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Biology subjects

Liu, L.

Publications and source records attributed to Liu, L..

At least 19 recordsLinked to original sources

CD4 T cell surface architecture is associated with response to anti-PD-1 therapy in non-small cell lung cancer

Anti-PD-1 therapy has substantially improved outcomes for patients with advanced non-small cell lung cancer (NSCLC), but clinical responses remain highly heterogeneous and are difficult to predict. Current immune profiling approaches primarily characterize immune cell composition and protein abundance, whereas the spatial organization of proteins at the cell surface has remained largely unexplored. Here, we demonstrate for the first time that cell surface protein organization is associated with clinical response to immune checkpoint inhibition therapy. Using the Proximity Network Assay (PNA), we simultaneously quantified cell frequencies, protein abundance, and protein organization in pretreatment peripheral blood mononuclear cells from 62 patients with advanced NSCLC treated with anti-PD-1 agents. While most cell populations were unchanged between responders and non-responders, pronounced response-associated alterations were identified within the CD4 T-cell compartment. Responders exhibited elevated expression of adhesion-associated proteins, and remodeling of a CD5-containing membrane domain. Increased colocalization within this domain was associated with poor clinical outcome and reduced survival. Machine learning analysis further identified CD4 T cell features as the strongest predictors of treatment response and demonstrated that protein organization provided greater predictive power than protein abundance alone. Together, these findings identify cell surface protein organization as a previously unexplored source of biomarkers and highlight its potential to improve immune profiling and biomarker discovery in cancer immunotherapy.

immunology↗

Pulmonary colonization of Candida albicans drives breast cancer lung metastasis via candidalysin

The intratumoral mycobiome is emerging as a key modulator of cancer progression, with specific fungal taxa as potential biomarkers. However, whether and how mycobiomes colonizing distant organs contribute to tumor evolution remains largely unexplored. Here, we identify selective enrichment of Candida albicans in breast cancer lung metastases. Mechanistically, the fungal virulence factor candidalysin activates pulmonary mast cells, which release chemotactic mediators that expand immunosuppressive populations and suppress cytotoxic lymphocyte activity, remodeling the lung into a metastasis-permissive microenvironment. Analysis of clinical isolates and isogenic mutants further demonstrates that candidalysin secretion levels dictate metastasis-promoting potential. Informed by these findings, we developed a combination regimen that concurrently eliminates fungal colonization, stabilizes mast cells, and reverses the immunosuppressive microenvironment, thereby significantly curtailing metastatic progression. Collectively, our study establishes pulmonary C. albicans colonization as a driver of breast cancer lung metastasis and provides a mechanistic framework for targeting mycobiome-host interactions in metastatic disease.

cancer biology↗

Engineering Upd-like to broadly restrict arbovirus infection and vector competence in mosquitoes

The global expansion of mosquito-borne viruses poses a growing threat to public health, yet the endogenous signals that activate antiviral immunity in mosquito vectors remain incompletely understood. Here, we identify Aedes aegypti Upd as an activator of JAK/STAT signaling that restricts arbovirus infection. Loss of Upd increased infection and dissemination of the flaviviruses ZIKV and DENV, as well as the alphavirus SINV, whereas blood meal inducible midgut overexpression reduced ZIKV and SINV infection. Mechanistically, Upd associated with the extracellular region of the Domeless (Dome) receptor, and Upd deficiency markedly reduced STAT phosphorylation and nuclear accumulation in the midgut. Upd expression was transiently induced in the midgut by an uninfected blood meal but remained elevated following ZIKV challenge, linking physiological responses to blood feeding with antiviral defense. In mammal mosquito transmission models, Upd overexpression reduced viral acquisition from infected hosts, whereas Upd deficiency enhanced viral dissemination and increased transmission following systemic infection. Together, these findings identify Upd as an endogenous regulator of mosquito JAK/STAT signaling and provide proof of principle that temporally targeted Upd expression can reduce arbovirus susceptibility and vector competence.

