The Effector RipAW Enhances Ralstonia solanacearum Invasion in Arabidopsis via CBP60g/SARD1-Dependent and -Independent Pathways
Wang, Huijuan (Northwest A&F University (Yangling, Xina))
Fu, Shouyang (Northwest A&F University (Yangling, Xina))
Cao, Tao (Northwest A&F University (Yangling, Xina))
Niu, Yang (Northwest A&F University (Yangling, Xina))
Cheng, Shengyang (Northwest A&F University (Yangling, Xina))
Gong, Qichang (Northwest A&F University (Yangling, Xina))
Ma, Hui (Northwest A&F University (Yangling, Xina))
Wang, Xiang (Northwest A&F University (Yangling, Xina))
Hu, JinXue (Northwest A&F University (Yangling, Xina))
Chen, Min (Southwest University (Chongqing, Xina))
Wang, Dongdong (Northwest A&F University (Yangling, Xina))
Zhang, Yong (Southwest University (Chongqing, Xina))
Sánchez Coll, Núria (Centre de Recerca en Agrigenòmica)
Valls, Marc (Universitat Autònoma de Barcelona. Departament de Genètica i de Microbiologia)
Chen, Qin (Northwest A&F University (Yangling, Xina))
Zhao, Cuizhu (Northwest A&F University (Yangling, Xina))
Chen, Yue (Northwest A&F University (Yangling, Xina))
Lu, Haibin (Northwest A&F University (Yangling, Xina))

Fecha:	2026
Resumen:	CaM-binding Protein 60-like G (CBP60g) and Systemic Acquired Resistance Deficient 1 (SARD1) are key immune signallingregulators that redundantly promote salicylic acid (SA) biosynthesis and plant immunity. Pathogen effectors often target theseimmune nodes to suppress plant defence. However, the role of bacterial effectors in disabling CBP60g and SARD1 to increaseplant susceptibility remains unclear. In this study, we show that RipAW, an E3 ligase effector from Ralstonia solanacearum,induces root architecture changes and enhances plant susceptibility to R. solanacearum in Est::RipAW transgenic plants. Theconstitutively expressed RipAW (C177S), lacking E3 ligase activity, did not affect root architecture or plant susceptibility, indi-cating that RipAW's E3 ligase activity is crucial for these phenotypes. Transcriptional profiling of Est::RipAW plants revealedstrong up-regulation of CBP60g and SARD1, while the SA signalling pathway remained in a basal state. Transient expression ofRipAW and CBP60g in Nicotiana benthamiana showed that RipAW associates with CBP60g and affects its stability. Genetic anal-ysis revealed that loss-of-function mutations in CBP60g and SARD1 increased plant susceptibility to R. solanacearum, but didnot enhance RipAW-mediated pathogen growth. Furthermore, growth of the R. solanacearum ΔRipAW null mutant strain wasreduced in wild-type plants but restored in cbp60g/sard1 mutant plants, confirming that the promotion of RipAW on bacterialgrowth is dependent on CBP60g and SARD1. Surprisingly, CBP60g and SARD1 were not involved in R. solanacearum-inducedand RipAW-triggered root architecture changes. Overall, our findings demonstrate that RipAW increases plant susceptibility toR. solanacearum via both CBP60g/SARD1-dependent and -independent pathways.
Derechos:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Lengua:	Anglès
Documento:	Article ; recerca ; Versió publicada
Publicado en:	Molecular plant pathology, Vol. 27, Num. 1 (January 2026) , art. e70207, ISSN 1364-3703

DOI: 10.1111/mpp.70207

17 p, 7.4 MB

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