Comprehensive isoform-level analysis reveals the contribution of alternative isoforms to venom evolution and repertoire diversity.

Animal venom systems have emerged as valuable models for investigating how novel polygenic phenotypes may arise from gene evolution by varying molecular mechanisms. However, a significant portion of venom genes produce alternative mRNA isoforms that have not been extensively characterized, hindering a comprehensive understanding of venom biology. In this study, we present a full-length isoform-level profiling workflow integrating multiple RNA sequencing technologies, allowing us to reconstruct a high-resolution transcriptome landscape of venom genes in the parasitoid wasp Pteromalus puparum Our findings demonstrate that more than half of the venom genes generate multiple isoforms within the venom gland. Through mass spectrometry analysis, we confirm that alternative splicing contributes to the diversity of venom proteins, acting as a mechanism for expanding the venom repertoire. Notably, we identified seven venom genes that exhibit distinct isoform usages between the venom gland and other tissues. Furthermore, evolutionary analyses of venom serpin3 and orcokinin further reveal that the co-option of an ancient isoform and a newly evolved isoform, respectively, contributes to venom recruitment, providing valuable insights into the genetic mechanisms driving venom evolution in parasitoid wasps. Overall, our study presents a comprehensive investigation of venom genes at the isoform level, significantly advancing our understanding of alternative isoforms in venom diversity and evolution and setting the stage for further in-depth research on venoms.

mDia formins form hetero-oligomers and cooperatively maintain murine hematopoiesis.

mDia formin proteins regulate the dynamics and organization of the cytoskeleton through their linear actin nucleation and polymerization activities. We previously showed that mDia1 deficiency leads to aberrant innate immune activation and induces myelodysplasia in a mouse model, and mDia2 regulates enucleation and cytokinesis of erythroblasts and the engraftment of hematopoietic stem and progenitor cells (HSPCs). However, whether and how mDia formins interplay and regulate hematopoiesis under physiological and stress conditions remains unknown. Here, we found that both mDia1 and mDia2 are required for HSPC regeneration under stress, such as serial plating, aging, and reconstitution after myeloid ablation. We showed that mDia1 and mDia2 form hetero-oligomers through the interactions between mDia1 GBD-DID and mDia2 DAD domains. Double knockout of mDia1 and mDia2 in hematopoietic cells synergistically impaired the filamentous actin network and serum response factor-involved transcriptional signaling, which led to declined HSPCs, severe anemia, and significant mortality in neonates and newborn mice. Our data demonstrate the potential roles of mDia hetero-oligomerization and their non-rodent functions in the regulation of HSPCs activity and orchestration of hematopoiesis.

Interferon-α regulates abnormally increased expression of RSAD2 in Th17 and Tfh cells in systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that often involves abnormal activation of regulatory IFN genes and regulation of B cells by CD4+ T cells. Radical S-adenosyl methionine domain containing 2 (RSAD2) is a viral suppressor protein regulated by type I IFN, and it has been proven to play an important regulatory role in SLE. However, the mechanism by which RSAD2 participates in the pathogenesis of SLE is unclear. In this study, we observed higher expression levels of RSAD2 in CD4+ T-cell subsets from the peripheral blood of SLE patients than in those from healthy controls by bioinformatics analysis and validation experiments. We analyzed the expression of RSAD2 in CD4+ T cells of patients with SLE and other autoimmune diseases. In addition, we found that the expression of RSAD2 in CD4+ T cells might be regulated by IFN-α, and RSAD2 significantly affected the differentiation of Th17 cells and T follicular helper (Tfh) cells. Our findings underlined that RSAD2 may promote B-cell activation by promoting the differentiation of Th17 and Tfh cells in SLE patients, a process that is regulated by IFN-α.

Optically pumped flexible GaN-based ultraviolet VCSELs.

