A Ralstonia effector RipAU impairs peanut AhSBT1.7 immunity for pathogenicity via AhPME-mediated cell wall degradation.

Bacterial wilt caused by Ralstonia solanacearum is a devastating disease affecting a great many crops including peanut. The pathogen damages plants via secreting type Ш effector proteins (T3Es) into hosts for pathogenicity. Here, we characterized RipAU was among the most toxic effectors as ΔRipAU completely lost its pathogenicity to peanuts. A serine residue of RipAU is the critical site for cell death. The RipAU targeted a subtilisin-like protease (AhSBT1.7) in peanut and both protein moved into nucleus. Heterotic expression of AhSBT1.7 in transgenic tobacco and Arabidopsis thaliana significantly improved the resistance to R. solanacearum. The enhanced resistance was linked with the upregulating ERF1 defense marker genes and decreasing pectin methylesterase (PME) activity like PME2&4 in cell wall pathways. The RipAU played toxic effect by repressing R-gene, defense hormone signaling, and AhSBTs metabolic pathways but increasing PMEs expressions. Furthermore, we discovered AhSBT1.7 interacted with AhPME4 and was colocalized at nucleus. The AhPME speeded plants susceptibility to pathogen via mediated cell wall degradation, which inhibited by AhSBT1.7 but upregulated by RipAU. Collectively, RipAU impaired AhSBT1.7 defense for pathogenicity by using PME-mediated cell wall degradation. This study reveals the mechanism of RipAU pathogenicity and AhSBT1.7 resistance, highlighting peanut immunity to bacterial wilt for future improvement.