Opioid-induced fragile-like regulatory T cells contribute to withdrawal.

Dysregulation of the immune system is a cardinal feature of opioid addiction. Here, we characterize the landscape of peripheral immune cells from patients with opioid use disorder and from healthy controls. Opioid-associated blood exhibited an abnormal distribution of immune cells characterized by a significant expansion of fragile-like regulatory T cells (Tregs), which was positively correlated with the withdrawal score. Analogously, opioid-treated mice also showed enhanced Treg-derived interferon-γ (IFN-γ) expression. IFN-γ signaling reshaped synaptic morphology in nucleus accumbens (NAc) neurons, modulating subsequent withdrawal symptoms. We demonstrate that opioids increase the expression of neuron-derived C-C motif chemokine ligand 2 (Ccl2) and disrupted blood-brain barrier (BBB) integrity through the downregulation of astrocyte-derived fatty-acid-binding protein 7 (Fabp7), which both triggered peripheral Treg infiltration into NAc. Our study demonstrates that opioids drive the expansion of fragile-like Tregs and favor peripheral Treg diapedesis across the BBB, which leads to IFN-γ-mediated synaptic instability and subsequent withdrawal symptoms.

STEEP mediates STING ER exit and activation of signaling.

STING is essential for control of infections and for tumor immunosurveillance, but it can also drive pathological inflammation. STING resides on the endoplasmic reticulum (ER) and traffics following stimulation to the ERGIC/Golgi, where signaling occurs. Although STING ER exit is the rate-limiting step in STING signaling, the mechanism that drives this process is not understood. Here we identify STEEP as a positive regulator of STING signaling. STEEP was associated with STING and promoted trafficking from the ER. This was mediated through stimulation of phosphatidylinositol-3-phosphate (PtdIns(3)P) production and ER membrane curvature formation, thus inducing COPII-mediated ER-to-Golgi trafficking of STING. Depletion of STEEP impaired STING-driven gene expression in response to virus infection in brain tissue and in cells from patients with STING-associated diseases. Interestingly, STING gain-of-function mutants from patients interacted strongly with STEEP, leading to increased ER PtdIns(3)P levels and membrane curvature. Thus, STEEP enables STING signaling by promoting ER exit.

Author Correction: STEEP mediates STING ER exit and activation of signaling.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

TMEFF1 is a neuron-specific restriction factor for herpes simplex virus.

The brain is highly sensitive to damage caused by infection and inflammation1,2. Herpes simplex virus 1 (HSV-1) is a neurotropic virus and the cause of herpes simplex encephalitis3. It is unknown whether neuron-specific antiviral factors control virus replication to prevent infection and excessive inflammatory responses, hence protecting the brain. Here we identify TMEFF1 as an HSV-1 restriction factor using genome-wide CRISPR screening. TMEFF1 is expressed specifically in neurons of the central nervous system and is not regulated by type I interferon, the best-known innate antiviral system controlling virus infections. Depletion of TMEFF1 in stem-cell-derived human neurons led to elevated viral replication and neuronal death following HSV-1 infection. TMEFF1 blocked the HSV-1 replication cycle at the level of viral entry through interactions with nectin-1 and non-muscle myosin heavy chains IIA and IIB, which are core proteins in virus-cell binding and virus-cell fusion, respectively4-6. Notably, Tmeff1-/- mice exhibited increased susceptibility to HSV-1 infection in the brain but not in the periphery. Within the brain, elevated viral load was observed specifically in neurons. Our study identifies TMEFF1 as a neuron-specific restriction factor essential for prevention of HSV-1 replication in the central nervous system.

A human embryonic limb cell atlas resolved in space and time.

