Fungal oxalic acid inhibits the deamidation of CERK1 ectodomain to dampen chitin-triggered plant immunity.

Botrytis cinerea and Sclerotinia sclerotiorum, two closely related necrotrophic fungal pathogens, secrete large amounts of oxalic acid (OA) into the plant apoplast to suppress host immunity, though the underlying mechanisms remain unclear. Here, we demonstrate that OA-induced virulence in Arabidopsis thaliana depends on CERK1, a coreceptor critical for fungal chitin-triggered immunity. Mass spectrometry analysis identified a site-specific deamidation at three asparagine residues (Asn70, Asn205, and Asn216) in CERK1's extracellular domain. Among these, only the deamidation-deficient N70A mutation impaired chitin-induced MPK4 activation, a process proven essential for plant resistance against both pathogens. OA treatment phenocopied the N70A mutation by suppressing chitin-elicited MPK4 activation. Consistently, acidic conditions mimicking the OA-acidified infection niche directly inhibited Asn70 deamidation. Notably, the N70A mutation of CERK1 triggered EDS1-dependent autoimmunity associated with senescence, which was mutually suppressed by the previously reported autoimmunity induced by the cerk1-4 (L124F) mutation. Our findings reveal that fungal OA dampens chitin-triggered immunity by exploiting pH-dependent inhibition of CERK1 Asn70 deamidation, establishing a mechanistic link between pathogen-derived acidity, post-translational modification of host immune receptors, and suppression of host immunity. Our data also suggest that the functional integrity of CERK1 is monitored by an endogenous immune surveillance system.