A large genetic screen for sos (for salt overly sensitive) mutants was performed in an attempt to isolate mutations in any gene with an sos phenotype. Our search yielded 28 new alleles of sos1 , nine mutant alleles of a newly identified locus, SOS2 , and one allele of a third salt tolerance locus, SOS3. The sos2 mutations, which are recessive, were mapped to the lower arm of chromosome V, ف 2.3 centimorgans away from the marker PHYC. Growth measurements demonstrated that sos2 mutants are specifically hypersensitive to inhibition by Na ؉ or Li ؉ and not hypersensitive to general osmotic stresses. Interestingly, the SOS2 locus is also necessary for K ؉ nutrition because sos2 mutants were unable to grow on a culture medium with a low level of K ؉ . The expression of several salt-inducible genes was superinduced in sos2 plants. The salt tolerance of sos1 , sos2 , and sos3 mutants correlated with their K ؉ tissue content but not their Na ؉ tissue content. Double mutant analysis indicated that the SOS genes function in the same pathway. Based on these results, a genetic model for salt tolerance mechanisms in Arabidopsis is presented in which SOS1 , SOS2 , and SOS3 are postulated to encode regulatory components controlling plant K ؉ nutrition that in turn is essential for salt tolerance.
INTRODUCTIONExcessive salt accumulation in soils affects the productivity of one-third of the world's limited arable land (Epstein et al., 1980). Much effort has been devoted toward understanding the mechanisms of plant salt tolerance with the eventual goal of improving the performance of crop plants in saline soils (Binzel and Reuveni, 1994). Equally important, these efforts continue to yield valuable knowledge about plant osmotic stress responses as well as cellular ion homeostasis (Bohnert et al., 1995;Niu et al., 1995;Zhu et al., 1997).A widely used approach to unravel plant salt tolerance mechanisms has been to identify cellular processes and genes whose activity or expression is regulated by salt stress (reviewed in Hasegawa et al., 1987;Cushman et al., 1990;Skriver and Mundy, 1990;Bray, 1993;Bohnert et al., 1995;Zhu et al., 1997). The underlying assumption is that salt-regulated processes and genes likely function in salt tolerance. Although this correlative approach has contributed to our appreciation of the complex nature of plant responses to salinity, it has failed, to a large extent, to establish salt tolerance determinants (Zhu et al., 1997). There are numerous documented changes in cellular activities in higher plants in response to salt stress. Such changes include, for example, cell wall alterations (Jones and Turner, 1978;Iraki et al., 1989), declines in photosynthesis (Seemann and Critchley, 1985;Locy et al., 1996), protein synthesis (Singh et al., 1985;Hurkman and Tanaka, 1987), and potassium content (Rains, 1972;Greenway and Munns, 1980), and increases in Na ϩ (Watad et al., 1983;Serrano and Gaxiola, 1994) and organic solutes, such as proline, glycinebetaine, and polyols (Greenway and Munns, 1980;Yancey et al., 19...