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Biology subjects

Jin, G.

Publications and source records attributed to Jin, G..

At least 19 recordsLinked to original sources

General Purpose AI for Public Data Analysis and Experimental Hypothesis Generation

Public molecular datasets can support biological questions beyond those addressed in the original studies. We examined how general-purpose AI could help generate and investigate such questions through four complementary investigations. Interactive single-cell analysis identified Apelin signaling as a candidate for promoting mesendoderm differentiation of human pluripotent stem cells, although subsequent experiments did not establish an effect under the tested conditions. Autonomous analyses then searched public single-cell data for tumor antigens that could be targeted by engineered immune cells. Three multiple-myeloma runs shared 50 candidates and repeatedly recovered BCMA and CD38, whereas three pancreatic ductal adenocarcinoma runs produced different exploratory results and nominated no target meeting their selection criteria. To examine whether published datasets could yield additional biological insights, we conducted two separate AI analyses of anonymized lung single-cell data without providing the original publication. One analysis was performed without information about the tissue type or disease status, while the other was provided with this information. Without tissue or disease information, the AI identified lung cell populations and inferred disease-associated tissue remodeling. The analyses also generated additional biological questions, eight of which showed statistical support in an independent patient dataset, including coordinated antioxidant-related expression across epithelial cell types and increased fibroblast CRYM expression. Finally, a broader public-data analysis integrated RNA expression, proteomics, CRISPR-based functional screening, and normal-tissue expression to prioritize 213 potential therapeutic targets for pancreatic cancer. Combining these measurements helped distinguish candidates with similar RNA evidence and assess their functional relevance and expression in normal tissues, although therapeutic selectivity remains to be established. Together, these investigations show how general-purpose AI can extend an experimental biologist's use of public data, generate testable hypotheses and identify biological relationships for further study. They also show why completing an analysis and obtaining a reproducible expression pattern are distinct from establishing an experimental or therapeutic effect.

bioinformatics↗

Targeting Cardiac Fibrosis with Chimeric Antigen Receptor Neutrophils Derived from Human Pluripotent Stem Cells

Heart failure remains a leading cause of global morbidity and mortality, with cardiac fibrosis contributing to disease progression. Following myocardial injury, activated cardiac fibroblasts orchestrate adverse extracellular matrix (ECM) remodeling, which leads to tissue stiffening and compromised contractility. Despite the clinical importance of cardiac fibrosis, current pharmacological interventions modulate disease progression without directly eliminating activated fibrogenic cells. To target these cells directly, we engineered human pluripotent stem cell (hPSC)-derived neutrophils expressing a chimeric antigen receptor (CAR) directed against fibroblast activation protein (FAP). In vitro, FAP CAR neutrophils exhibited increased reactive oxygen species-associated fluorescence during fibroblast co-culture and dose-dependent cytotoxicity in 2D cultures, while reducing fibroblast-associated fluorescence in 3D cardiac organoids without a significant reduction in cardiomyocyte-associated cardiac troponin T staining. FAP CAR neutrophils also showed increased iNOS and decreased Arginase-1 expression compared with unmodified neutrophils, consistent with a shift toward an N1-associated polarization profile. Analysis of public cardiac single-cell and single-nucleus RNA-sequencing datasets identified temporal patterns of immune-associated expression and fibroblast activation that informed treatment timing. In a murine myocardial infarction (MI) model, mice treated systemically with FAP CAR neutrophils showed higher day 7 left ventricular ejection fraction than PBS-treated mice in an exploratory comparison. Together, these findings support further evaluation of hPSC-derived FAP CAR neutrophils as an immunotherapeutic approach to cardiac fibrosis.

bioengineering↗

Coupling a developmental promoter to CRISPR interference for Wnt pathway regulation in human pluripotent stem cells

