Oxford University Press (OUP) Acta Medica Okayama 1347-6947 88 10 2024 Cytosolic acidification and oxidation are the toxic mechanisms of SO2 in Arabidopsis guard cells 1164 1171 EN Mahdi Mozhgani Institute of Plant Science and Resources, Okayama University Lia Ooi Institute of Plant Science and Resources, Okayama University Christelle Espagne Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC) Sophie Filleur Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC) Izumi C Mori Institute of Plant Science and Resources, Okayama University SO2/H2SO3 can damage plants. However, its toxic mechanism has still been controversial. Two models have been proposed, cytosolic acidification model and cellular oxidation model. Here, we assessed the toxic mechanism of H2SO3 in three cell types of Arabidopsis thaliana, mesophyll cells, guard cells (GCs), and petal cells. The sensitivity of GCs of Chloride channel a (CLCa)-knockout mutants to H2SO3 was significantly lower than those of wildtype plants. Expression of other CLC genes in mesophyll cells and petal cells were different from GCs. Treatment with antioxidant, disodium 4,5-dihydroxy-1,3-benzenedisulfonate (tiron), increased the median lethal concentration (LC50) of H2SO3 in GCs indicating the involvement of cellular oxidation, while the effect was negligible in mesophyll cells and petal cells. These results indicate that there are two toxic mechanisms of SO2 to Arabidopsis cells: cytosolic acidification and cellular oxidation, and the toxic mechanism may vary among cell types. No potential conflict of interest relevant to this article was reported.

© 2020 The Authors. Published by Elsevier Ltd. Acta Medica Okayama 00456535 247 2020 Application of the cellular oxidation biosensor to Toxicity Identification Evaluations for high-throughput toxicity assessment of river water 125933 EN Lia Ooi Institute of Plant Science and Resources, Okayama University Keisuke Okazaki Institute of Plant Science and Resources, Okayama University Carlos R. Arias-Barreiro nstitute of Plant Science and Resources, Okayama University Lee Yook Heng Southeast Asia Disaster Prevention Research Initiative (SEADPRI-UKM), Institute for Environment and Development (LESTARI), The National University of Malaysia Izumi C. Mori Institute of Plant Science and Resources, Okayama University Toxicity Identification Evaluation (TIE) is a useful method for the classification and identification of toxicants in a composite environment water sample. However, its extension to a larger sample size has been restrained owing to the limited throughput of toxicity bioassays. Here we reported the development of a high-throughput method of TIE Phase I. This newly developed method was assisted by the fluorescence-based cellular oxidation (CO) biosensor fabricated with roGFP2-expressing bacterial cells in 96-well microplate format. The assessment of four river water samples from Langat river basin by this new method demonstrated that the contaminant composition of the four samples can be classified into two distinct groups. The entire toxicity assay consisted of 2338 tests was completed within 12 h with a fluorescence microplate reader. Concurrently, the sample volume for each assay was reduced to 50 ƒÊL, which is 600 to 4700 times lesser to compare with conventional bioassays. These imply that the throughput of the CO biosensor-assisted TIE Phase I is now feasible for constructing a large-scale toxicity monitoring system, which would cover a whole watershed scale. No potential conflict of interest relevant to this article was reported.

Wiley Acta Medica Okayama 0140-7791 42 2 2018 The mechanism of SO2 -induced stomatal closure differs from O3 and CO2 responses and is mediated by nonapoptotic cell death in guard cells. 437 447 EN Lia Ooi Institute of Plant Science and Resources, Okayama University Takakazu Matsuura Institute of Plant Science and Resources, Okayama University Shintaro Munemasa Graduate School of Environmental and Life Science, Okayama University Yoshiyuki Murata Graduate School of Environmental and Life Science, Okayama University Maki Katsuhara Institute of Plant Science and Resources, Okayama University Takashi Hirayama Institute of Plant Science and Resources, Okayama University Izumi C. Mori Institute of Plant Science and Resources, Okayama University 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. No potential conflict of interest relevant to this article was reported.