Biology subjects

Liang, Q.

Publications and source records attributed to Liang, Q..

At least 19 recordsLinked to original sources

bioRxiv2026

Multimodal Connectome Markers of Disruptive Behavior Problems in Youth: Distinct Patterns of Concurrent Severity and Prospective Symptom Change

Disruptive behaviors problems, such as irritability/anger and maladaptive aggression, are associated with altered connectivity across networks supporting emotion regulation. However, multimodal connectome markers of concurrent severity and prospective symptom change, including sex-specific patterns, remain unclear. Using a large, sex-balanced sample from the Adolescent Brain Cognitive Development (ABCD) Study, we applied multimodal connectome-based predictive modelling (CPM) to test whether resting-state functional (n = 7,556; 49.3% female) and structural (N = 8,978; 48.4%) connectivity predicted baseline disruptive behavior severity (at ages 9-10) and 2-year symptom change (from ages 9-10 to 11-12). Models were adjusted for covariates, permutation-tested, and FDR corrected. Secondary analyses tested sex-stratified models separately in males and females. In models emerging as significant, follow-up analyses tested for distinct vs shared predictive edges. Functional and structural connectomes predicted baseline severity ({rho} = 0.087 and {rho} = 0.071, respectively). Functional connectivity also predicted prospective symptom change ({rho} = 0.038), whereas prospective structural prediction was predominately with negative edges ({rho} = 0.026). Functional connectivity models were significant in both sexes, while prospective structural connectivity models were significant in males, but not females. Frontoparietal, medial frontal, sensorimotor, salience, cerebellar, and visual networks contributed across models. Cross-sectional models showed a more distributed pattern while prospective models showed a more focal pattern. These findings identify complementary, largely distinct functional and structural connectome patterns associated with current disruptive behavior risk and subsequent symptom change, supporting the importance of developmental timing, sex, and imaging modality in developing brain-based biomarkers of disruptive behavior risk in youth.

neuroscience↗

bioRxiv2026

Inferential boundaries of age prediction: why prediction does not establish biological age measurement

Chronological-age clocks reconstruct age from biological measurements, yet their outputs are interpreted as biological age, gaps as ageing acceleration and intervention-associated decreases as rejuvenation. We show that age supervision identifies an age-task statistic, not a biological-age construct, and establish how this distinction changes biomarker construction and validation. Even at the population optimum, the same observable distribution and age-prediction performance admit incompatible biological-age interpretations. Resolving this ambiguity requires assumptions or evidence beyond the age task. Squared-error age loss penalizes within-age output dispersion without defining its biological direction. Given age and background, a gap re-expresses the compressed score; exact age recovery eliminates it even when heterogeneity remains in the measurements. Shared biological covariance permits genuine prognostic value without establishing construct identity. After allogeneic haematopoietic stem-cell transplantation, recipient-blood scores showed excess donor-lineage affiliation under a score-pairing null. In NHANES, age-trained scores improved held-out five-year mortality prediction beyond age and background, yet direct modelling of source measurements and mortality supervision at matched scalar capacity yielded further gains. The intended biological object must therefore guide study design, measurement selection and representation; validation must establish the claimed measurement relation rather than rely on age-prediction success alone.

bioinformatics↗

bioRxiv2026

Dynamic Control of Prokaryotic Chromosome Ploidy Rewires Metabolic Networks to Enhance Product Biosynthesis