While directed differentiation of human pluripotent stem cells commonly relies on the timed delivery of extracellular factors, these uniform treatments often yield heterogeneous responses across cell populations. Linking intracellular gene regulation directly to an emerging developmental state offers a complementary strategy to coordinate these differentiation signals from within the cell. Here, we explored this approach by coupling a T/Brachyury promoter to CRISPR interference targeting CTNNB1, which encodes the canonical Wnt signaling mediator {beta}-catenin. A T-promoter EGFP reporter line exhibited transiently increased activity during early differentiation, supporting the use of this promoter as a developmentally responsive input. We then combined the promoter with dCas9-KRAB and a CTNNB1-targeting guide RNA. Cas9-mediated integration was accompanied by indels at the CTNNB1 target site, whereas a Cas12a-mediated integration strategy yielded clones with no indels detected by ICE analysis. During differentiation, the selected T-dCas9 CTNNB1 clone showed reduced CTNNB1 expression and attenuated induction of Wnt associated genes. Together, these findings provide a proof of concept for combining a developmental promoter with a programmable intracellular regulator and identify a strategy for separating circuit integration from unintended target-site editing. This modular approach provides a foundation for developing genetic interventions whose expression is linked to developmental state.

synthetic biology↗

PD-1 regulates CD4+ T cell-mediated CD8+ T cell responses in the brain to balance viral control and neuroinflammation

Programmed cell death protein 1 (PD-1) is expressed by T cells during progressive multifocal leukoencephalopathy (PML), a life-threatening brain disease caused by the human-only JC polyomavirus. Why PD-1 blockade finds variable success in PML patients is unclear. Brain CD4+ and CD8+ T cells are PD-1high during mouse polyomavirus (MuPyV) encephalitis. Here, we show that PD-1 loss during MuPyV infection acts in a brain-autonomous manner to increase the magnitude of brain-infiltrating CD4+ and CD8+ T cells and the function of virus-specific CD8+ T cells; in concert, brain virus levels decline and neuroinflammation increases. Deletion of PD-1 in CD4+ T cells, but not CD8+ T cells, recapitulates effects of global PD-1 loss. Single-cell RNA sequencing shows that PD-1-deficient CD8+ T cells cluster as effectors while transcripts associated with proliferation and function are upregulated with loss of PD-1. Thus, CD4+ T cell-intrinsic PD-1 signaling balances antiviral defense against neural injury during polyomavirus CNS infection.

immunology↗

CART-GPT: A T Cell-Informed AI Linguistic Framework for Interpreting Neurotoxicity and Therapeutic Outcomes in CAR-T Therapy

Chimeric antigen receptor (CAR) T cell therapy holds transformative potential for hematologic malignancies, yet predicting patient-specific treatment efficacy and neurotoxicity remains a major clinical challenge due to the complex and heterogeneous nature of the infused CAR-T cell populations. Here, we introduce CART-GPT, a transformer-based model fine-tuned on a curated atlas of 1.12 million CAR-T single-cell RNA-seq profiles annotated with clinical outcomes. CART-GPT is the first AI model developed for CAR-T therapy that predicts both treatment response and the risk of immune effector cell-associated neurotoxicity syndrome (ICANS), achieving state-of-the-art performance (AUC ~0.8) and marking a significant advance in the field. The model provides interpretable insights, revealing that neither therapeutic efficacy nor neurotoxicity is driven by individual cell types alone, but by the combined influence of discrete, distinct subsets across diverse T cell states and transcriptional programs. A novel cell aggregation strategy links single-cell predictions to patient-level metrics, enhancing both accuracy and biological relevance. As a contribution to this ever-evolving field, we also release a comprehensive, annotated single-cell CAR-T atlas as a community resource to facilitate future research in immunotherapy. These advances demonstrate the potential of foundation models in single-cell biology to inform precision CAR-T treatment planning and facilitate the rational design of next-generation cell therapies.

bioinformatics↗

ODFormer: a Virtual Organoid for Predicting Personalized Therapeutic Responses in Pancreatic Cancer

