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Wang, L.

Publications and source records attributed to Wang, L..

At least 55 records · Page 3Linked to original sources

State-specific binding thermodynamics predicts ligand efficacy across ion-channel families.

Predicting ligand efficacy is a critical challenge in drug discovery, as a target's functional response is often determined by the way a ligand shifts conformational equilibria between different functional states, a process that is particularly intricate in ion channels. We classify ligands based on the difference of their binding free energies on putative active and inactive conformations, calculated via free energy perturbation (FEP) for 78 protein-ligand pairs across six ion channels from four structural superfamilies: GluA2, GABAAR {rho}1, 3{beta}4 nAChR, 5-HT3AR, TRPML1, and KCNQ2. This approach accurately distinguishes agonists from antagonists across all these ion-channel families with large or subtle structural differences, including at membrane-facing sites, and enables quantitative prediction of maximum response and partial agonism. Importantly, we find that local binding-pocket conformations encode the bound ligand's efficacy even when global channel states are ambiguous. Our results demonstrate that state-specific binding thermodynamics provides a robust framework for leveraging ion channel structures of diverse conformational states to elucidate mechanisms of action and to advance ion-channel drug discovery beyond simple affinity measurements, enabling the identification of new chemical matter with desired functional attributes.

biophysics↗

Microbes on the Mind: Multi-modal Neuroimaging Reveals Gut-Brain Axes in Infants

The gut microbiome develops from birth and is associated with cognition and mental health, but its relationship with early brain maturation remains unclear. We studied 223 typically developing infants aged 0-3 years using multimodal MRI and paired fecal shotgun metagenomics. Microbiome-wide association analysis linked microbial features to cortical morphology, white-matter microstructure, and functional networks. Regularized canonical correlation analysis identified structural-metabolic and functional-taxonomic covariance patterns. Sparse partial least-squares analysis recapitulated both full-sample CCA patterns and their defining structural and functional phenotypes, providing cross-method corroboration. Longitudinal canonical-score slopes did not significantly covary, whereas earlier neuroimaging CCA1 scores predicted microbiome CCA1 scores 1-6 months later in bidirectional autoregressive cross-lag models. These observational results identify coordinated developmental patterns and temporal ordering without establishing causality.

developmental biology↗

Leakage-controlled benchmarking reveals generalization limits of deep learning for protein-ligand binding affinity prediction

To address widespread data leakage and inconsistent evaluation in protein-ligand affinity prediction, we introduce PLABench, a leakage-controlled and target-centric benchmarking framework that enables standardized comparison across sequence- and structure-based models. We benchmark nine deep learning methods across blind CASP16 targets, leakage-controlled ChEMBL35 sets, and established Davis and KIBA datasets under rigorous data split settings, standardizing structural input via AlphaFold3 to ensure fair comparison. Although pretrained structure-based models achieve the highest overall accuracy, they show severe target-dependent variability, and increasing structural fidelity from predicted to experimental conformations yields no consistent gains. Meanwhile, sequence-based approaches surpass some structure-based methods on select targets, and protein family-level evaluations reveal uneven performance across families and substantial inter-model complementarity obscured by aggregate metrics. These findings demonstrate that training scale and structural input alone cannot guarantee cross-target generalization, highlighting the need for context-aware interaction modeling. PLABench provides an extensible open-source platform to facilitate these developments.

