Biology subjects

Zhou, W.

Publications and source records attributed to Zhou, W..

At least 37 records · Page 2Linked to original sources

bioRxiv2026

An organismal view of newborn cell dynamics in mammalian aging

Aging remodels tissue composition, yet static single-cell atlases cannot show which renewal processes drive this change across the organism. To address this gap, we applied TrackerSci to 21 mouse tissues at young, adult, and aged stages in both sexes, linking in vivo EdU labeling to single-nucleus chromatin accessibility. This produced approximately 3 million profiles of newborn cells matched to global cell populations from the same tissues and ages. Newborn-cell abundance varied widely across tissues and generally declined with age. Beyond abundance, the cell-type composition of newborn cells differed from that of the tissue as a whole. Reflecting this difference, they showed distinct chromatin states, including known renewal compartments and candidate progenitor or proliferation-active states. With age, they also shifted along inferred differentiation trajectories, with stalled-differentiation patterns emerging in multiple lineages. At the population level, age-related changes in newborn-cell abundance partially explained the broader shifts in cell-type composition during aging. Renewal-rate analysis further showed that age-related cell-type declines were driven by reduced replacement, while expansions reflected altered cell-state transitions. Together, these findings show how newborn cell dynamics across the whole organism reveal the routes by which aging remodels cellular composition.

genomics↗

bioRxiv2026

Human hindbrain organoids with segment-specific 5-HT neurons for motor modulation

The serotonergic system regulates human mood, reward, and motor control, and its impairment contributes to debilitating psychiatric disorders. Serotonergic neurons (SNs) arise predominantly in the hindbrain and acquire segment-specific identities and functions; however, the lack of human models remains a challenge to understanding the human serotonergic system. Here, we generate human serotonergic-enriched rostral and caudal hindbrain organoids (hsrHOs and hscHOs) that produce segment-specific SNs with regional identities corresponding to rhombomeres r2-r3 and r5-r8, respectively. hsrHOs and hscHOs produce SNs that recapitulate their in vivo counterparts in transcriptomic profiles, function, and ascending or descending projection preferences. Assembly with human neuromusculoskeletal organoids enables modeling of serotonergic modulation of motor control. This system further reveals that deficiency of the schizophrenia risk gene DISC1 disrupts human serotonergic development and impairs motor modulation. Together, our study establishes a human organoid platform for modeling development, circuit function and disease-associated dysfunction of the serotonergic modulatory system.

neuroscience↗

bioRxiv2026

Somatic-to-germline transmission of horizontally acquired extrachromosomal circular DNA in Brassica graft chimeras

Whether somatically acquired traits can contribute to heritable variation has remained an open question in plant biology for over a century. Here, using graft-induced periclinal chimeras between Brassica juncea and Brassica oleracea, we identified extrachromosomal circular DNA (eccDNA) as mobile genetic elements capable of crossing histological boundaries and entering the germline. We demonstrated that grafting could promote the horizontal transfer of eccDNA between somatic cell layers, enabling its stable maintenance in recipient tissues and permitting transmission through sexual reproduction across multiple generations. We found that transmitted eccDNA is non-randomly distributed across the genome, preferentially originating from gene-dense regions, and enriched for features associated with molecular persistence, such as inverted repeats, hairpin-forming sequences, and autonomously replicating sequence (ARS) consensus motifs. These genetic regions conferred replication competence, as evidenced by autonomous propagation in an ARS-less heterologous yeast system. Sexual progeny carrying graft-acquired eccDNA exhibited reproducible and lineage-dependent alterations in leaf morphology and drought tolerance, accompanied by coordinated transcriptional reprogramming. Notably, a subset of inherited eccDNA remained transcriptionally active in progeny, producing transcripts absent from self-grafted controls. Our findings establish eccDNA as heritable extrachromosomal elements that link graft-mediated somatic genetic transfer with stable germline transmission, thereby expanding the molecular scope of heritable variation in plants and providing a conceptual framework for graft-based trait transmission.