Pancreatic cancer (PC) patient-derived organoids (PDOs) faithfully recapitulate therapeutic responses but face clinical translation barriers, including high costs and technical complexity. To address these problems and the lack of frameworks for PDO-based drug-response assays, we developed ODFormer, a computational framework that simulates PC PDOs to predict clinically actionable, patient-specific drug responses by integrating transcriptomic and mutational profiles. ODFormer first employed two encoders, pretrained on 30,000 pan-cancer bulk transcriptomics and 1 million PC single-cell profiles respectively, to distil tissue-and organoid-specific representations. Then, trained on our curated 14,000 PDO drug-response assay (across 183 PDOs and 98 drugs) using a transformer-augmented hybrid contrastive network, ODFormer significantly outperformed state-of-the-art methods, notably achieving a PCC >0.9 in predicting standardized drug response. Multi-cohort retrospective analyses further demonstrated that ODFormer-guided personalized therapy significantly improves clinical outcomes, without requiring physical organoid assays. Furthermore, ODFormer identified novel clinico-biological PC subtypes and revealed therapy resistance biomarkers by stratifying predicted responders and non-responders. These were validated using independent datasets including TCGA-PDAC. Notably, ODFormer-guided treatment efficacy showed high concordance with prospective clinical responses by CA19-9.

bioinformatics↗

Targeting protein glycosylation and cholesterol metabolism in chemoresistant pancreatic cancer

Chemotherapy remains the cornerstone of pancreatic ductal adenocarcinoma (PDAC) treatment. However, most cases of PDAC finally progress to advanced chemoresistant disease. This highlights an urgent need to develop new pharmacological strategies to overcome chemotherapy resistance using clinical grade inhibitors. Here, we established a biobank comprising 260 organoid lines derived from 322 pancreatic cancer patients. These organoids underwent extensive multi-omics profiling and drug sensitivity testing for both chemotherapy and targeted therapy. Increased protein glycosylation and cholesterol metabolism signaling pathways were especially enriched in chemoresistant organoid lines. Importantly, chemoresistant PDAC organoids were effectively targeted with statins, inhibitors of cholesterol synthesis. Statins treatment attenuated protein glycosylation, cholesterol levels, and the epithelial-to-mesenchymal transition (EMT) signature in PDAC organoids. We further conducted a phase 2 clinical trial (NCT06241352) combining atorvastatin with chemotherapy in patients with advanced chemoresistant pancreatic cancer. Among 29 patients, 21 (72.4%) demonstrated a response, with tumor markers decreasing by more than 20%, suggesting durable responses and potential clinical benefits in this challenging patient population. ClinicalTrials.gov identifier: NCT06241352.

cancer biology↗

Single-Cell eQTL Mapping Reveals Cell Type-Specific Genetic Regulation in Lung Cancer

Genome-wide association studies (GWAS) have identified over 50 lung cancer risk loci; however, the precise cellular context of these genetic mechanisms remains unclear due to limitations in bulk tissue eQTL analyses. Here, we present the largest single-cell eQTL atlas of human lung tissue to date, profiling 222 donors using multiplexed scRNA-seq. We identified 16,785 eQTLs across 17 cell types, with over 90% of sc-eQTLs and 59% eGene being cell-type-specific, and fewer than 23% were detectable in paired bulk datasets. Integration with GWAS for non-small cell lung cancer highlighted epithelial and immune cells as key contributors to genetic susceptibility, identifying 28 candidate genes within known risk loci and 24 in novel regions. Notably, 47% of established NSCLC susceptibility loci exhibited cell-type-specific pleiotropic genetic regulation. This study provides a valuable resource of lung sc-eQTLs and illuminates how genetic variation modulates gene expression in a cell-type-specific fashion, contributing to lung cancer susceptibility.

genetics↗

NeoAtlas and NeoBert: A Database and A Predictive Model for Canonical and Noncanonical Tumor Neoantigens