Building high-performance microbial cell factories requires dynamic coordination of resource allocation among cellular growth, target-product biosynthesis, and endogenous host metabolism. However, existing polyploid engineering strategies rely primarily on static manipulation of chromosome copy number. Although increasing gene dosage can enhance biosynthetic capacity, static designs cannot readily accommodate the changing metabolic demands encountered during fermentation. Here, we developed a metabolite-responsive dynamic polyploid engineering strategy that couples chromosome ploidy to the cellular metabolic state. We first constructed a high-performance L-threonine biosensor and used it to sense intracellular L-threonine levels and regulate ftsZ expression, a key cell-division gene, thereby establishing a dynamic polyploid system that requires neither exogenous inducers nor antibiotics. This system enabled engineered cells to progressively transition from polyploid to haploid during fermentation, accompanied by stage-specific remodeling of cellular physiology and metabolism. Physiological characterization revealed a marked increase in cell size and alterations in cell-envelope properties during the polyploid phase, followed by a gradual decrease in chromosome copy number as fermentation progressed. Transcriptomic and metabolomic analyses further demonstrated that dynamic ploidy transitions induced global metabolic network rewiring, remodeling the tricarboxylic acid cycle and amino acid metabolism while redirecting carbon flux toward the biosynthesis of aspartate-family amino acids. Ultimately, dynamic polyploid engineering substantially enhanced L-threonine production, enabling the engineered strain to achieve an L-threonine titer of 183.1 g/L and a yield of 0.67 g/g glucose in 5-L fed-batch fermentation without antibiotics or exogenous inducers. These findings show that dynamic regulation of chromosome ploidy can couple gene-dosage control with remodeling of cellular physiology and metabolic networks, providing a new engineering strategy to overcome the limitations of static polyploid designs and build high-performance microbial cell factories.

synthetic biology↗

bioRxiv2026

Early origin of sugar sensing in jawed vertebrates

Sweet taste guides animals to consume carbohydrate-rich foods, and many different vertebrate groups, from fish to mammals, rely on sugar-rich fruits or nectar produced by flowering plants (angiosperms). Although the genes encoding T1R2-T1R3, the receptor pair that mammals use to sense sugars, exist in the genomes of many vertebrates, their functions are unclear--and whether sugar sensing arose once early in vertebrate evolution or independently in different lineages after angiosperms evolved is currently unknown. Here, we combined ancestral reconstruction and receptor functional profiling to examine the evolutionary history of T1R taste receptors--including recently-described non-canonical receptors--across all major vertebrate clades. Our results pinpoint the origin of sugar sensing to before the emergence of angiosperms and uncover a myriad of alternative T1R-based sugar-sensing mechanisms, suggesting multiple independent T1R trajectories and revealing uncharted sensory diversity across vertebrates.

evolutionary biology↗

bioRxiv2026

Host cell identity shapes the replication and evolution of Drosophila C virus

RNA viruses encounter diverse cellular environments within their hosts, yet how different host cell types influence viral evolution remains poorly understood. Here, we investigated the replication and experimental evolution of Drosophila C virus (DCV) in glial, mesodermal, and hemocyte-derived S2 cells. Mesodermal cells supported substantially higher viral RNA accumulation, viral protein production, and infectivity than glial or S2 cells, demonstrating pronounced cell type-dependent permissiveness. Comparative transcriptomic and proteomic analyses revealed distinct host responses to DCV infection despite the common mesodermal origin of mesodermal and S2 cells. Functional analyses showed that RNA interference, cGAS-STING signaling, viral binding and entry, and cellular ATP abundance could not account for the enhanced replication of DCV in mesodermal cells, whereas S2 cells displayed stronger cGAS-STING and JAK- STAT responses. Serial passage of DCV for 15 generations in mesodermal or S2 cells resulted in rapid phenotypic adaptation, with evolved viruses exhibiting improved replication in the corresponding cell type without altering infectivity in adult flies. Genome sequencing revealed distinct evolutionary patterns between nonstructural and structural protein-coding regions. Nonstructural proteins remained highly conserved with limited evidence of parallel evolution, whereas structural proteins accumulated more mutations and exhibited broader signatures of positive selection. A recurrent VP3 mutation (G8089A; R270H) independently emerged in three S2-passaged lineages, representing the only mutation consistently associated with adaptation to a specific cell type. Structural modeling suggested that this substitution is unlikely to substantially alter VP2-VP3 interactions, implying more subtle effects on capsid function. Together, our findings demonstrate that different Drosophila cell types impose distinct intracellular selective pressures that shape DCV replication and evolutionary trajectories, highlighting host cell identity as an important determinant of RNA virus evolution.

