Overexpression of CsRCI2H enhances salt tolerance in Camelina sativa (L.)

Abstract

Although plant rare cold inducible 2 (RCI2), a homolog of yeast PMP3, has been considered to play important roles in responses to abiotic stress in plants, the functional role of RCI2 in salt-stress tolerance remains largely unknown for crop plants. In this study, we determined the function of CsRCI2H from Camelina under salt stress. Subcellular localization analysis of the yellow fluorescent protein (YFP)-CsRCI2H fusion protein revealed that CsRCI2H localizes to the plasma membrane in tobacco leaves. Expression of CsRCI2H was greatly increased in the presence of 150 mM NaCl. CsRCI2H compensated for the salt sensitivity of the yeast mutant ∆pmp3 lacking the PMP3 gene. CsRCI2H-overexpressing transgenic Camelina showed improved seed germination, root growth and fresh weight under high salt stress. CsRCI2H-overexpressing transgenic Camelina displayed lower accumulation of Na⁺ in the roots and shoots but higher K⁺ and Ca²⁺ accumulation in the shoots than wild type plants under salt stress. Furthermore, CsRCI2H-overexpressing Camelina displayed higher stomatal conductance and lower malondialdehyde under salt stress. Transcript levels of ion-homeostasis related genes, such as CsSOS1, CsSOS3, and CsHKT1, were significantly increased in the CsRCI2H-overexpressing transgenic plants upon salt treatment. These results suggest that Na⁺ and K⁺ homeostasis can be controlled by the Na⁺ and K⁺ transport systems throughout the CsRCI2H-overexpressing transgenic Camelina plant under salt-stress conditions. Collectively, these results indicate that CsRCI2H contributes to salt tolerance in Camelina during seed germination and seedling growth by reducing Na⁺ toxicity in the plant cells via regulation of ion homeostasis.