Search bioRxiv⌕ Search

Biology subjects

Yu, X.

Publications and source records attributed to Yu, X..

At least 37 records · Page 2Linked to original sources

Model Validation Protocols for Machine Learning in Small Molecule Drug Discovery

Machine learning (ML) models for molecular property prediction are increasingly deployed in drug discovery, yet their adoption in real-world scenarios requires an understanding of the conditions in which a model succeeds or fails. While standardized benchmarks are powerful instruments to measure and unlock progress in ML research, they should not be blindly treated as the end goal. Especially static and retrospective benchmarks, in which no true unknown test set is employed, limit our ability to robustly validate a model's performance. Building on the collective expertise of a cross-industry consortium, we present a model validation framework consisting of five recommendations that would enable the community to move beyond aggregate metrics toward understanding where and why molecular property prediction models fail. We connect evaluation choices to real-world applications and case studies encountered in pharmaceutical research. The framework proposes splitting strategies that mimic realistic distribution shifts and expose common failure modes. We apply the recommended framework to a recently released dataset of absorption, distribution, metabolism, and excretion (ADME) properties. Across two complementary model algorithms, our case studies reveal four distinct failure modes (extrapolation, interpolation, representation, and evaluation), showing that model errors arise not only from distribution shift but also from limitations in molecular representations. Our results show that commonly used evaluation protocols can significantly overestimate performance and may not detect important model failure modes. All software and data are released via https://github.com/srijitseal/polaris.

bioinformatics↗

DYNAMIC CONFORMATIONS IN THE ACTIVATION OF PINK1 KINASE

Under mitochondrial stress, the mitochondrial kinase PINK1 is activated to phosphorylate ubiquitin, which in turn recruits the E3 ligase Parkin, thereby initiating clearance of damaged mitochondria. Dysregulation of the PINK1-Parkin signaling pathway is associated with early-onset autosomal recessive Parkinson's disease. However, the mechanisms governing PINK1 conformational dynamics and activation in response to mitochondrial stress remain poorly understood. Here, we report that Tribolium castaneum PINK1 (TcPINK1) forms specific symmetric dimers via interactions between the kinase N-lobe and the regulatory C-terminal domain. These dimers undergo dynamic conformational transitions across distinct states, including an autoinhibited state, an inactive intermediate state, a primed-activation state and an active state. Moreover, TcPINK1 undergoes lateral trans-phosphorylation through dimer-dimer interactions. Notably, symmetric dimer formation is essential for Parkin recruitment during mitophagy. These findings provide a framework for understanding the conformational plasticity and allosteric regulation of PINK1 in mitophagy.

biophysics↗

MOLECULAR BASIS FOR PINK1 MATURATION

Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1), a key regulator of mitophagy, has been linked to the pathogenesis of Parkinson's disease (PD). PINK1 recruits Parkin, an E3 ubiquitin ligase, triggering mitophagy in response to mitochondrial damage. During mitophagy, the quantity, stability, and activity of PINK1 must be strictly regulated; however, the mechanisms governing these parameters under cellular stress are still unclear. Herein, we determined the structural basis for PINK1 maturation mediated by heat shock protein 90/cell division cycle 37/FK506-binding protein 51 (HSP90/CDC37/FKBP51) chaperone complex. We identified PINK1-associated proteins using liquid chromatography-tandem mass spectrometry (LC-MS/MS) and determined the structures of the complexes using Cryo-Electron Microscopy (Cryo-EM). Results showed that FKBP51 potentially interacts with a conserved leucine-proline-phenylalanine (LPF) motif on the activation loop of PINK1 and negatively regulates PINK1 functions in mitophagy. A PINK1 mutation located at the FKBP51 recognition site is linked to mitophagy deficiency, which can be partially rescued by specific inhibition of FKBP51. These findings reveal a general mechanism for PINK1 recognition by the HSP90/CDC37/FKBP51 chaperone complex and suggest a potential approach for upregulating PINK1 activity, which is impaired in PD.

biophysics↗

PASTRI: Resolving Stage-Specific Cell-State Dynamics from Annotated Cell Lineage Trees