Human limbs emerge during the fourth post-conception week as mesenchymal buds, which develop into fully formed limbs over the subsequent months1. This process is orchestrated by numerous temporally and spatially restricted gene expression programmes, making congenital alterations in phenotype common2. Decades of work with model organisms have defined the fundamental mechanisms underlying vertebrate limb development, but an in-depth characterization of this process in humans has yet to be performed. Here we detail human embryonic limb development across space and time using single-cell and spatial transcriptomics. We demonstrate extensive diversification of cells from a few multipotent progenitors to myriad differentiated cell states, including several novel cell populations. We uncover two waves of human muscle development, each characterized by different cell states regulated by separate gene expression programmes, and identify musculin (MSC) as a key transcriptional repressor maintaining muscle stem cell identity. Through assembly of multiple anatomically continuous spatial transcriptomic samples using VisiumStitcher, we map cells across a sagittal section of a whole fetal hindlimb. We reveal a clear anatomical segregation between genes linked to brachydactyly and polysyndactyly, and uncover transcriptionally and spatially distinct populations of the mesenchyme in the autopod. Finally, we perform single-cell RNA sequencing on mouse embryonic limbs to facilitate cross-species developmental comparison, finding substantial homology between the two species.

Attenuated replication and pathogenicity of SARS-CoV-2 B.1.1.529 Omicron.

The Omicron (B.1.1.529) variant of SARS-CoV-2 emerged in November 2021 and is rapidly spreading among the human population1. Although recent reports reveal that the Omicron variant robustly escapes vaccine-associated and therapeutic neutralization antibodies2-10, the pathogenicity of the virus remains unknown. Here we show that the replication of Omicron is substantially attenuated in human Calu3 and Caco2 cells. Further mechanistic investigations reveal that Omicron is inefficient in its use of transmembrane serine protease 2 (TMPRSS2) compared with wild-type SARS-CoV-2 (HKU-001a) and previous variants, which may explain its reduced replication in Calu3 and Caco2 cells. The replication of Omicron is markedly attenuated in both the upper and lower respiratory tracts of infected K18-hACE2 mice compared with that of the wild-type strain and Delta (B.1.617.2) variant, resulting in its substantially ameliorated lung pathology. Compared with wild-type SARS-CoV-2 and the Alpha (B.1.1.7), Beta (1.351) and Delta variants, infection by Omicron causes the lowest reduction in body weight and the lowest mortality rate. Overall, our study demonstrates that the replication and pathogenicity of the Omicron variant of SARS-CoV-2 in mice is attenuated compared with the wild-type strain and other variants.

CELLULOSE SYNTHASE-LIKE C proteins modulate cell wall establishment during ethylene-mediated root growth inhibition in rice.

The cell wall shapes plant cell morphogenesis and affects the plasticity of organ growth. However, the way in which cell wall establishment is regulated by ethylene remains largely elusive. Here, by analyzing cell wall patterns, cell wall composition and gene expression in rice (Oryza sativa, L.) roots, we found that ethylene induces cell wall thickening and the expression of cell wall synthesis-related genes, including CELLULOSE SYNTHASE-LIKE C1, 2, 7, 9, 10 (OsCSLC1, 2, 7, 9, 10) and CELLULOSE SYNTHASE A3, 4, 7, 9 (OsCESA3, 4, 7, 9). Overexpression and mutant analyses revealed that OsCSLC2 and its homologs function in ethylene-mediated induction of xyloglucan biosynthesis mainly in the cell wall of root epidermal cells. Moreover, OsCESA-catalyzed cellulose deposition in the cell wall was enhanced by ethylene. OsCSLC-mediated xyloglucan biosynthesis likely plays an important role in restricting cell wall extension and cell elongation during the ethylene response in rice roots. Genetically, OsCSLC2 acts downstream of ETHYLENE-INSENSITIVE3-LIKE1 (OsEIL1)-mediated ethylene signaling, and OsCSLC1, 2, 7, 9 are directly activated by OsEIL1. Furthermore, the auxin signaling pathway is synergistically involved in these regulatory processes. These findings link plant hormone signaling with cell wall establishment, broadening our understanding of root growth plasticity in rice and other crops.

Conserved moonlighting protein pyruvate dehydrogenase induces robust protection against Staphylococcus aureus infection.

