Cyclic CMP and cyclic UMP mediate bacterial immunity against phages.

The cyclic pyrimidines 3',5'-cyclic cytidine monophosphate (cCMP) and 3',5'-cyclic uridine monophosphate (cUMP) have been reported in multiple organisms and cell types. As opposed to the cyclic nucleotides 3',5'-cyclic adenosine monophosphate (cAMP) and 3',5'-cyclic guanosine monophosphate (cGMP), which are second messenger molecules with well-established regulatory roles across all domains of life, the biological role of cyclic pyrimidines has remained unclear. Here we report that cCMP and cUMP are second messengers functioning in bacterial immunity against viruses. We discovered a family of bacterial pyrimidine cyclase enzymes that specifically synthesize cCMP and cUMP following phage infection and demonstrate that these molecules activate immune effectors that execute an antiviral response. A crystal structure of a uridylate cyclase enzyme from this family explains the molecular mechanism of selectivity for pyrimidines as cyclization substrates. Defense systems encoding pyrimidine cyclases, denoted here Pycsar (pyrimidine cyclase system for antiphage resistance), are widespread in prokaryotes. Our results assign clear biological function to cCMP and cUMP as immunity signaling molecules in bacteria.

Structural basis of microRNA biogenesis by Dicer-1 and its partner protein Loqs-PB.

In animals and plants, Dicer enzymes collaborate with double-stranded RNA-binding domain (dsRBD) proteins to convert precursor-microRNAs (pre-miRNAs) into miRNA duplexes. We report six cryo-EM structures of Drosophila Dicer-1 that show how Dicer-1 and its partner Loqs­PB cooperate (1) before binding pre-miRNA, (2) after binding and in a catalytically competent state, (3) after nicking one arm of the pre-miRNA, and (4) following complete dicing and initial product release. Our reconstructions suggest that pre-miRNA binds a rare, open conformation of the Dicer­1⋅Loqs­PB heterodimer. The Dicer-1 dsRBD and three Loqs­PB dsRBDs form a tight belt around the pre-miRNA, distorting the RNA helix to place the scissile phosphodiester bonds in the RNase III active sites. Pre-miRNA cleavage shifts the dsRBDs and partially closes Dicer-1, which may promote product release. Our data suggest a model for how the Dicer­1⋅Loqs­PB complex affects a complete cycle of pre-miRNA recognition, stepwise endonuclease cleavage, and product release.

A billion-year shift in the formation of Earth's largest ore deposits.

Banded iron formations (BIFs) archive the relationship between Earth's lithosphere, hydrosphere, and atmosphere through time. However, constraints on the origin of Earth's largest ore deposits, hosted by BIFs, are limited by the absence of direct geochronology. Without this temporal context, genetic models cannot be correlated with tectono-thermal and atmospheric drivers responsible for BIF upgrading through time. Utilizing in situ iron oxide U-Pb geochronology, we provide a direct timeline of events tracing development of all the giant BIF-hosted hematite deposits of the Hamersley Province (Pilbara Craton, Western Australia). Direct dating demonstrates that the major iron ore deposits in the region formed during 1.4 to 1.1 Ga. This is one billion to hundreds of millions of years later than previous age constraints based upon 1) the presence of hematite ore clasts in conglomerate beds deposited before ~1.84 Ga, and 2) phosphate mineral dating, which placed the onset of iron mineralization in the Province at ~2.2 to 2.0 Ga during the great oxidation event. Dating of the hematite clasts verified the occurrence of a ~2.2 to 2.0 Ga event, reflecting widespread, but now largely eroded iron mineralization occurring when the Pilbara and Kaapvaal cratons were proximal. No existing phosphate mineral dates overlap with obtained hematite dates and therefore cannot be related to hematite crystallization and ore formation. New geochronology conclusively links all major preserved hematite deposits to a far younger (1.4 to 1.1 Ga) formation period, correlated with the amalgamation of Australia following breakup of the Columbia supercontinent.

Boundary exchange completes the marine Pb cycle jigsaw.