Cellular transitions between phenotypic states are fundamental to development and disease, yet quantitative analysis of their dynamics remains challenging. Here we present PASTRI (Phylogenetic Adjacency-based State Transition Rate Inference), a computational framework that infers transition rates from cell lineages/phylogenies annotated with terminal phenotypic states, such as single-cell transcriptomes. We validate PASTRI using simulated lineages and the Caenorhabditis elegans embryonic lineage. Importantly, by leveraging cell pairs at varying phylogenetic distances, PASTRI accurately resolves stage-specific transition rates, circumventing the issue of developmental changes in dynamics. Applied to three cell phylogeny datasets from our lineage-tracing experiments spanning diverse developmental/disease models and tracing systems, PASTRI uncovers rate-limiting steps in the activation of hepatic stellate cells and the differentiation of primordial lung progenitors, as well as attractor states that support cancer cell proliferation. PASTRI thus opens up a venue for dissecting cell state transition dynamics from annotated cell lineage/phylogeny.

bioinformatics↗

PHOTORELEASE OF OXYTOCIN IN VIVO USING PHOTOSWITCHABLE NANOVESICLES MODULATES HIPPOCAMPAL CIRCUIT DYNAMICS AND SOCIAL BEHAVIOR

Achieving precise spatiotemporal control over neuropeptide delivery in vivo remains a major challenge, as conventional approaches lack temporal resolution and control over release kinetics or have limitations for in vivo applications. Here, we demonstrate that photoswitchable azobenzene-containing lipid nanovesicles ("azosomes") enable light-controlled release of neuropeptides in vivo in the brain of awake moving mice. Azosomes were infused into the hippocampus via optofluidic cannulas and activated using light stimulation in freely behaving mice. In vivo release kinetics were systematically characterized using calcein-loaded azosomes by varying light power, pulse duration, and post-infusion time. Oxytocin (OT)-loaded azosomes were used to assess bioactivity and receptor specificity using dual-color fiber photometry with the genetically encoded OT sensor (MTRIAOT), alongside pharmacological blockade with the oxytocin receptor antagonist OVTA (Ornithine-VasoTocin Analog). Azosomes enabled robust, repeatable, and light-dependent cargo release in vivo with tunable kinetics governed by stimulation parameters, with release efficiency controlled by light power and pulse duration. The system maintained functional stability for several hours post-infusion, with near-complete release achievable within a [~]2-hour window and minimal baseline leakage prior to stimulation. Controlled OT delivery produced rapid, receptor-specific increases in MTRIAOT signals and modulated CA2 hippocampal circuit activity, reducing excitatory neuronal transient frequency and amplitude while altering social interaction dynamics, including decreased latency to initiate contact. These findings establish, for the first time, photoswitchable nanovesicles as a versatile platform for spatiotemporally precise delivery of neuropeptides in vivo, overcoming key limitations of existing delivery strategies and providing a broadly applicable framework for manipulating neuromodulatory signaling with high temporal precision.

neuroscience↗

Plasma titration provides a physical ruler for cross-platform proteomics

Plasma proteomics is expanding across platforms and cohorts, and integrating these data for AI demands comparability at the protein level, not merely concordant associations1,2. Affinity and MS platforms use distinct probes (antibodies, aptamers, or peptides) and signal readouts, yielding contradictory cross-platform results3,4. Without a known quantitative truth, we cannot distinguish biology from measurement distortion, leaving no gold standard for integration. Here we introduce Plasmix--a plasma reference suite with predefined male:female ratios (M, 1:0; Y, 3:1; P, 1:1; X, 1:3; F, 0:1)--and show that preserving this quantitative titration gradient, not just technical repeatability, predicts cross-platform concordance and identifies protein measurements suitable for integration. Profiling Plasmix across five platforms (Olink, SomaScan, NULISA, AAgAtlas, and MS-DIA) and 12 protocols across 17 batches, we found discordance is dominated by signal generation, not sample identity, and platforms distort signals in a protein-specific manner. Crucially, proteins retaining the titration response showed stronger agreement in an independent cohort; anchoring to the Plasmix midpoint (P) via sample-to-reference ratios reduced distortions, extending harmonizable coverage by 10-20%. Plasmix thus provides a physical ruler to benchmark accuracy, identifying genuinely integrable measurements before pooling datasets or training AI models--a critical bottleneck for plasma proteomics.

molecular biology↗

A Principled Statistical Framework for Analyzing Spatial Patterns in Spatially Resolved Multi-Omics

