LAUSR

The methionine residues of proteins are the preferred targets of oxidation by reactive oxygen species resulting in the formation of methionine sulfoxide (MetSO), which impairs protein function. Methionine sulfoxide reductase A and B (MSR) catalyze the reduction of the MetSO S and R epimers back to Met residues, respectively. The roles of abscisic acid (ABA) and nitric oxide (NO) on the transcript levels of methionine sulfoxide reductase (MSR; EC 1.8.4.6) in the roots of 2-d-old etiolated rice (Oryza sativa L.) seedlings exposed to NaCl were examined. The OsMSR transcript levels increased upon exposure to NaCl, which increased as the NaCl concentrations increased. Fluridone (Flu) pretreatment inhibited the increases in ABA and NO contents and the OsMSRA4, OsMSRA5, OsMSRB1.1, OsMSRB3 and OsMSRB5 transcripts by NaCl, while ABA application reversed the effects of Flu. Flu did not affect the OsMSRA2 and OsMSRB1.2 transcripts. The application of the NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5,-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), to NaCl-treated roots inhibited the increase in all of the OsMSRs transcripts with the exception of OsMSRB1.2. Treatment with the NO donor sodium nitroprusside (SNP) increased all the OsMSRs transcripts. The inhibitory effect of Flu on the increase of the OsMSRA4, OsMSRA5, OsMSR1.1, OsMSRB 3, and OsMSRB5 transcripts in the NaCl-treated roots was reversed by SNP. cPTIO inhibited the expression of all the OsMSR genes. The OsMSRA2.1 and OsMSRB1.2 transcripts can be increased by SNP. The Flu-inhibited internal ABA contents cannot be recovered by treatment with cPTIO or SNP. In addition, NaCl-induced NO production can be divided into ABA-dependent and ABA-independent routes. Therefore, the ABA-dependent NO route regulated the expression of OsMSRA4, OsMSRA5, OsMSRB1.1, OsMSRB 3, and OsMSRB5 in the NaCl-treated rice roots, while the ABA-independent NO pathway modulated OsMSRA2.1, and the ABA-independent and NO-independent pathway modulated OsMSRB1.2 expression in response to NaCl treatment.