Material fluxes at the land-ocean interface impact seawater composition and global cycling of elements. However, most attention has been focused on the fluvial dissolved fluxes. For elements like lead (Pb), whose fluvial particulate flux into the ocean is two orders of magnitude higher than the dissolved counterpart, the role of particulates in elemental cycling is potentially important but currently less appreciated. Using both chemical analyses on samples collected from around equatorial Southeast Asia and model simulations, we show that particulate-dissolved exchange is an important mechanism controlling the concentration and isotopic composition of dissolved Pb in the ocean. Our model indicates that Pb contributed from particulate-dissolved exchange at ocean boundaries is larger than, or at least comparable to, other major Pb sources to the seawater before the Anthropocene, when the anthropogenic Pb was absent. Our work highlights the importance of boundary exchange in understanding marine element cycling and weathering-climate feedback.

Isotopes illustrate vertical transport of anthropogenic Pb by reversible scavenging within Pacific Ocean particle veils.

Reversible scavenging, the oceanographic process by which dissolved metals exchange onto and off sinking particles and are thereby transported to deeper depths, has been well established for the metal thorium for decades. Reversible scavenging both deepens the elemental distribution of adsorptive elements and shortens their oceanic residence times in the ocean compared to nonadsorptive metals, and scavenging ultimately removes elements from the ocean via sedimentation. Thus, it is important to understand which metals undergo reversible scavenging and under what conditions. Recently, reversible scavenging has been invoked in global biogeochemical models of a range of metals including lead, iron, copper, and zinc to fit modeled data to observations of oceanic dissolved metal distributions. Nonetheless, the effects of reversible scavenging remain difficult to visualize in ocean sections of dissolved metals and to distinguish from other processes such as biological regeneration. Here, we show that particle-rich "veils" descending from high-productivity zones in the equatorial and North Pacific provide idealized illustrations of reversible scavenging of dissolved lead (Pb). A meridional section of dissolved Pb isotope ratios across the central Pacific shows that where particle concentrations are sufficiently high, such as within particle veils, vertical transport of anthropogenic surface-dissolved Pb isotope ratios toward the deep ocean is manifested as columnar isotope anomalies. Modeling of this effect shows that reversible scavenging within particle-rich waters allows anthropogenic Pb isotope ratios from the surface to penetrate ancient deep waters on timescales sufficiently rapid to overcome horizontal mixing of deep water Pb isotope ratios along abyssal isopycnals.

Cambrian explosion condensed: High-precision geochronology of the lower Wood Canyon Formation, Nevada.

The geologically rapid appearance of fossils of modern animal phyla within Cambrian strata is a defining characteristic of the history of life on Earth. However, temporal calibration of the base of the Cambrian Period remains uncertain within millions of years, which has resulted in mounting challenges to the concept of a discrete Cambrian explosion. We present precise zircon U-Pb dates for the lower Wood Canyon Formation, Nevada. These data demonstrate the base of the Cambrian Period, as defined by both ichnofossil biostratigraphy and carbon isotope chemostratigraphy, was younger than 533 Mya, at least 6 My later than currently recognized. This new geochronology condenses previous age models for the Nemakit-Daldynian (early Cambrian) and, integrated with global records, demonstrates an explosive tempo to the early radiation of modern animal phyla.

African swine fever virus pB475L evades host antiviral innate immunity via targeting STAT2 to inhibit IFN-I signaling.

African swine fever virus (ASFV) causes severe disease in domestic pigs and wild boars, seriously threatening the development of the global pig industry. Type I interferon (IFN-I) is an important component of innate immunity, inducing the transcription and expression of antiviral cytokines by activating Janus-activated kinase-signal transducer and activator of transcription (STAT). However, the underlying molecular mechanisms by which ASFV antagonizes IFN-I signaling have not been fully elucidated. Therefore, using coimmunoprecipitation, confocal microscopy, and dual luciferase reporter assay methods, we investigated these mechanisms and identified a novel ASFV immunosuppressive protein, pB475L, which interacts with the C-terminal domain of STAT2. Consequently, pB475L inhibited IFN-I signaling by inhibiting STAT1 and STAT2 heterodimerization and nuclear translocation. Furthermore, we constructed an ASFV-B475L7PM mutant strain by homologous recombination, finding that ASFV-B475L7PM attenuated the inhibitory effects on IFN-I signaling compared to ASFV-WT. In summary, this study reveals a new mechanism by which ASFV impairs host innate immunity.

