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Guo, T.

Publications and source records attributed to Guo, T..

At least 19 recordsLinked to original sources

Reinforcement learning with evolutionary priors unlocks multi-site enzyme optimization from sparse experimental feedback

Industrial enzymes underpin sustainable manufacturing, yet natural proteins rarely combine the activity, robustness and application compatibility required for practical use. Engineering such properties requires identifying beneficial combinations of interacting mutations within vast sequence spaces that are too large to search exhaustively and too sparsely sampled to model reliably. Here we introduce AlphaVariant, a reinforcement-learning (RL) framework that couples a generative evolutionary prior with iteratively updated low-N fitness models to enable feedback-driven search of large combinatorial protein sequence spaces. Across six experimentally measured protein fitness landscapes, AlphaVariant ranked first on the three large, non-enumerable multi-site landscapes. In two successive rounds of savinase activity optimization, AlphaVariant-designed libraries yielded 75.4% and 83.8% activity-improved variants among experimentally characterized candidates even as the accessible mutation space expanded from 25 to 67 positions. The search identified beneficial mutation combinations involving up to 17 structurally dispersed sites and produced a variant with 7.1-fold higher activity than wild type after only two design-test cycles. We then extended AlphaVariant to jointly optimize activity, thermostability and a patent-informed constraint for intellectual-property freedom. This multi-objective search yielded variants that outperformed the commercial protease Uno 100 L in both biochemical assays and application-relevant detergent washing tests. These results demonstrate that generative RL can efficiently navigate vast protein fitness landscapes, progressively incorporate multiple engineering objectives and convert sparse experimental feedback into enzyme variants with industrially relevant performance, effectively resolving the limits of biocatalyst engineering.

bioinformatics↗

Collateral effects of bacteriophage resistance on antibiotic sensitivity in Pseudomonas aeruginosa

Collateral effect (CEs) of phage resistance can alter antibiotic sensitivity, leading to collateral sensitivity (CS). CS of phage resistance can potentially be used to design more effective phage--antibiotic combination treatments, yet insufficient knowledge on the occurrence of such phage resistance associated CS is currently available. Here, we characterized CEs across diverse Pseudomonas aeruginosa strains, antibiotics, and phages. For each of eight strains (seven clinical isolates and PAO1), we generated mutants resistant to phage PAO1-1 and, separately, mutants resistant to each of six antibiotics. Phage-resistant mutants were also generated using four additional phages (M32, NP1, NP3, and PNM), and double phage- and antibiotic-resistant mutants from one strain. We measured growth curves across antibiotic concentration ranges after which the area-under-the-curve (AUC) was quantified as a measure of bacterial burden. Dose-response curves for AUC against antibiotic concentrations were constructed to estimate a fold change in EC50 of mutants relative to their parental strains. PAO1-1-resistant mutants showed significant CS to colistin and polymyxin B. For other antibiotics, CEs varied by phage and parental strain: PAO1-1-resistant mutants showed CS to tobramycin, whereas mutants resistant to the other four phages tested were associated with CR. For double phage- and antibiotic resistant mutants we found CS to colistin and tobramycin relative to the parental strain. Resistance mutations occurred predominantly in genes involved in metabolism, virulence, and DNA replication. Antibiotic-resistant mutants also showed increased phage sensitivity, with the strongest effect in colistin-resistant mutants. In conclusion this study demonstrates collateral effects of phage resistance are most specific to both strain- and antibiotic-specific.

pharmacology and toxicology↗

Rice blast fungus hijacks a rice RALF peptide to initiate infection

Plant-derived peptides regulate immunity and host-microbe interactions, but whether fungal pathogens exploit endogenous plant peptides for infection-site selection remains largely unknown. Rapid alkalinization factors (RALFs) are a family of plant peptide hormones that contribute to plant development, reproduction, stress responses, and cell-wall organization. Here, we show that OsRALF7, which is an immune-activating peptide in rice (Oryza sativa), is co-opted by the rice blast fungus Magnaporthe oryzae as a host-derived cue for appressorium formation, specialized infection structures required for host penetration. While synthetic OsRALF7 peptide induced defense responses in rice suspension cells, the same peptide induced appressorium formation in M. oryzae. OsRALF7-induced appressorium formation was associated with activation of the cAMP/PKA and Pmk1 MAPK pathways and required a hydrophobic surface. M. oryzae inoculated onto Osralf7 knockout plants formed fewer appressoria, and the positioning of these appressoria relative to the boundaries between two adjacent plant epidermal cells was altered. These findings suggest that OsRALF7 provides positional information for infection initiation for M. oryzae. OsRALF7 localized to the plasma membrane and cell wall in rice, and its appressorium-inducing activity required a conserved YISY motif and cysteine residues. This activity was not conserved in Colletotrichum higginsianum, as RALF23 from Arabidopsis thaliana did not induce appressorium formation but instead showed antifungal activity. Together, these findings uncover a dual function of endogenous plant immune-modulating RALF peptides at the plant-pathogen interface, where they can be exploited by M. oryzae as a host-derived cue for infection initiation while also retaining antifungal activity against other fungal species.

