'Bending' models of halotropism: incorporating protein phosphatase 2A, ABCB transporters, and auxin metabolism

Abstract

Salt stress causes worldwide reductions in agricultural yields, a problem that is exacerbated by the depletion of global freshwater reserves and the use of contaminated or recycled water (i.e. effluent water). Additionally, salt stress can occur as cultivated areas are subjected to frequent rounds of irrigation followed by periods of moderate to severe evapotranspiration, which can result in the heterogeneous aggregation of salts in agricultural soils. Our understanding of the later stages of salt stress and the mechanisms by which salt is transported out of cells and roots has greatly improved over the last decade. The precise mechanisms by which plant roots perceive salt stress and translate this perception into adaptive, directional growth away from increased salt concentrations (i.e. halotropism), however, are not well understood. Here, we provide a review of the current knowledge surrounding the early responses to salt stress and the initiation of halotropism, including lipid signaling, protein phosphorylation cascades, and changes in auxin metabolism and/or transport. Current models of halotropism have focused on the role of PIN2- and PIN1-mediated auxin efflux in initiating and controlling halotropism. Recent studies, however, suggest that additional factors such as ABCB transporters, protein phosphatase 2A activity, and auxin metabolism should be included in the model of halotropic growth.

Keywords: Auxin; auxin metabolism; auxin transport; phosphatidic acid; phospholipase D; protein phosphatase 2A; salt stress.