Biology subjects

Li, H.

Publications and source records attributed to Li, H..

At least 217 records · Page 12Linked to original sources

bioRxiv2026

Multi-agent reasoning enables predictive design of living materials

Artificial intelligence is increasingly used to accelerate scientific discovery, but most successful frameworks operate within well-defined molecular, protein or materials spaces. Living materials present a more formidable computational problem because functions emerge from context dependent coupling among cells, matrices, fabrication processes and evaluation conditions. Here we introduce LiveMat, a multi-agent reasoning framework that transforms unstructured literature into a computable design space for living materials. LiveMat standardizes 34,215 living material records, integrating 16,769 microorganism and 17,446 polymer entries into a knowledge graph linking living components, abiotic matrices, functional outputs, evaluation contexts and performance metrics. Benchmarking across five large language models shows that living material reasoning is limited mainly by cross-domain feature integration rather than coarse classification. LiveMat overcomes this limitation through constraint decomposition, provenance-aware extraction, consistency checking and expert-anchored ranking. In a prospective wound-healing task, it prioritizes a four-component design with state-of-the-art in vivo performance, establishing a scalable infrastructure for interpretable, evidence-grounded living material discovery.

biochemistry↗

bioRxiv2026

VC-RDAgent: An efficient rare disease diagnosis agent via virtual case construction informed by hybrid statistical-metric and hyperbolic-semantic prioritization

While Large Language Models (LLMs) have shown promise in clinical decision support, current Retrieval-Augmented Generation (RAG) paradigms face a fundamental bottleneck in rare disease diagnosis: the scarcity, privacy restrictions, and extreme heterogeneity of real-world patient records. This reliance on sparse or inaccessible data leads to a severe "retrieval mismatch," where the lack of high-quality reference cases causes diagnostic performance to degrade sharply. To break this deadlock, we propose VC-RDAgent, a privacy-preserving and offline-capable framework that decouples diagnostic reasoning from sensitive real-world records by synthesizing virtual standardized cases. The system is powered by VC-Ranker, a multi-dimensional engine that integrates statistical-metric measures with hyperbolic-semantic embeddings to capture deep hierarchical ontology relationships. This approach allows for the dynamic generation of high-fidelity virtual references directly from authoritative knowledge bases. Extensive benchmarking across four diverse datasets demonstrates that VC-RDAgent effectively functions as a "performance equalizer." It boosts average Top-1 hit rates by 8.7% to 85.9% over zero-case baselines, enabling lightweight open-source models to rival frontier commercial systems. Notably, VC-Ranker alone achieved an aggregate Top-10 hit rate of 0.819, outperforming prior state-of-the-art methods by 6%. By eliminating the dependency on real-time web retrieval and private case sharing, VC-RDAgent provides a scalable, robust, and clinically deployable solution to shorten the diagnostic odyssey, which is made accessible through an intuitive, chat-based web application https://rarellm.service.bio-it.tech/rdagent/.

bioinformatics↗

bioRxiv2026

The Electromagnetic-Core-First Paradigm: A Mechatronic Co-Design Framework for High-Density Implantable Systems

The miniaturization of implantable mechatronic systems is fundamentally limited by a pervasive design conflict: within a rigid spatial envelope, the requirements for high electromagnetic power density, physiological fluid pathways, and perfect biocompatibility compete irreconcilably. To resolve this, we propose a paradigm shift--the Electromagnetic Core-First (ECF) co-design framework. Unlike traditional sequential approaches that force performance compromise, ECF establishes a maximized electromagnetic core (via NSGA-III optimization under manufacturing constraints) as the immutable foundation. Fluid and thermal structures are then co-optimized in parallel within this fixed boundary, achieving global system synergy. Demonstrating its efficacy, we realized a fully magnetically levitated Fontan blood pump (O38.2 mm). The ECF-designed prototype, featuring a novel nested magnet topology, achieves: (1) 57.4% higher air-gap flux density vs. baseline designs and an 18.4 N static suspension force at only 4 W; (2) physiological flow matching (8.8 mmHg at 3.2 L/min); and (3) exceptional biocompatibility, with a hemolysis index of 0.0061 g/100 L and surface temperature rise <1.9{degrees}C. This work transcends the presentation of a single device; it establishes a systematic, physics-driven design paradigm that transforms extreme miniaturization from a constraint into a catalyst for performance, applicable to next-generation implantable mechatronic systems.