plant biology↗

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↗

Super-Resolution Visual ProteomEx for Hard Tissues and Clinical Samples

Correlating nanoscale tissue architecture with unbiased molecular composition within the same specimen remains a fundamental challenge in spatial biology. Current spatial proteomics methods either lack the imaging resolution required to resolve nanoscale tissue architecture or achieve only limited proteome coverage, and untargeted approaches capable of deep protein identification have yet to be integrated with super-resolution imaging within a single workflow. Here, we present microProteomEx, an integrated platform that combines hydrogel-assisted tissue expansion with mass spectrometry-compatible fluorescence imaging, laser capture microdissection, and bottom-up proteomics to achieve simultaneous three-dimensional super-resolution imaging (effective lateral resolution down to [~]47 nm on conventional diffraction-limited microscopes) and spatially resolved proteomics at a scalable lateral resolution of 29-100 {micro}m (0.02-0.28 nL volumetric resolution). By optimizing fixation, protein anchoring, and a secondary re-embedding strategy, we extend the method to mechanically resilient tissues, including mouse kidney and heart, as well as to formalin-fixed, paraffin-embedded clinical specimens. We demonstrate single-glomerulus and single-plaque proteomics (450-1,000 proteins per structure), resolve proteomic differences between malignant melanoma and giant congenital melanocytic nevus in a rare pediatric case, and characterize the morphology-resolved molecular heterogeneity of cored versus diffuse amyloid-beta plaques in a mouse model of Alzheimers disease across two disease stages. microProteomEx establishes a broadly accessible framework for correlating tissue ultrastructure with deep spatial proteomics, with direct implications for disease biology, biomarker discovery, and precision medicine.

biochemistry↗

Drug-Prot: A query system for statistical inference of drug effects and interactions in dynamic proteomic networks

Understanding drug effects and drug-drug interactions is essential for developing combination therapies. We present Drug-Prot, a computational framework that leverages large-scale perturbation proteomics to quantify causal drug effects, drug-drug interactions, and dynamic protein relationships. Using data from 63 single drugs and 59 drug combinations applied to 18 breast cancer cell lines at 6, 24, and 48 hours, Drug-Prot estimates drug effects on protein expression and reconstructs directed temporal protein dependency networks. The publicly available software enables targeted analyses of user-defined protein sets, substantially reducing the multiple-testing burden. Through an interactive web application, users obtain corrected p-values for single-drug and combination effects, directed temporal dependency networks, and downloadable results without requiring access to the underlying proteomic dataset. As a use case, we apply invariance-regularized Random Forests to triple-negative breast cancer cell lines to identify proteins associated with drug response. Querying these proteins in Drug-Prot reveals drug-specific and interaction effects at the protein-network level, illustrating how the framework links candidate causal protein features to actionable drug combinations.

bioinformatics↗

Language Immersion Enhances Attentional Speech Processing via Low-Frequency Neural Tracking

Language experience is a powerful driver of neurocognitive plasticity, shown to modulate attentional and executive processing in speakers of multiple languages. This paper investigated how immersion in a second-language environment shapes attentional processing of speech. Fifty-eight bilingual Chinese-English speakers matched on their English language proficiency listened to competing continuous speech streams in a naturalistic listening task. They were immersed either in their native language environment (Beijing, China), or in the second language environment (Cambridge, UK). In an identical EEG experiment across the two immersion contexts, we assessed the listeners cortical tracking of attended and unattended speech and task-related attentional allocation using Temporal Response Function (mTRF) and Power Spectral Density (PSD) analyses. Behavioral comprehension of the attended narratives was uniformly high. PSD analyses showed no group difference in task-related attentional allocation, but mTRF results revealed robust differences in cortical tracking, with increased tracking of attended - but not unattended - streams in the immersed group, driven by the delta band (1-4 Hz). This boost in tracking of the attended signal declined with prolonged immersion, indicative of changes to attentional speech processing as the language environment stabilizes and consistent with the expansion-renormalization framework of neurocognitive adaptation. Jointly, these data imply that immersion in second-language environments shapes the way listeners encode speech, sharpening the brains ability to extract target auditory information from background noise. They furthermore suggest that, rather than being static or monotonous, this modulation reflects a flexible and dynamic process that is continuously shaped by changes in environmental demands and their duration. Key pointsO_LISecond language immersion boosts cortical tracking of attended speech, driven by the delta band (1-4 Hz). C_LIO_LIThis boost decreases with prolonged immersion, reflecting the dynamic, expansion-renormalization adaptation trajectory. C_LIO_LIImmersion does not influence task-related attentional allocation. C_LI

neuroscience↗

Activity of a three-phage combination against Mycobacterium tuberculosis in disease-relevant conditions

