Cytosolic acidification and oxidation are the toxic mechanisms of SO2 in Arabidopsis guard cells.
Autor: | Mozhgani M; Institute of Plant Science and Resources, Okayama University, Kurashiki, Okayama, Japan., Ooi L; Institute of Plant Science and Resources, Okayama University, Kurashiki, Okayama, Japan.; Plant & Microbial Research Unit (PMRU), Research, Technology & Value Creation Division, Nagase Viita Co. Ltd., Naka-ku, Okayama, Japan., Espagne C; Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC), Gif-sur-Yvette, France., Filleur S; Université Paris-Saclay, CEA, CNRS, Institute for Integrative Biology of the Cell (I2BC), Gif-sur-Yvette, France.; Université Paris Cité, UFR Sciences du Vivant, Paris, France., Mori IC; Institute of Plant Science and Resources, Okayama University, Kurashiki, Okayama, Japan. |
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Jazyk: | angličtina |
Zdroj: | Bioscience, biotechnology, and biochemistry [Biosci Biotechnol Biochem] 2024 Sep 20; Vol. 88 (10), pp. 1164-1171. |
DOI: | 10.1093/bbb/zbae092 |
Abstrakt: | 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. (© The Author(s) 2024. Published by Oxford University Press on behalf of Japan Society for Bioscience, Biotechnology, and Agrochemistry.) |
Databáze: | MEDLINE |
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