Wheat Oxophytodienoate Reductase GeneTaOPR1Confers Salinity Tolerance via Enhancement of Abscisic Acid Signaling and Reactive Oxygen Species Scavenging    

Abstract

The 12-oxo-phytodienoic acid reductases (OPRs) are classified into the two subgroups OPRI and OPRII. The latter proteins participate in jasmonic acid synthesis, while the function of the former ones is as yet unclear. We describe here the characterization of the OPRI gene TaOPR1, isolated from the salinity-tolerant bread wheat (Triticum aestivum) cultivar SR3. Salinity stress induced a higher level of TaOPR1 expression in the seedling roots of cv SR3 than in its parental cultivar, JN177. This induction was abolished when abscisic acid (ABA) synthesis was inhibited. The overexpression of TaOPR1 in wheat significantly enhanced the level of salinity tolerance, while its heterologous expression in Arabidopsis alleviated root growth restriction in the presence of salinity and oxidants and raised the sensitivity to ABA. In Arabidopsis, TaOPR1 promoted ABA synthesis and the ABA-dependent stress-responsive pathway, partially rescued the sensitivity of the Arabidopsis aba2 mutant defective in ABA synthesis to salinity, and improved the activities of reactive oxygen species scavengers and the transcription of their encoding genes while reducing malondialdehyde and reactive oxygen species levels. TaOPR1 did not interact with jasmonate synthesis or the jasmonate signaling pathway. Rather than serving purely as an antioxidant, we believe that TaOPR1 acts during episodes of abiotic stress response as a signaling compound associated with the regulation of the ABA-mediated signaling network.

A Wheat Allene Oxide Cyclase Gene Enhances Salinity Tolerance via Jasmonate Signaling

“…The loss of AtMYC2 function impairs the level of sensitivity to both ABA and JA (Abe et al, 2003). The constitutive expression of TaOPR1 up-regulated AtMYC2 and enhanced the plant's sensitivity to ABA (Dong et al, 2013). Similarly, the constitutive expression of TaAOC1 also induced AtMYC2, while the loss of this gene in the atmyc2-2 mutant abolished the salinity tolerance promotive effect of TaAOC1 (Fig.…”

“…The contribution of TaOPR1 to the salinity tolerance of the ABA synthesis mutant aba2-2 was partially impaired, even though the higher transcript abundance of TaOPR1 had no effect on either JA content or the transcription level of JAZ1, known to be a key upstream component of the JA signaling pathway (Dong et al, 2013). Here, TaAOC1 constitutive expression increased JA content (Figs.…”

“…In a previous study, the elevation of the OPRIcatalyzed branch, achieved by the constitutive expression of TaOPR1, enhanced salinity tolerance via promoting activity in an ABA-dependent pathway (Dong et al, 2013). The contribution of TaOPR1 to the salinity tolerance of the ABA synthesis mutant aba2-2 was partially impaired, even though the higher transcript abundance of TaOPR1 had no effect on either JA content or the transcription level of JAZ1, known to be a key upstream component of the JA signaling pathway (Dong et al, 2013).…”

“…After a 48-h exposure to each of the stress agents, RNA was extracted from root tissue and processed for quantitative reverse transcription-PCR (qPCR). The phenotypic effects of salinity stress were noted at 4 d after adding 50 mM NaCl in 4 consecutive days (Dong et al, 2013).…”

“…As applied similarly to genes encoding OPRI enzymes, these genes are characteristically up-regulated by pathogen invasion, wounding, and oxidative stress (Biesgen and Weiler, 1999;Agrawal et al, 2003). When expressed heterologously in Arabidopsis, the product of the bread wheat OPRI gene TaOPR1 has been shown to enhance salinity tolerance by the up-regulation of AtMYC2, thereby triggering an ABA-dependent signaling pathway in a JA-independent manner (Dong et al, 2013). Whether the JA synthesis branch of a-linolenic acid metabolism is also involved in the response to salinity stress remains to be resolved.…”