Abstract
Salt stress is a major environmental factor influencing plant growth and development. To identify salt tolerance determinants, a genetic screen for
salt overly sensitive
(
sos
) mutants was performed in Arabidopsis. We present here the characterization of
sos4
mutants and the positional cloning of the
SOS4
gene.
sos4
mutant plants are hypersensitive to Na
+
, K
+
, and Li
+
ions. Under NaCl stress,
sos4
plants accumulate more Na
+
and retain less K
+
compared with wild-type plants.
SOS4
encodes a pyridoxal kinase that is involved in the biosynthesis of pyridoxal-5-phosphate, an active form of vitamin B6. The expression of
SOS4
cDNAs complements an
Escherichia coli
mutant defective in pyridoxal kinase. Supplementation of pyridoxine but not pyridoxal in the growth medium can partially rescue the
sos4
defect in salt tolerance.
SOS4
is expressed ubiquitously in all plant tissues. As a result of alternative splicing, two transcripts are derived from the
SOS4
gene, the relative abundance of which is modulated by development and environmental stresses. Besides being essential cofactors for numerous enzymes, as shown by pharmacological studies in animal cells, pyridoxal-5-phosphate and its derivatives are also ligands for P2X receptor ion channels. Our results demonstrate that pyridoxal kinase is a novel salt tolerance determinant important for the regulation of Na
+
and K
+
homeostasis in plants. We propose that pyridoxal-5-phosphate regulates Na
+
and K
+
homeostasis by modulating the activities of ion transporters.