A stress-inducible plasma membrane protein 3 (AcPMP3) in a monocotyledonous halophyte, Aneurolepidium chinense, regulates cellular Na(+) and K(+) accumulation under salt stress.

Regulation of ion homeostasis is fundamental to physiological activities in plants. Here, we report on the functional characterization of AcPMP3 [Aneurolepidium chinense (a monocotyledonous halophyte) plasma membrane protein 3] under salt stress. Expression of AcPMP3-1 and AcPMP3-2 genes was highly induced by various abiotic stresses, such as salt, cold and drought. Furthermore, abscisic acid, H(2)O(2) and salicylic acid also triggered expression of AcPMP3 genes. In the Deltanha1 Deltapmr2 Deltapmp3 yeast mutant, which lacks the major Na(+) efflux systems (Na(+)/H(+) antiporter and Na(+)-ATPase), its salt-sensitive phenotype was restored by expressing the AcPMP3-1 gene, and the transformants accumulated lesser amounts of Na(+) and K(+) than mutant cells under 50 mM NaCl and 500 mM KCl conditions, respectively. These results suggested that AcPMP3-1 plays a role as a regulator of both Na(+) and K(+) accumulation in the cells. In situ hybridization showed that the AcPMP3-1 transcript was localized in cells of the root cap and root epidermis, which strongly suggested that AcPMP3-1 is essential for regulating Na(+)/K(+) transportation between plant roots and the outer environment under salt stress.

Osmotic stress in barley regulates expression of a different set of genes than salt stress does.

Under high salt conditions, plant growth is severely inhibited due to both osmotic and ionic stresses. In an effort to dissect genes and pathways that respond to changes in osmotic potential under salt stress, the expression patterns were compared of 460 non-redundant salt-responsive genes in barley during the initial phase under osmotic versus salt stress using cDNA microarrays with northern blot and real-time RT-PCR analyses. Out of 52 genes that were differentially expressed under osmotic stress, 11, such as the up-regulated genes for pyrroline-5-carboxylate synthetase, betaine aldehyde dehydrogenase 2, plasma membrane protein 3, and the down-regulated genes for water channel 2, heat shock protein 70, and phospholipase C, were regulated in a virtually identical manner under salt stress. These genes were involved in a wide range of metabolic and signalling pathways suggesting that, during the initial phase under salt stress, several of the cellular responses are mediated by changes in osmotic potential.