bioengineering↗

bioRxiv2026

Multimodal Profiling of Repair-associated Immune Dynamics in a Mouse Model of Menstruation

Despite the importance of inflammation to menstruation, we lack detailed understanding of how immune dynamics contribute to endometrial repair. We performed detailed phenotypic characterisation of uterine immune cells using single cell RNA sequencing, flow cytometry and multiplex immunohistochemistry in a mouse model of simulated menstruation. Uterine tissues were collected from age-matched controls or from key phases of menstruation, including tissue breakdown, repair and remodelling. Our findings reveal distinct compositional changes across different phases of menstruation and highlight predominant roles for monocytes, macrophages, and neutrophils in endometrial repair. Immunohistochemistry revealed the spatial association of these myeloid cell subsets with areas of tissue repair and remodelling. Bioinformatic analysis highlighted key roles for monocyte, macrophage and neutrophil signalling during endometrial repair with thrombospondin 1 and secreted phosphoprotein 1 emerging as key signalling pathways. These data significantly advance our understanding of menstrual physiology and identify potential therapeutic targets for menstrual disorders. summaryThis study investigates immune cell dynamics in a mouse model of menstruation, highlighting roles for monocytes, macrophages, and neutrophils in non-fibrotic endometrial repair, and identifies key signalling pathways as potential therapeutic targets for menstrual disorders.

immunology↗

bioRxiv2026

The Evolution of Biomineral Armor in Fungus-farming Ants

Biomineralization has enabled remarkable adaptations across the animal kingdom, including defensive structures and rock-grinding teeth. Although calcium carbonate is a common biogenically formed mineral found in all extant animal phyla, it is only recently known in insects and almost universally occurs with minimal magnesium content. A high-Mg calcite armor layer, covering most of the exoskeleton, was recently discovered in the fungus-farming ant Acromyrmex echinatior. Here, using a combination of scanning electron microscopy, energy-dispersive spectroscopy, and X-ray diffraction, paired with genome-scale phylogenetic analysis based on ultraconserved elements (UCEs), we characterize the evolution of biomineralization in fungus-farming ants. We show the presence of high-Mg calcite biomineral in 35 of 50 fungus-farming ant species studied, including taxa that span all major agricultural lineages. The biomineral is absent in all 16 myrmicine outgroup ant species, indicating an origin of the biomineral within ant agriculture, with ancestral state reconstruction analysis slightly supporting multiple origins within the fungus-farming ant clade. We then show that the occurrence of the biomineral is closely associated with the ancient mutualism with antimicrobial-producing Pseudonocardia, finding biomineral presence to be significantly correlated with the Pseudonocardia symbiont and the cuticular symbiotic structures that maintain these bacteria. Furthermore, we reveal significant inter-species variation in mineral composition and coverage, as well as intra-colony caste-specific differences, highlighting its adaptive complexity. Collectively, this work demonstrates that the innovation of a high-Mg calcite armor is strongly associated with the evolution of ant agriculture, revealing a rare biomineral to be widespread in the fungus-farming ants.

evolutionary biology↗

bioRxiv2026

The BELL-type homeobox transcription factor RLC3/OsBLH4 controls leaf rolling and drought tolerance via KNOX-BELL-lignin regulatory network in rice

O_LIModerate leaf rolling in rice is crucial for plant architecture and stress adaptation, but its molecular regulation remains unclear. We investigated the role of RLC3/OsBLH4, a BELL-type homeobox transcription factor, in controlling leaf rolling and drought tolerance, addressing gaps in lignin biosynthesis and cell wall development mechanisms. C_LIO_LIWe used gene map-based cloning (rlc3-1, rlc3-2), CRISPR/Cas9 knockout lines (rlc3-ko#11, rlc3-ko#12), and allelic complementation to validate RLC3s function. Additionally, we employed biochemical assays, gene expression analysis, and protein interaction studies to explore its regulatory network. C_LIO_LIRLC3 mutations impaired lignin biosynthesis and secondary cell wall formation, reducing bulliform cells area and causing midrib defects. These structural abnormalities accelerated water loss, leading to excessive leaf rolling and compromised drought tolerance. Mechanistically, RLC3 directly activates lignin synthesis genes (OsPAL5, OsCOMT5, OsCCR4, OsCAld5H1) and interacts with KNOX transcription factors (OSH1, OSH45, OSH71) to form a KNOX-BELL complex, further regulating lignin content and cell wall development. C_LIO_LIRLC3 orchestrates lignin deposition and secondary cell wall development to control leaf rolling, water transport, and drought tolerance. This study reveals a novel KNOX-BELL-lignin regulatory module governing leaf morphology and stress adaptation, offering targets for crop improvement under drought conditions. C_LI

plant biology↗

bioRxiv2026

Decomposing multi-scale dynamic regulation from single-cell multiomics with scMagnify