microbiology↗

bioRxiv2026

The endosomal trafficking protein Myopic differentially regulates Drosophila C virus infection in cultured cells and adult flies

Positive-sense RNA viruses extensively exploit host membrane trafficking pathways to establish intracellular replication organelles required for efficient viral replication. However, the contribution of endosomal trafficking proteins to infection by Drosophila C virus (DCV), a natural dicistrovirus of Drosophila melanogaster, remains poorly understood. Here, we investigated the role of Myopic (Mop), a conserved ESCRT-associated endosomal trafficking protein, during DCV infection. Knockdown of mop in cultured S2 cells significantly increased DCV RNA and viral protein accumulation without affecting viral binding or entry, indicating that Mop restricts DCV replication at a post-entry stage. In addition, depletion of mop altered the intracellular distribution of viral proteins, suggesting that Mop may influence the organization of DCV-associated intracellular membrane compartments. Unexpectedly, fat body-specific knockdown of mop in adult flies produced the opposite phenotype, resulting in reduced viral accumulation and prolonged survival following systemic DCV infection. This antiviral phenotype was not associated with enhanced activation of the STING or JAK-STAT pathways. Instead, transcriptomic and proteomic analyses revealed extensive remodeling of gene and protein expression, including altered abundance of proteins associated with autophagy and RNA interference. Together, our findings identify Mop as a previously unrecognized regulator of DCV infection and reveal distinct cell-autonomous and systemic functions of this conserved trafficking protein. These results highlight the importance of endosomal trafficking in antiviral defense and demonstrate that host membrane trafficking factors can exert fundamentally different effects on virus infection at the cellular and organismal levels.

microbiology↗

bioRxiv2026

scJET: Full-gene Space Single-cell Expression Generation with Patch-based Transformer Modeling

Most single-cell generative models rely on highly variable genes (HVGs) or low-dimensional latent representations, limiting their capacity to capture the complexity of full-gene features. We present scJET, a patch-based Transformer denoising framework that operates in full-gene space. scJET preserves global manifold structure, local neighborhood statistics, and gene-level expression programs. By combining scalable patch tokenization with full-gene denoising, scJET provides an efficient framework for transcriptome-wide single-cell matrix generation.

bioinformatics↗

bioRxiv2026

Dual-channel whole-brain imaging reveals distinct dopamine and calcium dynamics in walking Drosophila

Simultaneous recording of intra- and extracellular neuronal signals across the brain during behavior is crucial for unraveling brain information processing. In Drosophila, large-scale recordings have been explored, yet simultaneous dual-channel whole-brain imaging remains a significant challenge. We developed a system combining a Fourier light-field microscope with dual-focal microlens arrays optimized for adult walking flies, extending imaging volume while maintaining resolution requirements. This optical system is further combined with a cross-modal 3D registration and segmentation pipeline to integrate functional and structural data. Using this system, we simultaneously measured brain-wide intracellular calcium activity and extracellular dopamine release during locomotion. We found that functional maps and neural dynamics for dopamine and calcium are distinct across the brain and within specific compartments, particularly in the mushroom body and central complex, aligning with their anatomical bases. Both calcium and dopamine representations of locomotion are distributed, yet they exhibit different patterns. Mushroom body compartments can be functionally categorized into two types based on their responses to specific locomotive actions. Forward walking or acceleration boosts activity in compartments innervated by PAM dopaminergic neurons, while dampening activity in those targeted by PPL1 dopaminergic neurons. Conversely, backward walking or deceleration heightens PPL1 activity while reducing PAM activity, consistent with the functions of these neurons in encoding approach and avoidance choices. Notably, single-compartment activity can reliably decode behavior choices. Our findings, spanning whole-brain, brain-region, and single-compartment, demonstrate the capability of our system to uncover neural dynamics across multiple scales and channels in behaving animals.