microbiology↗

BiNVaST: niche boundary-preserving and synthetic data-guided variational autoencoders for concordant inference across high-resolution spatial transcriptomic platforms

High-resolution spatial transcriptomics (ST) enables subcellular spatially resolved transcript profiling but remains difficult to annotate in complex tissues because of gene coverage and super sparseness in expression. These challenges are amplified in cancer research, where neoplastic cell states and rare immune cells in tumor microenvironment are often poorly captured by generic references and/or cell typing tools exclusively built on molecular profile. Here, we present BiNVaST, a niche boundary-preserving and dual-branch variational autoencoder fused with statistical simulator for reliable cell typing across multiple spatial platforms. It generates platform-adjusted in silico training data by integrating query spatial profile and user-defined pre-annotated single-cell reference through Singular Value Decomposition and Optimal Transport, combining molecular similarity and spatial proximity to predict segmented cell labels. BiNVaST was benchmarked against existing methods across Xenium, CosMx, Stereo-seq, Visium HD platforms using six specimens from four tissue types. This tool is sensitive in detecting divergent tumor cell states and improves the cross-platform concordance, distinguishing disease-specific neoplastic and non-neoplastic cellular subpopulations and supporting robust cellular or niche inferences in heterogeneous tissues.

bioinformatics↗

Human brain white matter charts in international populations

Brain charts provide normative references for identifying neurodevelopmental milestones and clinically meaningful deviations. Existing white matter (WM) charts are derived predominantly from European and North American populations, limiting generalizability. Here, we established the first set of population-specific WM charts of 198 morphological and microstructural phenotypes for both Chinese (N=19,215) and Western (N=15,584) populations across the human lifespan. Developmental trajectories and spatial organization of WM maturation and degeneration were broadly conserved across the populations, whereas maturational timing varied across pathways and metrics. The Chinese population showed earlier maturation in several projection and sensorimotor pathways, but more protracted maturation in higher-order association and limbic pathways. Chinese population-matched charts more accurately predicted WM phenotypes and detected more extreme disease-related deviations in brain health in the Chinese population than Western-derived models. Individual deviation patterns further discriminated patients from healthy controls and predicted cognitive performance and plasma biomarkers. Our findings reveal population-specific WM maturation and show that reference-population mismatch can reduce the accuracy and clinical sensitivity of normative brain charts.

neuroscience↗

Venetoclax Resistance Creates Canonical Pyroptosis Vulnerability in AML

Venetoclax has transformed acute myeloid leukemia (AML) therapy, yet resistance is almost inevitable. Its diverse, often difficult-to-target drivers frequently converge on monocytic differentiation, a state that survives on MCL1 rather than BCL2. Here, we show that the very cells that escape BCL2 inhibition retain the canonical pyroptosis machinery of normal monocytes. Across 15 bulk and 4 single-cell cohorts, the canonical pyroptosis program was enriched in monocytic AML and monocytic leukemia stem cells, correlated with venetoclax resistance, and associated with inferior survival specifically after venetoclax-based therapy. In 24 cell lines and 142 patient specimens, both DPP8/9 inhibition by Val-boroPro and NLRP3 activation by lipopolysaccharide (LPS) plus nigericin preferentially killed monocytic AML cells through GSDMD-mediated pyroptosis, largely sparing non-monocytic AML and lymphoid leukemias. Venetoclax preferentially depleted primitive AML blasts but enriched a monocytic residuum vulnerable to canonical pyroptosis; combining venetoclax with Val-boroPro achieved deeper ex vivo clearance than either agent alone. In venetoclax-resistant xenografts, Val-boroPro suppressed leukemia progression, and adding venetoclax further reduced leukemia burden and prolonged survival beyond either monotherapy. Thus, venetoclax resistance itself exposes an alternative, druggable cell-death program that can be therapeutically exploited to overcome this resistance.

cancer biology↗

DiffRhyShiny: A Benchmarking-Informed Platform for Differential Rhythmicity Analysis with Dependence-Aware Evidence Integration

