The mechanism of SO 2 ‐induced stomatal closure differs from O 3 and CO 2 responses and is mediated by nonapoptotic cell death in guard cells

Plants closing stomata in the presence of harmful gases is believed to be a stress avoidance mechanism. SO 2 , one of the major airborne pollutants, has long been reported to induce stomatal closure, yet the mechanism remains unknown. Little is known about the stomatal response to airborne pollutants besides O 3 . SLOW ANION CHANNEL‐ASSOCIATED 1 ( SLAC1 ) and OPEN STOMATA 1 ( OST1 ) were identified as genes mediating O 3 ‐induced closure. SLAC1 and OST1 are also known to mediate stomatal closure in response to CO 2 , together with RESPIRATORY BURST OXIDASE HOMOLOG s ( RBOH s). The overlaying roles of these genes in response to O 3 and CO 2 suggested that plants share their molecular regulators for airborne stimuli. Here, we investigated and compared stomatal closure event induced by a wide concentration range of SO 2 in Arabidopsis through molecular genetic approaches. O 3 ‐ and CO 2 ‐insensitive stomata mutants did not show significant differences from the wild type in stomatal sensitivity, guard cell viability, and chlorophyll content revealing that SO 2 ‐induced closure is not regulated by the same molecular mechanisms as for O 3 and CO 2 . Nonapoptotic cell death is shown as the reason for SO 2 ‐induced closure, which proposed the closure as a physicochemical process resulted from SO 2 distress, instead of a biological protection mechanism.