In this study, a facile approach is used to enhance the broad orange emission efficiency and stability as well as monodispersity of Cs 2 AgInCl 6 nanocrystals (NCs) via doping Bi 3+ and surface passivation with potassium bromide. While the pristine Cs 2 AgInCl 6 NCs show an excitonic absorption peak at 280 nm, the doped NCs have an additional absorption peak at 365 nm, which is attributed to direct bismuth s−p transition. Compared to the low photoluminescence (PL) quantum yield (QY) of 0.04% for the pristine Cs 2 AgInCl 6 NCs due to parity forbidden transition, the doped NCs show a PLQY of 5.82%, a significant improvement due to breaking of the parity forbidden transition. The PLQY can be further increased to 8.59% for Cs 2 AgIn 0.9 Bi 0.1 Cl 6 when passivated with KBr. This work demonstrates that the combination of doping and surface passivation can substantially improve the PL of the Cs 2 AgInCl 6 double perovskite. A model is proposed to explain the observed enhancement in PL and stability.

Ophiobolins are a group of sesterterpenoids with a 5-8-5 tricyclic skeleton. They exhibit a significant cytotoxicity and present potential medicinal prospects. However, the biosynthesis and transport mechanisms of these valuable compounds have not been fully resolved. Herein, based on a transcriptome analysis, gene inactivation, heterologous expression and feeding experiments, we fully explain the biosynthesis pathway of ophiobolin K in Aspergillus ustus 094102, especially proved to be an unclustered oxidase OblCAu that catalyzes dehydrogenation at the site of C16 and C17 of both ophiobolin F and ophiobolin C. We also find that the intermediate ophiobolin C and final product ophiobolin K could be transported into a space between the cell wall and membrane by OblDAu to avoid the inhibiting of cell growth, which is proved by a fluorescence observation of the subcellular localization and cytotoxicity tests. This study completely resolves the biosynthesis mechanism of ophiobolins in strain A. ustus 094102. At the same time, it is revealed that the burden of strain growth caused by the excessive accumulation and toxicity of secondary metabolites is closely related to compartmentalized biosynthesis.