Three new red neutral and ionic iridium(III) complexes based on the same main ligand and auxiliary ligand but with different counterions for solution-processed organic light-emitting diodes

Three new neutral and ionic phosphorescent iridium(III) complexes were successfully prepared using 1-(6-methoxynaphthalen-2-yl)isoquinoline as the main ligand, while the auxiliary ligand was 2-(2-1H-imidazolyl)pyridine. Three complexes (Ir1, Ir2, Ir3) showed red emission, peaking at 610, 609, and 615 nm, respectively, and they exhibited good solubility and excellent photophysical properties in different solvents, which is suitable to prepare organic light-emitting diodes (OLEDs) by solution method. Among the three OLEDs prepared by iridium(III) complexes using the solution method, the device based on Ir2 possessed better electroluminescent properties, and its maximum brightness, current efficiency (CE), power efficiency (PE), and the maximum external quantum efficiency (EQE) were 507.2 cd m⁻², 0.14 cd A⁻¹, 0.06 lm W⁻¹, and 0.14%. respectively, proving that the three complexes have a certain of potential for OLEDs applications and are expected to expand the applications of iridium(III) complexes for OLEDs.     

Inhibiting Dendrite Formation and Electrode Corrosion via a Scalable Self-Assembled Mercaptan Layer for Stable Aqueous Zinc Batteries

The practical use of Zn metal anodes in aqueous zinc batteries is impeded by the growth of dendrites, anode corrosion, and hydrogen evolution reaction in aqueous electrolytes. In this study, a simple, energy-efficient, and scalable approach is reported to mitigate these detrimental issues effectively. Using 1-hexanethiol (HT), a hydrophobic self-assembled mercaptan layer (SAML) with a highly ordered structure is in situ created on the surface of the Zn anode. This ultrathin interfacial structure guides uniform Zn deposition and shields the Zn anode from water and oxygen-induced corrosion, thus effectively inhibiting dendrite formation and side reactions. Consequently, the HT-Zn electrode showcases impressive electrochemical stability and reversibility, and the as-assembled HT-Zn||I₂ full cell delivers increased specific capacity (from 112 to 155 mAh g⁻¹ at 1 A g⁻¹) and ultra-stable cyclability (zero capacity decay during the extended 1500 cycles at 4 A g⁻¹). To validate the effectiveness of this simple and scalable method, a large-sized pouch cell is prepared, which can be stably operated for 1000 cycles with a capacity decay of merely 0.0098% per cycle and Coulombic efficiency exceeding 99.1%. The presented SAML strategy highlights the potential of molecular engineering in improving the performance of aqueous zinc batteries.     

Room-Temperature Molten Salt-Mediated CsPbI3 Growth for Excellent Photovoltaic Performance

Defects within perovskite have been known to act as the nonradiative recombination centers, negatively impacting the carrier transport, which degrades the photovoltaic performance of perovskite solar cells (PSCs). Therefore, preparing a high-quality perovskite film is of vital significance. To this end, a room-temperature molten salt, dimethylamine formate (DMAFa), is introduced into perovskite precursor solution to regulate the crystallization process of CsPbI₃ films. DMAFa can coordinate with Pb²⁺ as HCOO⁻-Pb²⁺ in the early stages, then HCOO⁻-Pb²⁺ is gradually displaced by I⁻-Pb²⁺ due to its decomposition during the subsequent annealing, thus delaying the crystallization rate, meanwhile, the DMA⁺ can interact with the uncoordinated Pb²⁺ to passivate defects of perovskite films, thereby, forming a high-quality CsPbI₃ film with large grain size and low-defect density. As a result of this strategy, the power conversion efficiency is increased to 20.40%, and the open-circuit voltage is up to 1.21 V. These findings indicate that the introduction of DMAFa offers a fundamental way to achieve high-performance CsPbI₃ PSCs.     

Cytosolic phosphoglucose isomerase is essential for microsporogenesis and embryogenesis in Arabidopsis

Phosphoglucose isomerase (PGI) catalyzes the interconversion of fructose-6-phosphate and glucose-6-phosphate, which impacts cell carbon metabolic flow. Arabidopsis (Arabidopsis thaliana) contains two nuclear PGI genes respectively encoding plastidial PGI1 and cytosolic PGI (cPGI). The loss of PGI1 impairs the conversion of F6P of the Calvin–Benson cycle to G6P for the synthesis of transitory starch in leaf chloroplasts. Since cpgi knockout mutants have not yet been obtained, they are thought to be lethal. The cpgi lethality can be rescued by expressing CaMV 35S promoter (p35S)-driven cPGI; however, the complemented line is completely sterile due to pollen degeneration. Here, we generated a cpgi mutant expressing p35S::cPGI-YFP in which YFP fluorescence in developing anthers was undetectable specifically in the tapetum and in pollen, which could be associated with male sterility. We also generated RNAi-cPGI knockdown lines with strong cPGI repression in floral buds that exhibited reduced male fertility due to the degeneration of most pollen. Histological analyses indicated that the synthesis of intersporal callose walls was impaired, causing microsporocytes to fail to separate haploid daughter nuclei to form tetrads, which might be responsible for subsequent pollen degeneration. We successfully isolated cpgi knockout mutants in the progeny of a heterozygous cpgi mutant floral-dipped with sugar solutions. The rescued cpgi mutants exhibited diminished young vegetative growth, reduced female fertility, and impaired intersporal callose wall formation in a meiocyte, and, thus, male sterility. Collectively, our data suggest that cPGI plays a vital role in carbohydrate partitioning, which is indispensable for microsporogenesis and early embryogenesis.

The cPGI-mediated carbohydrate partition is essential for early pollen and embryo development in Arabidopsis.     

