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OsDMI3介导的OsUXS3磷酸化通过调节水稻中OsCATB蛋白丰度提高氧化应激耐受性。

OsDMI3-mediated OsUXS3 phosphorylation improves oxidative stress tolerance by modulating OsCATB protein abundance in rice.

作者信息

Ni Lan, Wang Qingwen, Chen Chao, Wang Shuang, Shen Tao, Jiang Jingjing, Cui Zhenzhen, Li Kaiyue, Yang Qiqing, Jiang Mingyi

机构信息

College of Life Sciences, National Key Laboratory of Crop Genetics and Germplasm Enhancement, Key Laboratory of Crop Physiology Ecology and Production Management, Ministry of Agriculture, Nanjing Agricultural University, Nanjing, 210095, China.

Southern Regional Collaborative Innovation Center for Grain and Oil Crops in China, Hunan Agricultural University, Changsha, 410128, China.

出版信息

J Integr Plant Biol. 2022 May;64(5):1087-1101. doi: 10.1111/jipb.13255. Epub 2022 Apr 29.

DOI:10.1111/jipb.13255
PMID:35348292
Abstract

Calcium (Ca )/calmodulin (CaM)-dependent protein kinase (CCaMK) is an important positive regulator of antioxidant defenses and tolerance against oxidative stress. However, the underlying molecular mechanisms are largely unknown. Here, we report that the rice (Oryza sativa) CCaMK (OsDMI3) physically interacts with and phosphorylates OsUXS3, a cytosol-localized UDP-xylose synthase. Genetic and biochemical evidence demonstrated that OsUXS3 acts downstream of OsDMI3 to enhance the oxidative stress tolerance conferred by higher catalase (CAT) activity. Indeed, OsUXS3 interacted with CAT isozyme B (OsCATB), and this interaction was required to increase OsCATB protein abundance under oxidative stress conditions. Furthermore, we showed that OsDMI3 phosphorylates OsUXS3 on residue Ser-245, thereby further promoting the interaction between OsUXS3 and OsCATB. Our results indicate that OsDMI3 promotes the association of OsUXS3 with OsCATB to enhance CAT activity under oxidative stress. These findings reveal OsUXS3 as a direct target of OsDMI3 and demonstrate its involvement in antioxidant defense.

摘要

钙(Ca )/钙调蛋白(CaM)依赖性蛋白激酶(CCaMK)是抗氧化防御和氧化应激耐受性的重要正向调节因子。然而,其潜在的分子机制在很大程度上尚不清楚。在此,我们报道水稻(Oryza sativa)CCaMK(OsDMI3)与定位于胞质溶胶的UDP-木糖合酶OsUXS3发生物理相互作用并使其磷酸化。遗传和生化证据表明,OsUXS3在OsDMI3的下游发挥作用,通过提高过氧化氢酶(CAT)活性来增强氧化应激耐受性。事实上,OsUXS3与CAT同工酶B(OsCATB)相互作用,并且这种相互作用是在氧化应激条件下增加OsCATB蛋白丰度所必需的。此外,我们表明OsDMI3使OsUXS3的丝氨酸-245位点磷酸化,从而进一步促进OsUXS3与OsCATB之间的相互作用。我们的结果表明,OsDMI3促进OsUXS3与OsCATB的结合,以增强氧化应激下的CAT活性。这些发现揭示了OsUXS3是OsDMI3的直接靶点,并证明了其参与抗氧化防御。

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