Flexible optoelectronic platforms, which integrate optoelectronic devices on a flexible substrate, are promising in more complex working environments benefiting from the mechanical flexibility. Herein, for the first time to the best of our knowledge, a flexible GaN-based vertical cavity surface-emitting laser (VCSEL) in the ultraviolet A (UVA) range was demonstrated by using a thin-film transfer process based on laser lift-off (LLO) and spin-coating of a flexible substrate. The lasing wavelength is 376.5 nm with a linewidth of 0.6 nm and threshold energy of 98.4 nJ/pulse, corresponding to a threshold energy density of 13.9 mJ/cm2. The flexible substrate in this study is directly formed by spin-coating of photosensitive epoxy resin, which is much simplified and cost-effective, and a 2-in. wafer scale GaN-based membrane can be successfully transferred to a flexible substrate through this method. Such flexible UVA VCSELs are promising for the development of next-generation flexible and wearable technologies.

InsectBase 2.0: a comprehensive gene resource for insects.

Insects are the largest group of animals on the planet and have a huge impact on human life by providing resources, transmitting diseases, and damaging agricultural crop production. Recently, a large amount of insect genome and gene data has been generated. A comprehensive database is highly desirable for managing, sharing, and mining these resources. Here, we present an updated database, InsectBase 2.0 (http://v2.insect-genome.com/), covering 815 insect genomes, 25 805 transcriptomes and >16 million genes, including 15 045 111 coding sequences, 3 436 022 3'UTRs, 4 345 664 5'UTRs, 112 162 miRNAs and 1 293 430 lncRNAs. In addition, we used an in-house standard pipeline to annotate 1 434 653 genes belonging to 164 gene families; 215 986 potential horizontally transferred genes; and 419 KEGG pathways. Web services such as BLAST, JBrowse2 and Synteny Viewer are provided for searching and visualization. InsectBase 2.0 serves as a valuable platform for entomologists and researchers in the related communities of animal evolution and invertebrate comparative genomics.

Unraveling the complex evolutionary history of lepidopteran chromosomes through ancestral chromosome reconstruction and novel chromosome nomenclature.

BACKGROUND: Lepidoptera is one of the most species-rich animal groups, with substantial karyotype variations among species due to chromosomal rearrangements. Knowledge of the evolutionary patterns of lepidopteran chromosomes still needs to be improved. RESULTS: Here, we used chromosome-level genome assemblies of 185 lepidopteran insects to reconstruct an ancestral reference genome and proposed a new chromosome nomenclature. Thus, we renamed over 5000 extant chromosomes with this system, revealing the historical events of chromosomal rearrangements and their features. Additionally, our findings indicate that, compared with autosomes, the Z chromosome in Lepidoptera underwent a fast loss of conserved genes, rapid acquisition of lineage-specific genes, and a low rate of gene duplication. Moreover, we presented evidence that all available 67 W chromosomes originated from a common ancestor chromosome, with four neo-W chromosomes identified, including one generated by fusion with an autosome and three derived through horizontal gene transfer. We also detected nearly 4000 inter-chromosomal gene movement events. Notably, Geminin is transferred from the autosome to the Z chromosome. When located on the autosome, Geminin shows female-biased expression, but on the Z chromosome, it exhibits male-biased expression. This contributes to the sexual dimorphism of body size in silkworms. CONCLUSIONS: Our study sheds light on the complex evolutionary history of lepidopteran chromosomes based on ancestral chromosome reconstruction and novel chromosome nomenclature.

Microtia, Branchial Cleft Fistula, and Tetralogy of Fallot: A Possible Association.

When searching over associations between congenital ear abnormalities, especially microtia and affiliated deformities like cleft lip or palate and congenital heart diseases, some clinical analysis and genetic theories are found. A 10-year-old boy sent to the plastic surgery hospital was puzzled by a congenital anterior auricular fistula with fluid trace for more than 9 years. The preoperative diagnoses were branchial cleft fistula and congenital left ear deformity with postoperation of TOF. By browsing over studies on genetic concerns and clinical performance, it may be attributed to a possible association between microtia, branchial cleft fistula, and tetralogy of Fallot, though whose fundamental mechanisms remain concerned.

