SHOU4/4L link cell wall cellulose synthesis to pattern-triggered immunity.

Area of Science:

• Plant immunity
• Molecular plant-microbe interactions
• Signal transduction

Background:

• Pattern recognition receptors (PRRs) initiate pattern-triggered immunity (PTI) by sensing molecular patterns.
• Receptor-like cytoplasmic kinases (RLCKs) are key signaling components downstream of PRRs, regulating plant defense responses through protein phosphorylation.
• Understanding RLCK substrates is vital for elucidating plant immune mechanisms.

Purpose of the Study:

• To identify and characterize RLCK-regulated substrate proteins involved in plant immunity.
• To investigate the role of SHOU4 and SHOU4L in plant resistance to pathogens.
• To elucidate the regulatory mechanism of SHOU4L by RLCKs.

Main Methods:

• Phosphorylation analysis of SHOU4 and SHOU4L upon pattern elicitation.
• Protein-protein interaction studies using co-immunoprecipitation.
• Phosphoproteomic analysis to identify phosphorylation sites.
• Functional analysis of SHOU4L variants in loss-of-function mutants.

Main Results:

• SHOU4 and SHOU4L are rapidly phosphorylated upon pattern elicitation and are essential for resistance to bacterial and fungal pathogens.
• BOTRYTIS-INDUCED KINASE 1 (BIK1), an RLCK-VII kinase, interacts with and phosphorylates SHOU4L.
• Reversible phosphorylation of SHOU4L is critical for both plant immunity and development, influencing its interaction with Cellulose Synthase 1 (CESA1).

Conclusions:

• SHOU4/4L are newly identified components of pattern-triggered immunity (PTI).
• BIK1-mediated phosphorylation of SHOU4L regulates plant immunity and development by modulating its interaction with CESA1 and cellulose synthesis.
• This study reveals a novel mechanism of plant immune signaling involving RLCK regulation of substrate protein function.