Disruption of the mRNA m⁶A writer complex triggers autoimmunity in Arabidopsis

Distinguishing self from non-self is crucial to direct immune responses against pathogens. Unmodified RNAs stimulate human innate immunity, but RNA modifications suppress this response. mRNA m⁶A modification is essential forArabidopsis thalianaviability. However, the molecular basis of the impact of mRNA m⁶A depletion is poorly understood. Here, we show that disruption of the Arabidopsis mRNA m⁶A writer complex triggers autoimmunity. Most gene expression changes in m⁶A writer complexvir-1mutants grown at 17°C are explained by defence gene activation and are suppressed at 27°C, consistent with the established temperature sensitivity of Arabidopsis immunity. Accordingly, we found enhanced pathogen resistance and increased premature cell death invir-1mutants at 17°C but not 27°C. Global temperature-sensitive mRNA poly(A) tail length changes accompany these phenotypes. Our results demonstrate that autoimmunity is a major phenotype of mRNA m⁶A writer complex mutants, which has important implications for interpreting this modification’s role. Furthermore, we open the broader question of whether unmodified RNA triggers immune signalling in plants.