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 HOMOLOGs (RBOHs). 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.