Motivation: Differential rhythmicity analysis identifies condition-specific changes in biological oscillations, but diverse algorithmic assumptions complicate method selection. Furthermore, integrating complementary evidence across different tools while accounting for statistical dependence remains an unresolved challenge. Results: We benchmarked seven algorithms across diverse rhythmic scenarios, revealing that optimal selection depends heavily on specific biological variations and experimental designs. To overcome single-algorithm limitations, we introduced Kost's Method, a dependence-aware p-value integration approach. Building on this framework, we developed DiffRhyShiny, an interactive web platform that automates robust differential rhythmicity analysis, consensus evaluation, and visualization. Furthermore, we validated the platform's performance and statistical rigor using both extensive simulated scenarios and real-world transcriptomic datasets. Availability and implementation: DiffRhyShiny is freely available at https://omicsai.shinyapps.io/diffrhyshiny, with the latest source code at https://github.com/liuchuan111/diffrhyshiny. The code and data to reproduce all benchmarking results are archived on Figshare at https://doi.org/10.6084/m9.figshare.33070100.

bioinformatics↗

Co-targeting KRAS and BCL-2 induces pyroptosis and antitumor tertiary lymphoid structures

Mutant KRAS drives lung tumorigenesis through both cell-intrinsic and cell-extrinsic mechanisms, yet mutation subtype-specific differences in metabolic regulation and immune evasion remain incompletely understood. Here we show that the KRAS G12D mutation, particularly in the KRAS/STK11 co-mutant (KL) context, is associated with poor prognosis and a suppressed immune microenvironment characterized by impaired antigen presentation. At the cell-intrinsic level, G12D exhibits weakened interaction with hexokinase 1 (HK1), reduced spare respiratory capacity, and diminished mitochondrial stress resistance compared with G12C. Based on this mitochondrial vulnerability, we screened a panel of clinically available agents that induce mitochondrial stress and identified that co-targeting KRAS and BCL-2 synergistically triggers GSDME-mediated pyroptosis predominantly in G12D tumors. This combination further induces functional tertiary lymphoid structures (TLS) in vivo. Immune cell depletion experiments further demonstrate that the antitumor efficacy is dramatically dependent on B cells. Moreover, this treatment strategy induced membrane attack complex (MAC) deposition in situ and elicited memory antitumor responses. Collectively, these findings establish that combined KRAS and BCL-2 inhibition elicits pyroptosis and TLS formation, leading to B-cell-dependent in situ and memory antitumor immunity, providing a mechanistic rationale for targeting mitochondrial-immune crosstalk in KRAS G12D-mutant lung cancer.

cancer biology↗

Metagenomic insights into dose-dependent alterations in the tobacco rhizosphere microbiome by pyrroloquinoline quinone

Pyrroloquinoline quinone (PQQ) is known to promote plant growth, yet how the rhizosphere microbiome varies with PQQ concentration remains poorly understood. We applied metagenomic sequencing to characterize the taxonomic composition and functional potential of the tobacco rhizosphere microbiome across PQQ treatments at 0.5, 1 and 2 mol/L plus an untreated control. The rhizosphere microbiome was dominated by Pseudomonadota and Actinomycetota and differed among treatments in a concentration-associated, non-monotonic manner. The most pronounced differences were observed at 1 mol/L, where alpha diversity showed dimension-specific variation and beta-diversity analysis resolved the most distinct community profile. Taxonomic and functional profiles varied concurrently, with Streptomyces, Sphingomonas, Rhodanobacter and Lysobacter, together with functions related to biosynthesis, energy metabolism, colonization and environmental sensing, showing higher relative abundance at this concentration. No broad-spectrum antimicrobial effect was detected at the community level, and antibiotic resistance gene abundance showed no significant differences among treatments after correction for multiple testing. These findings provide a basis for further evaluation of PQQ in modulating the rhizosphere microbiome in continuous cropping systems.

microbiology↗

A dsRNA Virus Converts Early Endosomes into Stable Replication Organelles Through Maturation Arrest and Retrograde Transport