Identification of a short sequence motif in the influenza A virus pathogenicity factor PB1-F2 required for inhibition of human NLRP3.

Influenza A virus infection activates the NLRP3 inflammasome, a multiprotein signaling complex responsible for the proteolytic activation and release of the proinflammatory cytokine IL-1ß from monocytes and macrophages. Some influenza A virus (IAV) strains encode a short 90-amino acid peptide (PB1-F2) on an alternative open reading frame of segment 2, with immunomodulatory activity. We recently demonstrated that contemporary IAV PB1-F2 inhibits the activation of NLRP3, potentially by NEK7-dependent activation. PB1-F2 binds to NLRP3 with its C-terminal 50 amino acids, but the exact binding motif was unknown. On the NLRP3 side, the interface is formed through the leucine-rich-repeat (LRR) domain, potentially in conjunction with the pyrin domain. Here, we took advantage of PB1-F2 sequences from IAV strains with either weak or strong NLRP3 interaction. Sequence comparison and structure prediction using Alphafold2 identified a short four amino acid sequence motif (TQGS) in PB1-F2 that defines NLRP3-LRR binding. Conversion of this motif to that of the non-binding PB1-F2 suffices to lose inhibition of NLRP3 dependent IL-1ß release. The TQGS motif further alters the subcellular localization of PB1-F2 and its colocalization with NLRP3 LRR and pyrin domain. Structural predictions suggest the establishment of additional hydrogen bonds between the C-terminus of PB1-F2 and the LRR domain of NLRP3, with two hydrogen bonds connecting to threonine and glutamine of the TQGS motif. Phylogenetic data show that the identified NLRP3 interaction motif in PB1-F2 is widely conserved among recent IAV-infecting humans. Our data explain at a molecular level the specificity of NLRP3 inhibition by influenza A virus. IMPORTANCE: Influenza A virus infection is accompanied by a strong inflammatory response and high fever. The human immune system facilitates the swift clearance of the virus with this response. An essential signal protein in the proinflammatory host response is IL-1b. It is released from inflammatory macrophages, and its production and secretion depend on the function of NLRP3. We had previously shown that influenza A virus blocks NLRP3 activation by the expression of a viral inhibitor, PB1-F2. Here, we demonstrate how this short peptide binds to NLRP3 and provide evidence that a four amino acid stretch in PB1-F2 is necessary and sufficient to mediate this binding. Our data identify a new virus-host interface required to block one signaling path of the innate host response against influenza A virus.

PB2 residue 473 contributes to the mammalian virulence of H7N9 avian influenza virus by modulating viral polymerase activity via ANP32A.

Since the first human infection reported in 2013, H7N9 avian influenza virus (AIV) has been regarded as a serious threat to human health. In this study, we sought to identify the virulence determinant of the H7N9 virus in mammalian hosts. By comparing the virulence of the SH/4664 H7N9 virus, a non-virulent H9N2 virus, and various H7N9-H9N2 hybrid viruses in infected mice, we first pinpointed PB2 as the primary viral factor accounting for the difference between H7N9 and H9N2 in mammalian virulence. We further analyzed the in vivo effects of individually mutating H7N9 PB2 residues different from the closely related H9N2 virus and consequently found residue 473, alongside the well-known residue 627, to be critical for the virulence of the H7N9 virus in mice and the activity of its reconstituted viral polymerase in mammalian cells. The importance of PB2-473 was further strengthened by studying reverse H7N9 substitutions in the H9N2 background. Finally, we surprisingly found that species-specific usage of ANP32A, a family member of host factors connecting with the PB2-627 polymorphism, mediates the contribution of PB2 473 residue to the mammalian adaption of AIV polymerase, as the attenuating effect of PB2 M473T on the viral polymerase activity and viral growth of the H7N9 virus could be efficiently complemented by co-expression of chicken ANP32A but not mouse ANP32A and ANP32B. Together, our studies uncovered the PB2 473 residue as a novel viral host range determinant of AIVs via species-specific co-opting of the ANP32 host factor to support viral polymerase activity.IMPORTANCEThe H7N9 avian influenza virus has been considered to have the potential to cause the next pandemic since the first case of human infection reported in 2013. In this study, we identified PB2 residue 473 as a new determinant of mouse virulence and mammalian adaptation of the viral polymerase of the H7N9 virus and its non-pathogenic H9N2 counterparts. We further demonstrated that the variation in PB2-473 is functionally linked to differential co-opting of the host ANP32A protein in supporting viral polymerase activity, which is analogous to the well-known PB2-627 polymorphism, albeit the two PB2 positions are spatially distant. By providing new mechanistic insight into the PB2-mediated host range determination of influenza A viruses, our study implicated the potential existence of multiple PB2-ANP32 interfaces that could be targets for developing new antivirals against the H7N9 virus as well as other mammalian-adapted influenza viruses.