Deciphering the highly coupled regulatory circuits that drive cellular dynamics remains a fundamental goal in biology. However, capturing the multi-scale time-lagged dynamics and combinatorial regulatory logic of gene regulation remains computationally challenging. Here we present scMagnify, a deep-learning-based framework that leverages multiomic single-cell assays of chromatin accessibility and gene expression via nonlinear Granger causality to reconstruct and decompose multi-scale gene regulatory networks (GRNs). Benchmarking on both simulated and real datasets demonstrates that scMagnify achieves superior performance. scMagnify employs tensor decomposition to systematically identify combinatorial TF modules and their activation profiles across different time-lags. It enables a hierarchical dissection of the regulatory landscape-- from the activity of individual regulator to the combinatorial logic of regulatory modules and intercellular communications. We applied scMagnify to human hematopoiesis and mouse pancreas development, where it successfully recovered known lineage-driving regulators and provided novel insights into the combinatorial logic that governs cell fate decisions. Furthermore, in the context of kidney injury, scMagnifys intracellular communication module mapped key signaling-to-transcription cascades linking microenvironment cues to pathological epithelial cell changes. In summary, scMagnify provides a powerful and versatile computational framework for dissecting the multi-scale regulatory logic that governs complex biological processes in development and disease.

bioinformatics↗

bioRxiv2026

SPCoral: diagonal integration of spatial multi-omics across diverse modalities and technologies

Spatial multi-omics is indispensable for decoding the comprehensive molecular landscape of biological systems. However, the integration of multi-omics remains largely unresolved due to inherent disparities in molecular features, spatial morphology, and resolution. Here we developed SPCoral for diagonal integration of spatial multiomics across adjacent slices. SPCoral extracts spatial covariation patterns via graph attention networks, followed by the use of optimal transport to identify high-confidence anchors in an unsupervised, feature-independent manner. SPCoral utilizes a crossmodality attention network to enable seamless cross-resolution feature integration alongside robust cross-omics prediction. Comprehensive benchmarking demonstrates SPCorals superior performance across different technologies, modalities and varied resolutions. The integrated multi-omics representation further improves spatial domain identification, effectively augments experimental data, enables cross-modal association analysis, and facilitates cell-cell communication. SPCoral exhibits good scalability with data size, reveals biological insights that are not attainable using a single modality. In summary, SPCoral offers a powerful framework for spatial multi-omics integration across various technologies and biological scenarios.

bioinformatics↗

bioRxiv2026

Neural subspace reorganization reflects value-based decision making

Value-based decision making requires maintaining and comparing multiple option representations associated with different values. Then, the chosen option must be communicated to downstream regions to drive behavior. The neural circuits involved in value-based decisions are increasingly well understood, but less understood is how decisions shape option representations. We recorded from lateral prefrontal cortex (LPFC), a central hub for transforming options into actions, while non-human primates (NHPs) held two sequentially presented option-value pairs (spatial targets and abstract reward cues) in working memory, then chose the option with the higher value. This revealed how decisions dynamically reorganize option representations in LPFC. We found that, once decisions could be made, representations of chosen and unchosen options rotated into orthogonal subspaces and the chosen option representation was expanded. Before decisions, the first- and second-presented options were maintained separately. After decisions, the chosen option was rotated into a subspace with a consistent representation of the prescribed action, regardless of its presentation order. This suggests a mechanism for value-based decisions where the decision drives a neural subspace reorganization that facilitates selective and efficient readout of the chosen action.

neuroscience↗

bioRxiv2026

cGAS-mediated IFN-I signaling contributes to disease progression in drug-refractory epilepsy