Developing an effective Staphylococcus aureus (S. aureus) vaccine has been a challenging endeavor, as demonstrated by numerous failed clinical trials over the years. In this study, we formulated a vaccine containing a highly conserved moonlighting protein, the pyruvate dehydrogenase complex E2 subunit (PDHC), and showed that it induced strong protective immunity against epidemiologically relevant staphylococcal strains in various murine disease models. While antibody responses contributed to bacterial control, they were not essential for protective immunity in the bloodstream infection model. Conversely, vaccine-induced systemic immunity relied on γδ T cells. It has been suggested that prior S. aureus exposure may contribute to the reduction of vaccine efficacy. However, PDHC-induced protective immunity still facilitated bacterial clearance in mice previously exposed to S. aureus. Collectively, our findings indicate that PDHC is a promising serotype-independent vaccine candidate effective against both methicillin-sensitive and methicillin-resistant S. aureus isolates.

Hidden hotspots of amphibian biodiversity in China.

Identifying and protecting hotspots of endemism and species richness is crucial for mitigating the global biodiversity crisis. However, our understanding of spatial diversity patterns is far from complete, which severely limits our ability to conserve biodiversity hotspots. Here, we report a comprehensive analysis of amphibian species diversity in China, one of the most species-rich countries on Earth. Our study combines 20 y of field surveys with new molecular analyses of 521 described species and also identifies 100 potential cryptic species. We identify 10 hotspots of amphibian diversity in China, each with exceptional species richness and endemism and with exceptional phylogenetic diversity and phylogenetic endemism (based on a new time-calibrated, species-level phylogeny for Chinese amphibians). These 10 hotspots encompass 59.6% of China's described amphibian species, 49.0% of cryptic species, and 55.6% of species endemic to China. Only four of these 10 hotspots correspond to previously recognized biodiversity hotspots. The six new hotspots include the Nanling Mountains and other mountain ranges in South China. Among the 186 species in the six new hotspots, only 9.7% are well covered by protected areas and most (88.2%) are exposed to high human impacts. Five of the six new hotspots are under very high human pressure and are in urgent need of protection. We also find that patterns of richness in cryptic species are significantly related to those in described species but are not identical.

Interfacial Robustness and Improved Kinetics of Single-Crystal Ni-Rich Co-Free Cathodes Enabled by Surface Crystal-Facet Modulation.

The elimination of Co from Ni-rich layered cathodes is critical to reduce the production cost and increase the energy density for sustainable development. Herein, a delicate strategy of crystal-facet modulation is designed and explored, which is achieved by simultaneous Al/W-doping into the precursors, while the surface role of the crystal-facet is intensively revealed. Unlike traditional studies on crystal structure growth along a certain direction, this work modulates the crystal-facet at the nanoscale based on the effect of W-doping dynamic migration with surface energy, successfully constructing the core-shell (003)/(104) facet surface. Compared to the (003) plane, the induced (104) facet at the surface can provide more space for Li+-activity, enabling lower interfacial polarization and higher Li+-transport rate. Additionally, bulk Al-doping is beneficial for enhancing the Li+-diffusion from the exterior surface to the interior lattice. With improved interfacial stability and restrained surface erosion, the product exhibits superior capacity retention and boosted rate performance under the elevated temperature.

ZnMn2(PO4)2·nH2O: An H2O-Imbedding-Activated Cathode for Robust Aqueous Zinc-Ion Batteries.

Component modulation endows Mn-based electrodes with prominent energy storage properties due to their adjustable crystal structure characteristics. Herein, ZnMn2(PO4)2·nH2O (ZMP·nH2O) was obtained by a hydration reaction from ZnMn2(PO4)2 (ZMP) during an electrode-aging evolution. Benefiting from the introduction of lattice H2O molecules into the ZMP structure, the ion transmission path has been expanded along with the extended d-spacing, which will further facilitate the ZMP → ZMP·nH2O phase evolution and electrochemical reaction kinetics. Meanwhile, the hydrogen bond can be generated between H2O and O in PO43-, which strengthens the structure stability of ZMP·nH2O and lowers the conversion barrier from ZMP to ZMP·4H2O during the Zn2+ uptake/removal process. Thereof, ZMP·nH2O delivers enhanced electrochemical reaction kinetics with robust structure tolerance (106.52 mA h g-1 at 100 mA g-1 over 620 cycles). This high-energy aqueous Zn||ZMP·nH2O battery provides a facile strategy for engineering and exploration of high-performance ZIBs to realize the practical application of Mn-based cathodes.

