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CYSTM3 negatively regulates salt stress tolerance in Arabidopsis

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Abstract

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CYSTM3, a small mitochondrial protein, acts as a negative regulator in salt stress response by preventing Na+ efflux and disturbing reactive oxygen species (ROS) homeostasis in Arabidopsis.

Abstract

Cysteine-rich transmembrane module (CYSTM) is a not well characterized small peptide family in plants. In this study, we identified a novel mitochondrion-localized CYSTM member CYSTM3 from Arabidopsis, which was ubiquitously expressed in different tissues and dramatically induced by salt stress. Transgenic plants overexpressing CYSTM3 (OE) displayed hypersensitivity to salt stress compared with wild type (WT) plants, whereas a knockout mutant cystm3 was more tolerant to high salinity than WT. Moreover, OE lines accumulated higher contents of Na+ and ROS than WT and cystm3 upon exposure to high salinity. Further analysis revealed that CYSTM3 could deter root Na+ efflux and inhibit the activities of a range of ROS scavenging enzymes in Arabidopsis. In addition, the transcripts of nuclear salt stress-responsive genes were over-activated in cystm3 than those in WT and OE lines. Taken together, Arabidopsis CYSTM3 acts as a negative regulator in salt stress tolerance.

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The data that support the findings of this study are available from the corresponding author upon request.

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Acknowledgements

This work was supported by the National Natural Science Foundation of China (Grant Nos. 31570271 and 31771878), and the Natural Science Foundation of Shandong Province (Grant No. ZR2016CM22).

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J.H. and C.Z. conceived the original screening and research plans; Z.Y., and Y.X. performed experiments; Z.Y., and Y.X. conceived the project and wrote the article; S.Z., C.W., G.Y. and K.Y. provided suggestions and proofed the article; J.H. and C.Z. supervised and complemented the writing.

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Correspondence to Chengchao Zheng or Jinguang Huang.

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Xu, Y., Yu, Z., Zhang, S. et al. CYSTM3 negatively regulates salt stress tolerance in Arabidopsis. Plant Mol Biol 99, 395–406 (2019). https://doi.org/10.1007/s11103-019-00825-x

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  • DOI: https://doi.org/10.1007/s11103-019-00825-x

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