Biology subjects

Zhu, P.

Publications and source records attributed to Zhu, P..

At least 19 recordsLinked to original sources

bioRxiv2026

mtDNA Activates AIM2-Mediated PANoptosis in Interstitial Macrophages to Promote Immune Checkpoint Inhibitor Pneumonitis

Immune checkpoint inhibitor pneumonitis (CIP) is a serious immune-related adverse event, yet its mechanisms remain unclear. Using a mouse model of anti-PD-1-induced CIP, we show that PD-1 blockade induces pulmonary inflammation and dysfunction, accompanied by accumulation of lung interstitial macrophages (IMs) and PANoptosis, preferentially in IMs rather than alveolar macrophages. Anti-PD-1 also causes mitochondrial stress and cytosolic mtDNA accumulation. AIM2 deficiency attenuates pulmonary inflammation, IM accumulation, and PANoptosis-associated signaling; NLRP3 or GSDMD deficiency similarly reduces inflammation and PANoptotic responses. In macrophages, TNF- plus IFN-{gamma} induces mitochondrial dysfunction and cytosolic mtDNA accumulation, and mtDNA amplifies cytokine-induced cell death and caspase-1/GSDMD activation, which is abolished by AIM2 deficiency. Thus, AIM2-mediated PANoptosis in lung IMs drives CIP, and mtDNA-associated innate immune signaling amplifies inflammatory macrophage death during CIP.

immunology↗

bioRxiv2026

A fast 2C-induction method reveals a barrier role of SP2 for totipotency

The acquisition of totipotency in vitro remains a major challenge, limiting our understanding of early embryogenesis and its clinical and translational applications. Here, we reported a robust and rapid chemical reprogramming system that converts mouse embryonic stem cells (mESCs) into totipotent-like cells (TLCs) within 36 hours, with efficiencies exceeding 70%. The induced cells exhibit transcriptomic, epigenomic, and functional features closely resembling 2-cell (2C) stage embryos, as confirmed by scRNA-seq, ATAC-seq, and chimeric embryo analyses. Single-cell trajectory construction revealed a branching reprogramming process that yields both successful totipotent-like and alternative, non-reprogrammed fates. Mechanistically, we identified the transcription factor SP2 as a barrier to totipotency acquisition, promoting lineage-specific gene expression while repressing totipotency networks. Collectively, our study has established a highly efficient in vitro model for totipotency induction and highlighted molecular barriers shaping cell fate decisions, providing a platform to dissect the mechanisms governing the pluripotency-to-totipotency transition.

developmental biology↗

bioRxiv2026

Ecosystem disservices are underrepresented in literature on annual crop agroecosystems

Maximising ecosystem service (ES) benefits while minimising ecosystem disservices (EDS) is essential for ecological intensification in annual crop systems. Yet ecosystem disservices are often underreported in the scientific literature, potentially biasing how agroecosystem functioning is understood. To test this, we built a predicted network of plausible links between ecosystem service providers (taxa or functional groups that can deliver ecosystem services or disservices), and the ES or EDS they may provide. We then compared this with a realised network based on systematic Scopus searches of annual crop literature. The predicted network contained 47 nodes and 103 links, whereas the realised network contained 33 nodes and 58 links, representing declines of 29.8% in nodes and 43.7% in links. Overall connectivity declined, especially for highly connected nodes, and four of the nine predicted disservice nodes were absent from the literature. ES links were more likely to be documented than EDS links, and EDS links were three times more likely to be absent. Across all links, ES were reported in 6.6 times more papers than EDS. Projected networks, which map indirect connections by linking ES directly to EDS if they share common providers, showed that these bundled interactions were strongly reduced, obscuring multifunctionality and trade-offs. This systematic underrepresentation of EDS, reflecting a cognitive bias, can inflate perceived benefits, distort the evaluation of key taxa and interactions, and create unrealistic expectations about intervention outcomes in biological crop protection. Addressing EDS alongside ES is therefore essential for more balanced assessments of crop-system management and better-informed decisions.

ecology↗

bioRxiv2026

Mechano-Initiated PIEZO1-VEGFR2 Interaction Governs CD34+ Cell Differentiation and Repair in Arteriovenous Fistula