plant biology↗

bioRxiv2026

piRNA direct the chromatin reader to its genomic targets

The chromatin reader Rhino (Rhi) is an HP1-paralog and master regulator of piRNA biogenesis in Drosophila that drives the transcription of piRNA precursors. While Rhi binds the heterochromatic mark H3K9me3, this interaction is insufficient to explain its specific occupancy, as Rhi is excluded from the majority of H3K9me3-enriched loci. Instead, we find that Rhi recruitment is orchestrated by several competing pathways, including the piRNA-guided protein Panoramix (Panx) and the DNA-binding protein Kipferl (Kipf). We demonstrate that Panx functions as a piRNA-guided modular scaffold that directs Rhi to its targets through a dual-mode mechanism: its N-terminus recruits the H3K9 methyltransferase machinery, while its C-terminus directly binds the Rhi chromodomain. While H3K9me3 deposition provides a necessary foundation, it acts in synergy with the direct Panx-Rhi physical bridge to drive robust Rhi occupancy. Furthermore, Rhi recruitment is amplified by the cytoplasmic inheritance of maternal piRNAs, forming a transgenerational feed-forward loop. Our results reveal that the piRNA pathway imparts sequence-specificity to the H3K9me3 code, utilizing a direct physical bridge to program the genomic distribution of the chromatin reader Rhi.

molecular biology↗

bioRxiv2026

Species and strain diversity in Staphylococcus drive divergent host responses in human skin

The skin microbiome regulates key skin processes, yet the functional diversity of a dominant genus, Staphylococcus, remains poorly resolved at the strain level for multiple species across its pathogenic and commensal continuum. It is likely that Staphylococcus effects on skin are diverse at these finest taxonomic resolutions, but current skin models lack the physiological relevance and scalability needed to profile this diversity. Using an organotypic 3D human skin model (reconstructed human epidermis, RHE), we profiled skin responses to 187 Staphylococcus strains across seven dominant species. Canonically pathogenic species (e.g., S. aureus) induced broad inflammatory responses, whereas prototypical commensal species (e.g., S. hominis) elicited more nuanced effects on innate immune and skin barrier responses. Strikingly, S. epidermidis displayed pronounced strain-level heterogeneity, with subsets inducing either commensal or pathogen-like responses despite lacking canonical virulence factors, suggesting pleiotropic effects. Comparative genomics, dual-transcriptomics, untargeted metabolomics, and growth phenotyping revealed species- and strain-specific traits underlying these differential effects on RHE, including the presence of select cell surface proteins and differential arginine metabolism. Together, our study provides the first high-throughput, species- and strain-resolved analysis of skin-Staphylococcus interactions, offering mechanistic insights and a platform for microbiome-based strategies to modulate skin inflammation and diseases. One-line summaryHigh-throughput profiling of Staphylococcus in a human skin model shows that species- and strain-level diversity underlies a continuum of host barrier and immune responses.

microbiology↗

bioRxiv2026

Population genomics of skin Staphylococcus reveals disease-associated restructuring of species and strain diversity

Whole genome sequences of microbial isolates are essential to link microbial diversity to population and community ecology, because metagenomics alone cannot resolve strain-level variation, particularly in complex and mobile genetic elements that confer strain-specific traits such as virulence. We cultured and whole-genome sequenced 2,920 Staphylococcus isolates from healthy subjects and patients with Dariers disease and congenital ichthyosis. Our results show that disease imposes selection at the species level, while strain populations within those species diversify across individuals in a manner consistent with ecological drift, resulting in increased interpersonal heterogeneity of strain composition. Despite this variability, strain populations converged on shared functional traits, suggesting constraints imposed by the disease environment. We further examined key functional elements of clinical and ecological relevance, including the agr quorum sensing system, the mobile genetic element SCCmec that carries methicillin resistance, and CRISPR/Cas systems, contextualizing these features both within isolate population structure and the surrounding microbial community using metagenomic data. We found disease-dependent enrichment of virulence genes, striking species-specific phylogenetic sorting of agr variants, unexpected modularity of previously undocumented SCCmec elements in diseased skin, and links between phages in the microbiota and CRISPR spacers in the isolate genomes. Taken together, our integrated, large-scale analysis of isolate genomics and metagenomics reveals that skin disease restructures staphylococcal strain populations through combined effects of selection, drift, and functional constraint. One line summaryWhole-genome sequencing of 2,920 skin Staphylococcus isolates shows that disease selects at the species level while reshaping strain populations and their functional diversity within hosts.

microbiology↗

bioRxiv2026

RVQ-Alpha: Bridging Single-Cell Transcriptomics and Large Language Models via Discrete Tokenization and Verifiable Reinforcement Learning

