|Cho, Daeshik -|
|Villiers, Florent -|
|Kroniewicz, Laetitia -|
|Lee, Sangmee -|
|Seo, You Jin -|
|Hirschi, Kendal -|
|Leonhardt, Nathalie -|
|Kwak, June -|
Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 28, 2012
Publication Date: August 29, 2012
Citation: Cho, D., Villiers, F., Kroniewicz, L., Lee, S., Seo, Y., Hirschi, K.D., Leonhardt, N., Kwak, J.M. 2012. Vacuolar CAX1 and CAX3 influence auxin transport in guard cells via regulation of apoplastic pH. Plant Physiology. 160(3):1293-1302. Interpretive Summary: A central problem in engineering plants for increased nutrient content is factoring in how these changes could impact plant growth. The movement of nutrients like calcium (Ca) in plants is thought to be important for how plants grow and adapt; however, the mechanisms associated with these changes have not been fully investigated. Work here suggests the movement of Ca is often associated with changes in the pH of the cell. Altering plant Ca transporters thus can boost nutrient content and also impacts how the plant grows by changing the pH within the cell. This work demonstrates a new way that altering nutrient levels impact the growth and yield of crops.
Technical Abstract: Cation exchangers CAX1 and CAX3 are vacuolar ion transporters involved in ion homeostasis in plants. Widely expressed in the plant, they mediate calcium transport from the cytosol to the vacuole lumen using the proton gradient across the tonoplast. Here, we report an unexpected role of CAX1 and CAX3 in regulating apoplastic pH and describe how they contribute to auxin transport using the guard cell's response as readout of hormone signaling and cross talk. We show that indole-3-acetic acid (IAA) inhibition of abscisic acid (ABA)-induced stomatal closure is impaired in "cax1", "cax3", and "cax1/cax3". These mutants exhibited constitutive hypopolarization of the plasma membrane, and time-course analyses of membrane potential revealed that IAA-induced hyperpolarization of the plasma membrane is also altered in these mutants. Both ethylene and 1-naphthalene acetic acid inhibited ABA-triggered stomatal closure in "cax1", "cax3", and "cax1/cax3", suggesting that auxin signaling cascades were functional and that a defect in IAA transport caused the phenotype of the "cax" mutants. Consistent with this finding, chemical inhibition of AUX1 in wild-type plants phenocopied the "cax" mutants. We also found that "cax1/cax3" mutants have a higher apoplastic pH than the wild type, further supporting the hypothesis that there is a defect in IAA import in the "cax" mutants. Accordingly, we were able to fully restore IAA inhibition of ABA-induced stomatal closure in "cax1", "cax3", and "cax1/cax3" when stomatal movement assays were carried out at a lower extracellular pH. Our results suggest a network linking the vacuolar cation exchangers to apoplastic pH maintenance that plays a crucial role in cellular processes.