Emerging spatial multi-omics technologies enable the profiling of molecular variation within its tissue context, yet existing methods for identifying spatially variable features lack principled approaches to experimental design and cross-sample inference. Here, we present STORM, a principled Statistical TOol for spatially Resolved Multi-omics, for rigorously analyzing spatial patterns in spatial multi-omics research. STORM incorporates a robust and efficient nonparametric test that quantifies local deviations in molecular feature measurements to detect spatial dependence across transcriptomic and proteomic data. It further estimates an interpretable spatial effect size, supports power calculations for both spatial locations and biological replicates, and enables formal group-level comparisons. In several simulated and experimental spatial multi-omics case studies, STORM demonstrates reliable performance in detecting spatial structures while offering quantitative support for study design decisions. Overall, STORM provides a principled statistical framework that unifies spatial hypothesis testing, effect size estimation, power analysis, and experimental design for spatial multi-omics data.

bioinformatics↗

Programmable Allosteric DNAzyme Coupled with CRISPR/Cas12a System for Multiplexed and Sensitive Detection of Extracellular Vesicle Derived MicroRNAs

Extracellular vesicle (EV)-derived microRNAs serve as important biomarkers for cancer diagnosis, yet their accurate detection remains limited by insufficient control of nucleic acid recognition and signal activation. Here, we identified a previously unrecognized feature of CRISPR/Cas12a, in which incorporation of ribonucleotides into single stranded DNA targets modulates Cas12a activation efficiency, revealing a hybrid DNA/RNA-dependent regulation of Cas12a activity. Leveraging this mechanism, we established a programmable detection strategy that enables sequence dependent tuning of Cas12a activation without the need for target amplification. By coupling DNAzyme mediated cleavage with Cas12a trans-cleavage, a cascade signal amplification system was established, enabling highly sensitive and selective detection of miRNAs. To facilitate clinical applications, an EV-based sample processing strategy was integrated to simplify isolation of EV associated miRNAs and allow direct miRNA detection without conventional RNA extraction. The resulting platform demonstrated robust discrimination of multiple miRNA targets in clinical cohorts and supported accurate classification of cancer subtypes according to expression signatures. By integrating machine learning analysis, the system accurate distinguished breast cancer (BC) patients from healthy donors (HD), as well as triple-negative breast cancer (TNBC) from BC. This study provides a mechanism-guided strategy for programmable CRISPR-based nucleic acid detection in complex biological samples.

bioengineering↗

Extracellular vesicles drive cross-genus mycovirus transmission and suppress two fungal diseases

Mycoviruses are typically transmitted vertically through fungal reproduction or horizontally via hyphal anastomosis, but identical viruses in phylogenetically divergent fungi hint at unknown inter-species transmission mechanisms. Here, we identify fungal extracellular vesicles (EVs) as mediators of cross-genus mycovirus transmission. Using the hypovirulent Botrytis cinerea strain IBc-374 (harboring 16 mycoviruses) as a donor, we show that up to 13 mycoviruses are horizontally transmitted to Sclerotinia sclerotiorum during dual culture or plant co-inoculation, even though these two fungi belong to different genera and are generally considered incapable of hyphal anastomosis. Electron microscopy reveals abundant vesicle structures in IBc-374 hyphae, and nanoparticle tracking analysis showed that the strain secretes >11-fold more EVs than a virus-free strain. RT-PCR detects genomic RNAs of 7 mycoviruses in purified EVs, and the full-length viral genome in EVs was further validated with BcHV5 as example by fluorescence in situ hybridization and RT-PCR. Incubation of protoplast-derived germlings of S. sclerotiorum or B. cinerea with IBc-374 EVs leads to infection by 4-6 donor mycoviruses, demonstrating EV-mediated cross-genus transmission. Injection of mycovirus-carrying EVs into tobacco leaves followed by fungal inoculation also transmits two hypoviruses to both species. Application of IBc-374 hyphal fragment suspension significantly reduces lesion sizes caused by both pathogens on plants, and rescued two pathogens carrying multiple mycoviruses exhibit hypovirulence and impaired growth. Our findings reveal EVs as a cell-free vector that bypasses vegetative incompatibility, providing a mechanistic basis for cross-species viral spread and opening avenues for EV-based virus cocktails to control multiple fungal diseases. IN BRIEFWu et al. discover that fungal extracellular vesicles (EVs) can package and transmit multiple mycoviruses across genera from Botrytis cinerea to Sclerotinia sclerotiorum. EV-mediated delivery overcomes vegetative incompatibility barriers and reduces disease caused by both fungal pathogens, offering a cell-free strategy for mycovirus-based biological control.

microbiology↗

INSM1 Regulates Neuroendocrine Plasticity and Tumor Progression in Prostate Cancer