Enterohemorrhagic Escherichia coli effector EspF triggers oxidative DNA lesions in intestinal epithelial cells.

Attaching/effacing (A/E) pathogens induce DNA damage and colorectal cancer by injecting effector proteins into host cells via the type III secretion system (T3SS). EspF is one of the T3SS-dependent effector proteins exclusive to A/E pathogens, which include enterohemorrhagic Escherichia coli. The role of EspF in the induction of double-strand breaks (DSBs) and the phosphorylation of the repair protein SMC1 has been demonstrated previously. However, the process of damage accumulation and DSB formation has remained enigmatic, and the damage response is not well understood. Here, we first showed a compensatory increase in the mismatch repair proteins MutS homolog 2 (MSH2) and MSH6, as well as poly(ADP-ribose) polymerase 1, followed by a dramatic decrease, threatening cell survival in the presence of EspF. Flow cytometry revealed that EspF arrested the cell cycle at the G2/M phase to facilitate DNA repair. Subsequently, 8-oxoguanine (8-oxoG) lesions, a marker of oxidative damage, were assayed by ELISA and immunofluorescence, which revealed the accumulation of 8-oxoG from the cytosol to the nucleus. Furthermore, the status of single-stranded DNA (ssDNA) and DSBs was confirmed. We observed that EspF accelerated the course of DNA lesions, including 8-oxoG and unrepaired ssDNA, which were converted into DSBs; this was accompanied by the phosphorylation of replication protein A 32 in repair-defective cells. Collectively, these findings reveal that EspF triggers various types of oxidative DNA lesions with impairment of the DNA damage response and may result in genomic instability and cell death, offering novel insight into the tumorigenic potential of EspF.IMPORTANCEOxidative DNA lesions play causative roles in colitis-associated colon cancer. Accumulating evidence shows strong links between attaching/effacing (A/E) pathogens and colorectal cancer (CRC). EspF is one of many effector proteins exclusive to A/E pathogens with defined roles in the induction of oxidative stress, double-strand breaks (DSBs), and repair dysregulation. Here, we found that EspF promotes reactive oxygen species generation and 8-oxoguanine (8-oxoG) lesions when the repair system is activated, contributing to sustained cell survival. However, infected cells exposed to EspF presented 8-oxoG, which results in DSBs and ssDNA accumulation when the cell cycle is arrested at the G2/M phase and the repair system is defective or saturated by DNA lesions. In addition, we found that EspF could intensify the accumulation of nuclear DNA lesions through oxidative and replication stress. Overall, our work highlights the involvement of EspF in DNA lesions and DNA damage response, providing a novel avenue by which A/E pathogens may contribute to CRC.

Genome-wide identification, characterization and expression pattern analysis of TIFY family members in Artemisia argyi.

BACKGROUND: Plant-specific TIFY proteins play crucial roles in regulating plant growth, development, and various stress responses. However, there is no information available about this family in Artemisia argyi, a well-known traditional medicinal plant with great economic value. RESULTS: A total of 34 AaTIFY genes were identified, including 4 TIFY, 22 JAZ, 5 PPD, and 3 ZML genes. Structural, motif scanning, and phylogenetic relationships analysis of these genes revealed that members within the same group or subgroup exhibit similar exon-intron structures and conserved motif compositions. The TIFY genes were unevenly distributed across the 15 chromosomes. Tandem duplication events and segmental duplication events have been identified in the TIFY family in A. argyi. These events have played a crucial role in the gene multiplication and compression of different subfamilies within the TIFY family. Promoter analysis revealed that most AaTIFY genes contain multiple cis-elements associated with stress response, phytohormone signal transduction, and plant growth and development. Expression analysis of roots and leaves using RNA-seq data revealed that certain AaTIFY genes showed tissue-specific expression patterns, and some AaTIFY genes, such as AaTIFY19/29, were found to be involved in regulating salt and saline-alkali stresses. In addition, RT-qPCR analysis showed that TIFY genes, especially AaTIFY19/23/27/29, respond to a variety of hormonal treatments, such as MeJA, ABA, SA, and IAA. This suggested that TIFY genes in A. argyi regulate plant growth and respond to different stresses by following different hormone signaling pathways. CONCLUSION: Taken together, our study conducted a comprehensive identification and analysis of the TIFY gene family in A. argyi. These findings suggested that TIFY might play an important role in plant development and stress responses, which laid a valuable foundation for further understanding the function of TIFY genes in multiple stress responses and phytohormone crosstalk in A. argyi.

