The present review focuses on two important aspects of Na
+ toxicity in rice (
Oryza sativa L.), (i) that Na
+ stress induces different changes in cytosolic Ca
2+, [Ca
2+]
cyt, and pH, [pH]
cyt, in tolerant and sensitive cultivars, and (ii) that cells from a tolerant cultivar can better maintain a low cytosolic Na
+ and/or Na
+/K
+ ratio. Experiments with single rice protoplasts, fluorescence microscopy and specific ion-selective dyes suggest that Na
+ must be sensed inside the cytosol, before any prolonged changes in [Ca
2+]
cyt and [pH]
cyt occur. Inhibitor analyses show that Na
+-induced increase in [pH]
cyt in the tolerant cv. Pokkali, and a decrease in [pH]
cyt in the sensitive cv. BRRI DHan29, likely are coupled to different H
+-ATPases. Expression analysis of OsHKT2;1 (previous name OsHKT1), OsHKT2;2 (previous name OsHKT2) and OsVHA transcripts in rice using RT-PCR and fluorescence
in situ-PCR, shows a variable and cell- specific induction in the two rice cultivars under salt stress condition. We conclude that the transient uptake of Na
+, which occurs only in the tolerant cultivar, and the fast compartmentalization of Na
+ into the vacuole, probably are the most important cellular traits for Na
+-tolerance in rice. The low [Na
+]
cyt in cv. Pokkali might depend on the fast down-regulation of OsHKT2;1, causing less uptake of Na
+, and fast up-regulation of the OsVHA transcript, and subsequent activation of the Na
+/H
+-anti-porter in the tonoplast. To decrease the cytosolic Na
+/K
+ ratio under Na
+ toxicity, cv. Pokkali may also induce increased uptake of K
+ through induction of OsHKT2;2, and other specific K
+-transporter genes.
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