AbstractNeuroendocrine prostate cancer (NEPC) is a highly aggressive and therapy-resistant subtype that arises from adenocarcinoma through lineage plasticity; however, the molecular mechanisms driving this transition remain incompletely defined. Insulinoma-associated protein 1 (INSM1), a zinc-finger transcription factor and established neuroendocrine lineage marker, has been implicated in a variety of neuroendocrine malignancies, yet its functional contribution to NEPC progression is not well understood. In this study, we demonstrate that INSM1 is consistently upregulated across NEPC patient tumors and experimental models, including both ASCL1 and NEUROD1 molecular subtypes, as revealed by integrated bulk and single-cell transcriptomic analyses. Functional studies revealed that INSM1 is sufficient to induce and necessary to maintain neuroendocrine lineage programs in prostate cancer, as overexpression promoted and depletion suppressed neuroendocrine-associated transcriptional networks. Mechanistically, pro-neural transcription factors, including ASCL1, NEUROD1, NEUROG3, and MYCN, directly or indirectly activate INSM1 expression, positioning it as a critical downstream effector of neuroendocrine lineage specification. Therapeutically, we identify homo-harringtonine (HHT), an FDA-approved protein synthesis inhibitor, as a potent suppressor of INSM1. HHT selectively reduces viability of INSM1-high NEPC cells at nanomolar concentrations, promotes ubiquitin-mediated degradation of INSM1, and significantly inhibits tumor growth in vivo. Notably, INSM1 depletion further enhances cellular sensitivity to HHT treatment. Collectively, our findings establish INSM1 as a key regulator of neuroendocrine plasticity and a promising therapeutic vulnerability in NEPC, providing a rationale for targeting INSM1 to suppress tumor progression.

cancer biology↗

Community diversity and interaction of bacterial, cyanobacteria and protist among aquatic and soil micro-food chains

Microorganisms, found in every environment, play an important role in recycling matter and providing energy to the ecosystem. Here, we used 18S and 16S metabarcoding to study bacteria, cyanobacteria and protist community diversity and functional ecology among different environments of typical lake, river, marine and soil from the Yangtze Delta of China. The results showed that the similarity of cyanobacteria and protozoa communities in soil and aquatic environments was both higher than that of bacteria and microalgae communities. While the diversity of cyanobacteria and bacteria in lake was higher than that in river, marine and soil, the diversity of microalgae and protozoa in river was higher than that in lake, marine and soil. The {beta} diversity of cyanobacteria and bacteria marked differences in lake from other environments. But The distribution of dominant families of cyanobacteria, bacteria, microalgae and protozoa is similar to diversity. While significant positive correlations were found among dominant species of cyanobacteria, protozoa, bacteria and microalgae in lake the dominant species among bacteria, microalgae and protozoa in river, marine and soil all showed more negative correlations. Our study provides the basis for understanding the functional ecology of microbes in the micro-food webs of different environments.

ecology↗

Evolutionary Origins and Synthetic Reconstruction of Gingerols

How new enzymatic activities become integrated with existing metabolic networks to generate lineage-restricted plant chemistry remains a central question in metabolic evolution, exemplified by gingerol biosynthesis in Zingiberaceae, whose complete enzymatic basis has remained elusive. Here, we resolve this problem by elucidating the evolutionary origins and the full biosynthetic pathway of gingerol through single-cell transcriptomics, functional screening, structural biology, comparative genomics and pathway reconstruction. A coordinated metabolic program operates in ginger oil cells, thereby guiding the identification of diketide-CoA synthases, gingerol synthases (GS) and gingerol reductases that together constitute the complete pathway. GS remodels the conserved type III polyketide synthase scaffold to organize a fatty acyl-CoA and a phenylpropanoid-derived intermediate for gingerol formation. Furthermore, GS arose through duplication and limited active-site remodeling of a curcumin synthase-like enzyme, accompanied by coordinated recruitment of precursor-supply and reduction pathways. Translating these principles into yeast achieves the first de novo microbial production of 6-gingerol from glucose at 12.4 mg/L. These findings reveal the evolutionary logic by which plants recruit and coordinate novel enzymatic activities to establish lineage-restricted metabolic program, providing a framework for understanding and engineering specialized metabolism across the plant kingdom.

synthetic biology↗

Seasonal Rebalancing of Assembly Processes and Cross-Domain Network Restructuring in Microbial Communities of a Large Eutrophic Lake

