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Feng, H.

Publications and source records attributed to Feng, H..

At least 19 recordsLinked to original sources

Overcoming segmentation bottlenecks in brain tissue for spatial proteomic inference at population scale

In spatial proteomics across large cohorts, downstream estimates from tens of thousands of images depend on accurate cell segmentation. Yet pretrained segmentation models struggle with morphologically complex cell bodies in human brain tissue, and how domain adaptation affects downstream discovery remains unclear. Here, we introduce SPInfer, a workflow for spatial proteomic inference developed using 5,832 manually annotated cell bodies from 120 immunofluorescence images of the human prefrontal cortex. After benchmarking eight segmentation methods spanning classical, convolutional, and foundation models, we adapted Cellpose-SAM, raising cell segmentation F1 from 0.37 to 0.84 and recovering cell compositions concordant with matched single-nucleus RNA-seq and spatial transcriptomics. Across 14,765 images from 69 postmortem donors, identical Alzheimer's disease pathology models found no significant associations after false discovery rate correction using zero-shot masks, versus four using fine-tuned masks; three linked higher OLIG2-positive fractions to greater neurofibrillary tangle and plaque burden. Using the fine-tuned masks, a graph attention network over nuclear neighborhoods classified four cell types without marker information, and differential expression analysis linked cell morphology to gene expression. This provides a pipeline for fine-tuning foundation models to segment complex tissues, enabling biological discovery in spatial proteomics at the population scale.

bioinformatics↗

NEIL2 regulates RNA polymerase II dynamics to suppress transcription replication conflicts in pancreatic cancer

Transcription replication conflicts (TRCs) arise from spatiotemporal interference between replication and transcription machinery and contribute to genome instability in cancer cells. In pancreatic ductal adenocarcinoma (PDAC) cells, oncogenic KRAS drives TRC formation, and base excision repair (BER) contributes to TRC resolution as an adaptive response. Here, we show that TRCs are enriched in pancreatic tumor sections from patients and are associated with malignant progression. We identify NEIL2, a bifunctional DNA glycosylase in the BER pathway, as a critical regulator of TRCs in PDAC cells. Mechanistically, NEIL2 loss causes aberrant RNA polymerase II (RNAPII) occupancy at transcription start sites and downstream of transcription end sites. Dysregulated RNAPII dynamics promote R-loop-dependent and -independent TRCs contributing to replication stress, DNA damage, and impaired cancer cell proliferation. Notably, the DNA-binding motif of NEIL2 necessary for canonical BER function is dispensable for TRC regulation. Together, these findings reveal an unrecognized role for NEIL2 in regulating RNAPII dynamics and mitigating TRCs in pancreatic cancer cells.

molecular biology↗

An Aphid Protein Interferes with Plant endomembrane Trafficking Machinery to Promote Aphid Survival and Plant Growth

Aphids deplete their host plants of amino acids and other essential nutrients by feeding on phloem sap. Autophagy, a conserved process across eukaryotes, maintains cellular homeostasis during starvation and environmental stress by recycling damaged or excess cellular components. Here, we identified and characterized a previously uninvestigated aphid salivary protein, termed Aphid Autophagy Related Factor 1 (AAF1), that is secreted into plant cells and manipulates plant physiology in a manner that benefits the aphid. We show that AAF1 interacts with four known or putative host autophagy related proteins: RABD1 and RABD2a (plant homologs of Ypt1/RAB1), ATG8, a ubiquitin like protein required for autophagosome formation, and PI3PT, a previously uncharacterized ER localized putative lipid binding or lipid transfer protein annotated as a phosphoinositide 3 phosphate transfer protein. We further demonstrate that the RAB binding domain of AAF1 and its interaction with RABD2a may be specifically required for AAF1 function. In addition, we identified unique, highly mobile compartments containing interacting AAF1 and RABD2a that are associated with the endoplasmic reticulum (ER) and dynamically traffic with autophagosomes. We propose that these compartments may be derived from endosomes or endosome to ER contact sites (EERCSs) and serve as platforms for autophagosome trafficking and/or biogenesis. We further propose that AAF1, RABD2a, and PI3PT function together to regulate the formation or function of these compartments, thereby supporting autophagosome formation and trafficking. Finally, we show that stable expression of AAF1 in plants enhances growth and biomass in an autophagy dependent manner.