bioinformatics↗

Transcription factors read a second regulatory code in chromatin

Transcription factors (TFs) decode gene regulatory information written in DNA, yet how this vocabulary is interpreted within chromatin remains largely unexplored. Here, using an upgraded NCAP-SELEX platform, we systematically map the nucleosomal DNA recognition landscapes of 269 human TFs. We uncover a widespread, chromatin-dependent mode of sequence recognition: many TFs recognize motifs on nucleosomal DNA that are distinct from their canonical naked-DNA binding sites, revealing that nucleosome architecture encodes a second gene regulatory code in chromatin. Cryo-electron microscopy structures of TF-nucleosome complexes demonstrate that this second code is read through a combination of nucleosome-induced DNA deformation and direct protein-histone contacts. Functional analyses show that these chromatin-encoded motifs actively promote chromatin accessibility and drive cell-type-specific cis-regulatory activity in vivo. Strikingly, a single TF can deploy its canonical and nucleosome-derived motif repertoires to partition and govern entirely distinct physiological programs. Together, our findings establish that TFs interpret two complementary layers of genomic information: the primary DNA sequence and a second code written into the nucleosome architecture. This chromatin-encoded layer of regulatory information fundamentally expands our understanding of how TF specificity is achieved and how gene regulatory networks are wired in multicellular organisms.

systems biology↗

Maleic acid adjuvates BCG to induce CD4+CD8+ T cells and sterilize tuberculosis

Anti-tuberculosis (TB) immunity typically emphasizes CD4+ T and CD8+ T cells that only provide limited protection against Mycobacterium tuberculosis (Mtb) infection. The anti-TB function of CD4+CD8+ T cells remains unexplored, mostly due to the dogma that ThPOK and Runx3 antagonize each other to block their development and their scarcity. Here, we show that immunization of BCG (Bacillus Calmette-Gu&eacuterin) with Complete Freund's Adjuvant (CFA) markedly induced CD4+CD8+ T cells through the gut microbiota Clostridium butyricum or its metabolite maleic acid. Mtb-specific CD4+CD8+ T cells exhibited a broad T-cell receptor repertoire and sterilized Mtb infection by inducing SLAMF1 and neutrophil responses. Mechanistically, maleic acid interacted with PAK2 to promote STAT5 phosphorylation at Ser127, thus upregulating Ets1 expression. Direct binding of Ets1 to the Runx3 and ThPOK promoters orchestrated their expression to redirect the CD8+ T cell differentiation towards the CD4+CD8+ lineage. Moreover, immunization of BCG plus Clostridium butyricum or maleic acid sterilized Mtb infection in mouse models. These findings establish CD4+CD8+ T cells as superior immune effectors against Mtb, a concept that could fundamentally redirect the current paradigm for anti-TB vaccine development.

microbiology↗

Mapping First In Vivo Ebolavirus Infection Events

Orthoebolaviruses, including Ebola virus (EBOV) and Bundibugyo virus (BDBV), cause sporadic outbreaks and devastating hemorrhagic infections in humans. A significant challenge that impedes the study of filoviruses is that the infectious virus can only be handled in biosafety level 4 (BSL4) facilities due to their extreme virulence. Life cycle modeling systems that use minigenomes and transcription/replication-competent virus-like particles (trVLPs) are powerful tools for studying these virus biology and to explore antiviral therapies under BSL2 conditions. To date, these powerful tools have only been utilized in vitro in cell culture systems. In this work, we demonstrate the use of EBOV trVLPs in vivo. We report the fine specificity of first infection events in a model of EBOV injection in the skin. Cre recombinase expressing monocistronic EBOV trVLPs were packaged and used to inject Cre reporter mice intradermally (ID). Initial infection events were monitored in living animals by luciferase imaging and then by flow cytometry to track cell-specific expression of Cre-activated GFP. By this approach, EBOV trVLPs were shown to directly infect T cells, monocytes, dendritic cells (DCs) with notably high first infections of skin-resident Langerhans cells (LCs) in the skin barrier and its draining lymph node. EBOV trVLPs were next tested as an in vivo tool to assess antiviral therapies by testing the ability of an EBOV vaccine to reduce trVLP luciferase levels after infection in the skin. This work demonstrates first in vivo use of EBOV trVLPs and provides proof of concept for their use as an in vivo BSL2 model to more rapidly develop antiviral agents and vaccines.