Facet-dependent transformation and toxicity of nanoscale zinc oxide in the synthetic saliva.

The nanoscale zinc oxide (n-ZnO) was used in food packages due to its superior antibacterial activity, resulting in potential intake of n-ZnO through the digestive system, wherein n-ZnO interacted with saliva. In recent, facet engineering, a technique for controlling the exposed facets, was applied to n-ZnO, whereas risk of n-ZnO with specific exposed facets in saliva was ignored. ZnO nanoflakes (ZnO-0001) and nanoneedles (ZnO-1010) with the primary exposed facets of {0001} and {1010} respectively were prepared in this study, investigating stability and toxicity of ZnO-0001 and ZnO-1010 in synthetic saliva. Both ZnO-0001 and ZnO-1010 partially transformed into amorphous Zn3(PO4)2 within 1 hr in the saliva even containing orgnaic components, forming a ZnO-Zn3(PO4)2 core-shell structure. Nevertheless, ZnO-1010 relative to ZnO-0001 would likely transform into Zn3(PO4)2, being attributed to superior dissolution of {1010} facet due to its lower vacancy formation energy (1.15 eV) than {0001} facet (3.90 eV). The toxicity of n-ZnO to Caco-2 cells was also dependent on the primary exposed facet; ZnO-0001 caused cell toxicity through oxidative stress, whereas ZnO-1010 resulted in lower cells viability than ZnO-0001 through oxidative stress and membrane damage. Density functional theory calculations illustrated that ·O2- was formed and released on {1010} facet, yet O22- instead of ·O2- was generated on {0001} facet, leading to low oxidative stress from ZnO-0001. All findings demonstrated that stability and toxicity of n-ZnO were dependent on the primary exposed facet, improving our understanding of health risk of nanomaterials.

A Stapled Peptide Inhibitor Targeting the Binding Interface of N6-Adenosine-Methyltransferase Subunits METTL3 and METTL14 for Cancer Therapy.

METTL3, a primary methyltransferase catalyzing the RNA N6-methyladenosine (m6A) modification, has been identified as an oncogene in several cancer types and thus nominated as a potentially effective target for therapeutic inhibition. However, current options using this strategy are limited. In this study, we targeted protein-protein interactions at the METTL3-METTL14 binding interface to inhibit complex formation and subsequent catalysis of the RNA m6A modification. Among candidate peptides, RM3 exhibited the highest anti-cancer potency, inhibiting METTL3 activity while also facilitating its proteasomal degradation. We then designed a stapled peptide inhibitor (RSM3) with enhanced peptide stability and formation of the α-helical secondary structure required for METTL3 interaction. Functional and transcriptomic analysis in vivo indicated that RSM3 induced upregulation of programmed cell death-related genes while inhibiting cancer-promoting signals. Furthermore, tumor growth was significantly suppressed while apoptosis was enhanced upon RSM3 treatment, accompanied by increased METTL3 degradation, and reduced global RNA methylation levels in two in vivo tumor models. This peptide inhibitor thus exploits a mechanism distinct from other small-molecule competitive inhibitors to inhibit oncogenic METTL3 activity. Our findings collectively highlight the potential of targeting METTL3 in cancer therapies through peptide-based inhibition of complex formation and proteolytic degradation.

Overexpressed CD44 is associated with B-cell activation via the HA-CD44-AIM2 pathway in lupus B cells.