plant biology↗

Mendel, a foundation model of human genetic variation, prioritizes regulatory variants and improves gene expression prediction

Human genome-wide association studies have identified hundreds of thousands of variant trait associations, but interpreting their mechanistic consequences at allele resolution remains a central bottleneck. DNA foundation models pretrained on genomic sequence corpora learn features predictive of regulatory activity, yet their training objectives are dominated by the conserved background common to all individuals, rather than the sparse variant sites at which human genetic variation is concentrated. Here we introduce Mendel, a DNA foundation model trained from scratch on human whole genome sequences using a variant-centric objective that concentrates supervision on allelic events within reference aligned sequence context. On held-out individuals, Mendel attains 0.984 micro-averaged SNV allele-prediction accuracy, compared with 0.311 for Evo 2. Mendel residual difficulty is selectively enriched at cis-eQTL variants, prioritizes fine-mapped causal variants (AUROC 0.731), where Evo 2 residuals performed near chance, and when converted into a cis-expression prior for modelling, improves prediction relative to an unweighted baseline in all 50 GTEx tissues.

genetics↗

AC-Diff: Anatomy-Contrast Disentangled Diffusion for Multi-Vendor Liver MRI Harmonization

Magnetic resonance imaging (MRI) exhibits substantial scanner and protocol dependent appearance variations, making harmonization challenging without distorting patient specific anatomy, particularly in abdominal imaging. We propose AC-Diff, an anatomy--contrast disentangled diffusion framework that formulates MRI harmonization as a factor-specific generative intervention. Using aligned multi-contrast supervision and cross-patient factor swapping, AC-Diff learns to separate anatomical structure from acquisition-dependent contrast. Unlike conventional image or latent diffusion, AC-Diff restricts stochastic generation to the contrast subspace while the source anatomy bypasses diffusion and is directly reused during reconstruction. Experiments on an in-house multi-vendor cohort and the external Duke Liver MRI dataset demonstrate improved target-domain alignment with strong structural preservation. In downstream liver segmentation, AC-Diff improves Dice from 0.942 for the original inputs to 0.954 for the harmonized images. These results support contrast-specific latent generation as a promising approach to anatomy-preserving MRI harmonization.

bioengineering↗

SMORE: joint dimension reduction and cell population discovery on single-cell methylome data

Single-cell DNA methylation profiling technology captures novel epigenetic data modality but are challenging to analyze because of their heterogeneity, high dimensionality, and ultra-sparsity. Here we present SMORE (Single-cell MethylOme Reduction and Embedding), a computational method for joint dimensionality reduction and cell population discovery dedicated to single-cell DNA methylation data. SMORE operates on a Bayesian framework that converts methylation proportions into ordered methylation states and jointly infers a low-dimensional representation, cell populations and their number. By using low-rank latent Gaussian factorization and adopting a mixture-of-finite-mixtures prior on latent cell scores, SMORE infers cell assignments without requiring a prespecified cluster number, and propagates uncertainty from methylation measurements to cell assignments. Across simulations spanning varying sample sizes, population imbalance, signal strengths and model misspecification, SMORE accurately recovered latent population structure and outperformed existing methods. Applied to human single-cell methylation datasets from lung, peripheral blood and primary motor cortex, SMORE recovered biologically supported cell population structures. SMORE provides an uncertainty-aware framework for dimension reduction and population discovery for single-cell methylomes.

bioinformatics↗

SGFP-Grid Split GFP Graphene Grids

Affinity graphene grids provide a promising approach for selective protein capture in cryo-EM. Here, we introduce a split-GFP graphene grid platform(SGFP-G), in which graphene-conjugated GFP 1-10 selectively captures GFP11 tagged proteins from low concentration samples or cell lysates. This platform enables rapid assessment of target protein enrichment and particle distribution before vitrification via fluorescence imaging, while the grid design positions captured proteins away from the graphene surface and air-water interface. We also introduce a unique strategy to minimize nonspecific protein adsorption, thereby improving the selective enrichment of target proteins on this grid. Using GFP11-tagged apoferritin, we demonstrate fluorescence guided protein capture and obtain a 2.58 [A] cryoEM reconstruction, establishing SGFP-G as an affinity grid platform for high resolution structural studies with reduced sample requirements.