microbiology↗

LRRC37A is essential for acrosomal ion homeostasis and male fertility

Mammalian spermatozoa face various challenges during their long march to the destination. As a specialized membrane-bound organelle in the sperm head, the acrosome is particularly sensitive to changes in ionic and osmotic conditions, yet how acrosomal ion homeostasis is maintained remains largely unknown. Here, we show that LRRC37A is required for acrosomal ion homeostasis. Loss of Lrrc37a causes complete male infertility, accompanied by pronounced enlargement and deformation of the acrosome in the sperm head. Acrosome biogenesis was not affected by Lrrc37a knockout during the early stages of spermiogenesis, whereas acrosomal enlargement emerged at later stages and became more pronounced in the epididymis. LRRC37A localized to the outer acrosomal region and interacted with the Na/K-ATPase -subunit isoforms ATP1A1 and ATP1A4. Loss of LRRC37A disrupted the spatial distribution of both isoforms and was accompanied by increased Na within the acrosomal region. In addition, pharmacological perturbation of Na/K-ATPase activity or cellular ion homeostasis induced acrosomal swelling. These findings establish an essential role for LRRC37A in acrosomal ion homeostasis, suggesting that its deficiency may be associated with a distinct form of teratozoospermia characterized by acrosomal enlargement.

cell biology↗

A mycovirus identified from an outbreak fungal species complex reveals a parallel antiviral system

Mycoviruses are prevalent across major fungal lineages, yet none have been reported in the Cryptococcus gattii species complex (CGSC), the causative agent of the largest known fungal outbreak in immunocompetent hosts. Consequently, the occurrence of mycoviruses and the host determinants governing their infection in this important pathogenic clade remain unexplored. Through screening of 386 Cryptococcus isolates, we identified a mycovirus, designated CgTV1, in an environmental isolate of the Cryptococcus gattii species complex (CGSC). CgTV1 is a double-stranded RNA (dsRNA) mycovirus of the genus Totivirus, with a genome encoding a capsid protein and an RNA-dependent RNA polymerase. We showed that CgTV1 establishes a cryptic infection, because neither viral presence nor its clearance significantly alters host transcriptomic profiles, suggesting the existence of mechanisms that maintain virus-host homeostasis. Population genomic analyses reveal that an intact RNAi pathway constitutes a critical genetic barrier, and CgTV1 persistence strictly requires loss of function mutations in both AGO1 and AGO2. By pan-transcriptomics across 43 CGSC strains, we further uncovered an RNase III gene, CAI1, which exhibits high expression in the mycovirus positive isolate. Biochemical analysis indicates that Cai1 directly recognizes and degrades CgTV1 dsRNA, thereby constraining excessive mycoviral proliferation. We further demonstrate that Dicer and Cai1 act in parallel to maintain virus-host homeostasis: their combined ablation results in higher viral loads and more pronounced changes in host gene expression than ablation of either factor alone. Collectively, our findings provide the evidence of the occurrence of a mycovirus in the CGSC and reveal parallel mechanisms that enable cryptic mycoviral infections.

genetics↗

Stability of Antibody Repertoires in Astronauts During Long-Term Spaceflight

Long-duration spaceflight is known to disrupt several aspects of immune function yet its impact on the antiviral antibody repertoire remains unclear. We analyzed longitudinal plasma samples from 11 astronauts participating in a 6-month long spaceflight, including preflight, inflight, and postflight timepoints. Using a high-throughput serological method based on phage display of linear peptides from thousands of viruses we assessed the stability of antiviral antibodies over time. Across two phage libraries expressing different pathogen panels, we detected antibodies against Alphainfluenzavirus, Betainfluenzavirus, Enterovirus, and Orthopneumovirus consistently with the highest abundancy in all astronauts over all timepoints. Antibody levels against these infectious agents remained remarkably stable within individuals during and after spaceflight. In contrast, substantial heterogeneity was observed among astronauts, reflecting individualized immune histories and baseline antibody profiles. These results were confirmed by a different immunoassay using whole protein from the most targeted viruses. Together, these findings demonstrate that the antiviral antibody repertoire is largely resilient during prolonged spaceflight, highlighting preserved humoral memory despite potential dysregulation in cellular immune compartments.

