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

Lia Ooi; Takakazu Matsuura; Shintaro Munemasa; Yoshiyuki Murata; Maki Katsuhara; Takashi Hirayama; Izumi C. Mori

doi:10.1111/pce.13406

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

Lia Ooi, Takakazu Matsuura, Shintaro Munemasa, Yoshiyuki Murata, Maki Katsuhara, Takashi Hirayama, Izumi C. Mori

Research output: Contribution to journal › Article › peer-review

11 Citations (Scopus)

Abstract

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 language	English
Pages (from-to)	437-447
Number of pages	11
Journal	Plant Cell and Environment
Volume	42
Issue number	2
DOIs	https://doi.org/10.1111/pce.13406
Publication status	Published - Feb 1 2019

Keywords

airborne pollutants
nonapoptotic cell death
stomatal closure
sulfur dioxide

ASJC Scopus subject areas

Physiology
Plant Science

Access to Document

10.1111/pce.13406

Cite this

Ooi, L., Matsuura, T., Munemasa, S., Murata, Y., Katsuhara, M., Hirayama, T., & Mori, I. C. (2019). 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 Plant Cell and Environment, 42(2), 437-447. https://doi.org/10.1111/pce.13406

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 . / Ooi, Lia; Matsuura, Takakazu; Munemasa, Shintaro et al.
In: Plant Cell and Environment, Vol. 42, No. 2, 01.02.2019, p. 437-447.

Research output: Contribution to journal › Article › peer-review

Ooi, L, Matsuura, T, Munemasa, S , Murata, Y , Katsuhara, M , Hirayama, T & Mori, IC 2019, ' 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 ', Plant Cell and Environment, vol. 42, no. 2, pp. 437-447. https://doi.org/10.1111/pce.13406

Ooi L, Matsuura T, Munemasa S , Murata Y , Katsuhara M , Hirayama T et al. 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 Plant Cell and Environment. 2019 Feb 1;42(2):437-447. doi: 10.1111/pce.13406

Ooi, Lia ; Matsuura, Takakazu ; Munemasa, Shintaro et al. / 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 In: Plant Cell and Environment. 2019 ; Vol. 42, No. 2. pp. 437-447.

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abstract = " 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. ",

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