Tandem Chemistry with Janus Mesopores Accelerator for Efficient Aqueous Batteries.

A reliable solid electrolyte interphase (SEI) on the metallic Zn anode is imperative for stable Zn-based aqueous batteries. However, the incompatible Zn-ion reduction processes, scilicet simultaneous adsorption (capture) and desolvation (repulsion) of Zn2+(H2O)6, raise kinetics and stability challenges for the design of SEI. Here, we demonstrate a tandem chemistry strategy to decouple and accelerate the concurrent adsorption and desolvation processes of the Zn2+ cluster at the inner Helmholtz layer. An electrochemically assembled perforative mesopore SiO2 interphase with tandem hydrophilic -OH and hydrophobic -F groups serves as a Janus mesopores accelerator to boost a fast and stable Zn2+ reduction reaction. Combining in situ electrochemical digital holography, molecular dynamics simulations, and spectroscopic characterizations reveals that -OH groups capture Zn2+ clusters from the bulk electrolyte and then -F groups repulse coordinated H2O molecules in the solvation shell to achieve the tandem ion reduction process. The resultant symmetric batteries exhibit reversible cycles over 8000 and 2000 h under high current densities of 4 and 10 mA cm-2, respectively. The feasibility of the tandem chemistry is further evidenced in both Zn//VO2 and Zn//I2 batteries, and it might be universal to other aqueous metal-ion batteries.

Glucagon-like peptide-1 receptor agonist exendin 4 ameliorates diabetes-associated vascular calcification by regulating mitophagy through the AMPK signaling pathway.

BACKGROUND: Vascular calcification (VC) is a complication in diabetes mellitus (DM) patients. Osteogenic phenotype switching of vascular smooth muscle cells (VSMCs) plays a critical role in diabetes-related VC. Mitophagy can inhibit phenotype switching in VSMCs. This study aimed to investigate the role of the glucagon-like peptide-1 receptor (GLP-1R) agonist exendin 4 (EX4) in mitophagy-induced phenotype switching. MATERIALS AND METHODS: The status of VC in T2DM mice was monitored using Von Kossa and Alizarin Red S (ARS) staining in mouse aortic tissue. Human aortic smooth muscle cells were cultured in high glucose (HG) and ß-glycerophosphate (ß-GP) conditioned medium. Accumulation of LC3B and p62 was detected in the mitochondrial fraction. The effect of EX4 in vitro and in vivo was investigated by knocking down AMPKα1. RESULTS: In diabetic VC mice, EX4 decreased the percentage of von Kossa/ARS positive area. EX4 inhibited osteogenic differentiation of HG/ß-GP-induced VSMCs. In HG/ß-GP-induced VSMCs, the number of mitophagosomes was increased, whereas the addition of EX4 restored mitochondrial function, increased the number of mitophagosome-lysosome fusions, and reduced p62 in mitochondrial frictions. EX4 increased the phosphorylation of AMPKα (Thr172) and ULK1 (Ser555) in HG/ß-GP-induced VSMCs. After knockdown of AMPKα1, ULK1 could not be activated by EX4. The accumulation of LC3B and p62 could not be reduced after AMPKα1 knockdown. Knockdown of AMPKα1 negated the therapeutic effects of EX4 on VC of diabetic mice. CONCLUSION: EX4 could promote mitophagy by activating the AMPK signaling pathway, attenuate insufficient mitophagy, and thus inhibit the osteogenic phenotype switching of VSMCs.

