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A defect-passivation strategy is proposed to fabricate efficient sky-blue perovskite light-emitting diodes (PeLEDs) by using three additives: 2-(4-fluorophenyl) ethylamine hydrobromide (p-F-PEABr), lithium bromide (LiBr), and diethylamine hydrobromide (DEABr). This strategy not only significantly reduces the nonradiative recombination loss caused by defects, but also preserves the energy cascade transfer efficiency by maintaining the phase dispersion of the low dimensional phases. In addition to the universal additive p-F-PEABr, LiBr is introduced to improve perovskite crystallinity and passivate defects. The third additive DEABr employed as a spacer ligand partially replacing p-F-PEABr not only passivates the defects, thereby reducing the nonradiative recombination loss, but also preserves the phase dispersion of the low dimensional phases, thereby maintaining the energy cascade transfer efficiency. Moreover, Auger recombination is reduced and the radiation recombination efficiency is improved. As a result, the sky-blue PeLEDs achieve a maximum external quantum efficiency (EQE) of 7.82% with an emission peak at 484 nmand a maximum brightness of 5127 cd m-2. [ABSTRACT FROM AUTHOR]

The plant cuticle is an important protective barrier on the plant surface, constructed mainly by polymerized cutin matrix and a complex wax mixture. Although the pathway of plant cuticle biosynthesis has been clarified, knowledge of the transcriptional regulation network underlying fruit cuticle formation remains limited. In the present work, we discovered that tomato fruits of the NAC transcription factor SlNOR-like1 knockout mutants (nor-like1) produced by CRISPR/Cas9 [clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9] displayed reduced cutin deposition and cuticle thickness, with a microcracking phenotype, while wax accumulation was promoted. Further research revealed that SlNOR-like1 promotes cutin deposition by binding to the promoters of glycerol-3-phosphate acyltransferase6 (SlGPAT6 ; a key gene for cutin monomer formation) and CUTIN DEFICIENT2 (SlCD2 ; a positive regulator of cutin production) to activate their expression. Meanwhile, SlNOR-like1 inhibits wax accumulation, acting as a transcriptional repressor by targeting wax biosynthesis, and transport-related genes 3-ketoacyl-CoA synthase1 (SlKCS1), ECERIFERUM 1-2 (SlCER1-2), SlWAX2 , and glycosylphosphatidylinositol-anchored lipid transfer protein 1-like (SlLTPG1-like). In conclusion, SlNOR-like1 executes a dual regulatory effect on tomato fruit cuticle development. Our results provide a new model for the transcriptional regulation of fruit cuticle formation. [ABSTRACT FROM AUTHOR]