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by aberrant development of B cells and excess production of autoantibodies. Our team previously reported that absent in melanoma 2 (AIM2) regulates B-cell differentiation via the Bcl-6-Blimp-1 axis. Notably, in keyhole limpet hemocyanin (KLH)-immunized CD19creAim2f/f mice, the frequency of CD19+CD44+ B cells was decreased, accompanied by a weakened KLH response, indicating that AIM2 deficiency suppressed the antigen-induced B-cell immune response by downregulating the expression of CD44. CD44, a surface marker of T-cell activation and memory, was overexpressed in T cells of SLE patients, but its roles and mechanism in B cells have not been elucidated. In the current work, we revealed that CD44 expression was upregulated in the B cells of SLE patients and MRL/lpr mice, accompanied by elevated AIM2 expression in CD19+CD44+ B-cell subsets, and that its ligand hyaluronan (HA) was also abnormally increased in the serum of SLE patients. Notably, the extrafollicular (EF) region serves as an important site of B-cell activation and differentiation separate from the germinal center, while CD44 expression is concentrated in EF B cells. In addition, in vitro experiments demonstrated that the HA-CD44 interaction stimulated B-cell activation and upregulated the expression of AIM2 and the transcription factor STAT3. Either blocking CD44, knocking down AIM2 expression or suppressing the activity of STAT3 in B cells suppressed B-cell activation and proliferation. Moreover, blocking CD44 downregulated the expression of STAT3 and AIM2, while suppressing the activity of STAT3 decreased the expression of CD44 and AIM2. In summary, overexpressed CD44 in B cells might participate in B-cell activation and proliferation in the EF region via the HA-CD44-AIM2 pathway, providing potential targets for SLE therapy.

Cryo-EM Structure and Functional Studies of EBNA1 Binding to the Family of Repeats and Dyad Symmetry Elements of Epstein-Barr Virus oriP.

Epstein-Barr nuclear antigen 1 (EBNA1) is a multifunctional viral-encoded DNA-binding protein essential for Epstein-Barr virus (EBV) DNA replication and episome maintenance. EBNA1 binds to two functionally distinct elements at the viral origin of plasmid replication (oriP), termed the dyad symmetry (DS) element, required for replication initiation and the family of repeats (FR) required for episome maintenance. Here, we determined the cryo-electron microscopy (cryo-EM) structure of the EBNA1 DNA binding domain (DBD) from amino acids (aa) 459 to 614 and its interaction with two tandem sites at the DS and FR. We found that EBNA1 induces a strong DNA bending angle in the DS, while the FR is more linear. The N-terminal arm of the DBD (aa 444 to 468) makes extensive contact with DNA as it wraps around the minor groove, with some conformational variation among EBNA1 monomers. Mutation of variable-contact residues K460 and K461 had only minor effects on DNA binding but had abrogated oriP-dependent DNA replication. We also observed that the AT-rich intervening DNA between EBNA1 binding sites in the FR can be occupied by the EBNA1 AT hook, N-terminal domain (NTD) aa 1 to 90 to form a Zn-dependent stable complex with EBNA1 DBD on a 2×FR DNA template. We propose a model showing EBNA1 DBD and NTD cobinding at the FR and suggest that this may contribute to the oligomerization of viral episomes important for maintenance during latent infection. IMPORTANCE EBV latent infection is causally linked to diverse cancers and autoimmune disorders. EBNA1 is the viral-encoded DNA binding protein required for episomal maintenance during latent infection and is consistently expressed in all EBV tumors. The interaction of EBNA1 with different genetic elements confers different viral functions, such as replication initiation at DS and chromosome tethering at FR. Here, we used cryo-EM to determine the structure of the EBNA1 DNA-binding domain (DBD) bound to two tandem sites at the DS and at the FR. We also show that the NTD of EBNA1 can interact with the AT-rich DNA sequence between tandem EBNA1 DBD binding sites in the FR. These results provide new information on the mechanism of EBNA1 DNA binding at DS and FR and suggest a higher-order oligomeric structure of EBNA1 bound to FR. Our findings have implications for targeting EBNA1 in EBV-associated disease.

Membrane skeleton modulates erythroid proteome remodeling and organelle clearance.