immunology↗

Division-Specific Organization of a Shared Functional Scaffold in the Early-Life Human Brain

Early cognition and behavior emerge from coordinated maturation of functional systems spanning the brain, making cross-division integration essential for defining whole-brain architecture and understanding its role in neurodevelopment. Yet early human functional development is still largely investigated through cortical networks or through isolated, coarsely resolved noncortical structures, leaving unclear how this integrated architecture is organized across the cerebral cortex, subcortex and cerebellum. Moving beyond structure-isolated and adult-derived maps, we create a reproducible, fine-grained Early-Life Whole-Brain Functional Parcellation (UNC-ELF) spanning birth to six years. Using this framework, we identify a shared functional scaffold expressed through distinct division-specific modes: differentiated and dual-polarity cortical organization, spatially graded cerebellar organization with blended functional transition zones, and nucleus-constrained subcortical mosaics of multi-system affiliation. Across early childhood, the scaffold is selectively refined through heterogeneous, nonlinear connectivity trajectories, with major inflections concentrated in infancy. Age-, sex- and prospective cognition-related variation is differentially encoded across distinct connectomic components. Together, these findings reframe early functional brain development as coordinated refinement of a shared but nonuniform whole-brain scaffold and establish UNC-ELF as a unified reference for resolving typical and atypical functional organization across the developing brain.

neuroscience↗

Deep reinforcement learning-driven discovery of a MsbA-targeted small-molecule antibiotic for the treatment of Acinetobacter baumannii infection

Antibiotics with new mechanisms are highly pursued to address the threat of infections caused by drug-resistant Gram-negative bacteria. Targeting MsbA, a key protein of the lipopolysaccharide biosynthesis pathway, represents a promising strategy to discover new classes of antibiotics. However, currently available MsbA-targeted molecules either lack sufficient potency or have unfavorable properties, necessitating expansion of chemical space. In this study, we chose the most promising cerastecin Cpd 4 as the template, and used two Artificial Intelligence (AI)-based tools, i.e. Link-INVENT and AutoMolDesigner for molecular design, performed chemical derivatization and antibacterial activity evaluation, which led to the discovery of Y-11 (MIC for A. baumannii: 0.5 g/mL). Encouragingly, Y-11 showed equivalent potency to Cpd4 for carbapenem-resistant A. baumannii, and less cytotoxicity and hemolysis as well as lower spontaneous resistance frequency. In vivo efficacy study demonstrated that Y-11 could effectively reduce bacterial loads in the mice infected by A. baumannii. The following mechanism study including molecular dynamics simulation, biochemical assay, and transmission electron microscope (TEM) analysis suggested that Y-11 inhibited the transport of lipooligosaccharide and impaired the formation of outer membrane, probably by competitively binding to the substrate binding site of MsbA and modulating ATPase activity. Taken together, we have discovered a MsbA-targeted small molecule Y-11 via AI-driven drug design, which provides a foundation for future antibiotic development.

biochemistry↗

Ileal Gpbar1 gates depressive phenotypes via gut to brain "vagal-NTS-PVN"GABAergic axis

