A YopJ-family effector from Ralstonia solanacearum is associated with auxin-responsive transcriptional reprogramming and bacterial wilt suppression

Abstract

Effector-triggered immunity (ETI) can reshape hormone-associated transcriptional programs during plant–pathogen interactions. However, how bacterial effectors are associated with hormone-responsive defense outputs in potato remains poorly understood. This study identifies RipBR, a previously uncharacterized YopJ-family effector from Ralstonia solanacearum, as an avirulence-associated determinant in the wild potato accession Solanum albicans ALB28-1. Loss- and gain-of-function analyses demonstrated that RipBR contributes to reduced bacterial wilt symptoms and restricts bacterial colonization in potato. Mutations in conserved residues H158 and C225 strongly impaired RipBR-associated hypersensitive response induction and disease suppression, indicating their importance for RipBR function. RipBR localized to both the nucleus and cytoplasm, whereas H158R and C225S mutations were associated with altered subcellular distribution and impaired immune-associated phenotypes. Transcriptome analysis revealed that RipBR recognition was accompanied by extensive auxin-responsive transcriptional reprogramming, including induction of AUX/IAA, ARF, GH3, and SAUR genes, together with activation of the defense-associated transcription factor SaTGA1. These responses occurred without detectable increases in endogenous indole-3-acetic acid (IAA) accumulation or major auxin biosynthetic gene expression, suggesting modulation of auxin signaling rather than enhanced auxin production. Exogenous 1-naphthaleneacetic acid (NAA) treatment alleviated bacterial wilt symptoms but did not significantly reduce bacterial colonization, indicating that auxin signaling activation alone is insufficient to establish enhanced resistance. Together, these findings identify RipBR as a YopJ-family effector associated with bacterial wilt suppression in potato and reveal an association between effector recognition and auxin-responsive transcriptional reprogramming during plant immunity.