Infectious bursal disease virus (IBDV) and infectious pancreatic necrosis virus (IPNV) are major animal pathogens that impose a heavy burden on the poultry and aquaculture industries. Yet, major aspects of their unique replication program remain unknown. IBDV is unusual among double-stranded RNA viruses in that it replicates in association with host endosomes. We previously demonstrated this association to be orchestrated by the viral protein VP3 and the early endosomal lipid phosphatidylinositol 3-phosphate [PtdIns(3)P], suggesting an essential role for VP3 in forming birnaviruses specialized replication compartments. Here, combining high-resolution fluorescence and correlative light-electron microscopy with diverse molecular and biochemical analyses, we define how the IBDV protein VP3 targets and remodels host endosomes, and establish that endosome-associated replication is conserved in members of the Birnaviridae family. We show that IBDV VP3 targets early endosomes via the PtdIns(3)P effector Early Endosomal Antigen 1 (EEA1) to arrest their maturation and prompt their association with the Golgi complex via ESCPE-1-mediated retrograde transport. We further show that IPNV also exploits endosomal membranes for replication in a PtdIns(3)P dependent manner, although for this virus VP3 engages endosomes through an EEA1-independent mechanism yet to be determined. This work uncovers how birnaviruses exploit a single viral protein to orchestrate endosome remodeling and intracellular trafficking to establish specialized replication compartments while revealing both conserved and host-adapted features of birnaviruses replication.

cell biology↗

Prime editing enables high-throughput identification and characterization of selective MutSβ inhibitors

DNA mismatch repair (MMR) maintains genome stability but paradoxically drives expansion of pathogenic repeats responsible for trinucleotide repeat disorders. Attenuating repeat instability through targeted inhibition of MMR is therefore a therapeutic strategy of interest; however, progress is constrained by a lack of robust methods for defining and isolating MMR subpathways. We exploited features of prime editing to profile the effects of core MMR genes on thousands of programmed DNA mispairs in cells and resolved distinct MMR processes, including a noncanonical, loop-directed mechanism. Guided by these results, we built a set of scalable reporters that detect loss of separable MMR processes and screened ~72,000 small molecules for activity against MutS{beta}-directed MMR. This effort identified a novel series of MutS{beta} inhibitors that reduced (CAG)n expansion in a cell model. Altogether, this study establishes several methods for systematically interrogating MMR, with demonstrated capacity to identify inhibitors of therapeutic value.

bioengineering↗

Developmental Convergence Across Diverse Genetic Architectures in Childhood Apraxia of Speech

Childhood apraxia of speech (CAS) is a neurodevelopmental disorder of speech-motor planning and programming, associated with literacy, academic, and psychosocial difficulties. We performed whole-exome sequencing in 11 families comprising 21 affected and 15 unaffected individuals with phenotyping spanning speech, language, cognition, literacy, and motor function. We identified 60 prioritized variant observations representing 22 unique variants across 20 genes with family-based segregation analysis assessed in informative relatives; 5 arose de novo. Our cohort included multiple affected siblings and extended relatives, with several families carrying multiple prioritized variants, suggesting cumulative or oligogenic susceptibility. Speech and literacy impairment co-occurred with oral-motor, feeding, and fine-motor difficulties. BrainSpan co-expression analysis identified MECP2 and ANK2 as the genes with the highest observed connectivity in the sampled postnatal network. Exploratory analysis of the KOLF2.1J perturbation atlas in undifferentiated human induced pluripotent stem cells identified a positive LMO3 expression-response score following NIPBL repression and opposing LMO3 and ANK2 response directions within a cohesin-associated perturbation cluster. These observations motivate testing in human neural cells. Functional enrichment, protein-association, and developmental-expression analyses supported shared biological themes involving chromatin regulation, neuronal signaling, and extracellular-matrix organization. Among six families, multiple affected relatives shared prioritized variants across a unique set of several genes, demonstrating multilocus candidate profiles whose individual and combined effects may contribute to CAS susceptibility. We propose four novel CAS candidate genes: LMO3 and PCDH10, previously linked to human accelerated regions, as well as MYCBP2 and PTPRS. Our work provides multiple testable hypotheses for future variant-specific functional validation in speech-motor development.

