J Integr Plant Biol ›› 2022, Vol. 64 ›› Issue (6): 1229-1245.DOI: 10.1111/jipb.13256

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  • 收稿日期:2022-03-08 接受日期:2022-03-24 出版日期:2022-06-01 发布日期:2022-06-15

Testing the polar auxin transport model with a selective plasma membrane H+-ATPase inhibitor

Yongqing Yang1†*, Xiaohui Liu2†, Wei Guo3, Wei Liu4, Wei Shao5, Jun Zhao1, Junhong Li1, Qing Dong1, Liang Ma1, Qun He6, Yingzhang Li1, Jianyong Han6 and Xiaoguang Lei2*   

  1. 1 State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100193, China
    2 Beijing National Laboratory for Molecular Sciences, Key Laboratory of Bioorganic Chemistry and Molecular Engineering of Ministry of Education, Department of Chemical Biology, College of Chemistry and Molecular Engineering, Synthetic and Functional Biomolecules Center, and Peking‐Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China
    3 Institute of Food Science and Technology, Chinese Academy of Agricultural Sciences, Beijing 100193, China
    4 Department of Dermatology, Peking University First Hospital, Beijing 100034, China
    5 Iomics Biosciences Inc., Beijing 100102, China
    6 College of Biological Sciences, China Agricultural University, Beijing 100193, China

    †These authors contributed equally to this work.
    *Correspondences: Yongqing Yang (yangyongqing@cau.edu.cn, Dr. Yang is fully responsible for the distribution of the materials associated with this article); Xiaoguang Lei (xglei@pku.edu.cn)
  • Received:2022-03-08 Accepted:2022-03-24 Online:2022-06-01 Published:2022-06-15

Abstract:

Auxin is unique among plant hormones in that its function requires polarized transport across plant cells. A chemiosmotic model was proposed to explain how polar auxin transport is derived by the H+ gradient across the plasma membrane (PM) established by PM H+-adenosine triphosphatases (ATPases). However, a classical genetic approach by mutations in PM H+-ATPase members did not result in the ablation of polar auxin distribution, possibly due to functional redundancy in this gene family. To confirm the crucial role of PM H+-ATPases in the polar auxin transport model, we employed a chemical genetic approach. Through a chemical screen, we identified protonstatin-1 (PS-1), a selective small-molecule inhibitor of PM H+-ATPase activity that inhibits auxin transport. Assays with transgenic plants and yeast strains showed that the activity of PM H+-ATPases affects auxin uptake as well as acropetal and basipetal polar auxin transport. We propose that PS-1 can be used as a tool to interrogate the function of PM H+-ATPases. Our results support the chemiosmotic model in which PM H+-ATPase itself plays a fundamental role in polar auxin transport.

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