Mitochondrial ß-Cyanoalanine Synthase Participates in flg22-Induced Stomatal Immunity

Area of Science:

• Plant Physiology
• Plant Immunology
• Cellular Signaling

Background:

• Guard cells regulate plant gas exchange and defense responses.
• Stomatal immunity, triggered by pathogen-associated molecular patterns (PAMPs), involves reactive oxygen species (ROS) and hydrogen sulfide (H₂S).
• While cytosolic H₂S sources are studied, mitochondrial H₂S roles in stomatal immunity remain unclear.

Purpose of the Study:

• To investigate the role of the mitochondrial H₂S source, β-cyanoalanine synthase CAS-C1, in flagellin (flg22)-induced stomatal immunity.
• To explore the involvement of mitochondrial H₂S in ROS production and susceptibility to bacterial pathogens.

Main Methods:

• Analysis of stomatal closure and apoplastic ROS production in cas-c1 mutant plants and wild-type.
• Treatment with a mitochondrial H₂S donor (AP39) and assessment of RBOHD-dependent ROS production.
• Pharmacological inhibition of mitochondrial electron transport chain activity and its effect on stomatal closure.

Main Results:

• Plants lacking CAS-C1 exhibited impaired flg22-triggered stomatal closure and reduced apoplastic ROS production, leading to increased susceptibility to bacterial inoculation.
• Mitochondrial H₂S donor AP39 induced stomatal closure in an RBOHD-dependent manner.
• Disruption of mitochondrial electron transport chain activity affected flg22-induced stomatal closure.

Conclusions:

• Mitochondrial H₂S, produced by CAS-C1, is essential for effective stomatal immunity against bacterial PAMPs.
• Mitochondrial H₂S signaling is linked to RBOHD-mediated ROS production in guard cells.
• Intracellular organelles, particularly mitochondria, play a significant role in orchestrating plant stomatal signaling and immune responses.