Implantation of human urine stem cells promotes neural repair in spinal cord injury rats associated cadeharin-1 and integrin subunit beta 1 expression.

BACKGROUND: The aim of this study was to determine the effect of human urine-derived stem cells (HUSCs) for the treatment of spinal cord injury (SCI) and investigate associated the molecular network mechanism by using bioinformatics combined with experimental validation. METHODS: After the contusive SCI model was established, the HUSC-expressed specific antigen marker was implanted into the injury site immediately, and the Basso, Beattie and Bresnahan locomotor rating scale (BBB scale) was utilized to evaluate motor function so as to determine the effect of HUSCs for the neural repair after SCI. Then, the geneCards database was used to collect related gene targets for both HUSCs and SCI, and cross genes were merged with the findings of PubMed screen. Subsequently, protein-protein interaction (PPI) network, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment, as well as core network construction, were performed using Cytoscape software. Lastly, real-time quantitative polymerase chain reaction (PCR) and immunofluorescence were employed to validate the mRNA expression and localization of 10 hub genes, and two of the most important, designated as cadherin 1 (CDH1) and integrin subunit beta 1 (ITGB1), were identified successfully. RESULTS: The immunophenotypes of HUSCs were marked by CD90+ and CD44+ but not CD45, and flow cytometry confirmed their character. The expression rates of CD90, CD73, CD44 and CD105 in HUSCs were 99.49, 99.77, 99.82 and 99.51%, respectively, while the expression rates of CD43, CD45, CD11b and HLA-DR were 0.08, 0.30, 1.34 and 0.02%, respectively. After SCI, all rats appeared to have severe motor dysfunction, but the BBB score was increased in HUSC-transplanted rats compared with control rats at 28 days. By using bioinformatics, we obtained 6668 targets for SCI and 1095 targets for HUSCs and identified a total of 645 cross targets between HUSCs and SCI. Based on the PPI and Cytoscape analysis, CD44, ACTB, FN1, ITGB1, HSPA8, CDH1, ALB, HSP90AA1 and GAPDH were identified as possible therapeutic targets. Enrichment analysis revealed that the involved signal pathways included complement and coagulation cascades, lysosome, systemic lupus erythematosus, etc. Lastly, quantificational real-time (qRT)-PCR confirmed the mRNA differential expression of CDH1/ITGB1 after HUSC therapy, and glial fibrillary acidic protein (GFAP) immunofluorescence staining showed that the astrocyte proliferation at the injured site could be reduced significantly after HUSC treatment. CONCLUSIONS: We validated that HUSC implantation is effective for the treatment of SCI, and the underlying mechanisms associated with the multiple molecular network. Of these, CDH1 and ITGB1 may be considered as important candidate targets. Those findings therefore provided the crucial evidence for the potential use of HUSCs in SCI treatment in future clinic trials.

Asymmetric Kosmotropism-Stabilized Double-Layer Hydrogel for Low-Cost Neutral Zinc-Air Battery.

Zinc air battery (ZAB) provides a low-cost and high-energy density power source, particularly in wearable and portable devices. Despite the extensive research on air cathode catalysts, their practical application is hindered by low zinc utilization rate and severe corrosion and passivation in liquid-based alkaline electrolytes. Herein, a double-layer gel (DLKgel) is developed by leveraging the distinct kosmotropic properties of ZnCl2 and ZnSO4. Through phase separation induced by the kosmotropic differentiation (instead of membrane in decoupled systems), this DLKgel electrolyte serves a dual purpose of shielding cathode from irreversible reaction products and protecting Zn anode from passivation. Neutral ZABs with DLKgel demonstrate high zinc utilization rate of 89.3% and stable cycling over 800 h under a current density of 0.1 mA cm-2. The integration of DLKgel-based ZABs into a flexible GPS tracking device is demonstrated, highlighting the potential for broad adoption of flexible ZABs in wearable and logistics applications.