Single-cell RNA sequencing yields continuous expression profiles, whereas large language models operate over discrete autoregressive sequences, leaving no shared computational interface for language-model reasoning over cell states. Existing approaches either keep cellular information outside the LLM vocabulary, consume context per listed gene, or learn reconstruction codes without gene-level grounding. We introduce RVQ-Alpha, which systematically adapts four stages of LLM training (tokenization, supervised fine-tuning, reinforcement learning, and distillation) to single-cell analysis. Multi-codebook Residual Vector Quantization (RVQ) lexicalizes each profile into a compact, hierarchical cellular alphabet in the models native token stream, while a paired decoder reconstructs the corresponding expression profile. Evidence-First supervision grounds these symbols in named genes and expression-linked evidence; Fact-Aware RLVR then penalizes contradictory claims to support auditable reasoning. Task-specific RLVR yields strong experts, but a single Mixed policy underperforms them across all four task families. To recover specialist competence in a unified model, we adopt Multi-Teacher On-Policy Distillation (MOPD), which consolidates these experts into one All-in-One checkpoint without retaining a separate policy for each task. On the CAPSTONE benchmark, a four-task suite with explicit biological shifts and deterministic ontology-aware graders, the unified checkpoint improves over Mixed on all 12 metrics and remains within 0.005 of the task-routed specialist reference on every primary metric. Overall, RVQ-Alpha provides a unified pipeline for grounded, auditable multi-task single-cell analysis.

bioinformatics↗

bioRxiv2026

Computational and Proteomic Analyses Reveal Cardiac Dysfunction and Heart Failure-Associated Biomarker Secretion from Venezuelan Equine Encephalitis Virus TC83-infected human IPSC-derived Cardiomyocytes

Arthropod-borne pathogens, many of which are neurotropic, can disseminate beyond the central nervous system to infect peripheral organs. In recent years, an increasing number of cardiac dysfunctions have been reported following arthropod-borne viral infections; however, the mechanism underlying these cardiac manifestations remains poorly understood. In this study, we investigated the impact of Venezuelan Equine Encephalitis Virus (VEEV) TC-83 infection on cardiac function and immune-response of human induced-pluripotent stem cell (hIPSC)-derived cardiomyocytes (hIPSC-CMs). We first confirmed the successful differentiation of hIPSCs into spontaneously beating hIPSC-CMs. We then demonstrated that these cells are highly susceptible to VEEV TC-83 infection, which induced pronounced arrhythmias and complete cessation of beating within 24 hours post-infection. To quantify these functional changes, we developed a segmentation-free computational pipeline that converts frame-to-frame motion in brightfield time-lapse movies into a one-dimensional signal reflecting contractile activity and extracts beat timing, beat rate, and rhythm-regularity features in the time and frequency domains. This analysis revealed progressive disruption of beating dynamics following VEEV TC-83 infection, with early rhythm instability and complete loss of coordinated beating by 24 hours post-infection. Furthermore, mass spectrometry analysis of VEEV TC-83-infected hIPSC-CMs supernatants revealed the presence of biomarkers typically associated with heart failure in patients, underscoring a virus-induced cardiac functional impairment. Together, these findings provide new insight into cardiac complications associated with arthropod-borne viral infections and may support advances in preventive medicine.

cell biology↗

bioRxiv2026

Neuronal EphB2 signaling drives persistent neuropathic pain following spinal cord injury

Neuropathic pain after spinal cord injury reflects persistent hyperexcitability in the spinal cord dorsal horn, yet the molecular drivers sustaining this maladaptive state are unknown. Using an antibody microarray of dorsal horn tissue from mice six weeks after cervical contusion spinal cord injury, we found persistent upregulation of Eph-ephrin signaling, including increased EphB1, EphB2 and EphB3 expression and phosphorylation. Reversible chemogenetic inhibition of EphB kinase activity, using an EphB1/2/3 analog-sensitive knock-in mouse, selectively reversed established mechanical allodynia without affecting thermal hyperalgesia or motor function and also shifted dorsal horn signaling away from pain sensitization-associated pathways. Among EphB receptors, EphB2 showed the most consistent and robust injury-induced increase in expression within dorsal horn. Although EphB2 transcript levels increased in both dorsal horn neurons and astrocytes, conditional deletion of EphB2 only in dorsal horn neurons, but not in astrocytes, reversed established mechanical allodynia and reduced dorsal horn neuronal activation. These findings identify EphB signaling, and neuronal EphB2 in particular, as a mechanism that actively maintains pain hypersensitivity after spinal cord injury.