Neoantigens are classified into canonical and noncanonical types. Noncanonical neoantigens include those derived from noncoding regions, transposable elements (TE), and intron retention events, and they have recently gained considerable attention in cancer immunity. We curated 35,574 non-redundant neoantigen-HLA pairs from 14 immunopeptidomes studies, by analyzing unique features and differences across various sources of neoantigens. This knowledge enabled us to develop machine learning models for the prediction of different types of neoantigens. Our data and models are available at a public portal (https://ngdc.cncb.ac.cn/neoatlas) to facilitate broad access and future research. This resource offers advanced functionalities, including integration with epigenome browsers which allow easy navigation of epigenomic datasets to support and confirm the expression of neoantigens. We further demonstrate that combining our database with mass spectrometry analysis can identify noncanonical neoantigens. The resource we constructed holds significant value and promise for the development of neoantigen-based vaccines.

systems biology↗

Heterogeneous Sox2 transcriptional dynamics mediate pluripotency maintenance in mESCs in response to LIF signaling perturbations

The LIF signaling pathway and its regulation of internal factors like Sox2 is crucial for maintaining self-renewal and pluripotency in mESCs. However, the direct impact of LIF signaling on Sox2 transcriptional dynamics at the single-cell level remains elusive. Here, we employ PP7/PCP-mediated live imaging to analyze the transcriptional dynamics of Sox2 under perturbation of the LIF signaling pathway at single-cell resolution. Removal of the LIF ligand or addition of a JAK inhibitor heterogeneously affects the cell population, reducing the number of Sox2-active cells, rather than completely abolishing Sox2 expression. Moreover, Sox2-active cells under LIF perturbation exhibit significant reductions in mRNA production per cell. This reduction is characterized by decreased size and frequency of transcriptional bursting, resulting in shorter duration of Sox2 activity. Notably, cells with reduced or absent Sox2 expression demonstrate a significant loss in pluripotency, indicating that a reduction in Sox2 transcription (rather than a complete loss) is sufficient to trigger the transition from embryonic to an early differentiated state. In LIF-perturbed cells with Sox2 expression reduced to about 50% of non-perturbed levels, we observe a binary behavior, with cells either retaining or losing pluripotency-associated traits. Lastly, we find Sox2 expression is transcriptionally inherited across cell cycles, with Sox2-active mother cells more likely to reactivate Sox2 after mitosis compared to Sox2-inactive cells. This robust transcriptional memory is observed independent of LIF signaling perturbation. Our findings provide new insights into the transcriptional regulation of Sox2, advancing our understanding of the quantitative thresholds of gene expression required for pluripotency maintenance and highlighting the power of single-cell approaches to unravel dynamic regulatory mechanisms.

molecular biology↗

The CD4 T cell-independent IgG response during persistent virus infection favors emergence of neutralization-escape variants

How changes in the quality of anti-viral antibody (Ab) responses due to pre-existing or acquired CD4 T cell insufficiency affect virus evolution during persistent infection are unknown. Using mouse polyomavirus (MuPyV), we found that CD4 T cell depletion before infection results in short-lived plasma cells secreting low-avidity antiviral IgG with limited BCR diversity and weak virus-neutralizing ability. CD4 T cell deficiency during persistent infection incurs a shift from a T-dependent (TD) to T-independent (TI) Ab response, resembling the pre-existing TI Ab response. CD4 T cell loss before infection or during persistent infection is conducive for emergence of Ab-escape variants. Cryo-EM reconstruction of complexes of MuPyV virions with polyclonal IgG directly from infected mice with pre-existing or acquired CD4 T cell deficiency enabled visualization of shortfalls in TI IgG binding. By debilitating the antiviral IgG response, CD4 T cell deficiency sets the stage for outgrowth of variant viruses resistant to neutralization. ONE SENTENCE SUMMARYPre-existing and acquired CD4 T cell deficiency facilitates outgrowth of Ab-escape viral variants during persistent infection.

immunology↗

Liprin-α/RIM complex regulates the dynamic assembly of presynaptic active zones via liquid-liquid phase separation

