Silicon transcriptionally regulates sulfur and ABA metabolism and delays leaf senescence in barley under combined sulfur deficiency and osmotic stress

Abstract

Several studies have revealed that both sulfur (S) and silicon (Si) nutrition play a pivotal role in alleviating drought stress tolerance in plants. Additionally, Si application has also been reported to mitigate plant nutrient deficiency. However, to date there is no report that evaluates the performance and relevance of Si nutrition under S deficiency. In the present study, we explored the role of supplemental Si on S metabolism under combined S deficiency and osmotic stress. Barley plants were simultaneously subjected to polyethylene glycol (PEG)-induced osmotic stress under low or high S supply and Si nutrition. The results showed that Si supply regulated S and ABA metabolism at the transcriptional level under combined S deficiency and osmotic stress. The induction of the genes involved in S metabolism further contributed to the balance of redox potential by lowering the GSSG/GSH ratio and reducing H2O2 level in shoots. The transcriptional regulation of the genes involved in ABA biosynthesis and degradation pathways by Si reduced the level of shoot ABA under combined stress. Additionally, Si resulted in delayed leaf senescence under combined stresses by increasing chlorophyll levels, suppressing the expression of barley senescence gene HvS40, and reducing IAA levels. Therefore, shoots showed enhanced tolerance to osmotic stress under S deficiency as supported by higher sucrose concentrations, higher relative water content and higher shoot biomass. In roots under combined stress, Si induced the expression of the sulfur transporter HvST1;1 which resulted in a higher uptake of SO42− and NO3−. The higher root NO3- increased both glutamine and proline concentration. The higher sucrose in roots also increased root biomass, reflecting the tolerance of roots to osmotic stress. Our investigation reveals an important role of Si in transcriptionally regulating S and ABA metabolism under collective stress conditions manifested by S deficiency and osmotic stress.