Bacterial XopR subverts RIN4 complex-mediated plant immunity via plasma membrane-associated percolation

Area of Science:

• Plant-microbe interactions
• Molecular plant pathology
• Cellular microbiology

Background:

• Phytopathogenic bacteria employ type 3 effectors (T3Es) to suppress plant immunity.
• T3Es often contain intrinsically disordered regions (IDRs) crucial for function, but their role in subverting plant defenses is not fully understood.
• Plant immune receptors, like the RPM1-interacting protein 4 (RIN4) complex, are key targets for bacterial effectors.

Purpose of the Study:

• To elucidate the mechanism by which T3E XopR, utilizing its IDRs, manipulates plant immune complexes.
• To investigate the role of macromolecular condensation in the interaction between XopR and the RIN4-RPM1 immune complex.
• To understand how XopR disrupts plant defense signaling at the plasma membrane.

Main Methods:

• Investigated XopR's behavior on the plant plasma membrane using biophysical techniques.
• Analyzed the formation of XopR-mediated macromolecular condensates.
• Studied the impact of XopR on RIN4 phosphorylation and RPM1-activated defense in Arabidopsis.
• Examined the interaction between XopR, RIN4, and RPM1-interacting protein kinase (RIPK).

Main Results:

• XopR forms dynamic, spatiotemporal networks on the plant plasma membrane through percolation clustering and spanning.
• These XopR networks efficiently manipulate plant surface immune regulators, including the RIN4-RPM1 complex.
• XopR disrupts the RIN4-RPM1 condensate, leading to reduced RIN4 phosphorylation and diminished plant defense.
• XopR impairs RIN4 phosphorylation by RIPK, a key step in RPM1-mediated immunity.

Conclusions:

• Plant plasma membrane-associated macromolecular condensation is a critical mechanism for T3E function.
• T3E XopR subverts plant immunity by forming a network that disrupts the RIN4-RPM1 immune complex and inhibits defense signaling.
• This study reveals a novel strategy employed by bacteria to overcome plant defenses through effector-driven condensate modulation.