Anti‐hsa‐miR‐59 alleviates premature senescence associated with Hutchinson‐Gilford progeria syndrome in mice

Hutchinson‐Gilford progeria syndrome (HGPS) is a lethal premature aging disorder without an effective therapeutic regimen. Because of their targetability and influence on gene expression, microRNAs (miRNAs) are attractive therapeutic tools to treat diseases. Here we identified that hsa‐miR‐59 (miR‐59) was markedly upregulated in HGPS patient cells and in multiple tissues of an HGPS mouse model (Lmna ^G609G/G609G ), which disturbed the interaction between RNAPII and TFIIH, resulting in abnormal expression of cell cycle genes by targeting high‐mobility group A family HMGA1 and HMGA2. Functional inhibition of miR‐59 alleviated the cellular senescence phenotype of HGPS cells. Treatment with AAV9‐mediated anti‐miR‐59 reduced fibrosis in the quadriceps muscle, heart, and aorta, suppressed epidermal thinning and dermal fat loss, and yielded a 25.5% increase in longevity of Lmna ^G609G/G609G mice. These results identify a new strategy for the treatment of HGPS and provide insight into the etiology of HGPS disease.     

Adaptive behaviors of Drosophila larvae on slippery surfaces

Friction is ubiquitous but an essential force for insects during locomotion. Insects use dedicated bio-mechanical systems such as adhesive pads to modulate the intensity of friction, providing a stable grip with touching substrates for locomotion. However, how to uncover behavioral adaptation and regulatory neural circuits of friction modification is still largely understood. In this study, we devised a novel behavior paradigm to investigate adaptive behavioral alternation of Drosophila larvae under low-friction surfaces. We found a tail looseness phenotype similar to slipping behavior in humans, as a primary indicator to assess the degree of slipping. We found a gradual reduction on slipping level in wild-type larvae after successive larval crawling, coupled with incremental tail contraction, displacement, and speed acceleration. Meanwhile, we also found a strong correlation between tail looseness index and length of contraction, suggesting that lengthening tail contraction may contribute to enlarging the contact area with the tube. Moreover, we found a delayed adaptation in rut mutant larvae, inferring that neural plasticity may participate in slipping adaptation. In conclusion, our paradigm can be easily and reliably replicated, providing a feasible pathway to uncover the behavioral principle and neural mechanism of acclimation of Drosophila larvae to low-friction conditions.     

Characterization and acceleration of genome shuffling and ploidy reduction in synthetic allopolyploids by genome sequencing and editing

Polyploidy and the subsequent ploidy reduction and genome shuffling are the major driving forces of genome evolution. Here, we revealed short-term allopolyploid genome evolution by sequencing a synthetic intergeneric hybrid (Raphanobrassica, RRCC). In this allotetraploid, the genome deletion was quick, while rearrangement was slow. The core and high-frequency genes tended to be retained while the specific and low-frequency genes tended to be deleted in the hybrid. The large-fragment deletions were enriched in the heterochromatin region and probably derived from chromosome breaks. The intergeneric translocations were primarily of short fragments dependent on homoeology, indicating a gene conversion origin. To accelerate genome shuffling, we developed an efficient genome editing platform for Raphanobrassica. By editing Fanconi Anemia Complementation Group M (FANCM) genes, homoeologous recombination, chromosome deletion and secondary meiosis with additional ploidy reduction were accelerated. FANCM was shown to be a checkpoint of meiosis and controller of ploidy stability. By simultaneously editing FLIP genes, gene conversion was precisely introduced, and mosaic genes were produced around the target site. This intergeneric hybrid and genome editing platform not only provides models that facilitate experimental evolution research by speeding up genome shuffling and conversion but also accelerates plant breeding by enhancing intergeneric genetic exchange and creating new genes.     

Construction of a cross-species cell landscape at single-cell level

Individual cells are basic units of life. Despite extensive efforts to characterize the cellular heterogeneity of different organisms, cross-species comparisons of landscape dynamics have not been achieved. Here, we applied single-cell RNA sequencing (scRNA-seq) to map organism-level cell landscapes at multiple life stages for mice, zebrafish and Drosophila. By integrating the comprehensive dataset of > 2.6 million single cells, we constructed a cross-species cell landscape and identified signatures and common pathways that changed throughout the life span. We identified structural inflammation and mitochondrial dysfunction as the most common hallmarks of organism aging, and found that pharmacological activation of mitochondrial metabolism alleviated aging phenotypes in mice. The cross-species cell landscape with other published datasets were stored in an integrated online portal—Cell Landscape. Our work provides a valuable resource for studying lineage development, maturation and aging.     

Interaction of human HelQ with DNA polymerase delta halts DNA synthesis and stimulates DNA single-strand annealing

DNA strand breaks are repaired by DNA synthesis from an exposed DNA end paired with a homologous DNA template. DNA polymerase delta (Pol δ) catalyses DNA synthesis in multiple eukaryotic DNA break repair pathways but triggers genome instability unless its activity is restrained. We show that human HelQ halts DNA synthesis by isolated Pol δ and Pol δ-PCNA-RPA holoenzyme. Using novel HelQ mutant proteins we identify that inhibition of Pol δ is independent of DNA binding, and maps to a 70 amino acid intrinsically disordered region of HelQ. Pol δ and its POLD3 subunit robustly stimulated DNA single-strand annealing by HelQ, and POLD3 and HelQ interact physically via the intrinsically disordered HelQ region. This data, and inability of HelQ to inhibit DNA synthesis by the POLD1 catalytic subunit of Pol δ, reveal a mechanism for limiting DNA synthesis and promoting DNA strand annealing during human DNA break repair, which centres on POLD3.