BackgroundEndothelial cell (EC) injury induced by disturbed flow drives neointimal hyperplasia in arteriovenous fistulas (AVFs), where CD34+ cell-mediated repair may be involved. PIEZO1 and VEGFR2 are important mechanosensors with critical role in maintaining endothelial function. However, whether PIEZO1 interacts with VEGFR2 during CD34+ cell differentiation to orchestrate the vascular repair remains unknown. MethodsAVF model was established in several mouse strains. Single cell RNA sequencing was performed for human and mouse samples. Cd34-CreERT2; R26-tdTomato; Piezo1flox/flox mice were used to investigate the effect of Piezo1 deletion on endothelial repair in AVFs. CD34-high human umbilical vein ECs (CD34high HUVECs) was sorted and exposed to different flow patterns to determine the role of shear stress in CD34high cell differentiation. Co-immunoprecipitation, proximal ligation assay and complementary approaches were performed to delineate mechanotransduction initiated by PIEZO1-VEGFR2 interaction. ResultsSingle cell RNA sequencing and immunostaining showed abundant CD34high cells in the vessel wall of AVFs in humans and animal models. Exposure of CD34high HUVECs to different flow patterns showed that laminar shear stress downregulated CD34 while upregulating VE-cadherin and claudin-5 expression. In contrast, oscillatory flow produced the opposite effects, indicating impaired endothelial maturation. PIEZO1 knockdown in CD34high HUVECs attenuated shear stress-induced endothelial marker expression. In Cd34 conditional Piezo1 knockout mouse model of AVF, we observed decreased number of CD34-derived cells, more compact cellular arrangement, and attenuated neointimal hyperplasia. Mechanistically, we found PIEZO1 interacts with VEGFR2, thereby mediating the distinct effects of laminar and oscillatory shear stress on AKT-FoxO1 axis, which critically regulates endothelial marker expression. Furthermore, pharmacological activation of AKT signaling in AVF mouse model enhanced CD34+ cell-mediated endothelial repair and attenuated neointimal hyperplasia. ConclusionPIEZO1-VEGFR2 complex-mediated mechanotransduction plays a key role in regulating CD34+ cell-derived endothelial repair in AVFs via AKT-FoxO1 axis. AKT activation enhances endothelial maturation, thereby attenuating neointimal hyperplasia in AVFs. Novelty and SignificanceO_ST_ABSWhat Is Known?C_ST_ABSO_LIIn arteriovenous fistulas (AVFs), abnormal shear stress induces endothelial cell injury, and the resulting neointimal hyperplasia is a major cause of anastomotic stenosis. C_LIO_LICD34 cells actively participate in vascular endothelial repair. C_LIO_LIPIEZO1 is a mechanoreceptor mediating endothelial sensing of hemodynamic shear stress, contributing to the maintenance of atheroprotective endothelial phenotype under laminar shear stress, whereas its activation induces pro-inflammatory effects under disturbed shear stress. C_LI What New Information Does This Article Contribute?O_LICD34 cells participate in repairing endothelial injury induced by abnormal shear stress in AVFs. PIEZO1 knockout in CD34+ cells improve endothelial repair and attenuates neointimal hyperplasia in AVF. C_LIO_LILaminar shear stress induces CD34 downregulation and upregulates VE-cadherin and claudin-5 expression in CD34-high human umbilical vein endothelial cells, whereas oscillatory shear stress upregulates CD34 expression and suppresses VE-cadherin and claudin-5 expression. C_LIO_LIMechano-stimuli lead to PIEZO1-VEGFR2 complex formation regulating CD34 cell-mediated endothelial repair through the downstream AKT-FoxO1 axis. C_LI Abnormal hemodynamic shear stress-induced endothelial injury initiates neointimal hyperplasia in AVFs. The present study identifies PIEZO1 as a key mechanosensor that regulates CD34+ cell-derived endothelial repair in response to distinct blood flow patterns. PIEZO1 promotes CD34+ cell differentiation into mature ECs for endothelial repair under laminar shear stress, whereas it disrupts the differentiation of CD34+ cells into mature endothelium under oscillatory shear stress. Mechanistically, a novel shear stress-sensing complex comprising PIEZO1 and VEGFR2 was identified in regulating flow-induced differentiation of CD34+ cells into mature ECs via the AKT-FoxO1 signaling axis, thereby controlling the expression of endothelial maturation markers VE-Cadherin and Claudin-5. These findings define a novel PIEZO1-VEGFR2 mechanotransduction axis in CD34+ cell-mediated endothelial repair and support AKT pathway activation as a potential therapeutic strategy against neointimal hyperplasia in AVFs.

