The F-box Containing Bacterial Effector RipG6 Destabilizes a Receptor-Like Cytoplasmic Kinase Involved in Plant...

Area of Science:

• Plant Pathology
• Molecular Plant-Microbe Interactions
• Cellular Immunity

Background:

• Bacterial pathogens use type III secreted effectors to manipulate host immunity.
• Ralstonia solanacearum causes bacterial wilt, utilizing RipG effectors for virulence.
• RipG effectors are proposed to interact with host ubiquitin-ligase complexes via their F-box motif.

Purpose of the Study:

• Investigate the function of RipG6 effector in plant immunity.
• Identify host interactors of RipG6.
• Elucidate the mechanism by which RipG6 suppresses plant immunity.

Main Methods:

• Utilized surrogate type III delivery and heterologous expression systems.
• Performed yeast and plant cell co-expression assays to identify interactors.
• Assessed SlRLCK-VIII-6 stability upon co-expression with RipG6 variants.

Main Results:

• RipG6 suppressed plant pattern-triggered immunity in an F-box-dependent manner.
• Identified tomato receptor-like cytoplasmic kinase (SlRLCK-VIII-6) as a RipG6 interactor.
• RipG6 co-expression reduced SlRLCK-VIII-6 stability, an effect dependent on the F-box motif.
• Homologs of SlRLCK-VIII-6 positively regulate plant immune signaling.

Conclusions:

• RipG6 destabilizes SlRLCK-VIII-6, likely by recruiting it to a host ubiquitin-ligase complex.
• This destabilization mechanism suppresses plant immunity, contributing to Ralstonia solanacearum virulence.
• Understanding SlRLCK-VIII-6 function is crucial for deciphering pathogen effector strategies.