Epilepsy is a prevalent neurological disease with a third of patients becoming non-responsive to antiepileptic drugs and developing drug-refractory epilepsy (DRE). Here we report that DRE disease progression is contributed by overactive cyclic GMP-AMP synthase (cGAS), a double-stranded DNA sensor that induces type I interferon (IFN-I) signaling. In human DRE microglia, we observe a robust IFN-I signature and the activation of upstream cGAS-STING signaling. Further, in mouse models of Dravet syndrome, a genetic form of DRE, we observe the activation of the cGAS pathway. We show that microglial cGAS can be activated by DNA released from hyperexcitable neurons. Genetic reduction and pharmacological inhibition of cGAS reduces epileptic phenotypes, glial inflammatory signatures, and neuronal transcriptomic changes, underscoring the therapeutic potential of targeting cGAS for DRE treatment.

neuroscience↗

bioRxiv2026

Notch signaling in the embryonic ectoderm promotes periderm cell fate and represses mineralization of vibrissa hair follicles

The Notch signaling pathway is a critical means to regulate cell fate choice in animals. Appropriate regulation of this pathway is also required for human face formation as both loss and gain of function mutations of Notch signaling can cause syndromes with craniofacial abnormalities. Here we examine the consequences of manipulation of Notch signaling in the early mouse embryonic ectoderm by either removing the transcriptional effector Rbpj or expressing a constitutively active form of the Notch1 intracellular domain. Loss of Rbpj resulted in cleft secondary palate but strikingly was also associated with the ectopic mineralization of vibrissa follicles. In contrast, activation of Notch signaling resulted in multiple embryonic defects including a fully penetrant bilateral cleft lip and palate. Further, single cell RNA-seq data indicated a switch from a basal epithelial cell identity towards periderm when Notch signal transduction was elevated. These cell fate changes were accompanied by misregulation of genes and pathways known to impact human and mouse orofacial clefting including Grhl3, Irf6, and Wnt pathway. Together, these findings provide insight into human craniofacial conditions caused by misregulated Notch activity. SUMMARY STATEMENTOur studies demonstrate that Notch signaling in the embryonic ectoderm stimulates periderm cell fate while also repressing transformation of the inner root sheath of whisker follicles into mineralized tissue.

developmental biology↗

bioRxiv2026

ProMeta: A meta-learning framework for robust disease diagnosis and prediction from plasma proteomics

The plasma proteome offers a dynamic window of human health, capturing the real-time intersections between genetics and physiology. However, the application of deep learning to proteomics is currently hindered by a reliance on large-scale labeled datasets, rendering standard models ineffective for rare or novel diseases where patient samples are inherently scarce. Here, we present ProMeta, a meta-learning framework designed to enable robust disease modeling under extreme data restrictions. By integrating knowledge-guided pathway encoding with bi-level meta-optimization, ProMeta projects unstructured proteomic profiles into biologically interpretable functional tokens. This architecture allows the model to learn a global initialization containing transferable biological priors from biobank-scale data, facilitating rapid adaptation to novel tasks. Through comprehensive benchmark experiments, ProMeta consistently outperformed transfer learning and traditional machine learning baselines in both disease diagnosis and prediction tasks. In the most challenging 4-shot scenarios (utilizing only 2 cases and 2 controls), the model achieved robust generalization with an average AUROC of [~] 0.69, representing a 24.6% relative improvement over the best-performing baseline methods. Mechanistic investigation revealed that ProMeta disentangles cases from controls in the latent space prior to task-specific adaptation, confirming the acquisition of universal biological rules rather than rote memorization. Furthermore, gradient-based interpretation identified disease-specific protein biomarkers and functional pathways consistent with known pathophysiology. Collectively, ProMeta overcomes the data-scarcity bottleneck in precision medicine, providing a scalable, interpretable framework for characterizing the full spectrum of human diseases, particularly for rare conditions lacking extensive clinical cohorts.

bioinformatics↗

bioRxiv2026

Shared Maturation Pathways of HIV-1 Envelope-reactive V3-glycan bnAb Lineages in Human and Rhesus Macaque