Uni-GBSA: an open-source and web-based automatic workflow to perform MM/GB(PB)SA calculations for virtual screening.

Binding free energy calculation of a ligand to a protein receptor is a fundamental objective in drug discovery. Molecular mechanics/Generalized-Born (Poisson-Boltzmann) surface area (MM/GB(PB)SA) is one of the most popular methods for binding free energy calculations. It is more accurate than most scoring functions and more computationally efficient than alchemical free energy methods. Several open-source tools for performing MM/GB(PB)SA calculations have been developed, but they have limitations and high entry barriers to users. Here, we introduce Uni-GBSA, a user-friendly automatic workflow to perform MM/GB(PB)SA calculations, which can perform topology preparation, structure optimization, binding free energy calculation and parameter scanning for MM/GB(PB)SA calculations. It also offers a batch mode that evaluates thousands of molecules against one protein target in parallel for efficient application in virtual screening. The default parameters are selected after systematic testing on the PDBBind-2011 refined dataset. In our case studies, Uni-GBSA produced a satisfactory correlation with the experimental binding affinities and outperformed AutoDock Vina in molecular enrichment. Uni-GBSA is available as an open-source package at https://github.com/dptech-corp/Uni-GBSA. It can also be accessed for virtual screening from the Hermite web platform at https://hermite.dp.tech. A free Uni-GBSA web server of a lab version is available at https://labs.dp.tech/projects/uni-gbsa/. This increases user-friendliness because the web server frees users from package installations and provides users with validated workflows for input data and parameter settings, cloud computing resources for efficient job completions, a user-friendly interface and professional support and maintenance.

A phased small interfering RNA-derived pathway mediates lead stress tolerance in maize.

Phased small interfering RNAs (phasiRNAs) are a distinct class of endogenous small interfering RNAs, which regulate plant growth, development and environmental stress response. To determine the effect of phasiRNAs on maize (Zea mays L.) tolerance to lead (Pb) stress, the roots of 305 maize lines under Pb treatment were subjected to generation of individual databases of small RNAs. We identified 55 high-confidence phasiRNAs derived from 13 PHAS genes (genes producing phasiRNAs) in this maize panel, of which 41 derived from nine PHAS loci were negatively correlated with Pb content in the roots. The potential targets of the 41 phasiRNAs were enriched in ion transport and import. Only the expression of PHAS_1 (ZmTAS3j, Trans-Acting Short Interference RNA3) was regulated by its cis-expression quantitative trait locus and thus affected the Pb content in the roots. Using the Nicotiana benthamiana (N. benthamiana) transient expression system, 5'-rapid amplification of cDNA ends, and Arabidopsis heterologously expressed, we verified that ZmTAS3j was cleaved by zma-miR390 and thus generated tasiRNA targeting ARF genes (tasiARFs), and that the 5' and 3' zma-miR390 target sites of ZmTAS3j were both necessary for efficient biosynthesis and functional integrity of tasiARFs. We validated the involvement of the zma-miR390-ZmTAS3j-tasiARF-ZmARF3-ZmHMA3 pathway in Pb accumulation in maize seedlings using genetic, molecular, and cytological methods. Moreover, the increased Pb tolerance in ZmTAS3j-overexpressed lines was likely attributed to the zma-miR390-ZmTAS3j-tasiARF-ZmARF3-SAURs pathway, which elevated indole acetic acid levels and thus reactive oxygen species scavenging capacity in maize roots. Our study reveals the importance of the TAS3-derived tasiRNA pathway in plant adaptation to Pb stress.