biochemistry↗

Dual-Mode Bio-CM2: Multimodal Computational Miniature Mesoscope for Fluorescence and Label-Free Imaging

Understanding biological function often requires complementary information on molecular identity, morphology, behavior, and physiology acquired simultaneously from the same specimen. Achieving this capability in miniature microscopes remains challenging because integrating multiple imaging contrasts typically increases optical complexity while compromising field of view (FOV), spatial resolution, or form factor. Here we present dual-mode Bio-CM2, a multimodal computational miniature mesoscope that simultaneously captures fluorescence and label-free reflectance through a shared optical architecture based on distributed computational optics. The system enables frame-interleaved, co-registered dual-mode imaging over a [~]7.5 x 10 mm2 FOV with [~]6 m lateral resolution. We demonstrate the versatility of dual-mode Bio-CM2 across diverse biological systems. In freely moving Caenorhabditis elegans, reflectance captures body posture and locomotor behavior that contextualize fluorescently labeled protein aggregates. In freely swimming larval zebrafish, reflectance captures whole-body morphology and swimming behavior, while fluorescence visualizes cardiac activity. In head-fixed mice, simultaneous fluorescence and reflectance imaging across the bilateral dorsal cortex provides complementary measurements of neuronal calcium activity and intrinsic hemodynamic signals. By integrating molecularly specific fluorescence with complementary reflectance contrast, dual-mode Bio-CM2 extends distributed computational optics into a scalable platform for multimodal miniature imaging.

bioengineering↗

Host insect microRNAs are translocated to an obligate endosymbiont

Many insects rely on intimate interactions with bacterial symbionts housed in specialized cells called bacteriocytes. While host and symbiont gene expression in bacteriocytes appears highly integrated, the underlying regulatory mechanisms remain largely unknown. MicroRNAs regulate gene expression and are emerging as mediators of cross-kingdom communication. Here, in the pea aphid, Acyrthosiphon pisum, and the green peach aphid, Myzus persicae, we demonstrate cross-kingdom translocation of aphid miRNAs into their obligate endosymbiont, Buchnera aphidicola. miRNA fluorescence in situ hybridization in aphid embryos provides direct evidence that four out of five candidate miRNAs (miR-1, miR-10, miR-29, and miR-927) localize inside Buchnera cells. To investigate how these miRNAs may regulate Buchnera gene expression, we further demonstrated the cross-kingdom translocation of aphid argonuate 1 protein (Ago1), into Buchnera using immunolocalization. Given the translocation of both Ago1 and miRNAs, we applied a eukaryotic miRNA target prediction framework and found that all cross-kingdom-translocated miRNAs are predicted to target Buchnera genes involved in symbiotic functions. Although the precise in vivo functions of translocated miRNAs remain challenging to determine, our findings suggest a previously unrecognized layer of regulation between insect host and its obligate endosymbiont, offering new insight into the molecular dialogue that supports insect-microbe interactions, highlighting potential targets for miRNA-based pest management. Significance statementMany insects have evolved bacteriocyte cells to house essential bacterial endosymbionts. However, how bacteriocytes are specified and how gene expression is coordinated between host and symbiont remain largely unknown. Here, we identify that aphid microRNAs, along with an argonaute protein, are translocated into the obligate bacterial endosymbiont Buchnera, revealing a previously unrecognized regulatory layer mediating host and obligate endosymbiont interactions. This discovery provides evidence of miRNA cross-kingdom movement into an obligate endosymbiont, filling a key knowledge gap in how eukaryotic host small RNAs can influence microbial partners. Given the critical role of Buchnera in aphid survival and reproduction, these findings not only advance fundamental knowledge of insect-microbe interactions but also point to new molecular targets for innovative pest management strategies.