ABSTRACTUnderstanding broadly neutralizing antibody (bnAb) lineage development in rhesus macaques (RMs) infected with Simian-HIV (SHIV) may inform HIV-1 vaccine designs. We analyzed HIV-1 envelope-antibody coevolution in 18 RMs infected by SHIV.BG505 (subtype A) and found highly conserved patterns of antibody recognition and Env escape, including in three animals that developed V3-glycan bnAbs. From one RM with V3-glycan targeted plasma breadth, we isolated 203 members of a single clonal Ab lineage designated DH1030. DH1030 Abs demonstrated striking genetic, functional and structural similarities with the human V3-glycan bnAb lineage DH270, which was isolated from an individual with subtype C HIV-1 CH848 infection. Notably, human-DH270 and macaque-DH1030 bnAbs shared early improbable mutations in HCDR2 that were critical for bnAb development. Thus, key improbable mutations and convergent patterns of antibody evolution and epitope recognition were shared across primate species and distinct HIV-1 subtypes, findings that may be leveraged in new HIV-1 vaccine designs. ONE SENTENCE SUMMARYBroadly neutralizing antibodies targeting HIV-1 envelope surface protein develop via a common maturation pathway across primate phylogeny.

immunology↗

bioRxiv2026

Wetness modulates the effects of grazing on net ecosystem productivity in global grasslands

Overgrazing has induced widespread grassland degradation globally. However, how grazing intensity affects ecosystem carbon dioxide (CO2) fluxes with wetness fluctuations in grasslands at a global scale remains poorly understood. Here we measured ecosystem CO2 fluxes covering the 7th to 11th years of a continuous grazing experiment in a typical steppe, and conducted a meta-analysis of 585 observations by collecting relevant data in global grasslands. Our experimental results showed that mean gross primary productivity (GPP) and ecosystem respiration (ER) were decreased under heavy grazing (HG) compared with control without grazing (CK), whereas net ecosystem productivity (NEP) was not different between HG and CK in the typical steppe. The NEP was higher under light grazing in the wetter years, but it was not different between LG and CK under drier years in the typical steppe. The structural equation model showed that grazing altered NEP by increasing soil temperature and relative growth rate, while decreasing AGB. In contrast, grazing decreased GPP, ER and NEP, respectively, in global grasslands. Both our field experiment and the meta-analysis revealed that the response of NEP to light grazing, rather than heavy grazing, was lineally correlated with the wetness index. Higher wetness and aboveground biomass (AGB) increased the response of NEP to grazing in global grasslands. However, heavy grazing reduced NEP and AGB even under higher wetness indices in global grasslands, resulting from a loss of their resilience in long-term heavy grazing. These findings indicate that light grazing appears to be a promising management to promote plant relative growth rate and carbon sequestration. Overall, the meta-analysis and field experiment jointly provide global perspectives on the response of ecosystem CO2 fluxes to grazing intensity and improve our understanding of the factors influencing the response of ecosystem CO2 fluxes to grazing intensity.

ecology↗

bioRxiv2026

Endothelin 2-Mediated Neuroinflammation Drives Hypertension-Associated Retinal Dysfunction

Systemic hypertension is a significant risk factor for glaucoma, a leading cause of irreversible blindness, yet the mechanistic basis connecting the two conditions remains elusive. Here, we demonstrate that hypertensive rats develop accelerated retinal degeneration characterized by retinal thinning, functional impairment, reduced perfusion, and progressive neuroinflammation. Critically, these changes occur despite persistently lower intraocular pressure (IOP), indicating an IOP-independent mechanism of pathology. Transcriptomic and biochemical analyses identified a robust activation of the retinal endothelin system, with endothelin-2 (EDN2) being the earliest and most significantly upregulated component. AAV-delivered retinal Edn2 knockdown completely restored retinal function, ameliorated neuroinflammation, and enhanced retinal blood flow in hypertensive rats. Pharmacological blockade of endothelin receptor type A (EDNRA), but not type B, replicated these protective effects without altering IOP. Our findings establish EDN2 as a central, IOP-independent driver of hypertension-associated retinal neurodegeneration and identify the endothelin-EDNRA axis as a potential therapeutic target to prevent vision loss in hypertensive patients.

neuroscience↗

bioRxiv2026

Data-Driven Retrieval of Effective Point Spread Functions for Super-Resolution Optoacoustic Imaging