cell biology↗

bioRxiv2026

Visualization of the architecture of flexible chromatin and the binding of chromatin regulators

Chromatin organization plays a central role in regulating genome accessibility and gene expression in eukaryotic cells. However, the inherent flexibility and structural heterogeneity of chromatin pose significant challenges for its structure determination. Here, we use a Nuc-back strategy with cryo-electron tomography (cryo-ET) and subtomogram averaging methods to visualize chromatin at the nucleosome level by averaging nucleosome at moderate-to-high resolution, classifying the fundamental unit of chromatin, i.e., nucleosome, into distinct classes, and linking different nucleosome structures to chromatin architecture. We reveal that nucleosome heterogeneity is a key factor in chromatin flexibility which disrupts interactions between nucleosomes. In addition, this strategy allows for the localization and visualization of chromatin regulators and their structure on chromatin. These results provide a foundation for future research in 3D genome and epigenetic process visualization. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=82 SRC="FIGDIR/small/730377v1_ufig1.gif" ALT="Figure 1"> View larger version (23K): org.highwire.dtl.DTLVardef@1b003c8org.highwire.dtl.DTLVardef@c86543org.highwire.dtl.DTLVardef@7033f5org.highwire.dtl.DTLVardef@635485_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗

bioRxiv2026

Presenilin 1 (PS1) located at mitochondrial inner membrane regulates mitochondrial cristae junction proteins arrangement and cristae formation in HEK293 cells

Presenilin 1 (PS1), a key pathogenic factor in familial Alzheimers disease, is implicated in regulation of mitochondrial functions, yet its precise sub-mitochondrial localization and underlying mechanisms remain poorly understood. In this study, we generated PS1 knockout (PS1 KO) cell lines to investigate the role of PS1 in mitochondrial structure and function. Our results demonstrated that PS1 is directly localized to the mitochondrial inner membrane. PS1 deficiency led to reduced ATP production, impaired mitochondrial respiration capacity, decreased mitochondrial membrane potential, disrupted Ca2+ homeostasis, and elevated reactive oxygen species (ROS) accumulation. Moreover, loss of PS1 caused abnormal mitochondrial cristae structure. Further analysis revealed that PS1 interacts with mitochondrial inner membrane proteins. Its absence promotes ATAD3A oligomerization and disrupts its arrangement at mitochondrial cristae junctions, leading to expansion of the mitochondria-associated membrane (MAM) and instability of mitochondrial DNA (mtDNA). Our findings demonstrate that PS1 acts as a central regulator of mitochondrial cristae morphogenesis by modulating protein interaction networks at cristae junctions, thereby illuminating fundamental molecular mechanisms contributing to mitochondrial dysfunctions in Alzheimers disease.

cell biology↗

bioRxiv2026

Histology-Aware Graph for Modeling Intercellular Communication in Spatial Transcriptomics

Cell-cell communication (CCC) is essential to how life forms and functions. Recent tools achieve single-cell-resolved CCC inference utilizing spatial transcriptomics (ST). However, most ignore the modeling of tissue contexts surrounding cells, causing high false-positive/negative rates. Here, we propose HARMONIC, a CCC inference method integrating multimodal ST and hematoxylin and eosin (H&E)-stained images. HARMONIC causally modeling the transcriptomic-to-contextual relationships for CCC inference. The state-of-the-art performance was verified across ST platforms, species and healthy/diseased status, on both synthetic and biological samples. HARMONIC was applied in various real-world scenarios, especially on tissues with clear morphological boundaries, including cortical layers in mouse brain, medullary-cortex structures in mouse kidney, as well as tumor-stromal/immune interface. Significant refinement of false-positive/negative predictions was observed compared to ST-only CCC tools.