The final stages of mammalian erythropoiesis involve enucleation, membrane and proteome remodeling, and organelle clearance. Concomitantly, the erythroid membrane skeleton establishes a unique pseudohexagonal spectrin meshwork that is connected to the membrane through junctional complexes. The mechanism and signaling pathways involved in the coordination of these processes are unclear. The results of our study revealed an unexpected role of the membrane skeleton in the modulation of proteome remodeling and organelle clearance during the final stages of erythropoiesis. We found that diaphanous-related formin mDia2 is a master regulator of the integrity of the membrane skeleton through polymerization of actin protofilament in the junctional complex. The mDia2-deficient terminal erythroid cell contained a disorganized and rigid membrane skeleton that was ineffective in detaching the extruded nucleus. In addition, the disrupted skeleton failed to activate the endosomal sorting complex required for transport-III (ESCRT-III) complex, which led to a global defect in proteome remodeling, endolysosomal trafficking, and autophagic organelle clearance. Chmp5, a component of the ESCRT-III complex, is regulated by mDia2-dependent activation of the serum response factor and is essential for membrane remodeling and autophagosome-lysosome fusion. Mice with loss of Chmp5 in hematopoietic cells in vivo resembled the phenotypes in mDia2-knockout mice. Furthermore, overexpression of Chmp5 in mDia2-deficient hematopoietic stem and progenitor cells significantly restored terminal erythropoiesis in vivo. These findings reveal a formin-regulated signaling pathway that connects the membrane skeleton to proteome remodeling, enucleation, and organelle clearance during terminal erythropoiesis.

Optical gain at 1.55 µm of Er(TMHD)3 complex doped polymer waveguides based on the intramolecular energy transfer effect.

Based on the intramolecular energy transfer mechanism between organic ligand TMHD (2, 2, 6, 6-tetramethyl-3, 5-heptanedione) and central Er3+ ions, optical gains at 1.55 µm were demonstrated in three structures of polymer waveguides using complex Er(TMHD)3-doped polymethylmethacrylate (PMMA) as the active material. With the excitation of two low-power UV light-emitting diodes (LEDs) instead of 980 or 1480 nm lasers, relative gains of 3.5 and 4.1 dB cm-1 were achieved in a 1-cm-long rectangular waveguide with an active core of Er(TMHD)3-doped PMMA polymer. Meanwhile, relative gain of 3.0 dB cm-1 was obtained in an evanescent-field waveguide with cross-section of 4 × 4 µm2 using passive SU-8 polymer as core and a ∼1-µm-thick Er(TMHD)3-doped PMMA as upper cladding. By growing a 100 nm thick aluminum mirror and active lower cladding, the optical gain was doubled to 6.7 dB cm-1 in evanescent-field waveguides because of the stimulated excitation of Er3+ ions in the upper and lower cladding and the improved absorption efficiency.

Improvement of optical properties of InGaN-based red multiple quantum wells.

The realization of red-emitting InGaN quantum well (QW) is a hot issue in current nitride semiconductor research. It has been shown that using a low-Indium (In)-content pre-well layer is an effective method to improve the crystal quality of red QWs. On the other hand, keeping uniform composition distribution at higher In content in red QWs is an urgent problem to be solved. In this work, the optical properties of blue pre-QW and red QWs with different well width and growth conditions are investigated by photoluminescence (PL). The results prove that the higher-In-content blue pre-QW is beneficial to effectively relieve the residual stress. Meanwhile, higher growth temperature and growth rate can improve the uniformity of In content and the crystal quality of red QWs, enhancing the PL emission intensity. Possible physical process of stress evolution and the model of In fluctuation in the subsequent red QW are discussed. This study provides a useful reference for the development of InGaN-based red emission materials and devices.

Two-step spin coating CsPbBr3 thin films and photodetectors in the atmosphere.