Localization-based super-resolution techniques have revolutionized biomedical imaging by surpassing classical diffraction limits. However, their performance is fundamentally constrained by distortions of the point spread function (PSF) induced by the system and the sample, which are particularly prominent in the case of spatially under-sampling. Here we introduce a data-driven effective point spread function retrieval (DEPR) method that directly learns continuous, field-dependent system responses from experimental point source datasets. Through statistical aggregation of thousands of targets and iterative self-supervised refinement, DEPR captures spatially variant imaging characteristics in situ without prior assumptions or external calibrations. When integrated into the localization optoacoustic tomography (LOT) pipeline, DEPR achieves accurate sub-pixel localization despite under-sampled conditions, thus enhancing resolution while reducing computational burden. We demonstrate its efficacy by in vivo imaging of the murine brain microvasculature using microparticle contrast agents in the first (NIR-I) and second (NIR-II) near-infrared windows, achieving significant improvement in data utilization efficiency and substantial reduction of gridded artifacts compared to conventional approaches. The method resolves vascular structures with [~]41 m separation across a [~]3 mm imaging depth range. This framework addresses fundamental challenges shared across diverse localization-based imaging modalities, offering a robust and generalizable strategy for high-precision imaging in complex biological systems.

neuroscience↗

bioRxiv2026

OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway

Osteoclastogenesis-associated transmembrane protein 1 (OSTM1) is a glycosylated, membrane-integral protein that regulates lysosomal homeostasis, with loss-of-function mutations causing autosomal recessive osteopetrosis. Through a whole-genome CRISPR/Cas9 screen, we identified OSTM1 as a previously unrecognized tumor suppressor in B-cell malignancies. Consistent with this role, OSTM1 is frequently deleted or downregulated across a broad spectrum of human B-cell cancers. In mice, B-cell-specific monoallelic or biallelic ablation of Ostm1 cooperates with Cdkn2a loss to drive lymphomagenesis with near-complete penetrance. Mechanistically, we uncover a cytosolic, non-glycosylated fraction of OSTM1 that functions as a ubiquitin E3 ligase to promote proteasomal degradation of phosphodiesterase 3B (PDE3B). As PDE3B hydrolyzes cAMP and suppresses the tumor-protective PKA/CREB/CREBBP signaling axis, loss of OSTM1 leads to PDE3B stabilization, attenuation of cAMP signaling, and enhanced oncogenic transformation. Together, our findings establish OSTM1 as a critical suppressor of B-cell lymphomagenesis through regulation of the cAMP/PKA/CREB pathway.

cancer biology↗

bioRxiv2026

Small brown planthopper infestation enhances it reproduction and insecticide tolerance by manipulating glucose distribution and levels in rice

The evolutionary arms race between plants and insects involves not only direct defense and counter-defense but also sophisticated resource manipulation. However, how herbivorous insects respond to host nutritional signals to modulate their fitness traits remains unclear. This study investigates how the small brown planthopper (SBPH, Laodelphax striatellus) manipulates host plant carbohydrate allocation, and to elucidate the molecular mechanisms by which the acquired glucose enhances SBPH fecundity and insecticide tolerance. Using molecular, pharmacological, and biochemical approaches, we found that SBPH infestation induced systemic carbohydrate reallocation in rice, elevating whole-plant glucose levels by promoting aerial accumulation while depleting root reserves. Host-derived glucose enhanced SBPH fecundity by activating the target of rapamycin (TOR) pathway, upregulating juvenile hormone (JH) signaling, and increasing vitellogenin production. For imidacloprid tolerance, glucose boosted glutathione S-transferase (GST) activity via two synergistic mechanisms: by upregulating glutamate cysteine ligase (GCL) to increase glutathione synthesis, and transcriptionally via the glucose-TOR-JH axis to induce LsGSTe1 (SBPH epsilon class GST) and LsGSTo1 (SBPH omega class GST) expression. Our findings establish host-derived glucose as a central signaling molecule that SBPH utilizes to modulate conserved pathways for simultaneous optimization of reproduction and insecticide resistance. This reveals a multifaceted nutrient-responsive mechanism in insect pests and identifies the glucose-TOR-JH axis as critical molecular targets for developing nutrient-based pest control strategies, such as disrupting insect nutrient-sensing pathways or modulating host carbohydrate metabolism. HighlightsO_LISBPH infestation elevates whole-plant glucose levels by promoting aerial accumulation while suppressing root abundance. C_LIO_LISBPH-induced glucose in the rice aerial tissues boosts reproduction of SBPH via TOR-JH-Vg pathway. C_LIO_LISBPH-induced glucose in the rice aerial tissues enhances imidacloprid tolerance of SBPH through GCL-GSH-GST and TOR-JH-GST axis. C_LI Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=152 SRC="FIGDIR/small/701313v2_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@39e084org.highwire.dtl.DTLVardef@1c310cborg.highwire.dtl.DTLVardef@1838575org.highwire.dtl.DTLVardef@1aedebe_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