bioinformatics↗

bioRxiv2026

Fungal volatiles drive lifestyle-dependent, systemic metabolic reprogramming in poplar

O_LIRationale: Although trees encounter diverse fungal communities, it is unclear how they adjust their physiology in response to fungal ecological strategies before physical contact. We tested whether volatile organic compounds (VOCs) emitted by fungi are sufficient to induce systemic, lifestyle-consistent metabolic states in poplar roots and leaves. C_LIO_LIMethods: Populus x canescens roots were exposed to VOCs from a pathogen (Heterobasidion annosum), a saprotroph (Postia placenta) or an ectomycorrhizal mutualist (Laccaria bicolor) for six weeks in a contact-free pot-in-pot system. Untargeted LC-MS metabolomics characterized VOC-induced metabolic reprogramming in roots and leaves. C_LIO_LIKey results: Fungal VOC exposure alone reconfigured the metabolomes of roots and leaves, with strong discrimination between treatments despite belowground exposure. Poplar revealed a shared VOC-responsive component, but also fungus-specific programmes: pathogen VOCs produced a suppression-dominated systemic phenotype; saprotroph VOCs promoted lipid-centred metabolic activation; and mutualist VOCs elicited restrained, compatibility-consistent shifts with targeted pathway modulation. C_LIO_LIMain conclusion: Volatile-mediated surveillance allows trees to anticipate fungal lifestyle-associated cues and adjust systemic metabolism before physical contact occurs. This links airborne fungal cues to whole-plant physiological configuration and extends plant-fungal recognition beyond contact-dependent mechanisms. C_LI One-sentence summaryVolatile-mediated surveillance allows trees to anticipate fungal lifestyle and adjust systemic metabolism before physical contact occurs.

plant biology↗

bioRxiv2026

EOLA1, a novel mitochondria-localized protein critical for heart functions via regulating mitochondrial translation

Mitochondria possess their own mRNA translation system, mediated by specialized mitoribosomes. Dysregulation of mitochondrial translation disrupts metabolic homeostasis and is linked to various pathologies, including metabolic syndromes, neurological disorders, and cardiac diseases. Using CRISPR/Cas9 screening, we identified EOLA1 (endothelial-overexpressed lipopolysaccharide-associated factor 1) as a novel mitochondrial matrix protein essential for metabolic homeostasis. Knockout of Eola1 severely affects mitochondrial translation and consequently the oxidative phosphorylation in mammalian cells. Mechanistically, EOLA1 physically interacts with mitochondrial 12S ribosomal RNA (12S mt-rRNA) and the mitochondrial Tu translation elongation factor (TUFM), facilitating efficient translation elongation of mitochondrial-encoded mRNAs. Furthermore, genetic ablation of Eola1 in mice induced severe cardiac dysfunction, demonstrating its indispensable role in maintaining heart function through mitochondrial translation control. Together, our findings establish EOLA1 as a key regulator of mitochondrial translation via its interactions with 12S mt-rRNA and TUFM, highlighting its importance in cellular metabolism and a potential role in cardiac disease pathogenesis.

molecular biology↗

bioRxiv2025

A Foundational Generative Model for Cross-platform Unified Enhancement of Spatial Transcriptomics

Spatial transcriptomics (ST) platforms are limited by spatial resolution, sensitivity to low expression levels, alignment with tissue structures, and the balance across tissue complexity. Computational enhancement typically targets a single challenge, e.g., super-resolution using hematoxylin and eosin (H&E) images or sensitivity enhancement with single-cell RNA sequencing (scRNA-seq). However, most ignore the interdependence across challenges, yielding biologically inconsistent enhancement. Here we introduce FOCUS, a foundational generative model for unified ST enhancement, conditioned on H&E images, scRNA-seq references, and spatial co-expression priors. With large-scale pretrained encoders, FOCUS uses a modular design for multimodal integration and a cross-challenge coordination strategy to target co-occurring challenges, enabling joint optimization. FOCUS was trained and comprehensively benchmarked on >1.7 million H&E-ST pairs and >5.8 million single-cell profiles, demonstrating state-of-the-art performance across ten ST platforms, on both individual and coupled challenges. The real-world utility and generalizability were validated on a rare suprasellar tumor, papillary craniopharyngioma, and an unseen ST platform (Open-ST) for primary and metastatic head and neck squamous cell carcinoma.