Synergistic dual conversion reactions assisting Pb-S electrochemistry for energy storage.

SignificanceBased on the analysis of three thermodynamic parameters of various M-S systems (solubility of metal sulfides [MxSy] in aqueous solution, volume change of the metal-sulfur [M-S] battery system, and the potential of S/MxSy cathode redox couple), an aqueous Pb-S battery operated by synergistic dual conversion reactions (cathode: S⇄PbS, anode: Pb2+⇄PbO2) has been officially reported. Benefitting from the inherent insolubility of PbS and a conversion-type counter electrode, the aqueous Pb-S battery exhibited two advantages: it is shuttle effect free and has a dendrite-free nature. Moreover, the practical value of the Pb-S battery was further certified by the prototype S|Pb(NO3)2ǁZn(NO3)2|Zn hybrid cell, which afforded an energy density of 930.9 Wh kg-1sulfur.

Viral PB1-F2 and host IFN-γ guide ILC2 and T cell activity during influenza virus infection.

Functional plasticity of innate lymphoid cells (ILCs) and T cells is regulated by host environmental cues, but the influence of pathogen-derived virulence factors has not been described. We now report the interplay between host interferon (IFN)-γ and viral PB1-F2 virulence protein in regulating the functions of ILC2s and T cells that lead to recovery from influenza virus infection of mice. In the absence of IFN-γ, lung ILC2s from mice challenged with the A/California/04/2009 (CA04) H1N1 virus, containing nonfunctional viral PB1-F2, initiated a robust IL-5 response, which also led to improved tissue integrity and increased survival. Conversely, challenge with Puerto Rico/8/1934 (PR8) H1N1 virus expressing fully functional PB1-F2, suppressed IL-5+ ILC2 responses, and induced a dominant IL-13+ CD8 T cell response, regardless of host IFN-γ expression. IFN-γ-deficient mice had increased survival and improved tissue integrity following challenge with lethal doses of CA04, but not PR8 virus, and increased resistance was dependent on the presence of IFN-γR+ ILC2s. Reverse-engineered influenza viruses differing in functional PB1-F2 activity induced ILC2 and T cell phenotypes similar to the PB1-F2 donor strains, demonstrating the potent role of viral PB1-F2 in host resistance. These results show the ability of a pathogen virulence factor together with host IFN-γ to regulate protective pulmonary immunity during influenza infection.

Developmental Pb exposure increases AD risk via altered intracellular Ca2+ homeostasis in hiPSC-derived cortical neurons.

Exposure to environmental chemicals such as lead (Pb) during vulnerable developmental periods can result in adverse health outcomes later in life. Human cohort studies have demonstrated associations between developmental Pb exposure and Alzheimer's disease (AD) onset in later life which were further corroborated by findings from animal studies. The molecular pathway linking developmental Pb exposure and increased AD risk, however, remains elusive. In this work, we used human iPSC-derived cortical neurons as a model system to study the effects of Pb exposure on AD-like pathogenesis in human cortical neurons. We exposed neural progenitor cells derived from human iPSC to 0, 15, and 50 ppb Pb for 48 h, removed Pb-containing medium, and further differentiated them into cortical neurons. Immunofluorescence, Western blotting, RNA-sequencing, ELISA, and FRET reporter cell lines were used to determine changes in AD-like pathogenesis in differentiated cortical neurons. Exposing neural progenitor cells to low-dose Pb, mimicking a developmental exposure, can result in altered neurite morphology. Differentiated neurons exhibit altered calcium homeostasis, synaptic plasticity, and epigenetic landscape along with elevated AD-like pathogenesis markers, including phosphorylated tau, tau aggregates, and Aß42/40. Collectively, our findings provide an evidence base for Ca dysregulation caused by developmental Pb exposure as a plausible molecular mechanism accounting for increased AD risk in populations with developmental Pb exposure.

Genome-wide identification and characterization of NAC transcription factor family members in Trifolium pratense and expression analysis under lead stress.