evolutionary biology↗

Oxidized protein states define metastatic fitness in lung cancer

AbstractReactive oxygen species (ROS) are a pervasive feature of human cancers, yet the protein targets through which ROS-regulated cell states shape tumor biology remains poorly understood. Here, using cysteine chemical proteomics, we define signatures of protein states under distinct cellular ROS environments that capture protein oxidation and conformational changes. Quantifying these signatures in primary lung tumors and brain metastases revealed a surprising enrichment of oxidative states in metastasis. To determine how these states support fitness, we performed genome-wide CRISPR screens and identified the mitochondrial Complex I subunit NDUFA10 as a key oxidation-dependent vulnerability. Oxidation of NDUFA10*Cys253 supports Complex I function through a previously unrecognized nucleotide kinase activity that maintains mitochondrial DNA levels. Enforcing a reduced conformation in NDUFA10 disrupts brain metastatic colonization in vivo. These findings establish ROS regulated protein states as a functional layer of tumor fitness, providing a framework for identifying redox-dependent mechanisms that support cancer progression.

Cancer Biology↗

Genetic characterisation and aggressiveness of the Fusarium oxysporum Species Complex in tomato plants and irrigation water from Australian processing fields

Fusarium oxysporum Species Complex (FOSC) includes important soilborne pathogens of a range of crops worldwide. In Victoria (VIC) and New South Wales (NSW), Australia, FOSC has been identified as the cause of stunting and poor growth in processing tomato fields, resulting in significant yield losses. A total of 40 FOSC isolates were obtained from symptomatic tomato plants, irrigation water samples and culture collections, which were confirmed to be FOSC by multi-gene phylogenetic analyses based on four genomic loci: beta tubulin, calmodulin, the second largest subunit of nuclear RNA polymerase II, and translation elongation factor one-alpha. There was a high level of genetic diversity among isolates, with multiple phylogenetic lineages detected. Glasshouse bioassays demonstrated that all isolates were pathogenic to processing tomato, resulting in significant reductions in plant growth, with above ground height reduced by 11 to 26% and root dry weight by 44 to 83% compared with the control (p < 0.05). Although aggressiveness varied among isolates, growth reduction occurred irrespective of their phylogenetic placement. Moreover, the shared genetic background of isolates from irrigation water and plant samples highlights the role of irrigation water as a potential source of inoculum in Fusarium epidemics, underscoring its significance for disease management in Australian processing tomato systems.

plant biology↗

Genomic Decoding of Specialized Aromatic Hydrocarbon Degradation in Mangrove-Derived Gordonia sp. B7 2

Petroleum pollution has increased worldwide, driving the search for microorganisms with efficient hydrocarbon-degrading capabilities. Here, we report a novel bacterium, Gordonia sp. B7-2, isolated from mangrove sediments in Hainan, China. Phylogenetic analysis based on the 16S rRNA gene and whole-genome sequences, together with digital DNA-DNA hybridization and average nucleotide identity values, supported its classification as a new species within the genus Gordonia. The complete genome of strain B7-2 consists of a single circular chromosome of 5.39 Mb with a G+C content of 65.99%, and encodes 4,887 protein-coding genes. Genomic annotation revealed a complete pathway for aromatic hydrocarbon degradation, including genes encoding protocatechuate 3,4-dioxygenase and biphenyl-2,3-diol 1,2-dioxygenase, whereas genes involved in the initial oxidation of alkanes were absent. Consistent with these genomic predictions, strain B7-2 degraded 64.33% of crude oil (300 mg/L) within 28 days, with rapid degradation during the initial 14 days, followed by a slower phase thereafter, reflecting the dynamics of complex hydrocarbon mixtures. Together, these results demonstrate that strain B7-2 is specialized for the degradation of aromatic hydrocarbons and highlight its potential for targeted petroleum bioremediation. IMPORTANCEMangrove ecosystems are highly vulnerable to petroleum contamination, yet the microorganisms responsible for hydrocarbon turnover in these environments remain poorly characterized. This study describes a new bacterial species, Gordonia sp. B7-2, that exhibits a strong metabolic specialization for aromatic hydrocarbon degradation. Unlike many known oil-degrading bacteria that preferentially utilize alkanes, strain B7-2 targets aromatic components of crude oil, which are among the most persistent and toxic fractions.Its ability to efficiently degrade crude oil highlights its potential in the bioremediation of contaminated coastal environments and expands our understanding of microbial contributions to hydrocarbon cycling in mangrove sediments

microbiology↗

Distinct functions of PBRM1 and BAP1 reconcile the course of kidney cancer evolution and disease progression

