Testing the polar auxin transport model with a selective plasma membrane H<sup>+</sup>‐ATPase inhibitor
Yongqing Yang, Xiaohui Liu, Wei Guo, Wei Liu, Wei Shao, Jun Zhao, Junhong Li, Qing Dong, Liang Ma, Qun He, Ying-Zhang Li, Jianyong Han, Xiaoguang Lei
Abstract
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.