Recently, inorganic halide perovskites, especially CsPbBr3, have been attracting attention because of their high efficiency, wide color gamut, and narrow luminescent spectrum. To elevate the perovskite devices' performance, optimizations of crystalline quality, device structures, and fabrication process are essential. Currently, the state-of-the-art fabrication approach of CsPbBr3 is spin-coating in an inert environment (nitrogen, argon, etc.), which requires temperature and humidity control. In this work, a CsPbBr3-based visible photodetector (PD) is realized in a humid atmosphere, whose performances were comparable to those reported in an inert glovebox. The dependencies of responsivity and transient time on CsBr coating layer numbers and electrode period were also investigated. The best device performance was obtained with 4 layers of CsBr coating with a responsivity of 107.2 mA/W, detectivity of 4.29 × 1010 Jones, and quantum efficiency of 25.4%. The rise time of the 3-4-layer CsBr-coated PD was reduced by the higher crystalline quality and carrier mobility, while the decay time of the 1-layer CsBr-coated PD was faster since the dense defect induced non-radiative recombination centers. With the period T increasing, the responsivity decreased, while the transient times increased. We believe that our results could benefit the future optimization of perovskite materials and PDs.

Flexible GaN-based ultraviolet microdisk lasers on PET substrate.

Flexible optoelectronics is a technique for fabricating optoelectronic devices on a flexible substrate. Compared with conventional devices, flexible optoelectronic devices can be used in more complex working environments benefiting from the mechanical flexibility. Herein, for the first time to the best of our knowledge, a flexible GaN-based microdisk laser on a polyethylene terephthalate (PET) substrate in the ultraviolet A (UVA) range was demonstrated by using thin film transfer process based on laser lift-off (LLO). The lasing wavelength is 370.5 nm with a linewidth of 0.15 nm and a threshold power density of 200 kW/cm2. Additionally, a distributed Bragg reflector (DBR) was deposited on the backside of the microdisk as the bottom mirror between GaN microdisk and PET substrate, which can provide better mode confinement inside the microdisk and increases the oscillation intensity. The lasing wavelength of the flexible laser shows a 2-nm redshift under different bending curvature of the substrate, which is promising for applications such as mechanical sensing.

Current spreading structure of GaN-based vertical-cavity surface-emitting lasers.

Indium tin oxide (ITO) is often used as a current spreading layer in the GaN-based vertical-cavity surface-emitting lasers (VCSELs). However, the absorption coefficient of ITO is significant, which reduces the laser output power, raises the threshold, and makes VCSELs hardly lase in the ultraviolet range. To find a transparent conductive structure that can replace ITO, we propose a periodic p-AlGaN/u-GaN/p-GaN structure. In the simulation of light-emitting diodes, the optimized parameter is obtained with multi-period 10 nm p-Al0.1Ga0.9N/2 nm u-GaN/8 nm p-GaN combined with n-GaN/n-Al0.2Ga0.8N in the n region. Applying the structure to 435 nm VCSELs and comparing it to a common VCSEL with the ITO current spreading layer, it can be found that the new structure reduces the threshold from 9.17 to 3.06 kA/cm2. The laser power increases from 1.33 to 15.4 mW. The optimized structure has a high laser power and a lower threshold, which can be used in future investigations.

Linking Transthyretin-Binding Chemicals and Free Thyroid Hormones: In Vitro to In Vivo Extrapolation Based on a Competitive Binding Model.

Large numbers of pollutants competitively inhibit the binding between thyroid hormones and transthyretin (TTR) in vitro. However, the impact of this unintended binding on free thyroid hormones in vivo has not yet been characterized. Herein, we established a quantitative in vitro to in vivo extrapolation (QIVIVE) method based on a competitive binding model to quantify the effect of TTR-binding chemicals on free thyroid hormones in human blood. Twenty-five TTR-binding chemicals including 6 hydroxyl polybromodiphenyl ethers (OH-PDBEs), 6 hydroxyl polychlorobiphenyls (OH-PCBs), 4 halogenphenols, 5 per- and polyfluorinated substances (PFASs), and 4 phenols were selected for investigation. Incorporating the in vitro binding parameters and human exposure data, the QIVIVE model could well predict the in vivo effect on free thyroid hormones. Co-exposure to twenty-five typical TTR-binding chemicals resulted in median increases of 0.080 and 0.060% in circulating levels of free thyroxine (FT4) and free triiodothyronine (FT3) in the general population. Individuals with occupational exposure to TTR-binding chemicals suffered 1.88-32.2% increases in free thyroid hormone levels. This study provides a quantitative tool to evaluate the thyroid-disrupting risks of TTR-binding chemicals and proposes a new framework for assessing the in vivo effects of chemical exposures on endogenous molecules.