Depression represents a typical mental condition, yet whether intestinal metabolic signals drive central neural circuits remains unclear. Here we identify ileal enteric neuronal Gpbar1 as a previously unrecognized peripheral node that coordinates gut-to-brain communication to prevent depression-like behavior through a vagus-dependent, nucleus tractus solitaries (NTS)-paraventricular nucleus (PVN) signaling axis. The enteric plexus Gpbar1 is predominantly expressed on a subpopulation of GAD1-positive GABAergic neurons. Chronic restraint stress suppresses Gpbar1 expression, triggers glycolytic reprogramming and mitochondrial distress in both ileum and hypothalamus. Oral Gpbar1 agonism with INT-777 reverses hypothalamic HK2/TOM20 alterations and behavioral abnormalities by enhanced ileal mTOR/HIF-1 alpah signaling and glycolysis-related metabolite shifts, an effect specifically abolished by subdiaphragmatic vagotomy or chemogenetic silencing of PVN GABAergic neurons. Our findings establish ileal Gpbar1 as a gut-derived metabolic sensor that engages a defined vagal-brainstem-hypothalamic inhibitory circuit to regulate depressive phenotypes, shifting the roadmap from brain-centered to gut-initiated antidepressant mechanisms and unveiling a compelling peripheral therapeutic strategy that bypasses intractable central brain-directed intervention.

neuroscience↗

Physicochemical compatibility and stability of urapidil-propofol admixtures during simulated Y-site Administration

Background/Objectives: Urapidil with propofol is clinically efficient against elevated blood pressure during sedation. However, their physicochemical compatibility and emulsion stability upon continuous infusion remain unclear. This study aimed to evaluate different mixing ratios and diluents, thereby proving the safety limits for their co-administration. Methods: Urapidil solutions prepared with either sodium chloride (NS) or glucose injection (GS), and emulsified with propofol at different ratios (v/v), were stored for 12 h. Physical compatibility was assessed by visual inspection, pH, osmolality, mean droplet diameter (MDD), polydispersity index (PDI), zeta potential, and percentage of fat globules larger than 5 m (PFAT5). Chemical stability was quantified using high-performance liquid chromatography. Results: pH and osmolality stabilized. Urapidil hydrochloride and propofol contents remained pure at > 95%, MDD was < 500 nm, and PDI was < 0.2. Urapidil proportion in NS was significantly negatively correlated with the zeta potential. PFAT5 was > 0.05% after 2-8 h. In contrast, in GS at a 1:2 ratio, PFAT5 remained < 0.05%, which increased slightly in the 1:1 group at 8 h. PFAT5 stabilized in the high-propofol group (10:1) under all conditions. Conclusions: The chemical compatibility of the admixture was acceptable after 12 h of storage. However, physical compatibility was influenced by the mixing ratio, diluent type, and storage time. For clinical Y-site co-administration, a 10:1 mixing ratio or dilution in 5% GS is recommended. Enhanced proportions must be mixed with NS, while continuous infusion time must be < 2 h to mitigate fat embolism risk.

pharmacology and toxicology↗

Systematic CRISPRi perturbation of 1,408 autism risk genes maps multilevel transcriptional convergence in human cortical neurons

Genetic heterogeneity in autism spectrum disorder (ASD) complicates the identification of shared molecular pathways amenable to therapeutic intervention. Here, we perform a CRISPRi Perturb-seq screen targeting 1,408 ASD risk genes in human embryonic stem cell-derived immature cortical neurons and profile the resulting transcriptomic effects by single-cell RNA sequencing. We identify 215 ASD risk genes whose repression induces significant global transcriptomic dysregulation. Leveraging this functional atlas, we characterize candidate genes based on transcriptional similarity to established ASD hub genes. We identify gene programs recurrently dysregulated across perturbations, anchored by processes governing microtubule dynamics, neuron differentiation, cell migration, and transmembrane transport. We further identify CHAMP1 as a previously unrecognized regulator of Wnt signaling and define specific ASD risk genes that modulate the rate of cortical neuron differentiation. Analysis of differentially expressed genes reveals both convergent and perturbation-specific downstream transcriptional responses. Together, these findings provide a multilevel map of transcriptomic convergence in ASD and establish a framework for identifying both pathway-level and genotype-specific therapeutic strategies.

neuroscience↗

Attenuated Salmonella-Mediated Delivery of GSDMD Potentiates PD-1 Blockade Therapy against Melanoma