Harmful algal bloom (HAB) succession in eutrophic lakes arises from seasonal rebalancing of selection, dispersal, and drift across interacting microbial domains, yet process attribution remains limited due to the scarcity of cross-domain analyses. Using multi-marker eDNA metabarcoding (16S rRNA, 18S rRNA, 23S rRNA), we show that bacterioplankton, cyanobacteria, phytoplankton, and zooplankton in Lake Taihu undergo coordinated spring-summer transitions, with inter-seasonal turnover far exceeding spatial heterogeneity. Assembly regimes shifted coherently across domains: spring communities were dominated by strong homogeneous selection--especially among cyanobacteria and microeukaryotes--whereas summer communities moved toward drift- or neutrality-like dynamics under bloom-stage mixing that enhanced dispersal. Null- and neutral-model diagnostics supported these trends. Cross-domain co-occurrence networks restructured seasonally, with summer networks becoming more connected and substantially more robust, indicating that bloom conditions foster cohesive, robust interaction structures rather than destabilization. These findings provide evidence that bloom progression restructures aquatic microbiomes through a seasonal rebalance of selection, drift, and dispersal coupled with adaptive strengthening of cross-domain connectivity, providing a process-explicit framework for understanding community stability and ecosystem resilience in eutrophic lakes.

ecology↗

Uncovering key genes related to potato tuber starch concentration from the tuber bulking, maturation stage to storage

Potato is the worlds fourth major staple crop, and tuber starch is a critical dietary energy source and a food processing raw material. In this study, hybrid progenies of the high-starch cultivar Huasheng No.7 and China main commercial varieties were used as materials, high-throughput sequencing was performed on tuber samples at tuber bulking, maturation and storage stages. Combined with bioinformatics analysis, parent-progeny resequencing, SNP screening, the regulatory mechanism of tuber starch metabolism was explored. The results showed significant stage-specific transcriptional reprogramming in potato tubers: few differentially expressed genes (DEGs) were identified at tuber bulking and maturation stages, but massive transcriptional changes occurred during storage. XET family genes regulated cell wall remodeling and carbon translocation across all stages, and WRKY transcription factors specifically controlled starch homeostasis in stored tubers. The DEGs at different stage were induced by the SNPs from their parent, and the allele from the high-starch parent, Huasheng 7 may contribute the high-starch allele to the offsprings. One key gene, Soltu.DM.02G019910, which encoded {beta}-glucosidase, have a negatively relationship with tuber starch concentration. The low-starch potato breeding tubers shown higher significantly {beta}-glucosidase activity than high-starch breeding population at maturation stage. This study clarifies the molecular regulatory network of potato tuber starch metabolism and screens core regulatory genes from the tuber bulking stage to tuber storage, thereby providing theoretical support and genetic resources for molecular breeding of high-starch and storage-resistant potato varieties.

plant biology↗

Targeting neutrophil signaling networks in immune complex-mediated autoimmune disease

Fragment crystallizable gamma receptor (Fc{gamma}R)-induced signaling is a crucial process that determines the cellular response to immune complexes (IC) in autoimmune diseases. In several diseases including pemphigoid diseases (PD), such as epidermolysis bullosa acquisita (EBA), or rheumatoid arthritis (RA), neutrophils are prominently involved as effector cells, while others such as immune thrombocytopenia (ITP) are independent of neutrophils. At the same time, most diseases are commonly treated by broad-range immunosuppression accompanied by severe risk for adverse effects. Signal transduction inhibitors (STIs) have been successfully applied in cancer therapy. However, their use in autoimmune diseases is an emerging, but so far understudied potential treatment avenue. Therefore, we screened a target-selective compound library consisting of 155 STIs in a neutrophil-based assay and conducted a multiplex kinase activity profiling with IC-stimulated neutrophils. Thus, we found novel potential therapeutic targets that were validated both in vitro in functional neutrophil assays and in vivo in murine models of EBA Here, we demonstrate that both systemic and topical treatment with several individual STIs is effective in a prophylactic approach in these models. Furthermore, therapeutic treatment with the BTK inhibitor ibrutinib in the immunization-induced EBA model reduced disease severity by approximately 85 % and showed efficacy in additional experimental models of EBA, arthritis, and ITP. Together, the present study contributes to the elucidation of Fc{gamma}R-dependent signaling in neutrophils and identifies multiple novel promising treatment options including inhibition of PLC, PDK-1, PKC, p38, DNA-PK, KSP, c-Met, TBK-1 and BTK for IC-mediated autoimmune diseases.