neuroscience↗

bioRxiv2026

Endogenous mutational mechanisms and metabolic context shape endometrial cancer

Uterine corpus endometrial carcinoma (UCEC) is a common gynecologic malignancy with rising mortality, yet its genome-wide mutational architecture remains incompletely understood. Here we analyze deep whole-genome sequencing data from 440 UCEC tumors from The Cancer Genome Atlas, integrated with transcriptomic and clinical data, to define subtype-specific mutational processes and genomic architectures. We uncover pronounced molecular subtype-specific differences in endogenous mutational mechanisms, retrotransposition activity, structural variation, and chromosomal instability. LINE-1 retrotransposition emerges as a key contributor to genome instability in UCEC, acting as a prominent source of structural variation in copy-number stable tumors and associating with chromothripsis and ecDNA-mediated oncogene amplification in copy-number high tumors. Mutational signature SBS28 contributes significantly to mutations in POLE-deficient tumors and is strongly correlated with SBS10a and SBS10b. Mismatch repair-deficient tumors exhibit a previously unrecognized doublet base substitution signature and a defining imbalance between ID2 and ID1 indel processes, reflecting pervasive DNA template-strand replication slippage and associated with increased tumor immunogenicity. Copy-number low tumors follow a distinct low-mutagenesis evolutionary trajectory characterized by reduced replication stress, low proliferative activity, genomic stability and enrichment of SBS18 associated with oxidative damage. Notably, we identify a consistent inverse association between body mass index and tumor mutational burden in UCEC, suggesting that host metabolic state may influence fundamental cellular processes governing mutation accumulation, promoting tumor development through non-mutagenic mechanisms rather than elevated genomic instability. Together, these findings establish a mutagenesis-centric framework for UCEC that links endogenous mutational mechanisms to tumor architecture and host metabolic context, uncovering previously unrecognized subtype-specific genomic features with important implications for refined risk stratification and therapeutic strategies.

genomics↗

bioRxiv2026

Identification of SNARE Genes in Cucumber and the Role of CsSYP121 in Salt Stress Response

Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are essential regulators of plant growth, development, and stress adaptation. In this study, we performed a comprehensive genome-wide identification of SNARE genes in cucumber (Cucumis sativus L.), uncovering 51 putative members designated as CsSNAREs. Phylogenetic analysis confirmed that these genes cluster into five major clades: Qa-CsSNARE (14), Qb-CsSNARE (9), Qc-CsSNARE (10), Qb+c-CsSNARE (3), and R-CsSNARE (15). Bioinformatic analysis of their promoter regions, coupled with expression profiling under diverse abiotic stress conditions, highlighted a heightened responsiveness within the Qa-CsSNARE subfamily. To validate this, we selected representative Qa-CsSNARE genes for quantitative real-time PCR analysis under drought and salt stress. Among these, CsSYP121 was notably induced by salt treatment. We subsequently generated transgenic cucumber lines overexpressing CsSYP121 and challenged them with salinity. Phenotypic assessment, combined with measurements of reactive oxygen species (ROS) accumulation and K+/Na+ ratios, demonstrated that CsSYP121 overexpression (OE) confers enhanced salt tolerance and boosts antioxidant capacity. We propose a model wherein CsSYP121 mitigates ROS-induced cellular damage under salt stress, potentially through promoting K+/Na+ homeostasis, thereby improving plant performance under saline conditions. Our findings identify CsSYP121 as a promising candidate gene for breeding salt-tolerant crops.

plant biology↗

bioRxiv2026

WTR: A Toolkit for Functional Anterograde Transsynaptic Circuit Mapping

The brain coordinates animal physiology and behavior via neuronal circuits. To understand and simulate brain functions, it is essential to delineate the synaptic connectivity between neurons. Transsynaptic tracers serve as powerful tools for such purposes. In response to the demand for anterograde tracers for circuit mapping and functional interrogation, we developed WTR, a fusion protein of mammalian codon-optimized WGA, TEV-protease cleavage sequence, and Recombinase. WTR expressed via AAV vectors in cell-type-specific starter neurons reaches their postsynaptic neurons and releases Cre/Flpo upon exposure to TEV-protease expressed in downstream neurons. Accompanied by Cre/Flpo-dependent expression of EGFP, GCaMP7s, or ChR2, the toolkit enables labeling, recording, or manipulation of downstream neurons. We utilized WTR to characterize downstream neurons of either glutamatergic or GABAergic neurons in the preoptic area of anterior hypothalamus for their differential actions in thermoregulation or stress responses, respectively. These results establish WTR as a versatile platform for functional anterograde circuit mapping.

