Fermi level alignment by copper doping for efficient ITO/perovskite junction solar cells

Different from band edge alignment, the Fermi level mismatch induced by band bending can manipulate charge collection at the ITO/(CH_3NH_3)_(1−x)Cu_xPbI_3 heterojunctions. In this work, we employed a feasible spin-coating process to prepare copper defect compensation in CH_3NH_3PbI_3. The related work function was shown to shift with the copper doping density by Kelvin probe force microscopy (KPFM). Next, we applied transient surface photovoltage (TSPV) spectroscopy and first-order series reactions simulations to confirm that interface charge recombination at the ITO/perovskite junction can be eliminated through Cu+ doping. Nanoelectric photoconductive AFM analysis showed enhanced charge transfer and a higher photovoltage at the ITO/Cu-perovskite junction. Owing to efficient Fermi level alignment, the ITO/(CH_3NH_3)_(1−x)Cu_xPbI_3/PCBM/Ag devices displayed high power conversion efficiencies of 15.14 ± 0.67% at ambient conditions for inverted perovskite solar cells without any hole transport layer

Fermi level alignment by copper doping for efficient ITO/perovskite junction solar cells

Different from band edge alignment, the Fermi level mismatch induced by band bending can manipulate charge collection at the ITO/(CH_3NH_3)_(1−x)Cu_xPbI_3 heterojunctions. In this work, we employed a feasible spin-coating process to prepare copper defect compensation in CH_3NH_3PbI_3. The related work function was shown to shift with the copper doping density by Kelvin probe force microscopy (KPFM). Next, we applied transient surface photovoltage (TSPV) spectroscopy and first-order series reactions simulations to confirm that interface charge recombination at the ITO/perovskite junction can be eliminated through Cu+ doping. Nanoelectric photoconductive AFM analysis showed enhanced charge transfer and a higher photovoltage at the ITO/Cu-perovskite junction. Owing to efficient Fermi level alignment, the ITO/(CH_3NH_3)_(1−x)Cu_xPbI_3/PCBM/Ag devices displayed high power conversion efficiencies of 15.14 ± 0.67% at ambient conditions for inverted perovskite solar cells without any hole transport layer

Tulp1 deficiency causes early-onset retinal degeneration through affecting ciliogenesis and activating ferroptosis in zebrafish

Mutations in TUB-like protein 1 (TULP1) are associated with severe early-onset retinal degeneration in humans. However, the pathogenesis remains largely unknown. There are two homologous genes of TULP1 in zebrafish, namely tulp1a and tulp1b. Here, we generated the single knockout (tulp1a(−/−) and tulp1b(−/−)) and double knockout (tulp1-dKO) models in zebrafish. Knockout of tulp1a resulted in the mislocalization of UV cone opsins and the degeneration of UV cones specifically, while knockout of tulp1b resulted in mislocalization of rod opsins and rod-cone degeneration. In the tulp1-dKO zebrafish, mislocalization of opsins was present in all types of photoreceptors, and severe degeneration was observed at a very early age, mimicking the clinical manifestations of TULP1 patients. Photoreceptor cilium length was significantly reduced in the tulp1-dKO retinas. RNA-seq analysis showed that the expression of tektin2 (tekt2), a ciliary and flagellar microtubule structural component, was downregulated in the tulp1-dKO zebrafish. Dual-luciferase reporter assay suggested that Tulp1a and Tulp1b transcriptionally activate the promoter of tekt2. In addition, ferroptosis might be activated in the tulp1-dKO zebrafish, as suggested by the up-regulation of genes related to the ferroptosis pathway, the shrinkage of mitochondria, reduction or disappearance of mitochondria cristae, and the iron and lipid droplet deposition in the retina of tulp1-dKO zebrafish. In conclusion, our study establishes an appropriate zebrafish model for TULP1-associated retinal degeneration and proposes that loss of TULP1 causes defects in cilia structure and opsin trafficking through the downregulation of tekt2, which further increases the death of photoreceptors via ferroptosis. These findings offer insight into the pathogenesis and clinical treatment of early-onset retinal degeneration

Cross-species single-cell landscapes identify the pathogenic gene characteristics of inherited retinal diseases

Introduction: Inherited retinal diseases (IRDs) affect ∼4.5 million people worldwide. Elusive pathogenic variants in over 280 genes are associated with one or more clinical forms of IRDs. It is necessary to understand the complex interaction among retinal cell types and pathogenic genes by constructing a regulatory network. In this study, we attempt to establish a panoramic expression view of the cooperative work in retinal cells to understand the clinical manifestations and pathogenic bases underlying IRDs.Methods: Single-cell RNA sequencing (scRNA-seq) data on the retinas from 35 retina samples of 3 species (human, mouse, and zebrafish) including 259,087 cells were adopted to perform a comparative analysis across species. Bioinformatic tools were used to conduct weighted gene co-expression network analysis (WGCNA), single-cell regulatory network analysis, cell–cell communication analysis, and trajectory inference analysis.Results: The cross-species comparison revealed shared or species-specific gene expression patterns at single-cell resolution, such as the stathmin family genes, which were highly expressed specifically in zebrafish Müller glias (MGs). Thirteen gene modules were identified, of which nine were associated with retinal cell types, and Gene Ontology (GO) enrichment of module genes was consistent with cell-specific highly expressed genes. Many IRD genes were identified as hub genes and cell-specific regulons. Most IRDs, especially the retinitis pigmentosa (RP) genes, were enriched in rod-specific regulons. Integrated expression and transcription regulatory network genes, such as congenital stationary night blindness (CSNB) genes GRK1, PDE6B, and TRPM1, showed cell-specific expression and transcription characteristics in either rods or bipolar cells (BCs). IRD genes showed evolutionary conservation (GNAT2, PDE6G, and SAG) and divergence (GNAT2, MT-ND4, and PDE6A) along the trajectory of photoreceptors (PRs) among species. In particular, the Leber congenital amaurosis (LCA) gene OTX2 showed high expression at the beginning of the trajectory of both PRs and BCs.Conclusion: We identified molecular pathways and cell types closely connected with IRDs, bridging the gap between gene expression, genetics, and pathogenesis. The IRD genes enriched in cell-specific modules and regulons suggest that these diseases share common etiological bases. Overall, mining of interspecies transcriptome data reveals conserved transcriptomic features of retinas across species and promising applications in both normal retina anatomy and retina pathology