Wheat cis-zeatin-O-glucosyltransferase cZOGT1 interacts with the Ca2+-dependent lipid binding protein TaZIP to regulate senescence.

Premature senescence is an important factor affecting wheat yield and quality. Wheat yield can be increased by delaying senescence and prolonging the effective photosynthetic time. Previously, we found that the cis-zeatin-O-glucosyltransferase (cZOGT1) gene plays an important role in the stay-green wheat phenotype. In this study, cZOGT1-overexpressing lines exhibited a delayed senescence phenotype, despite a significant reduction in the total cytokinin content. Further, we found that cZOGT1 interacted with the Ca2+-dependent lipid binding protein TaZIP (cZOGT1-interacting protein), and that a high level of cZOGT1 expression led to the suppression of TaZIP expression, which in turn, reduced abscisic acid (ABA) content. The synergistic reduction in cytokinins and ABA levels eventually caused the stay-green phenotype in cZOGT1-overexpressing lines. This study provides a new theoretical basis to explain the mechanism underlying the wheat stay-green phenotype and provides a genetic resource for wheat molecular-design breeding.

Role of reactive oxygen species in lesion mimic formation and conferred basal resistance to Fusarium graminearum in barley lesion mimic mutant 5386.

This study investigated the barley lesion mimic mutant (LMM) 5386, evidenced by a leaf brown spot phenotype localized on the chromosome 3H, and its conferred basal resistance to Fusarium graminearum. RNA-seq analysis identified 1453 genes that were differentially expressed in LMM 5386 compared to those in the wild type. GO and KEGG functional annotations suggested that lesion mimic formation was mediated by pathways involving oxidation reduction and glutathione metabolism. Additionally, reactive oxygen species (ROS) accumulation in brown spots was substantially higher in LMM 5386 than in the wild-type plant; therefore, antioxidant competence, which is indicated by ROS accumulation, was significantly lower in LMM 5386. Furthermore, the reduction of glycine in LMM 5386 inhibited glutathione biosynthesis. These results suggest that the decrease in antioxidant competence and glutathione biosynthesis caused considerable ROS accumulation, leading to programmed cell death, which eventually reduced the yield components in LMM 5386.