neuroscience↗

bioRxiv2026

Subjective, not objective, socialness drives activity in the brain's third visual pathway

Recent work, including the third visual stream hypothesis, frames social perception as a largely automatic visual process. Simple animations of shapes engaged in "social" behaviors such as chasing have long been used to study social perception; however, both behavioral and neural responses are typically modeled against discrete, experimenter-assigned stimulus labels. This approach is insufficient, given that perceptions of such stimuli vary not only between people but also across trials. Here, we directly compared the neural responses to objective (stimulus-based) and subjective (response-based) socialness in an fMRI study in which the degree of chase between two agents was varied algorithmically. Participants (n=24) rated their perception of a chase on a continuous scale. Subjective ratings better predicted activity in visuo-social brain regions, predominantly in area MT, even after controlling for optic flow. Our findings underscore the visual nature of social cognition and highlight the importance of analyses sensitive to idiosyncrasies in perception.

neuroscience↗

bioRxiv2026

The Hidden Landscape of Missed Effects in Human Functional Neuroimaging

Functional neuroimaging aims to uncover brain processes underlying behavior and disease, yet studies are often underpowered to detect these effects. How this literature has shaped our understanding of brain function remains unknown, and little guidance exists for planning better powered studies. An underappreciated barrier is that commonly reported effect sizes across the brain are inflated, biasing study planning. Here, we introduce a correction for this inflation bias and show how more accurate studies can be planned using corrected effect size benchmarks from a mega-analysis of 63 typical studies across seven large datasets (52,979 participants). We find that common methods of planning studies based on uncorrected effects lead to roughly half the expected detections at typical sample sizes, with limited spatial overlap with original findings. These missed effects collectively explain meaningful additional variance in the desired outcome. We show how to recover missed effects by planning not only for power but also for a target number of detections via corrected benchmarks, or by taking a whole-brain approach with multivariate effects that individual research groups can detect (n < 50 compared to n > 1,000 for a typical univariate effect). These findings lay the groundwork for more informed study planning and a richer understanding of the widespread nature of brain effects, with implications for shared challenges (and solutions) across biomedicine.

neuroscience↗

bioRxiv2026

Three-dimensional Virtual Adult Cardiomyocyte Transcriptomics

Obtaining transcriptomes of adult cardiomyocytes at single-cell resolution remains challenging due to their large size, elongated morphology, and frequent multinucleation. Although spatial transcriptomics preserves tissue architecture and captures gene expression in situ, current analytical frameworks largely rely on nuclear-based segmentation and are therefore poorly suited to adult cardiomyocytes. Furthermore, individual tissue sections capture only a fraction of a cardiomyocyte, preventing reconstruction of complete cell-level transcriptomes. Here we present three-dimensional virtual cardiomyocyte (3D-VirtualCM), a membrane-guided framework that integrates cell-contour similarity and optimal transport to reconstruct volumetric cardiomyocyte transcriptomes from consecutive spatial transcriptomic sections. Applying 3D-VirtualCM to infarcted adult mouse hearts, we generated a panoramic transcriptomic atlas spanning 100 m thickness at single-cell resolution. 3D-VirtualCM identified spatially and transcriptionally distinct cardiomyocyte populations within the infarct border zone, enabled high-throughput quantification of cardiomyocytes re-entering the cell cycle together with their associated molecular signatures, and revealed heterogeneous RNA distribution along the longitudinal axis of individual cardiomyocytes. By integrating three-dimensional cellular morphology with in situ transcriptomic data, 3D-VirtualCM provides a scalable approach for resolving cardiomyocyte states and spatial organization in physiological and pathological cardiac remodeling.

bioinformatics↗

bioRxiv2026

Plant-derived soft electrophiles upregulate pro-resolving oxylipins in a paraquat-induced Drosophila model of Parkinson's disease.