bioengineering↗

bioRxiv2025

6mA demethylase Mi-NMAD-1 modulates nematode development and parasitism through the transcription factor Mi-nhr-118

N6-methyladenine (6mA) DNA methylation has emerged as an important epigenetic mark in eukaryotes, but its biological role in plant-parasitic nematodes remains largely unexplored. Here, we demonstrate that 6mA methylation is essential for the embryonic development and parasitic ability of Meloidogyne incognita. Silencing of the 6mA demethylase genes minmad-1 significantly reduced egg hatching, revealing that 6mA-mediated regulation is required for nematode development. Transcriptome analyses showed that minmad-1 knockdown downregulated genes involved in embryogenesis, RNA biosynthesis, and cell differentiation, suggesting a critical role of 6mA in developmental gene regulation. Among the transcription factors affected by minmad-1 silencing, Mi-nhr-118, a nuclear hormone receptor orthologous to C. elegans nhr-118, was identified as a key regulator of embryonic development. Functional assays confirmed that RNAi or host-induced gene silencing (HIGS) of Mi-nhr-118 led to developmental arrest, reduced gall and egg mass formation, and impaired infectivity across multiple Meloidogyne species. ChIP-seq analysis revealed that Mi-nhr-118 directly binds to promoters of genes associated with cellular regulation and developmental signaling. Several downstream targets, including transcription factors (Mi_23621.1, Mi_39647.1) and genes implicated in metabolic and signaling processes (Mi_03067.1, Mi_08398.1), were shown to be essential for both embryogenesis and parasitism. Functional enrichment analyses of Mi-nhr-118 target genes indicated suppression of immune-related signaling, carbohydrate recognition, and glycoprotein biosynthetic pathways following gene silencing. Collectively, these findings establish Mi-nhr-118 as a central regulator linking 6mA-mediated epigenetic control to development and parasitism in M. incognita.

molecular biology↗

bioRxiv2025

The cloacal outgrowth orchestrates co-development of the bladder and umbilical arteries

The urinary bladder is an innovation of eutherian mammals to manage liquid wastes. However, bladder development and its embryonic function remain poorly understood. Here, we report that in both humans and mice the bladder emerges from the cloaca as the rostral outgrowth, which is flanked by the umbilical arteries. Arrest of the outgrowth, as seen in Shh-null mouse embryos, causes bladder agenesis and unexpected severe defect of the umbilical arteries, suggesting that the outgrowth epithelial signal Shh coordinates development of both the bladder and umbilical arteries. Wnt2 signaling molecule is restricted to the rostral outgrowth mesenchyme; and its expression is dramatically down-regulated in Shh-null mutants. Furthermore, Wnt2-null mutants develop small bladder and single umbilical artery defects. Findings here uncover an unexpected co-development mechanism of the bladder and umbilical arteries orchestrated by the cloacal outgrowth signals. The co-development paradigm offers a conceptual framework to understand evolution and development of the bladder. Significance StatementThe urinary bladder is found in the eutherian mammals but largely absent from other vertebrates. Innovation of the bladder has been viewed as a necessity to manage liquid metabolic wastes on dry land. In this study, we report that the bladder emerges from the rostral outgrowth of the cloaca. We also report an unexpected developmental link between the bladder and umbilical arteries and, demonstrate that their co-development is orchestrated by the outgrowth epithelial signal Shh and mesenchymal signal Wnt2. Findings here highlight a possibility that, in addition to managing metabolic wastes, normal bladder development is required for growth of mammalian embryos by supporting development of the umbilical arteries.

developmental biology↗

bioRxiv2025

Global Mapping of circRNA-Target RNA Interactions Reveals P-Body-Mediated Translational Repression

