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

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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.

Original languageEnglish
Pages (from-to)437-447
Number of pages11
JournalPlant Cell and Environment
Issue number2
Publication statusPublished - Feb 1 2019


  • airborne pollutants
  • nonapoptotic cell death
  • stomatal closure
  • sulfur dioxide

ASJC Scopus subject areas

  • Physiology
  • Plant Science


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