genetics↗

A genetic screen to identify novel interactions of the phosphatidylinositol phosphate signaling pathway in Drosophila spermatogenesis

Phosphatidylinositol (PI) phosphates (PIPs) are membrane lipids with crucial roles in intracellular signaling, membrane trafficking and cytoskeletal organization. To perturb PIP function in Drosophila melanogaster sperm development, we previously expressed the Salmonella PIP phosphatase SigD (also known as SopB) under control of a spermatocyte- specific promoter. SigD expression results in reduced levels of plasma membrane PI 4,5-bisphosphate [PI(4,5)P2; henceforth PIP2] and male sterility. Transgenic lines expressing high levels of SigD (SigD-high) exhibit defects in spermatocyte cytokinesis, ciliary transition zone maturation and spermatid elongation, whereas lines expressing low levels of SigD (SigD-low) have defects in nuclear shaping and spermatid cell polarization. To further investigate the role of PIPs during Drosophila sperm development, we conducted a sensitized genetic screen to identify suppressors and enhancers of SigD-low phenotypes. From a screen of 760 chromosomal deficiencies spanning 83.6% of chromosomes 2 and 3, we identified 80 interacting regions that were further narrowed down to 40 individual suppressors. Among the strongest interactors were genes involved in microtubule dynamics, nucleocytoplasmic transport and membrane trafficking. The novel genetic interactions identified by our screen pave the way for further investigation into molecular mechanisms underlying the affected aspects of sperm development.

genetics↗

Immune Reconstitution and Antigenic Exposure History Shape Virus-Specific Humoral Immunity in People with HIV

CD4+ T-cell recovery is widely used to assess immune reconstitution in people with HIV, but its relationship to virus-specific humoral immunity across pathogens remains unclear. We characterized neutralizing activity against SARS-CoV-2, HIV-1, and influenza viruses in ART-treated, virologically suppressed individuals spanning distinct CD4+ T-cell levels. BA.5 was the dominant SARS-CoV-2 neutralization target across CD4 strata, whereas D614G neutralization increased with greater immune reconstitution. This gradient was largely absent for the antigenically divergent NB.1.8.1 and XFG variants. HIV-1 neutralization was inversely associated with CD4+ T-cell count, while influenza showed strain-dependent patterns. Neutralization-to-protection bridging preserved a CD4-associated gradient for D614G but not for highly immune-evasive variants. These findings show that immune reconstitution does not translate uniformly into antiviral humoral function. Instead, antibody profiles reflect host immune status, prior antigenic exposure, and viral antigenic evolution, supporting pathogen-specific functional assessment alongside conventional immune monitoring.

immunology↗

SOX4 Reprograms Adipose Stromal Cells into a Cancer-Associated Fibroblast-like State to Drive Metabolic Disease

Pathogenic adipose tissue remodeling promotes metabolic disease in obesity, but the mechanisms that establish this unhealthy tissue state remain poorly understood. Here, we show that obesity drives SOX4-dependent reprogramming of mesenchymal stromal cells (MSCs) into cancer-associated fibroblast-like (CAF-like) cells that promote adipose tissue dysfunction. TGF{beta} signaling is elevated in obesity and activates SOX4 in mouse and human MSCs, inducing their conversion to a CAF-like state. In mice, MSC-specific SOX4 activation induces the CAF-like program and exacerbates adipose tissue inflammation and glucose intolerance, whereas Sox4 deletion attenuates inflammation and improves glucose homeostasis during obesity. We further identify the growth factor Midkine (MDK) as a SOX4-regulated paracrine effector produced by CAF-like cells. MDK inhibition in obese mice reduces adipose tissue inflammation and improves metabolic function. Together, these findings define a TGF{beta}-SOX4-MDK stromal signaling axis that drives pathological adipose tissue remodeling in obesity and highlight this pathway as a potential therapeutic target for improving metabolic health.

cell biology↗

A Context-Aware 14-3-3 Binding Predictor Enabled by Data Augmentation, Multi-Scale Biological Features, and Protein Language Model Embeddings