Clear cell renal cell carcinoma (ccRCC) progresses along two predominant evolutionary trajectories, defined by PBRM1 ([~]40%) or BAP1 ([~]15%) mutations on a VHL-inactivated background. They have distinct patterns of evolutionary tempo and mode, and vastly different clinical outcomes, yet the underlying genotype-specific molecular phenotypic programmes are unknown. We established a patient-derived preclinical model biobank that captures the genetic diversity of ccRCC. Through integrative analyses of preclinical models and tumour bulk and single cell profiling, we identified transcriptional and epigenetic changes specific to PBRM1- and BAP1-driven ccRCC. Modelling PBRM1 loss in vitro demonstrates that it reinforces renal lineage identity and maintains progenitor-like cell state. In contrast, BAP1 loss drives inflammatory signalling and chromosomal instability. These insights reconcile the distinct evolutionary modes (branched versus punctuated), tempo (slow versus fast) and clinical outcomes associated with PBRM1 and BAP1 mutations, respectively, establishing a framework for patient stratification and genotype-directed therapeutic development.

cancer biology↗

Auxin promotes GPI-anchored protein-mediated trafficking of ABP1 to enable cell-surface auxin signaling

Rapid auxin responses are triggered by Auxin-Binding Protein 1 (ABP1) signaling; however, the coupling of hormone perception to signaling activation is unclear. ABP1, a cell surface auxin receptor, is localized to endoplasmic reticulum (ER), raising a fundamental question of where auxin is perceived and how signaling-competent receptors are mobilized to cell surface. Herein, we established a dark-induced auxin synthesis system in Arabidopsis hypocotyl; abp1 mutants showed pronounced elongation. Auxin dose-dependently stimulates LORELEI-like glycosyl-phosphatidylinositol-anchored protein 1 (GPI-AP, LLG1) interaction with ABP1, driving their outward trafficking from ER. However, this complex dissociated in acidic apoplast, facilitating H+-ATPase-mediated auxin signaling. Our findings reveal how intracellular auxin perception is converted into rapid cell-surface signaling, establishing a mechanistic framework for fast auxin responses and uncovering a GPI-AP-mediated trafficking mechanism for ER-retained receptors.

plant biology↗

DNA-triggered AIM2 condensation orchestrates immune activation and regulation

The innate immune sensor AIM2 detects cytosolic DNA and initiates inflammatory responses, yet its activation mechanism remains incompletely understood. Here, we show that AIM2 undergoes liquid-liquid phase separation upon DNA binding, forming dynamic condensates both in vitro and in cells. These condensates serve as platforms for inflammasome and PANoptosome assembly, promoting immune activation across multiple pathways. Direct structural determination from condensates reveals the assembly of active-form ASC filaments. Mechanistically, liquid-phase condensation is governed by multivalent interactions involving different AIM2 domains, including previously uncharacterized regions and species-specific elements. In vitro and in vivo assays show that mutants specifically disrupting condensation impair immune complex assembly, cell death initiation, antimicrobial defense, and intestinal homeostasis. Moreover, AIM2-DNA condensates function as regulatory hubs targeted by host- and pathogen-derived factors to balance immune homeostasis or facilitate immune evasion. These findings establish liquid-phase condensation as a fundamental mechanism of AIM2 activation and a potential therapeutic target.

