Abstract
Brassinosteroid (BR)-deficient or -insensitive mutants exhibited altered plant architecture with the potential to impact yield, the underlying physiological and molecular mechanisms are still to be explored. In this study, we cloned three BR receptor homologous genes TaBRI1-A1, -B1 and -D1 from hexaploid wheat (Triticum estivum L.) and further isolated the TaBRI1-A1, TaBRI1-D1 deletion mutants from the ion beam-induced mutants of variety Xiaoyan81, TaBRI1-A1 and TaBRI1-D1 in which the expression of total receptor TaBRI1 was significantly decreased. The TaBRI1 knock-down mutants exhibited relatively erect leaves and a significant decrease in the 1000-grain weight. Further studies showed that TaBRI1 knock-down mutants showed a significant reduction in photosynthetic rate during the whole grain-filling stage. TaBRI1 knock-down plants generated by TaBRI1-A1, TaBRI1-D1 deletion or using virus-induced gene silencing exhibited the reduction in the efficiency of photosystem II (PSII) (Fv/Fm, Φ(PSII) and electron transport rate, ETR) especially under high light and high temperature stresses. The 24-epibrassinolide (EBR) treatment increased CO(2) assimilation rate in the wild type under both normal and high light and high temperature stresses conditions, but this increasing effect was not observed in the TaBRI1 knock-down mutants. Meanwhile, the expression levels of BR biosynthetic genes including TaDWARF4, TaCPD1 and TaCPD90C1 is not decreased or decreased to a lesser extent in the TaBRI1 knock-down mutants after EBR treatment. These results suggested that TaBRI1 is required for maintaining photosynthesis and tolerance to high light and high temperature stresses both of which are important for grain yield and will be a possible engineered target to control plant photosynthesis and yields in wheat.