Arabidopsis thaliana possesses two different ion-export mechanisms in the plastid inner envelope membrane. Due to a genome duplication, the transport proteins are encoded by partly redundant loci: K+-efflux antiporter1 (KEA1) and KEA2 and mechanosensitive channel of small conductance-like2 (MSL2) and MSL3. Thus far, a functional link between these two mechanisms has not been established. Here, we show that kea1msl2 loss-of-function mutants exhibit phenotypes such as slow growth, reduced photosynthesis and changes in chloroplast morphology, several of which are distinct from either single mutants and do not resemble kea1kea2 or msl2msl3 double mutants. Our data suggest that KEA1 and MSL2 function in concert to maintain plastid ion homeostasis and osmoregulation. Their interplay is critical for proper chloroplast development, organelle function, and plant performance.
Keywords: chloroplast; ion channels; ion homeostasis; membrane proteins; plant physiology; stress and development.
© 2024 The Authors. FEBS Letters published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.