BACKGROUND: The NAC TF family is widely involved in plant responses to various types of stress. Red clover (Trifolium pratense) is a high-quality legume, and the study of NAC genes in red clover has not been comprehensive. The aim of this study was to analyze the NAC gene family of red clover at the whole-genome level and explore its potential role in the Pb stress response. RESULTS: In this study, 72 TpNAC genes were identified from red clover; collinearity analysis showed that there were 5 pairs of large fragment replicators of TpNAC genes, and red clover was found to be closely related to Medicago truncatula. Interestingly, the TpNAC genes have more homologs in Arabidopsis thaliana than in soybean (Glycine max). There are many elements in the TpNAC genes promoters that respond to stress. Gene expression analysis showed that all the TpNAC genes responded to Pb stress. qRT-PCR showed that the expression levels of TpNAC29 and TpNAC42 were significantly decreased after Pb stress. Protein interaction network analysis showed that 21 TpNACs and 23 other genes participated in the interaction. In addition, the TpNAC proteins had three possible 3D structures, and the secondary structure of these proteins were mainly of other types. These results indicated that most TpNAC members were involved in the regulation of Pb stress in red clover. CONCLUSION: These results suggest that most TpNAC members are involved in the regulation of Pb stress in red clover. TpNAC members play an important role in the response of red clover to Pb stress.

NK92 cells and peripheral blood NK cells respond oppositely upon dasatinib treatment.

Natural killer (NK) cell is a valuable tool for immunotherapy in cancer treatment, both the cultured cell line NK92 and primary NK cells are widely studied and used in research and clinical trials. Clinical observations witnessed the improvement of patients' NK cells in terms of cell counts and cytotoxic activity upon dasatinib treatment, an approved drug for chronic myeloid leukaemia and Ph+ acute lymphocytic leukaemia. Several studies supported the clinical observations, yet others argued a detrimental effect of dasatinib on NK cells. Due to the complex conditions in different studies, the definite influence of dasatinib on NK92 and primary NK cells remains to be settled. Here, we used a well-defined in vitro system to evaluate the effects of dasatinib on NK92 cells and peripheral blood (PB)-NK cells. By co-culturing NK cells with dasatinib to test the cell counts and target cell-killing activities, we surprisingly found that the chemical influenced oppositely on these two types of NK cells. While dasatinib suppressed NK92 cell proliferation and cytotoxic activity, it improved PB-NK-killing tumour cells. RNA sequencing analysis further supported this finding, uncovering several proliferating and cytotoxic pathways responding invertedly between them. Our results highlighted an intrinsic difference between NK92 and PB-NK cells and may build clues to understand how dasatinib interacts with NK cells in vivo.

Flavonoid metabolism plays an important role in response to lead stress in maize at seedling stage.

BACKGROUND: Pb stress, a toxic abiotic stress, critically affects maize production and food security. Although some progress has been made in understanding the damage caused by Pb stress and plant response strategies, the regulatory mechanisms and resistance genes involved in the response to lead stress in crops are largely unknown. RESULTS: In this study, to uncover the response mechanism of maize to Pb stress phenotype, physiological and biochemical indexes, the transcriptome, and the metabolome under different concentrations of Pb stress were combined for comprehensive analysis. As a result, the development of seedlings and antioxidant system were significantly inhibited under Pb stress, especially under relatively high Pb concentrations. Transcriptome analysis revealed 3559 co-differentially expressed genes(co-DEG) under the four Pb concentration treatments (500 mg/L, 1000 mg/L, 2000 mg/L, and 3000 mg/L Pb(NO3)2), which were enriched mainly in the GO terms related to DNA-binding transcription factor activity, response to stress, response to reactive oxygen species, cell death, the plasma membrane and root epidermal cell differentiation. Metabolome analysis revealed 72 and 107 differentially expressed metabolites (DEMs) under T500 and T2000, respectively, and 36 co-DEMs. KEGG analysis of the DEMs and DEGs revealed a common metabolic pathway, namely, flavonoid biosynthesis. An association study between the flavonoid biosynthesis-related DEMs and DEGs revealed 20 genes associated with flavonoid-related metabolites, including 3 for genistin and 17 for calycosin. CONCLUSION: In summary, the study reveals that flavonoid metabolism plays an important role in response to Pb stress in maize, which not only provides genetic resources for the genetic improvement of maize Pb tolerance in the future but also enriches the theoretical basis of the maize Pb stress response.