neuroscience↗

bioRxiv2026

Repetitive extragenic palindrome (REP) elements are local, context-dependent, dual 3'UTR regulators in Escherichia coli

Repetitive extragenic palindromes (REPs) are the most abundant repetitive noncoding elements in the E. coli genome. Despite their abundance, the primary function of REPs has remained unclear. At different times, REPs have been proposed to contribute to chromosome organization, mRNA decay regulation, and transcription termination, among other functions. Here, we show that the model REP, REP325, does not measurably compact the chromosome but instead acts as a 3UTR-associated transcription regulator within the yjdMN operon, functioning both as a partially Rho-dependent terminator that limits transcription into the downstream yjdN gene and as an mRNA stabilizer that protects the upstream yjdM transcript from degradation. This dual role in controlling both transcriptional readthrough and susceptibility to decay provides a framework that reconciles several previously conflicting observations about REP function. Our genome-wide RNA-seq analysis further reveals that REPs with more canonical sequence and hairpin structures are more often associated with upstream-biased expression in tandem gene pairs, and that REPs positioned between convergent genes correlate with elevated expression of both genes. The large variance in expression patterns in both gene pair configurations is consistent with context-dependent termination and degradation blocking. Similarly, REPs do not uniformly affect mRNA half-lives. Because REP locations vary between E. coli strains, REPs likely contribute to regulatory diversity by tuning gene expression without altering protein-coding sequences or promoter regions, opening new avenues for modulating gene expression through REP-mediated transcription regulation.

biophysics↗

bioRxiv2026

Bacillus velezensis-derived muropeptide promotes growth of zebrafish via NOD2-mediated induction of IGF1 signaling

The role of gut microbiome in regulating vertebrate metabolism has been well-recognized. However, the effects of gut bacteria on growth have been less studied. Bacillus is a prevalent genus in the gut microbiota of human and animals. In this study, the effect of gut-derived Bacillus velezensis T23 on growth was investigated in zebrafish. B. velezensis T23 improved the growth of zebrafish and promoted IGF1 production in the liver and muscle, with a concomitant activation of the AKT/mTOR signaling pathway. The growth-promoting effect of B. velezensis T23 was not dependent on lipopeptides and polyketides. Cell wall peptidoglycan isolated from B. velezensis T23, as well as muramyl dipeptide (MDP), was sufficient to stimulate IGF1 signaling and growth. Further, the effect of B. velezensis T23 on growth and IGF1 production was abrogated in nod2-/- zebrafish, confirming that B. velezensis T23 promoted growth via MDP-NOD2 signaling. Gut transcriptomic analysis indicated that B. velezensis T23 promoted renewal and differentiation of intestinal cells, suggesting an involvement of gut-liver axis in the effect of B. velezensis T23 on systemic IGF1 production. Together, our results revealed an effect of gut Bacillus-derived muropeptide on growth via NOD2-IGF1 signaling, and provided novel mechanistic insights in the beneficial effect of Bacillus spp. as probiotics.

microbiology↗

bioRxiv2026

Hypothalamic Orexin Input to the Medial Amygdala Links Vigilance to Arousal

Arousal circuits govern anesthetic state transitions, but emergence is often complicated by agitation, and the neural circuits linking anesthetic arousal to vigilance remain unclear. Here, we identify a lateral hypothalamic orexin-to-medial amygdala pathway (LHAOx[->]MeA) that links anesthetic state transitions to vigilance-like behavioral bias. Synaptic labeling and slice recordings revealed dense LHAOx innervation in the MeA, and RNAscope showed predominant Ox2R expression in MeA GABAergic (MeAvGAT) neurons. LHAOx[->]MeA terminal activation increased local orexin release, promoted arousal from isoflurane anesthesia, delayed loss of righting reflex during induction, and accelerated recovery during emergence. In vigilance assays, stimulation acutely suppressed open-field exploration and produced real-time place preference without conditioned reinforcement. Fiber photometry demonstrated preferential recruitment of MeAvGAT neurons across anesthetic states. Direct MeAvGAT activation recapitulated cortical engagement, arousal, and vigilance phenotypes, whereas TeLC-mediated silencing of MeAvGAT output abolished induction delay and reversed vigilance-like bias while sparing light-anesthesia arousal and emergence acceleration.

