Impact of Leifsonia xyli subsp. xyli titer on nutritional status, and metabolism of sugar cane

Aims Sugarcane plants infected with Leifsonia xyli subsp. xyli ( Lxx ) have their primary metabolism affected with decreased levels of sugars and amino acids. Cysteine and methionine are sulfur-containing essential amino acids used for bacterial growth and the Lxx titer in sugar cane leaves could affect the animo acid concentrations. The goal of this study was to evaluate how the increase in Lxx titer affects the nutritional status and sulfur metabolism in sugar cane leaves. Methods Susceptible sugar cane ( Saccharum officinarum ) genotype: CB49260 was used in this study with low (256 cells) and high (2090 cells) Lxx titers and macronutrients and primary metabolites assessed from leaves and culms. Results Plants with high Lxx titers accumulated more biomass in the main culm, leaves, and shoots than plants with low Lxx titers. Additionally, plants with high Lxx titers had 26% more sulfur content in leaves than plants with low Lxx titers. Higher levels of sulfate, sucrose, maltose, raffinose, shikimic acid, malate, putrescine, glycerol, and, erythritol were also present in plants with high Lxx titers; but decreased levels of methionine and glutathione in leaves. In the culm, plants with high Lxx titers also had increased levels of maltose; but decreased levels of threonine, ornithine, phenylalanine and myo -inositol when compared with plants with low Lxx titers. Conclusions This study demonstrated that high bacterial titers increase sulfur demand in sugar cane; however, the increased S content in the leaf did not result in higher sulfur assimilation, verified by increased sulfate but decreased methionine and glutathione levels. Therefore, our study showed that lower methionine availability, and methionine catabolism to putrescine in the leaves may fail to meet the increased sulfur organic compound demand of Lxx . The decrease in glutathione biosynthesis may reflect impaired biosynthesis or a drain on this antioxidant resulting from oxidative stresss by pathogenesis of Lxx .