Age-accompanied chronic, low-grade systemic inflammation (inflammaging) drives the onset and progression of neurodegenerative disorders like Parkinsons disease (PD). Currently, no disease-modifying therapies are available for PD. Exposure to environmental toxicants, including paraquat (PQ), rotenone, and neurotoxic metals, increases disease risk. Conversely, sustained consumption of dietary soft electrophiles, such as flavonoids, carotenoids, vitamin E vitamers, and essential fatty acids, has been associated with increased lifespan and delayed age-related neurological decline. Omega-3 and select omega-6 fatty acids also serve as precursors of lipid-derived specialized pro-resolving mediators (SPMs), which exert potent anti-inflammatory and inflammation-resolving activities. Here, we report the development of a robust analytical method to quantify pro-resolving oxylipins in a PQ-induced Drosophila melanogaster model of PD, enabling investigation of how dietary phytochemicals modulate anti-inflammatory and pro-resolving lipid metabolism in vivo. We hypothesized that plant-derived soft electrophiles promote active resolution of neuroinflammation by enhancing the production of pro-resolving oxylipins derived from essential fatty acids, and that their neuroprotective effects are linked to their soft electrophilic properties. Our results demonstrate that specific lipophilic plant-derived soft electrophiles significantly upregulate pro-resolving oxylipins in Drosophila heads following PQ exposure. We identify a subset of flavones and structurally related phytochemicals that selectively enhance SPM biosynthesis and show that this response involves the NF-{kappa}B orthologue relish. Additionally, feeding modality and sex-specific dimorphisms were found to influence oxylipin production. Collectively, these findings indicate that structurally related dietary soft electrophiles enhance endogenous pro-resolving lipid pathways, promote resolution of toxin-induced neuroinflammation, and have potential preventive and therapeutic relevance for neuroinflammation-associated neurodegenerative diseases. HighlightsO_LIQuantification of pro-resolving lipids in a Drosophila Parkinsons model. C_LIO_LISpecific structural features of phytochemicals contribute to in vivo bioactivity. C_LIO_LILipophilic soft electrophiles show therapeutic potential against neuroinflammation. C_LIO_LIFeeding modality and sexual dimorphism also regulate oxylipin production. C_LI Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=105 SRC="FIGDIR/small/714080v1_ufig1.gif" ALT="Figure 1"> View larger version (43K): org.highwire.dtl.DTLVardef@2088cforg.highwire.dtl.DTLVardef@1f5d026org.highwire.dtl.DTLVardef@134aa44org.highwire.dtl.DTLVardef@965e28_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

bioRxiv2026

Mechano-activation of synovial fibroblasts and macrophages during OA progression in the dynamically stiffening synovial microenvironment

ObjectiveDuring osteoarthritis (OA) progression, the synovial membrane undergoes profound structural and compositional remodeling and fibrosis. We sought to elucidate how evolving synovial microenvironmental mechanics during fibrotic remodeling influence cell behavior and drive the progression of synovial pathology. MethodsSkeletally-mature male C57BL/6J mice were subjected to destabilization of the medial meniscus (DMM). To control for surgical confounders, both sham-operated and unoperated mice were included, with evaluation at 4- and 8-weeks. Synovial micromechanics were quantified via atomic force microscopy (AFM). Single-cell RNA sequencing (scRNA-seq), RNA fluorescence in situ hybridization (FISH), and flow cytometry were employed to investigate cellular heterogeneity, spatial organization, and crosstalk within fibrotic and non-fibrotic synovial niches. ResultsProgressive fibrotic remodeling and marked matrix stiffening were observed in DMM-operated synovium but absent in sham- and un-operated controls. While both sham and DMM joints mounted an acute stromal and immune response to surgery, these changes resolved over time in sham conditions but persisted in DMM synovium. During disease progression, distinct functional subsets of synovial fibroblasts and immune cells emerged, with mechanosignalling pathways and distinct immune cell-fibroblast crosstalk robustly activated within DMM-induced fibrotic microenvironments. ConclusionThis study demonstrates the complex cellular dynamics and crosstalk that differentiate the evolution of the pathological synovial response in the fibrotic DMM condition relative to surgical sham controls. Our findings highlight mechanotransduction as a central mechanism driving OA synovial pathogenesis and underscore the utility of the DMM model as a platform to dissect the molecular underpinnings of synovial fibrosis.