neuroscience↗

bioRxiv2026

Streptomyces enrichment in roots during drought is uncoupled from plant benefit and is driven by host suppression of iron uptake and immunity

Drought reshapes plant root microbiota, yet the mechanistic drivers and consequences of this observation remain unclear. We discovered that suppression of host immunity and iron homeostasis is required for Streptomyces enrichment in roots during drought across diverse soils. Genetic and physiological manipulation of these host pathways confirmed their requirement in modulating Streptomyces root enrichment. Drought-induced suppression of iron uptake was conserved across the [~]160 My monocot-eudicot divergence. Some Streptomyces strains enhanced plant growth and rescued iron uptake under drought. These benefits were uncoupled from Streptomyces root enrichment. They were instead shaped by intra-Streptomyces antagonism. We propose a two-step model: drought-driven down regulation of host iron and immune pathways enriches Streptomyces, while intra-genus dynamics fine-tune strain-level assembly and functional outcomes. Our data refine the idea that Streptomyces are enriched in roots during drought in response to a plant cry for help and consequently contribute to alleviation of this abiotic stress.

plant biology↗

bioRxiv2026

Connectome lateralization in autism across the first 14 years: heterogeneity related to developmental stage, hemisphere, and pathophysiology

Hemispheric lateralization is fundamental feature to neurodevelopment, yet its dynamic evolution in autism across childhood and underlying molecular mechanisms remain unknown. Thus, using a large-scale resting-state fMRI dataset (n = 1553, ages 1-14), we investigated developmental heterogeneity in connectome lateralization. At the group level, abnormalities in dynamic connectome lateralization strength (DCLS) progressed from focal patterns in early childhood ([≤] 6 years) to widespread distributions by late childhood ([≤] 14 years), independent of symptom severity. The late-stage patterns were validated using the ABIDE dataset (n=153). Late childhood also showed marked increases in inter-individual heterogeneity. These alterations were significantly associated with clinical phenotypes, transcriptomic profiles, and multiple neurotransmitter systems, with distinct patterns across childhood groups. Our findings reveal a developmentally dynamic trajectory of connectome lateralization in autism and highlight late childhood as a critical window for stage- and individual-specific interventions tailored to substantial individual heterogeneity.

neuroscience↗

bioRxiv2026

The LIF-LIFR Axis Promotes Liver Regeneration via Modulation of Angiogenesis and HGF Release from LSECs

Liver sinusoidal endothelial cells (LSECs) play essential roles in liver regeneration after injury, but the underlying mechanisms remain incompletely defined. Here we report that leukemia inhibitory factor (LIF), which is rapidly induced after liver injury, acts as a key regulator of LSECs-driven liver regeneration through interaction with LSECs-enriched LIF receptor (LIFR). LIF directly stimulates LSECs proliferation and induces hepatocyte growth factor (HGF) release in a dose-dependent manner via LIFR signaling in LSECs, thereby indirectly promoting hepatocyte proliferation. Systemic LIF neutralization or endothelial cells (ECs)-specific Lifr loss impairs liver regeneration, whereas low-titer AAV-mediated LIF expression increases vascular density, elevates circulating HGF, and improves early liver recovery after partial hepatectomy (PHx) in mice. Together, these findings establish LIF-LIFR as a previously unrecognized endothelial axis to promote hepatocyte proliferation and suggest potential therapeutic strategies to enhance liver repair in patients. HighlightsO_LILIF is upregulated after liver injury and LIF neutralization impairs liver recovery. C_LIO_LILIFR displays the highest expression in ECs; endothelial-specific Lifr deletion delays liver regeneration after injury. C_LIO_LILIF mediates a positive feedback loop including LSECs proliferation as well as HGF release via LIFR pathway. C_LIO_LILIF overexpression increases liver-to-body weight ratio in a dose-dependent manner and accelerates liver regeneration at early stage. C_LI Abstract Graphic O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=151 SRC="FIGDIR/small/707802v1_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@13b42feorg.highwire.dtl.DTLVardef@1ab6390org.highwire.dtl.DTLVardef@115c157org.highwire.dtl.DTLVardef@1486993_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