Genome of the parasitoid wasp Cotesia chilonis sheds light on amino acid resource exploitation.

BACKGROUND: A fundamental feature of parasitism is the nutritional exploitation of host organisms by their parasites. Parasitoid wasps lay eggs on arthropod hosts, exploiting them for nutrition to support larval development by using diverse effectors aimed at regulating host metabolism. However, the genetic components and molecular mechanisms at the basis of such exploitation, especially the utilization of host amino acid resources, remain largely unknown. To address this question, here, we present a chromosome-level genome assembly of the parasitoid wasp Cotesia chilonis and reconstruct its amino acid biosynthetic pathway. RESULTS: Analyses of the amino acid synthetic pathway indicate that C. chilonis lost the ability to synthesize ten amino acids, which was confirmed by feeding experiments with amino acid-depleted media. Of the ten pathways, nine are known to have been lost in the common ancestor of animals. We find that the ability to synthesize arginine was also lost in C. chilonis because of the absence of two key genes in the arginine synthesis pathway. Further analyses of the genomes of 72 arthropods species show that the loss of arginine synthesis is common in arthropods. Metabolomic analyses by UPLC-MS/MS reveal that the temporal concentrations of arginine, serine, tyrosine, and alanine are significantly higher in host (Chilo suppressalis) hemolymph at 3 days after parasitism, whereas the temporal levels of 5-hydroxylysine, glutamic acid, methionine, and lysine are significantly lower. We sequence the transcriptomes of a parasitized host and non-parasitized control. Differential gene expression analyses using these transcriptomes indicate that parasitoid wasps inhibit amino acid utilization and activate protein degradation in the host, likely resulting in the increase of amino acid content in host hemolymph. CONCLUSIONS: We sequenced the genome of a parasitoid wasp, C. chilonis, and revealed the features of trait loss in amino acid biosynthesis. Our work provides new insights into amino acid exploitation by parasitoid wasps, and this knowledge can specifically be used to design parasitoid artificial diets that potentially benefit mass rearing of parasitoids for pest control.

Regulated Ion/Electron-Conducting Interphase Enables Stable Zinc-Metal Anodes for Aqueous Zinc-Ions Batteries.

Metallic Zinc (Zn) is considered as a remarkably promising anode for aqueous Zn-ion batteries due to its high volumetric capacity and low redox potential. Unfortunately, dendritic growth and severe side reactions destabilizes the electrode/electrolyte interface, and ultimately reduce the electrochemical performance. Here, an artificial protective layer (APL) with a regulated ion and electron-conducting interphase is constructed on the Zn-metal anode to provide excellent interfacial stability in high-rate cycling. The superior ionic and moderate electronic conductivity of the APL derives from the co-embedding of MXene and Zn(CF3 SO3 )2 salts into the polyvinyl alcohol hydrogel, which enables a synergistic effect of local current density reduction during plating and ion transport acceleration during stripping for Zn anode. Furthermore, the high Young's modulus of the protective layer and dendrite-free deposition morphology during cycling suppresses hydrogen evolution reactions (2.5 mmol h-1 cm-2 ) and passivation. As a result, in symmetrical cell tests, the modified battery presents a stable life of over 2000 cycles at ultra-high current density of 20 mA cm-2 . This research presents a new insight into the formation and regulation of stable electrode-electrolyte interface for the Zn-metal anode.