The mechanism of SO2-induced stomatal closure differs from O-3 and CO2 responses and is mediated by nonapoptotic cell death in guard cells

摘要

Plants closing stomata in the presence of harmful gases is believed to be a stress avoidance mechanism. SO2, 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 CO2, together with RESPIRATORY BURST OXIDASE HOMOLOGs (RBOHs). The overlaying roles of these genes in response to O-3 and CO2 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 SO2 in Arabidopsis through molecular genetic approaches. O-3- and CO2-insensitive stomata mutants did not show significant differences from the wild type in stomatal sensitivity, guard cell viability, and chlorophyll content revealing that SO2-induced closure is not regulated by the same molecular mechanisms as for O-3 and CO2. Nonapoptotic cell death is shown as the reason for SO2-induced closure, which proposed the closure as a physicochemical process resulted from SO2 distress, instead of a biological protection mechanism.