Immunotherapy has emerged as a core therapeutic strategy for melanoma. Programmed death protein 1 (PD-1) is a critical immune checkpoint molecule that restrains host anti-tumor immunity, and therapeutic agents blocking the PD-1 signaling pathway have been widely deployed in clinical practice. Nevertheless, single-agent PD-1 blockade fails to elicit robust clinical responses in the majority of patients. Therefore, there is an urgent unmet need to develop combinatorial regimens capable of augmenting the anti-tumor efficacy of PD-1 inhibition. Gasdermin D (GSDMD), a pore-forming effector protein that orchestrates pyroptosis, exerts inherent anti-tumor activities upon overexpression. However, whether GSDMD can synergize with PD-1 blockade to enhance therapeutic outcomes against melanoma remains poorly defined. To address this question, we established an attenuated Salmonella engineered strain for targeted delivery of GSDMD, and further investigated the anti-melanoma therapeutic efficacy of combining this engineered bacterium with anti-PD-1 antibody via immunofluorescence staining, flow cytometry and other analytical approaches. Our in vivo results demonstrated that combinatorial treatment markedly suppressed melanoma progression in tumor-bearing mice relative to monotherapy with either GSDMD-expressing bacteria or anti-PD-1 antibody alone. Mechanistically, co-treatment upregulated intratumoral expression of GSDMD and the pro-apoptotic protein BAX, while simultaneously downregulating PD-1 expression. In addition, the GSDMD/anti-PD-1 combination significantly elevated the proportions of CD4 and CD8 T lymphocytes in both peripheral blood and splenic tissues, and facilitated robust tumor infiltration by these two T cell subsets. Compared with phosphate-buffered saline (PBS) and scramble control groups, combinatorial therapy promoted tumor infiltration of M1-type tumor-associated macrophages (TAMs) and repolarized TAMs away from the immunosuppressive M2 phenotype. Consistently, serum levels of the pro-inflammatory cytokines TNF- and IFN-{gamma} were markedly elevated following combined intervention. Collectively, this study verifies that attenuated Salmonella carrying GSDMD synergizes with anti-PD-1 antibody to elicit potent anti-tumor effects in melanoma-bearing mice by amplifying systemic and intratumoral anti-tumor immune responses, which provides a preclinical rationale for novel combinatorial therapeutic strategies against melanoma.

cancer biology↗

Cardiomyocyte-specific loss of Smyd5 leads to a robust activation of inflammatory signaling and heart failure in mice.

Background: Cardiomyocytes respond to stress by undergoing hypertrophic growth driven by dynamic changes in gene expression. Epigenetic mechanisms, including histone methylation, play critical roles in regulating these transcriptional programs, yet the enzymes controlling these modifications during cardiac disease remain largely unknown. The SMYD family of histone methyltransferases regulates gene expression in multiple biological contexts, but the function of SMYD5 in the mammalian heart has never been investigated. Methods: SMYD5 expression was assessed in human heart failure samples and in a mouse model of cardiac hypertrophy. To define its functional role in vivo, we generated inducible cardiomyocyte-specific Smyd5 knockout mice and characterized their cardiac phenotype using molecular, histological, and functional analyses. Chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR) was performed to examine histone H4 lysine 20 trimethylation (H4K20me3) at the Il-6 promoter. Results: SMYD5 expression was altered in diseased human and mouse hearts. Under basal conditions, cardiomyocyte-specific deletion of Smyd5 resulted in baseline structural cardiac remodeling and transcriptional signatures characteristic of pathological stress. Smyd5-deficient hearts exhibited marked inflammatory activation resembling a cytokine storm with immune cell infiltration and heart failure. Notably, Smyd5 knockout mice displayed a 100-fold increase in Il-6 expression, accompanied by a global reduction in H4K20me3. ChIP-qPCR analysis of the Il-6 promoter, together with loss- and gain-of-function analysis of SMYD5, supports a direct epigenetic role of SMYD5 in regulating Il-6 expression through H4K20me3 in cardiomyocytes. Conclusions: SMYD5 is a previously unrecognized epigenetic regulator of cardiac homeostasis that restrains inflammatory signaling in cardiomyocytes under normal conditions. Loss of Smyd5 disrupts H4K20me3, leading to derepression of Il-6 in cardiomyocytes and a robust inflammatory response characterized by immune cell recruitment and fibrosis, accompanied by rapid progression of cardiac remodeling and heart failure. These findings identify SMYD5 as a critical regulator of intrinsic cardiomyocyte inflammatory signaling and reveal a novel chromatin-based mechanism contributing to inflammatory cardiomyopathies.

