Na+ and K+ homeostasis control occurs through direct modulation of transport protein properties resulting from the physiological and biochemical status of cells or as an output of a responsive signal relay system(s) that mediates transcriptional or posttranscriptional regulation (Hasegawa et al., 2000a; Zhu, 2002, 2003). Conductance through transport systems is affected directly by pH, membrane potential, hyper- or hypoosmolarity, Ca2+ , cyclic nucleotides, phosphorylation/ dephosphorylation, as well as protein interaction and modification (Cherel et al., 2002; Demidchik et al., 2002; Qui et al., 2002; Quintero et al., 2002; Talke et al., 2003; Tester and Davenport, 2003; Vera-Estrella et al., 1999). There is substantial evidence for transcriptional regulation by salinity or osmotic stresses of plasma membrane and vacuolar H+ pumps, as well, additional posttranslational regulation of the resident proton pumps by phosphorylation with participation of 14:3:3 proteins (Dambly and Boutry, 2001; Hasegawa et al., 2000b; Shi et al., 2000). Also, transcription of genes encoding Na+ and K+ channels and transporters are modulated by salt and osmotic stresses (Aharon et al., 2003; Pilot et al., 2003; Rains and Epstein, 1967; Shi and Zhu, 2002; Su et al., 2001, 2002, 2003; Tester and Davenport, 2003; Zhu, 2003). sos1 mRNA stability is enhanced by salt stress. NaCl regulates Ca2+ modulation of Na+ uptake, attributable to the inhibition of unidirectional Na+ influx across the plasma membrane through nonselective cation channels (NSCCs) (Davenport and Tester, 2000; Demidchik and Tester, 2002; Epstein, 1961; Essah et al., 2003; Roberts and Tester, 1997). Although unconfirmed, prediction is that these transport proteins are cyclic nucleotide-gated channels (CNGC) whose gating properties are controlled by numerous effectors, including pharmacological agents known to inhibit similar channels in animal models, and whose Na+ conductance is blocked by Ca2+ (Cheng et al., 2003; Hirschi, 2004; Tester and Davenport, 2003). Genetic modulation of intracellular Ca2+ levels affects numerous ion homeostatic processes (Matsumoto et al., 2002).
Models for osmotic and ionic stress signal recognition assume that distinct sensors activate discrete signal transduction pathways that effect transcriptional and/or posttranscriptional control over determinants that mediate ion homeostasis, osmotic regulation, and obviate or attenuate stress pathologies (Cheng et al., 2003; Shinozaki et al., 2003; Zhu, 2002, 2003). Ca2+ and abscisic acid (ABA) are focal regulatory intermediates in hypersaline stress signaling that controls adaptation. Since it is the agricultural goal to enhance yield stability in saline environments, hypersaline stress effects on metabolic, cell division, growth, and development programs combinatorially increases the genetic determinants that become involved.
The search continues for the osmotic and/or the Na+ sensors. As indicated, hyper- or hypoosmolarity might affect directly the gating of ion channels that initiate a signal transduction pathway (Zhu, 2003). Hyperosmotically induced Ca2+ transients activate signaling through calcineurin resulting in the transcription of ENA1 (encoding a plasma membrane Na+ /H+ antiporter) increasing salt tolerance of yeast cells and in transformed plant cells (Marin et al., 2003; Nakayama et al., 2004). Alternatively, electrophoretic ion flux dissipates the membrane potential resulting in a cascade that controls osmotic or ion homeostasis. AtHK1 is implicated as a two component histidine kinase (Hik) that functions as a phospho-relay transducer controlling ABA-independent or dependent signaling that activates expression of genes encoding putative tolerance determinants (Shinozaki et al., 2003). Synechocystis sp. PCC 6803 Hiks, Hik16, Hik33, Hik34, and Hik41 implicated in salt and ion perception, while K+ and ionic strength activate autophosphorylation of KdpD, the putative turgor sensor expression of an operon encoding for a high affinity K+ transport system (Chinnusamy et al., 2004; Jung et al., 2000).
The Ca2+ -activated sos signal transduction and response pathway facilitates Na+ and perhaps K+ homeostasis in planta (Zhu, 2003). It is presumed that hypersaline stress induces a Ca2+ transient that is decoded by components of the sos pathway to facilitate Na+ homeostasis (Shinozaki et al., 2003; Zhu, 2003). sos3 recognizes Ca2+ signals and binds the divalent cation. sos3 then activates the serine/threonine kinase sos2, which phosphorylates the plasma membrane localized sos1 to induce its Na+ /H+ antiporter capacity. sos1 has been suggested to be a Na+ sensor but the determinant(s) responsible for the salt-induced Ca2+ transient is not yet identified.
The sos mutants (sos1, sos2, and sos3) are NaCl sensitive and exhibit K+ deficiency. The later phenotype indicates that the sos signaling pathway has a positive regulatory effect on K+ acquisition, although neither the regulatory components nor the regulated determinants have been identified. sos1 does not possess innate K+ transport capacity. Pretreatment of seedlings with 50 mM NaCl reduces K+ permeability of root cell plasma membranes isolated from sos1-1 but not of wild-type seedlings (Qiu et al., 2003). Reduced K+ uptake into (and consequential K+ deficiency) sos1 plants is attributed to elevated cytosolic Na+ levels that occur because of the defective Na+ efflux system (Guo et al., 2001; Qiu et al., 2003; Talke et al., 2003). htkt1 Mutations suppress K+ deficiency of sos1, 2 or 3 plants by reducing the intracellular Na+ accumulation (Rus et al., 2004). Mutations to other loci that suppress Na+ accumulation also attenuate the K+ deficient phenotype of sos3–1 plants.
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