We have earlier discussed the sos pathway under the aspect of controlling
sodiumhomeostasis, but detection of the pathway provides an example of another
kind because sos genes were first found in a salt-sensitive, glycophytic species.
Indeed, it has become clear that the cells of virtually all plants possess the capability
to sense and respond to a saline environment. Tolerance is, to a species specific
and widely varying degree, genetically possible (Serrano and Rodriguez-Navarro,
2002). Although the salt tolerance of many halophytes is constitutive, the tolerance
of others is induced by the salinity level of the environment (facultative halophytes)
but functions that determine halophytism are ubiquitous. From many
physiological and biochemical studies, it has also become clear that the plant
adaptive response to salinity involves four basic co-coordinated adjustments,
outlined in Fig. 12.3: ion homeostasis, osmotic compensation (water homeostasis),
injury repair or avoidance, and growth reduction (Zhu, 2001). Yet, the mechanisms
and precise genetic components involved in adaptation to salinity have remained
a mystery for long. Our understanding of how plants perceive the salinity of their
environment and adjust appropriately has improved tremendously with the introduction
and use of Arabidopsis as a model system. Although Arabidopsis is not
salt tolerant in the sense of halophytic tolerance, screening for mutants with lower
tolerance than the wild type in Arabidopsis in the mid 1990s has been successful and
much work has confirmed that Arabidopsis does have genetic components that
control the ability to survive and grow in a salinized environment (Ishitani et al., 1997; Warren et al., 1996; Werner and Finkelstein, 1995; Xiong et al., 2002b). Our
present understanding of plant signal transduction for adaptation to salinity has
become possible based on common ancestry of land plants. The approach has been
successful
because the advantages of well-developed genetic and molecular tools
developed for Arabidopsis could be exploited.