Ternary-Metal Sn-Pb-Zn Perovskite to Reconstruct Top Surface for Efficient and Stable Less-Pb Perovskite Solar Cells.

Though Sn-Pb alloyed perovskite solar cells (PSCs) achieved great progress, there is a dilemma to further increase Sn for less-Pb requirement. High Sn ratio (>70%) perovskite exhibits nonstoichiometric Sn:Pb:I at film surface to aggravate Sn2+ oxidation and interface energy mismatch. Here, ternary metal alloyed (FASnI3 )0.7 (MAPb1- x Znx I3 )0.3 (x = 0-3%) is constructed for Pb% < 30% perovskite. Zn with smaller ionic size and stronger ionic interaction than Sn/Pb assists forming high-quality perovskite film with ZnI6 4- enriched at surface to balance Sn:Pb:I ratio. Differing from uniform bulk doping, surface-rich Zn with lower lying orbits pushes down the energy band of perovskite and adjusts the interface energy for efficient charge transfer. The alloyed PSC realizes efficiency of 19.4% at AM1.5 (one of the highest values reported for Pb% < 30% PSCs). Moreover, stronger bonding of Zn─I and Sn─I contributes to better durability of ternary perovskite than binary perovskite. This work highlights a novel alloy method for efficient and stable less-Pb PSCs.

Efficient Tin-Lead Perovskite Solar Cells with a Ultrawide Usage Windows of Precursor Solution Opened by SnF2.

High quality tin-lead perovskite solar cells (Sn─Pb PSCs) can be fabricated via simple solution processing methods. However, the instability of precursor solutions and their narrow usage windows still pose challenges in manufacturing efficient and reproducible Sn─Pb PSCs, hindering the commercialization of PSCs. Fluorine tin (SnF2) is widely used as an antioxidant to improve the crystallinity of perovskite. In this study, another role of SnF2 as a stabilizer is found to restrain the deprotonation of methylammonium iodide (MAI) in the precursor solution, which improves their stability and expands their usage windows. Due to the inhibition of SnF2 on oxidation and deprotonation, stable large-sized colloidal clusters form gradually in perovskite precursor solution during aging, leading to uniform nucleation/crystallization during film growth, significantly reducing the roughness and defect density in the films. Because of the competitive deprotonation and oxidation process of Sn2+, the benefit of larger cluster maximizes after about ten days storage of precursor solution. The champion efficiency of Sn─Pb PSCs prepared with 10 days aged precursor solution is 22.00%. High performance of devices fabricated with precursor solution stored for even ≈40 days discloses the wide usage windows of precursor solution with SnF2 additive.

Progress of Hole-Transport Layers in Mixed Sn-Pb Perovskite Solar Cells.

Hybrid organic-inorganic lead halide perovskite solar cells (PSCs) have rapidly emerged as a promising photovoltaic technology, with record efficiencies surpassing 26%, approaching the theoretical Shockley-Queisser limit. The advent of all-perovskite tandem solar cells (APTSCs), integrating Pb-based wide-bandgap (WBG) with mixed Sn-Pb narrow-bandgap (NBG) perovskites, presents a compelling pathway to surpass this limit. Despite recent innovations in hole transport layers (HTLs) that have significantly improved the efficiency and stability of lead-based PSCs, an effective HTL tailored for Sn-Pb NBG PSCs remains an unmet need. This review highlights the essential role of HTLs in enhancing the performance of Sn-Pb PSCs, focusing on their ability to mitigate non-radiative recombination and optimize the buried interface, thereby improving film quality. The distinct attributes of Sn-Pb perovskites, such as their lower energy levels and accelerated crystallization rates, necessitate HTLs with specialized properties. In this study, the latest advancements in HTLs are systematically examined for Sn-Pb PSCs, encompassing organic, self-assembled monolayer (SAM), inorganic materials, and HTL-free designs. The review critically assesses the inherent limitations of each HTL category, and finally proposes strategies to surmount these obstacles to reach higher device performance.