Strong Oxidizing Molten Salts for Strengthening Structural Restoration Enabling Direct Regeneration of Spent Layered Cathode.

As a mainstream technology for recycling spent lithium-ion batteries, direct regeneration is rapidly developed due to its high efficiency and green characteristics. However, efficient reuse of spent LiNixCoyMn1- x - yO2 cathode is still a significant challenge, as the rock salt/spinel phase on the surface hinders the Li replenishment and phase transformation to the layered structure. In this work, the fundamental understanding of the repair mechanism is confirmed that the oxidizing atmosphere is the crucial factor that can greatly improve the rate and degree of phase restoration. Particularly, a ternary-component molten salt system (LiOH-Li2CO3-LiNO3) is proposed for direct regeneration of LiNi0.5Co0.2Mn0.3O2 (NCM523), which can in situ generate the strong oxidizing intermediate of superoxide radicals. Additionally, it shows a liquid-like reaction environment at a lower temperature to acceclerate the transport rate of superoxide-ions. Therefore, the synergistic effect of LiOH-Li2CO3-LiNO3 system can strengthen the full restoration of rock salt/spinel phases and achieve the complete Li-supplement. As anticipated, the regenerated NCM523 delivers a high cycling stability with a retention of 91.7% after 100 cycles, which is even competitive with the commercial NCM523. This strategy provides a facile approach for the complete recovery of layer structure cathode, demonstrating a unique perspective for the direct regeneration of spent lithium-ion batteries.

Vapor-Solid Interface Synthesis of Highly Crystalline Covalent Triazine Frameworks for Use as Efficient Photocatalysts.

Harsh synthetic conditions for crystalline covalent triazine frameworks (CTFs) and associated limitations on structural diversities impede not only further development of functional CTFs, but also practical large-scale synthesis. Herein, a mild and universal vapor-solid interface synthesis strategy is developed for highly crystalline CTFs employing trifluoromethanesulfonic acid vapor as catalysts. A series of highly ordered simple and functional CTFs (CTF-TJUs) can be facilely produced. In particular, the porphyrin-involved functional CTF (CTF-TJU-Por1) with high crystallinity is synthesized for the first time via this universal approach. The mechanism of vapor-catalyzed trimerization of nitrile monomers is thoroughly investigated through semi in situ characterizations. As a proof of concept, the photocatalytic performance of synthesized CTFs for water splitting is evaluated. CTF-TJU-133 exhibits significantly greater photocatalytic rates for hydrogen (4.35 µmol h-1) and oxygen (2.18 µmol h-1) evolutions during overall water splitting under visible light irradiations compared to other CTF-TJUs, representing one of the highest values among reported CTF photocatalysts. Further studies reveal that enhanced photocatalytic performance of CTF-TJU-133 results from optimized band structure, extended visible-light absorption, and high carrier separation efficiency. This study provides a promising strategy to synthesize various simple and functional CTFs, which significantly enriched diversities of CTF family for different application purposes.

ZmWAK02 encoding an RD-WAK protein confers maize resistance against gray leaf spot.

Gray leaf spot (GLS) caused by Cercospora zeina or C. zeae-maydis is a major maize disease throughout the world. Although more than 100 QTLs resistant against GLS have been identified, very few of them have been cloned. Here, we identified a major resistance QTL against GLS, qRglsSB, explaining 58.42% phenotypic variation in SB12×SA101 BC1 F1 population. By fine-mapping, it was narrowed down into a 928 kb region. By using transgenic lines, mutants and complementation lines, it was confirmed that the ZmWAK02 gene, encoding an RD wall-associated kinase, is the responsible gene in qRglsSB resistant against GLS. The introgression of the ZmWAK02 gene into hybrid lines significantly improves their grain yield in the presence of GLS pressure and does not reduce their grain yield in the absence of GLS. In summary, we cloned a gene, ZmWAK02, conferring large effect of GLS resistance and confirmed its great value in maize breeding.