Abstract

Salt stress is one of the major factors impacting crop productivity worldwide. Through a variety of effector and signaling pathways, plants achieve survival under salinity stress by maintaining high cytosolic potassium/sodium ion (K+/Na+) ratios, preventing Na+ cytotoxicity, and retaining osmotic balance. Ras‐related protein 5 (Rab5) members are involved in the trafficking of endosomes to the vacuole or plasma membrane (PM). The vacuolar protein sorting‐ associated protein 9 (vps9a) encodes the single guanine nucleotide exchange factor (GEF) that activates all three known Rab5 proteins in Arabidopsis thaliana. Previous work from our group has reported the critical function of vps9a for the operation of salt‐induced endocytic pathway, as well as the expansion of endomembrane compartments under saline stress conditions. Here we show an additional role of vps9a in plant response to salt stress via maintenance of K+ status of the cell rather than Na+ homeostasis. Our results show that roots from vps9a‐2 mutant, subjected to 100 mM NaCl, display alterations in transcript levels of genes involved in the K+ homeostasis pathway. Concurrent with the observed sensitivity of vps9a‐2 mutant under NaCl stress, exposure to low K+ environments resulted in growth retardation, and reduced rate of endocytosis. Furthermore, vps9a‐2 mutant displays reduced expression of auxin reporter, Direct Repeat‐5 (DR5), and alterations in polarity and abundance of auxin efflux carrier PIN‐ FORMED2 (PIN2). Imposition of NaCl stress was found to be restrictive to the elongation capacity of cells in the root elongation zone of vps9a‐2 mutant. Together our results indicate that alterations in K+ homeostasis and associated cellular changes causing increased cell wall pH, contribute to diminished root growth and compromised survival of vps9a‐2 mutant under salt stress conditions.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.