immunology↗

Learning to read a second language establishes a parallel L2 representation alongside the native one in the VWFA

Learning to read a second language requires the brain to incorporate a new writing system into an already established native-language reading network, yet how this process reshapes the Visual Word Form Area (VWFA) remains poorly understood. Using fMRI with a passive viewing paradigm, we systematically investigated how VWFA responses to Chinese (L1) and English (L2) words evolved across three groups of native Mandarin-speaking children at distinct stages of L2 literacy acquisition: L2 pre-readers, L2 beginning readers, and L2 advanced readers. We combined univariate activation analyses, representational similarity analysis, and supervised machine learning classification to investigate two theoretical accounts of VWFA reorganization: the Overlay Model, which predicts stable L1 responses as L2 responses emerge, and the Competing Model, which predicts competitive reallocation of neural resources from L1 to L2. We found that although the VWFA already exhibited robust selective responses to L1 words, L2-word selectivity was absent in L2 pre-readers but emerged robustly in beginning readers, with L1-word selectivity remaining stable throughout. Representational similarity analysis further revealed that robust L2 word representations within the VWFA emerged only after children began learning to read L2, while L1 word representations remained stable across all three groups. Finally, supervised machine learning analyses successfully discriminated among the three L2 literacy groups on the basis of L2 but not L1 activation patterns, indicating that VWFA responses to L2 alone were sufficient to capture childrens stages of L2 literacy acquisition, whereas responses to L1 were insensitive to L2 learning experience, providing no support for the Competing Models prediction of competitive neural reallocation away from L1. Together, these findings support the Overlay Model, demonstrating that the VWFA incorporates a new writing system within its existing cortical resources without compromising L1 print processing.

neuroscience↗

Sustained epigenetic rejuvenation of serially engrafting human iPSC-derived HSCs

Hematopoietic stem cell (HSC) function declines with age, contributing to immunosenescence and inferior transplantation outcomes. Here, we generated iPSC-derived HSCs (iHSCs) from multiple adult donors and performed integrated epigenetic, transcriptional, telomeric, and functional analyses to see if they retain youthful identity across differentiation and serial transplantation. Longitudinal DNA methylation profiling revealed that, independent of donor age, epigenetic age was reset to near zero in iPSCs and remained under seven years across differentiation and transplantation. In contrast, hematopoietic identity was established through a two-phase process: directional remodeling during in vitro differentiation extinguished pluripotency programs and initiated hematopoietic regulatory networks, while long-term engraftment was associated with a second wave of promoter methylation differences that converged toward primary adult HSCs. Notably, methylation at age-associated sites and global entropy remained stable across both phases, and single-cell telomere analysis demonstrated restoration of telomere length in iHSCs compared to primary adult HSCs. Youthful epigenetic features were maintained through secondary transplantation. These findings demonstrate that long-term HSC identity can be achieved independently of epigenetic aging and establish a framework for evaluating rejuvenated stem cell-derived grafts in regenerative medicine.

cell biology↗

Bone Mechanosensing Dictates Hematopoietic Stem Cell Fate and Immune Homeostasis

The vertebrate water-to-land transition was accompanied by a six-fold increase in gravitational force, followed by the migration of hematopoietic stem cells (HSCs) from kidney or liver to the bone marrow, and the acquisition of enhanced immune functions to cope with novel environmental pressures. Bone senses mechanical loading and provides a microenvironment for HSC development, yet whether bone mechanosensation affects immune cell development and immune homeostasis remains unclear. Here, we unveil bone as a mechanosensory organ that translates mechanical force into hematopoietic instructions. Mechanical loading of bone directs HSCs toward lymphoid lineages in mice and non-human primates, whereas unloading favors myeloid commitment. This process requires osteocyte mechanosensor Piezo1, which induces loading-responsive bone-derived factors such as IL1R2, SERPINC1 and INMT, thereby restraining inflammatory signaling and guiding HSC differentiation. Osteocyte Piezo1 deficiency recapitulates the hematopoietic and immune alterations observed during unloading. Functionally, this pathway enhances acute infection resistance and suppresses immunosenescence in mice and in aged long-tailed macaques. Notably, skeletal mechanoregulation of immune homeostasis is conserved across vertebrate species. Our research defines the mechano-bone-immune axis (mechano-osteoimmunology), offering a novel evolutionary perspective on the interconnected development of the skeletal and immune systems and presenting a promising non-pharmacological target to address immune dysfunction.

immunology↗