immunology↗

Neurocognitive deficits in controlling aversive memory among insomnia disorders

BackgroundInsomnia disorder is a common sleep disturbance characterized by adverse daytime cognitive and emotional impairments, such as repetitive negative thinking and increased psychological distress. Memory control, a key self-regulatory ability to control or inhibit unwanted thoughts and memories, plays an essential role in supporting cognitive functions and emotional well-being. Here, we delineate the neurocognitive mechanisms underlying memory control among individuals with insomnia. Methods41 participants meeting DSM-5 criteria for insomnia disorder and 40 healthy sleepers completed an emotional Think/No-Think task, during which participants either retrieved (Think) or suppressed the retrieval (No-Think) of aversive memories in response to memory cues while electroencephalograms were recorded. ResultsLinear mixed model analyses with age and depression scores as covariates showed that participants with insomnia exhibited impaired memory control abilities, as evidenced by reduced suppression-induced forgetting in memory recall when compared to healthy sleepers. Electrophysiologically, healthy sleepers showed enhanced right prefrontal theta power in retrieval suppression than in retrieval, indicating elevated needs of inhibitory control during memory control. In sharp contrast, this difference was absent among those with insomnia. Notably, the greater the severity of insomnia symptoms, the smaller the retrieval vs. retrieval suppression theta power differences across participants, linking inefficient top-down control of unwanted memories with low sleep qualities. ConclusionIndividuals with insomnia showed impaired memory control of aversive memories and aberrant electrophysiological activities during retrieval suppression. Future research shall investigate the causal relationship between memory control abilities and insomnia symptoms.

neuroscience↗

Structural basis for repurposing a flexible phage tail into an Intraspecific bacterial competition weapon

The rise of multidrug-resistant bacteria poses a major threat to human health. Tailocins, which are phage tail-like bacteriocins, offer a way to kill specific bacteria without the risks of horizontal gene transfer found in phage therapy. While the mechanism of contractile R-type tailocins is well-established, the bactericidal action of non-contractile F-type tailocins remains unresolved. Here, we report the high-resolution cryo-EM structure of the F-pyocin from Pseudomonas aeruginosa. The structure reveals a complex nanomachine made of a terminator cap (AlpD/PA0910), a helical tube (PA0633), and a tail tip that mediates a symmetry transition from sixfold to threefold. Notably, the tail tip connects to an elongated central fiber (PA0641) decorated with trimeric side fibers (PA0643/PA0646) involved in host recognition. Through genetic deletion studies and proteomic analysis, we delineate the F-pyocin assembly pathway, establishing that the tape-measure protein (PA0636) serves as a central scaffold coordinating the assembly of the tube, cap, and tail-tip modules. Structural analysis reveals a localized register shift in the central fibers coiled-coil shaft, suggesting a metastable state that may facilitate conformational changes upon host recognition. Our findings detail the atomic structure of an F-type tailocin, uncovering its coordinated assembly pathway and specialized tail-fiber architecture, which establishes a structural framework for engineering next-generation, precision antimicrobials.

biophysics↗

A mediterranean-mimicking diet harnesses gut microbiota-derived 3-IAA to rejuvenate T cell

Diet profoundly shapes the tumor microenvironment through metabolite modulation, yet the mechanisms linking diet, gut microbiota, and antitumor immunity remain unclear. Here, we demonstrate that a mediterranean-mimicking diet (MedDiet) suppresses tumor growth by orchestrating a microbiota-metabolite-immune axis. MedDiet selectively enriched Bacteroides thetaiotaomicron (B. thetaiotaomicron) in the gut, whose administration recapitulated tumor suppression. Both MedDiet and B. thetaiotaomicron elevated plasma levels of the tryptophan metabolite indole-3-acetic acid (3-IAA). Mechanistically, 3-IAA enhanced CD8+ T cell cytotoxicity and alleviated exhaustion by inhibiting the integrated stress response, sustaining antitumor immunity in vivo. Importantly, 3-IAA synergized with anti-PD-1 therapy to further restrain tumor progression. Finally, we developed a MedDiet Score to predict patient survival and response to immunotherapy. These findings reveal that dietary modulation of gut microbiota can reshape systemic metabolites to potentiate T cell-mediated antitumor responses. Our study identifies 3-IAA as a metabolite-based adjuvant for immune checkpoint therapy and highlights the translational potential of diet-driven immunomodulation in cancer treatment.

cancer biology↗