bioengineering↗

bioRxiv2026

Intestinal epithelial Casd1 influences mucus sialic acid O-acetylation and tissue damage susceptibility toward large-intestinal mucosal insults.

The intestinal mucus network, primarily composed of O-glycosylated MUC2 mucin polymers, is essential for protecting the gastrointestinal tract from microbial threats. Sialic acid (Sia), a terminal monosaccharide on complex O-glycans, plays a key role in maintaining mucus integrity and is frequently modified by Casd1-dependent O-acetylation (OAc). Despite its prevalence, the biological significance of sialic acid OAc (OAc-Sia) modifications in human and murine mucus remains unclear. We hypothesized that OAc-Sia variants on mucus interact with the microbiota and are required for optimal mucus barrier function and host-microbe homeostasis in the colon. To test this, we profiled OAc-Sia on human and mouse MUC2 in situ using viral-derived probes with bacterial FISH and confocal microscopy; generated intestinal epithelial cell (IEC)-specific Casd1 null mice (IEC Casd1-/-); performed sialylomic and O-glycomic HPLC-MS analyses; assessed microbial communities by 16S rRNA sequencing with quantitative microbial profiling (QMP); and evaluated disease susceptibility using DSS colitis and Citrobacter rodentium infection models. Results revealed that both human and murine mucins are extensively O-acetylated and interact with the microbiota, suggesting biological relevance. IEC Casd1-/- mice were viable and displayed a complete loss of mucin OAc-Sia, indicating Casd1 is the sole contributor to OAc-status. Unexpectedly, mucus function was intact in IEC Casd1-/- mice, with no difference in structure or quality vs. WT co-housed littermates.16S rRNA analysis showed a modest but significant sex-specific reduction of microbial loads in male IEC Casd1-/-mice, and a clear trend toward reduced Turicibacter spp. vs. WT mice in both male and females, without impacting overall short-chain fatty acid (SCFA) production. DSS treatment led to more severe and extensive tissue damage in IEC Casd1-/- mice. C. rodentium infection led to increased damage in the cecum and distal colon of IEC Casd1-/- mice without affecting pathogen load, suggesting that OAc-Sia status has a role in tolerance defense. These findings establish intestinal epithelial Sia O-acetylation as a component dispensable for mucus and host-microbe homeostasis at baseline, but important in limiting damage to mucosal inflammatory insults.

cell biology↗

bioRxiv2026

AI-driven discovery and engineering of human endogenous nanocage proteins for mRNA delivery

Safe and effective gene delivery remains a central challenge for therapeutic applications. While non-viral and viral vectors have enabled substantial progress, their reliance on non-human components often triggers immune responses, limiting their use in chronic treatments. Here, we developed DeepDelivery, an artificial intelligence-driven platform to repurpose human proteins for mRNA delivery. An unbiased screening of the human proteome nominated 512 candidates, with experimental validation confirming that 80% of top-ranked hits form mRNA-encapsulating particles and mediate efficient functional delivery in human cells without provoking detectable inflammation. Notably, multiple tripartite motif (TRIM) family proteins, typically linked to antiviral responses, exhibited strong assembly and delivery activity. Quantitative analysis and interpretation of the model revealed structural domains that govern nanocage formation, enabling domain-guided engineering of TRIM25 variants with enhanced function. Our work establishes a generalizable framework for discovering human-derived delivery vehicles and provides a path toward programmable, non-immunogenic mRNA therapeutics.

