The mechanism of SO2-induced stomatal closure differs from O3 and CO2 responses and is mediated by nonapoptotic cell death in guard cells

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3 Citations (Scopus)

Abstract

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 O3. SLOW ANION CHANNEL-ASSOCIATED 1 (SLAC1) and OPEN STOMATA 1 (OST1) were identified as genes mediating O3-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 O3 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. O3- 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 O3 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.

Original languageEnglish
JournalPlant Cell and Environment
DOIs
Publication statusAccepted/In press - Jan 1 2018

Fingerprint

guard cells
sulfur dioxide
Plant Stomata
Anions
cell death
Cell Death
Chemical Phenomena
carbon dioxide
Chlorophyll
Arabidopsis
Genes
Molecular Biology
Cell Survival
Gases
stomata
anions
pollutants
distress
molecular genetics
cell viability

Keywords

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

ASJC Scopus subject areas

  • Physiology
  • Plant Science

Cite this

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title = "The mechanism of SO2-induced stomatal closure differs from O3 and CO2 responses and is mediated by nonapoptotic cell death in guard cells",
abstract = "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 O3. SLOW ANION CHANNEL-ASSOCIATED 1 (SLAC1) and OPEN STOMATA 1 (OST1) were identified as genes mediating O3-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 O3 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. O3- 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 O3 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.",
keywords = "airborne pollutants, nonapoptotic cell death, stomatal closure, sulfur dioxide",
author = "Lia Ooi and Takakazu Matsuura and Shintaro Munemasa and Yoshiyuki Murata and Maki Katsuhara and Takashi Hirayama and Izumi Mori",
year = "2018",
month = "1",
day = "1",
doi = "10.1111/pce.13406",
language = "English",
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T1 - The mechanism of SO2-induced stomatal closure differs from O3 and CO2 responses and is mediated by nonapoptotic cell death in guard cells

AU - Ooi, Lia

AU - Matsuura, Takakazu

AU - Munemasa, Shintaro

AU - Murata, Yoshiyuki

AU - Katsuhara, Maki

AU - Hirayama, Takashi

AU - Mori, Izumi

PY - 2018/1/1

Y1 - 2018/1/1

N2 - 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 O3. SLOW ANION CHANNEL-ASSOCIATED 1 (SLAC1) and OPEN STOMATA 1 (OST1) were identified as genes mediating O3-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 O3 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. O3- 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 O3 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.

AB - 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 O3. SLOW ANION CHANNEL-ASSOCIATED 1 (SLAC1) and OPEN STOMATA 1 (OST1) were identified as genes mediating O3-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 O3 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. O3- 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 O3 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.

KW - airborne pollutants

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