molecular biology↗

How thermostable direct haemolysin (TDH) diverges from TDH-related haemolysin (TRH)? Reassessing haemolysins in Vibrio parahaemolyticus through functional and structural representation learning

Vibrio parahaemolyticus (Vp) is the major foodborne pathogen transmitted via shellfish products, which has posed significant threats to modern public health and resulted in significant economic damage to the seafood industry. Numerous studies have documented diverse aspects of Vp pathogenicity, among which thermostable direct haemolysin (TDH) and TDH related haemolysin (TRH) are considered as the major virulence biomarkers of Vp. Despite their established roles as key biomarkers, a systematic understanding of the divergence of TDH and TRH across sequence, structure, and function remains limited. In this study, a multi scale analysis of TDH and TRH was performed using publicly available (2131 and 99 records from NCBI and Uniprot database, respectively) amino acid sequence data combined with representation learning and structure prediction. Global alignment of curated TDH and TRH sequences revealed extensive, distributed mutations and clear separation between TDH and TRH at the amino acid level (percentage identity of between TDH and TRH ranging from 56.1 to 67.4%). In contrast, protein language model derived embeddings showed high global functional similarity while preserving distinct clustering patterns, indicating conserved core functionality alongside nuanced divergence echoed with the structural inference by AlphaFold. Importantly, modeling of mutation trajectories demonstrated that the transition from TDH to TRH is driven by accumulated, genome-wide residue changes rather than a small set of key mutations. Together, these results suggested that TDH and TRH represent functionally conserved yet evolutionarily diverged toxins driven by accumulated sequence variation throughout the full-length amino acid sequence. These accumulated point mutations lead to major structural difference: TRH forms an alpha-helical tail that TDH lacks, which suggests that TDH and TRH disrupt host membranes by different mechanisms despite their conserved core function, such as pore-forming and ion flux induction capability. These methods provided unprecedented detailed insights into the functional and structural properties of Vp haemolysin, offering critical information on how multi-dimensional variations in sequence might influence their role in Vp pathogenicity. Insights from this study reinforce the rationale for using Vp strains harboring tdh and trh genes in experimental design for environmental fitness investigation.

microbiology↗

Nuclear Myosin VI stabilises Ku-associated DNA ends during non-homologous end joining

DNA double-strand breaks (DSBs) require rapid signalling and physical stabilisation of broken DNA ends to preserve genome integrity. Here, we identify myosin VI (MVI) as an ATM-regulated component of the DSB response. DNA damage induces rapid nuclear accumulation and nanoscale reorganisation of MVI across multiple cell models, in an ATM-dependent manner. Pharmacological or genetic perturbation of MVI attenuates {gamma}H2AX signalling and disrupts Ku80 organisation, while DNA damage persists. This leads to increased sensitivity to cisplatin and bleomycin. Super-resolution imaging reveals spatial association of MVI with Ku80-containing repair structures, implicating MVI in non-homologous end joining (NHEJ). In a minimal reconstituted system, MVI and actin enhance the proximity of Ku70/80-bound DNA ends. Together, our findings identify MVI as a regulator of DSB repair that links ATM signalling to Ku-associated DNA-end stabilisation and suggest that targeting MVI may sensitise tumour cells to genotoxic therapy.

cancer biology↗