synthetic biology↗

bioRxiv2026

Immunoregulatory gene GIMAP6 suppresses lethal atherosclerotic vasculopathy and ischemic heart failure

Controlling hyperlipidemia has reduced but not eliminated atherosclerotic cardiovascular disease as a predominant cause of human mortality. Here, we report that loss of the immunoregulatory gene GTPase of immunity-associated protein 6 (GIMAP6), causes an inflammatory vasculopathy and accelerated atherosclerosis in the absence of hyperlipidemia. These pathologic changes in turn result in progressive cardiac ischemia, myocardial infarction, and heart failure, culminating in early death. In humans, rare deleterious GIMAP6 variants are associated with premature severe cardiovascular disease. These findings reveal GIMAP6 to play an important protective role against atherosclerotic cardiovascular disease whose identification offers opportunities for improved risk management and a target for new therapies.

immunology↗

bioRxiv2026

Cooperative Regulation of Membrane Domain Registration by Lipid Headgroup Size and Cholesterol Dynamics

The lateral organization of lipid domains and their coupling across the two leaflets are central to the structure of plasma membranes, yet the molecular determinants of domain registration and anti-registration remain incompletely understood. Here, we employ coarse-grained molecular dynamics simulations to investigate how lipid headgroup properties and cholesterol (CHOL) concentration regulate domain registration and anti-registration in symmetric model bilayers. Using a free energy perturbation (FEP)-like headgroup-interpolation approach to continuously interpolate between headgroup representations characteristic of phosphatidylethanolamine (PE) and phosphatidylcholine (PC) lipids at a fixed tail composition, we show that headgroup properties and CHOL concentration act cooperatively through their effects on lipid packing and membrane curvature. Simulations with restrained CHOL flip-flop further demonstrate that transbilayer CHOL exchange actively strengthens interleaflet coupling and promotes domain registration. These results identify headgroup-dependent packing, CHOL-induced curvature, and CHOL flip-flop as cooperative determinants of domain organization in model membranes. TOC Graphic O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=114 SRC="FIGDIR/small/699701v2_ufig1.gif" ALT="Figure 1"> View larger version (43K): org.highwire.dtl.DTLVardef@1a78635org.highwire.dtl.DTLVardef@15c17f7org.highwire.dtl.DTLVardef@1295adaorg.highwire.dtl.DTLVardef@ba80a_HPS_FORMAT_FIGEXP M_FIG C_FIG

biophysics↗

bioRxiv2025

Rapid ecosystem collapse and biofilter formation following seabed methane leakage

Globally, vast amounts of methane are trapped within subseafloor gas hydrates. Recent evidence suggests that climate- and human-induced perturbations can destabilize gas hydrates and trigger methane release, yet the response of deep-sea ecosystems to these changes remains poorly understood. Here we show multi-year in situ monitoring of seabed ecosystem following methane leakage induced by hydrate exploration activities. Within just two years, benthic microbial and eukaryotic diversity in the affected areas declined significantly, while microbial and macrofaunal abundance increased. Integrated geochemical and omics analyses reveal the rapid successional shift of seabed ecosystem to a novel chemosynthetic system. Aerobic methanotrophs (Methyloprofundus) co-established with unexpectedly fast growing anaerobic methanotrophic archaea (ANME-3), accompanied by a rapid recruitment of opportunistic polychaetes that bioirrigated the seabed to >50 cm depths. The active animal-microbe interactions sustained exceptionally high rates of methane oxidation that utilized diverse electron acceptors. We demonstrate that methane hydrate destabilization can trigger rapid collapse of native seabed ecosystem while driving the formation of an effective methane biofilter consuming this potent greenhouse gas much faster than previously estimated. Understanding seabed ecosystem response and feedback is critical for predicting benthic methane cycling under ongoing global change and for developing sustainable strategies for methane hydrate resource management.

ecology↗