The dawn of plant salt tolerance genetics

Abstract

Recent reports from Jian Kang Zhu et al. have provided clear evidence for a signal transduction pathway that mediates salt tolerance of plants by controlling ion homeostasis. Earlier research had identified several salt overly sensitive (sos) mutants of Arabidopsis thaliana ecotype Columbia, based on Na+/Li+ hypersensitivity. Genetic complementation studies allowed the mutants to be placed into five allelic groups, sos 1–sos 5. Phenotypic additivity analyses indicate that SOS1, SOS2 and SOS3 function in a common pathway, with SOS1 being epistatic to the other loci. Recently, mapped-based cloning and gene complementation has identified the genes at these three loci. SOS3 is a Ca2+-binding protein that contains EF-hand structures and a myristoylation site in the N terminus. It has greatest sequence homology with yeast calcineurin subunit B and with animal neuronal Ca2+ sensors. SOS2 encodes a serine/threonine kinase with a catalytic domain similar to the yeast sucrose nonfermenting (SNF1) kinase and the mammalian AMP-activated protein kinase (AMPK), but is regulated differently through a distinctive C-terminal regulatory domain. SOS1 is a putative plasma membrane Na+/H+ antiporter resembling the mammalian NHE and bacterial NhaP exchangers.