Presynaptic scaffold proteins, including liprin-, RIM, and ELKS, are pivotal to the assembly of the active zone and regulating the coupling of calcium signals and neurotransmitter release, yet the underlying mechanism remains poorly understood. Here, we determined the crystal structure of the liprin-2/RIM1 complex, revealing a multifaceted intermolecular interaction that drives the liprin-/RIM assembly. Neurodevelopmental disease-associated mutations block the formation of the complex. Disrupting this interaction in neurons impairs synaptic transmission and reduces the readily releasable pool of synaptic vesicles. Super-resolution imaging analysis supports a role for liprin- in recruiting RIM1 to the active zone, presumably by promoting the liquid-liquid phase separation (LLPS) of RIM1. Strikingly, the liprin-/RIM interaction modulates the competitive distribution of ELKS1 and voltage-gated calcium channels (VGCCs) in RIM1 condensates. Disrupting the liprin-/RIM interaction significantly decreased VGCC accumulation in the condensed phase and rendered release more sensitive to the slow calcium buffer EGTA, suggesting an increased physical distance between VGCC and vesicular calcium sensors. Together, our findings provide a plausible mechanism of the liprin-/RIM complex in regulating the coupling of calcium channels and primed synaptic vesicles via LLPS for efficient synaptic transmission and uncover the pathological implication of liprin- mutations in neurodevelopmental disorders.

neuroscience↗

The AP2/ERF transcription factor HcERF5 confers drought tolerance via ABA-mediated signaling in kenaf

The APETALA2/ethylene response factor (AP2/ERFs) are pivotal in regulating abiotic stress responses in plants. However, the specific role of ERFs in kenafs response to drought stress remains unclear. In this study, a transcription factors HcERF5 was isolated from kenaf and its role in drought stress tolerance was analyzed. HcERF5 was found to localize in both nucleus and cytoplasm and could be significantly induced by polyethylene glycol-6000 (PEG-6000) and abscisic acid (ABA) in kenaf seedlings. In transgenic Arabidopsis expressing the HcERF5 promoter-driven {beta}-glucuronidase (GUS), strong GUS activity was observed in roots, stems, and leaves. Overexpression of HcERF5 in Arabidopsis enhanced seed germination rates under drought or ABA stress and improved drought tolerance in seedlings by increasing antioxidant enzyme activities, whereas aterf5 knockout lines exhibited the opposite trend. Additionally, HcERF5 overexpressing Arabidopsis showed significantly increased drought tolerance and reduced sensitivity to ABA. Furthermore, virus-induced gene silencing (VIGS) of HcERF5 in kenaf reduced drought tolerance, as evidenced by decreased antioxidant enzyme activity, increased stomatal aperture, and elevated levels of malondialdehyde (MDA), reactive oxygen species (ROS), and proline under drought stress. RNA-seq analysis further revealed that HcERF5 directly regulated ABA signaling pathway. Yeast-two-hybrid (Y2H) assays revealed 29 proteins that interact with HcERF5. Among them, the expression of downstream drought stress-related genes HcPRK, HcRD22, HcMAP2, HcCAB, HcCS, and HcCCoAOMT3 were significantly reduced in HcERF5-silenced plants. Overall, this study highlights the significant potential of HcERF5 in enhancing drought tolerance in kenaf. HighlightO_LIHcERF5 overexpression enhanced drought tolerance in kenaf, however silencing increased drought sensitivity. C_LIO_LIHcERF5 regulates ABA synthesis and increases kenaf stomatal conductance and density under drought stress. C_LIO_LIHcERF5 regulates plant hormone signal transduction, MAPK signalling, and phenylpropanoid biosynthesis in kenaf under drought stress. C_LIO_LIProtein interaction revealed HcERF5 interacts with six stress-response genes. C_LI

molecular biology↗

Identification of a Novel Ferroptosis Inducer with Dual Modulatory Effects on GPX4 Activity and Stability

Ferroptosis is a unique form of intracellular iron-dependent cell death that differs from apoptosis, necrosis, and autophagy. GPX4, an antioxidant defense enzyme, plays a pivotal role as regulator of ferroptosis. Extensive researches suggest that targeting GPX4 holds promise for cancer therapy. However, the current GPX4 inhibitors face challenges due to unfavorable drug-like properties, which hinder their progress in clinical development. In this study, we identified a novel inhibitor called MI-2, demonstrating potent ferroptosis-inducing capacity. Mechanistically, MI-2 effectively inhibits the activity of GPX4 by direct interaction. Furthermore, MI-2 promotes the degradation of GPX4 through its well-established target, MALT1. In multiple cancer models, MI-2 has demonstrated synergistic effects when combined with sorafenib or regorafenib, resulting in enhanced ferroptosis induction. These findings highlight the dual modulatory effects of MI-2 on GPX4 activity and stability, offering a promising starting point for the development of drug-like GPX4 inhibitors with translational potential.