Circular RNAs (circRNAs) are primarily produced through pre-mRNA back-splicing, yet their target repertoire and functional mechanisms remain elusive. Here, we present circTargetMap, a computational framework for globally mapping circRNA targets using RNA-RNA interactomes obtained via RNA in situ conformation sequencing (RIC-seq) in the hippocampus and ten human cell lines. This approach identified 117,163 high-confidence circRNA-target RNA interactions, with 83% of target mRNAs bound by multiple circRNAs. Functionally, CDR1as and circRMST repress target mRNA translation by sequestering them into processing bodies (P-bodies)--membraneless granules--through sequence-specific base-pairing, probably independent of AGO2, DICER, and miRNAs. To directly capture granule-associated interactions, we developed granule RIC-seq (GRIC-seq) method, revealing the broad role of circRNA-target RNA interactions in translational repression. Moreover, pathogenic variants are significantly enriched around circRNA-target RNA interaction sites, suggesting potential roles in disease. Our study provides valuable resources for circRNA functional exploration and a framework for investigating RNA-RNA interactions within membraneless organelles.

molecular biology↗

bioRxiv2025

Volatile cues from pathogenic, mutualistic and saprotrophic fungi cause specific, fungus-dependent responses in poplar

Plants are exposed to complex interactions with belowground organisms, yet how they differentiate between mutualistic and pathogenic fungi before physical contact remains largely unknown. We exposed the roots of young Populus x canescens to volatile organic compounds (VOCs) emitted by either a pathogenic (Heterobasidion annosum), a saprotrophic (Postia placenta), or an ectomycorrhizal (Laccaria bicolor) fungus. VOC analysis of the shared rhizosphere headspace and leaf emissions revealed that poplar plants could perceive and respond to fungal identity solely through airborne cues. The root-zone headspace contained fungus-specific sesquiterpene fingerprints that remained similar after three and six weeks of co-cultivation: Pathogen-derived VOCs induced constant high sesquiterpene emissions from the root-zone, whereas mycorrhiza caused low but targeted emissions of specific sesquiterpenes. In contrast, saprotrophic VOCs caused a temporal shift in root-zone VOC pattern, with increased sesquiterpene emissions after six weeks. Fungal VOC exposure also altered leaf VOC emissions, enriching alkanes, esters and monoterpenes. Initially, leaf VOC emissions were fungal lifestyle-specific but they converged over time, indicating systemic signal integration of belowground signals. These findings demonstrate that trees can discriminate "friend-versus-foe" through VOCs alone, extending pattern-recognition theory beyond contact-dependent cues. Multivariate analyses suggested organ-specific chemical strategies: roots function as chemosensors decoding fungal volatilomes, while systemic adjustments shape aboveground VOC profiles. Understanding the plant response to fungal VOCs may offer potential for developing early pathogen diagnostics and further elucidate the volatile-mediated plant-fungal interactions.

plant biology↗

bioRxiv2025

Heme drives cardiac endothelial senescence in sepsis via STING activation

Sepsis-induced cardiac dysfunction is a major contributor to sepsis-related mortality, and many patients continue to experience long-term cardiac complications after recovery. Here, we demonstrate that cardiac senescence is a key feature of sepsis-associated cardiac dysfunction, with endothelial cells identified as the predominant senescent population in septic cardiac tissue. Yet, the pathogenic drivers of endothelial senescence in sepsis remain poorly characterized. Among potential mediators, we found that elevated levels of heme, a byproduct of hemolysis, strongly correlate with increased endothelial senescence and impaired cardiac function. Mechanistic studies revealed that heme acts as a novel ligand for STING, exacerbating bacterial infection induced STING polymerization and activation, thereby promoting endothelial senescence. Notably, either STING inhibition or enhanced heme clearance via increased hemopexin expression significantly alleviated cardiac endothelial senescence and facilitated cardiac functional recovery in septic mice. These findings identify heme as a critical pathogenic driver of endothelial senescence and highlight heme clearance as a promising therapeutic strategy for mitigating sepsis induced cardiac dysfunction.

cell biology↗

bioRxiv2025

Cryo-ET Analysis Unveils the Minimum Structural Unit and Hierarchical Ultrastructure of Silk Fibers in Silkworm and Spider

