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Overexpression of Arabidopsis thaliana malonyl-CoA synthetase gene enhances cold stress tolerance by activating mitogen-activated protein kinases in plant cells

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Abstract

Malonyl-CoA synthetases may modulate cell responses to abiotic stress by regulating stress-related signaling transduction pathways or activating expression of transcription factors. However, the molecular mechanism of cold stress tolerance enhanced by malonyl-CoA synthetase is not fully understood. Here, we report that overexpression of the Arabidopsis thaliana malonyl-CoA synthetase gene AAE13.1 resulted in increased cell viability and growth rate and decreased thiobarbituric acid reactive substances under cold stress in rice (Oryza sativa L.), tobacco (Nicotiana tabacum), and slash pine (Pinus elliottii Engelm.). AAE13.1 was associated with cold stress tolerance by increasing the activity of ascorbate peroxidase, catalase, polyphenol oxidase, and peroxidase and the accumulation of acid phosphatase and alkaline phosphatase. Among six rice mitogen-activated protein kinase (MAPK) genes examined, AAE13.1 overexpression increased the expression of OsMAPK genes during cold stress. AAE13.1 activated expression of stress-response genes OsMAPK1, OsMAPK2, and OsMAPK3, indicating that AAE13.1 enhances cold stress tolerance by regulating expression of MAPK genes in plant cells. These results increase our understanding of cold stress tolerance in species of monocotyledons, dicotyledons, and gymnosperms.

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Acknowledgements

The authors are grateful to Dr. T. Bradshaw, Dr. R. Lischewski, and Dr. D. Thompson for their critical reading and suggestions during the preparation of this manuscript.

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Correspondence to Wei Tang.

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Project funding: The work was supported by USDG Grant R31270740.

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Corresponding editor: Tao Xu.

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Tang, W., Tang, A.Y. Overexpression of Arabidopsis thaliana malonyl-CoA synthetase gene enhances cold stress tolerance by activating mitogen-activated protein kinases in plant cells. J. For. Res. 32, 741–753 (2021). https://doi.org/10.1007/s11676-020-01140-8

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