cell biology↗

One infusion of engineered long-lasting and multifunctional T cells cures asthma in mice

The majority of common chronic human diseases are incurable, which affect a large portion of population and require life-long treatments that impose huge disease, economic and social burden. For example, asthma is the most common respiratory disease affecting over 300 million people and accounts for > 250,000 death annually, for which there is no cure. Unlike traditional therapyies, engineered T cells, such as chimeric antigen receptor CAR T (CAR-T) cells, function as living drugs and can cure some hematological malignancies, but whether engineered T cells can cure common diseases beyond cancer remains elusive. Here, we develop a curative therapy for asthma based on enginerred T cell. With IL-5 as the targeting domain and depletion of BCOR and ZC3H12A, we produce long-lasting CAR-T cells eradicating IL-5R+ eosinophils, termed Immortal-like and Functional IL-5 CAR-T cells (5TIF) cells. We further enginerred 5TIF cells to secrete an IL-4 mutein that blocks the singaling of both IL-4 and IL-13, two driver inflammatory cytokines in asthma, named as 5TIF4 cells. In multiple models of asthma, one infusion of 5TIF4 cells in fully immunocompetent mice, in the absence of any conditioning regimen, confers long-term depletion of pathological eosinophils and blockade of IL-4/IL-13 actions, resulting in sustained repression of type 2 inflammation and asthmatic symptoms. Furthurmore, 5TIF4 cells can also be induced in human T cells in NSG mice. Our data demonstrate that asthma, a common noncancerous disease, can be cured by a single infusion of engineered long-lasting and multifunctional T cells, which paves the way for curing common chronic diseases by engineered long-lived T cells.

immunology↗

Induction of immortal-like and functional CAR-T cells by defined factors

Long-term antitumor efficacy of chimeric antigen receptor (CAR)-T cells depends on their functional persistence in vivo. T cells with stem-like property show better persistence, but factors conferring T cells bona fide stemness remain to be determined. Here, we demonstrate the induction of CAR-T cells into an immortal-like and functional state, termed TIF. The induction of CAR-TIF cells depends on repression of two factors: BCOR and ZC3H12A, and requires antigen or CAR tonic signaling. The reprogrammed CAR-TIF cells possess almost infinite stemness resembling induced pluripotent stem cells but retain functionality of mature T cells, which exhibit superior antitumor effect. CAR-TIF cells enter a metabolically dormant state after elimination of target cells, which persist in vivo with a saturable niche and mediate memory protection. CAR-TIF cells represent a novel state of T cells with unprecedented stemness conferring long-term functional persistence of CAR-T cells in vivo, which have broad potentials in T cell therapies.

immunology↗

A muscle hypertrophy-derived myokine reprograms the stromal vascular fractions differentiation towards thermogenic adipocytes in subcutaneous adipose tissue