Silkworm silk and spider silk are renowned for their exceptional mechanical properties, with the toughness of spider dragline silk exceeding that of silkworm silk and even outperforming high-performance synthetic fibers such as Kevlar and nylon. The mechanical properties of silk fibers are determined by their ultrastructure, including the size, morphology, and arrangement of their fundamental structural units. In this study, we employed the state-of-the-art cryo-electron tomography to investigate the in situ ultrastructure of silkworm silk, spider silk, and artificial silk. Our findings reveal that the fundamental structural unit of silkworm silk is a nanofibril approximately 3.6 nm in diameter, connected by numerous bridges, representing the smallest structural unit currently observable. These nanofibrils are aligned parallel to the fiber axis and organized into a herringbone pattern oriented in a specific direction. Multiple layers of this herringbone pattern stack together to form the final micron-scale fiber. In spider silk, a dense structure featuring nanofibrils is clearly visible, with their long axes tightly aligned parallel to the flow direction, leaving no discernible gaps. By contrast, silkworm silk exhibits larger, regionally varying gaps between nanofibrils, while artificial silk lacks the highly ordered arrangement characteristic of natural silks. Our study provides new insights into silk formation and offers valuable principles for designing ultrastrong silk.

biophysics↗

bioRxiv2025

Volatile-Mediated Plant Defense Networks: Field Evidence for Isoprene as a Short-Distance Immune Signal

Isoprene, the most abundant hydrocarbon emitted by vegetation, protects photosynthesis against oxidative and thermal stress and significantly impacts atmospheric chemistry. While laboratory studies suggest a role for isoprene in plant defense, its function in plant-plant communication under natural conditions remains unclear. Here, we demonstrate that isoprene acts as a signaling molecule, triggering systemic immune responses in neighboring plants against bacterial pathogens under field conditions. We established an experimental system using wild-type and transgenic silver birch (Betula pendula) lines engineered to emit varying levels of isoprene. Over two growing seasons, we examined the effects of birch-emitted volatile organic compounds on neighboring Arabidopsis thaliana, including wild-type and immune signaling mutants (llp1: legume lectin-like protein 1; jar1: jasmonate resistant 1). Isoprene emission rates positively correlated with systemic resistance in receiver plants, with higher emissions enhancing inhibition of Pseudomonas syringae growth. This immune response occurred independently of jasmonate signaling but required functional LLP1, suggesting a specific recognition pathway. By combining Arabidopsis mutant responses with birch volatile profiles, we confirmed that isoprene, rather than other terpenoids, mediates this effect. These findings reveal an unrecognized ecological function of isoprene as an airborne immune signal, establishing transgenic birch as a robust model for studying volatile-mediated plant defense networks in natural environments. Our results provide new insights into the molecular mechanisms underlying plant volatile perception and expand our understanding of chemical communication in terrestrial ecosystems. Significance StatementIsoprene, the most abundant volatile organic compound released by plants, protects against abiotic stress. Here, we demonstrate that isoprene also functions under ambient atmosphere as a short-distance immune signal, enhancing neighboring plants resistance to bacterial pathogens. This finding reveals a putative ecological role of isoprene in plant defense networks and suggests strategies for sustainable agriculture and forest management under environmental stress.

plant biology↗

bioRxiv2025

Insights into the spool-like architecture and infectionstrategy of the archaeal virus SEV1

Archaeal viruses are well known for their diverse morphologies and extreme stability. In this study, we used cryo-electron tomography to analyze the structure of SEV1 and its infection strategies in its native state. The results show that SEV1 nucleocapsid adopts a coil-stacking architecture which displays a degree of flexibility. VP4, whose homologues are widespread in the thermo-acidic environment globally, is identified as the major capsid protein and binds genomic DNA forming a "beads-on-a-string" arrangement. Simulations in various extreme environments indicate that the envelope of SEV1 is crucial to the thermostability. SEV1 infects the host by membrane fusion revealed by the membrane fusion assay. The infected cell undergoes cytoplasm condensation to form a "viral factory", leading to the successive production of nascent virions. A series of assembly intermediates of SEV1 are identified revealing an integrated picture of the virus assembly process. The nascent virions are found to be released through virus-associated pyramids (VAPs), composed of unique proteins encoded by SEV1 distinct from other known VAP proteins. Our study provides novel insights to the survival strategies of SEV1, a flexible and enveloped archaeal virus, by using the unique "coil-stacking" architecture and the characteristic infection strategies.

microbiology↗