromised CBP60g^D252N variant completely suppressed it. Unexpectedly, we found that functional loss of canonical effector-triggered immunity (ETI) pathways only partially suppressed the autoimmunity of the cbp60b;c;d;e;f quintuple mutant. Although simultaneously disrupting the ETI pathways and introducing CBP60g^D252N further suppressed the autoimmunity of cbp60b;c;d;e;f, it still failed to achieve complete suppression. These results indicate that the autoimmunity in cbp60b;c;d;e;f mutant is mediated by both canonical ETI-dependent and ETI-independent pathways. These results provide new insights and raise further questions regarding the signalling mechanisms of plant autoimmunity.