Skeletal muscle plays a significant role in both local and systemic energy metabolism; however, the cross-talk between skeletal muscle and adipose tissue remains largely unexplored. In this study, we identify the HIF2-Bambi-Thbs4 axis as a critical driver of muscle hypertrophy and metabolic improvement. Deletion of Bambi induces muscle hypertrophy and oxidative switching, thereby enhancing local and systemic metabolism under conditions of rodent chow and high-fat diets (HFD). Other than the metabolic regulation of skeletal muscle hypertrophy, we hypothesize that a portion of this improvement may be attributed to the metabolic reprogramming of the stromal vascular fraction (SVFs) of iWAT, promoting the development of beige adipocytes. Leveraging multi-omics approaches, we establish Thbs4 as a newly identified, muscle hypertrophy-derived myokine that serves as an essential regulator of this metabolic reprogramming. Thbs4 is upregulated in skeletal muscle during hypertrophy and aerobic exercise, localizes to the iWAT membrane, and facilitates the transformation of white adipocytes into beige adipocytes under conditions such as cold exposure, muscle hypertrophy, or aerobic exercise. Moreover, overexpression of Thbs4 elevates its plasma levels and leads to the transformation of white to beige adipocytes, therefore offering long-term protection against HFD-induced metabolic disorders. Conversely, Thbs4 knockout (Thbs4-KO) disrupts the metabolic reprogramming of SVFs and exacerbates metabolic syndromes induced by an HFD, mirroring the observed decline in Thbs4 levels in aged mice. Therefore, our findings underscore Thbs4s potential as both a long-term metabolic protective factor and a therapeutic target for the treatment of metabolic disorders. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=197 HEIGHT=200 SRC="FIGDIR/small/558627v1_ufig1.gif" ALT="Figure 1"> View larger version (63K): org.highwire.dtl.DTLVardef@1178e6org.highwire.dtl.DTLVardef@1184d4eorg.highwire.dtl.DTLVardef@7b592aorg.highwire.dtl.DTLVardef@1b0b03_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIBambi, a direct target gene of HIF2 in skeletal muscle, when deleted, triggers muscle hypertrophy and the transformation of white into beige adipocytes, improving systemic energy metabolism. C_LIO_LIThe metabolic reprogramming of stromal vascular fractions (SVFs) contributes to the observed improvements in energy metabolism and adipocyte hyperplasia. C_LIO_LIThbs4, a novel myokine produced in skeletal muscle during hypertrophy and aerobic exercise, plays a key role in the transformation of white into beige adipocytes. C_LIO_LIOverexpression of Thbs4 provides enduring protection against high-fat diet (HFD)-induced metabolic disorders, demonstrating its potential as a therapeutic target. C_LIO_LIThbs4 deletion abrogates the beneficial metabolic reprogramming of SVFs and exacerbates HFD-induced metabolic syndromes, further underlining its crucial role in metabolic regulation. C_LI

physiology↗

Phospholipase A2 activity is required for immune defense of European (Apis mellifera) and Asian (Apis cerana) honeybees against the American foulbrood pathogen, Paenibacillus larvae

Honeybees require a functioning immune system to defend against microbial pathogens. The American foulbrood pathogen, Paenibacillus larvae, is lethal to honeybees and one of the main causes of colony collapse. This study investigated the immune responses of Apis mellifera and Apis cerana honeybees against the bacterial pathogen P. larvae. Both species of honeybee larvae exhibited significant mortalities even at 102 [~] 103 cfu/mL of P. larvae by diet-feeding, although A. mellifera appeared to be more tolerant to the bacterial pathogen than A. cerana. Upon bacterial infection, the two honeybee species expressed both cellular and humoral immune responses. Hemocytes of both species exhibited characteristic spreading behaviors by cytoskeletal extension along with F-actin growth, and formed nodules upon P. larvae infection. Larvae of both species also expressed an antimicrobial peptide called apolipophorin III (ApoLpIII) in response to bacterial infection. However, these immune responses were significantly suppressed by a specific inhibitor to phospholipase A2 (PLA2). Each honeybee genome encodes four PLA2 genes (PLA2A [~] PLA2D), representing four orthologous combinations between the two species. In response to P. larvae infection, both species significantly up-regulated PLA2 enzyme activities and the expression of all four PLA2 genes. To determine the roles of the four PLA2s in the immune responses, RNA interference (RNAi) was performed by injecting gene-specific double stranded RNAs (dsRNAs). All four RNAi treatments significantly suppressed the immune responses, and specific inhibition of the two secretory PLA2s (PLA2A and PLA2B) potently suppressed nodule formation and ApoLpIII expression. These results demonstrate the cellular and humoral immune responses of A. mellifera and A. cerana against P. larvae. This study suggests that eicosanoids play a crucial role in mediating common immune responses in two closely related honeybees.

immunology↗