Identifying phosphorylated serine/threonine residues that mediate 14-3-3 interactions remain a major challenge in understanding phospho-dependent 14-3-3 regulation. Existing predictors largely rely on local sequence features surrounding candidate phosphosites, owing in part to the limited number of experimentally validated 14-3-3 binding sites, while broader contextual determinants of binding remain insufficiently explored. Here, we show that 14-3-3 binding sites are defined not only by local motif patterns but also by multi-scale biological context. We found that 14-3-3-binding proteins are enriched for condensation-related properties, that 14-3-3 docking sites preferentially localize to compact intrinsically disordered regions, and that protein language model embeddings provide informative representations for this task. To address both limited data availability and incomplete site representation, we developed CAMP-14-3-3 (Context-Aware Multi-scale Predictor for 14-3-3 binding), a framework that integrates multi- scale biological features with protein language model embeddings, together with a phylogeny-based data augmentation strategy and distribution-matched negative sampling. This integrated framework outperformed motif-based approaches and existing predictors on independent data. Our results support a context-aware view of 14-3-3 recognition and provide a general strategy for modeling phospho-dependent protein interactions under limited-data conditions.

bioinformatics↗

Controlling membrane tension by dynamic DNA nanorings

Membrane tension, defined as the energy cost to expand the membrane surface area, is a fundamental mechanical property of the lipid bilayer and an important modulator of various cellular processes. Liposomes provide model systems to study protein-mediated membrane dynamics, where membrane tension can be controlled by osmotic pressure and micropipette aspiration. However, it is challenging to individually control membrane tension of nanometer-sized liposomes, such as small unilamellar vesicles (SUVs), that are widely used for modeling subcellular membrane structures and drug delivery. To bridge this technological gap, we present reconfigurable DNA origami rings for dynamically controlling membrane tension of sub-100 nm liposomes. The DNA nanorings template the formation of uniformly sized SUVs and undergo trigger-responsive dilation and contraction, thus applying controlled and reversible mechanical stress to the SUV membranes. Electron microscopy analyses show deformed liposomes with ~2.5% expanded membrane area following ring dilation. The corresponding increase in membrane tension opens a mechanosensitive ion channel MscL with gating tension of ~10 mN/m. Selectively manipulating a mixture of SUV populations enables timed release of their distinct molecular cargos, either concurrently or one at a time. Furthermore, vesicles with expanded membranes are more conducive to SNARE-mediated fusion. The nanomechanical device thus provides a programmable platform for engineering the mechanics of synthetic nano-vesicles and studying membrane tension modulated processes at the molecular level.

biophysics↗

Architecture and Energy Transfer of the Bacterial Photosynthetic Unit

In phototrophic organisms, pigment-protein membrane complexes are densely packed to form photosynthetic units (PSUs) that capture solar energy and convert it into chemical energy. Although the structures of many individual photosynthetic complexes have been resolved, how they are arranged and interact with others within photosynthetic membranes to enable efficient excitation energy transfer (EET) remains poorly understood. Here, we report cryo-electron microscopy structures of PSU supercomplex assemblies from the phototrophic a-proteobacterium Rhodovulum viride, including an RC-LH1 core associated with one or two peripheral LH2 complexes and a curved LH2 tetramer. These membrane-derived assemblies define the relative positions and orientations of neighboring photosynthetic complexes and place their pigment arrays in proximity across antenna-antenna and antenna-core interfaces. Structure-based simulations identify potential EET pathways within the PSU assemblies and reveal rapid energy transfer across both LH2-LH2 and LH2-LH1 interfaces. Collectively, these findings provide insights into the assembly and structural modularity of bacterial PSUs and elucidate how the lateral organization of membrane protein complexes facilitates efficient energy transfer. This work extends structural studies of bacterial photosynthesis from individual complexes to their native higher-order assembly, providing a framework for understanding how photosynthetic supercomplex organization shapes energy migration and for guiding the design of artificial photosynthesis.

biochemistry↗