Phage therapy offers promise to combat antimicrobial resistance, including drug-resistant tuberculosis (TB). Understanding phage activity against Mycobacterium tuberculosis (Mtb) adapted to physiologic microenvironments, such as hypoxia and acidity in granulomas, is essential since these conditions induce non-replicating states. We evaluated a phage combination against Mtb under hypoxic, acidic (pH 5.5), and stationary-phase conditions in vitro. In planktonic Mtb growth conditions, phage concentrations increased around day seven followed by a significant reduction in Mtb H37Rv load, which was maintained over 31 days. Phage addition prevented regrowth was observed with rifampicin and isoniazid alone. Individual phage stability was differentially affected by acidic media conditions, resulting in variability of antimycobacterial activity. In hypoxic conditions and stationary growth experiments, phage titers remained stable over time with no change in mycobacterial load compared to controls. Model-based predictions were able to adequately capture phage-mycobacterial interactions with and without rifampicin. The lack of antimycobacterial activity in assays with non-replicating mycobacteria suggest that phages need actively replicating mycobacteria to exert lytic activity. Stable phage concentrations in assays with non-replicating mycobacteria suggests low grade phage replication in these conditions. Established models can support future study design through simulations of different experimental scenarios.

microbiology↗

Lamellar Normative Modelling of the Hippocampus Across the Human Lifespan

The hippocampus is a central hub of human memory and cognition and is closely associated with brain disorders. Studies have shown that it exhibits complex structural variation across the lifespan, yet the details of hippocampal morphology changes remain poorly understood. Here, we establish norms over the hippocampal geometry that resolve lamellar morphology and map lifespan trajectories across more than 27,000 individuals from 158 scanning sites. Hippocampal geometry shows spatially non-uniform developmental and ageing patterns across the lifespan, with lamellar thickness, width and length following dissociable trajectories. Across multiple brain disorders, this representation reveals localized and heterogeneous alterations beyond conventional subfield-level summaries, and uncovers a dichotomy in disease-associated patterns, with neurodegenerative conditions and schizophrenia showing predominant atrophy, whereas some other disorders exhibit focal or regionally selective hypertrophy. Transfer to a longitudinal Alzheimers Disease Neuroimaging Initiative cohort further supports out-of-sample generalization of our approach and enables individual-level tracking and conversion risk stratification. Overall, this work establishes a population-scale geometric reference for the hippocampus, extends normative brain mapping from coarse regional phenotypes to anatomically organized subcortical structure, and enables anatomically grounded characterization of disease-related alterations and individual-level deviation mapping, providing a principled basis for understanding and stratifying brain disorders across the lifespan in health and disease.

neuroscience↗

Transcription Factor-Mediated Reprogramming of Cancer-Associated Fibroblasts Reveals Targetable Vulnerabilities in Solid Tumors

Cancer-associated fibroblasts (CAFs) contribute to immune exclusion and therapy resistance in solid tumors, limiting the efficacy of chimeric antigen receptor (CAR) T cell and immune cell therapy. To overcome this, we developed a transcription factor (TF)-based strategy to reprogram prostate-derived CAFs (pCAFs) into normal fibroblast-like cells (NFs). We prioritized TFs enriched in quiescent stellate cells--Vitamin D receptor (VDR), Peroxisome Proliferator-Activated Receptor gamma (PPAR{gamma}), and p53--and selected VDR for proof-of-concept studies. Lentiviral VDR expression in pCAFs produced VDR-reprogrammed NFs (VDR-rpNFs) with reduced CAF markers, increased ATP, and suppressed TGF-{beta} and IL6, indicating phenotypic and metabolic reversion. In both in vitro 3D co-cultures and in vivo, VDR-rpNFs disrupted tumor architecture, enhanced CAR T cell infiltration, and reduced necrosis. PPAR{gamma}- and p53-rpNFs showed similar reprogramming effects. These results suggest TF-guided fibroblast reprogramming as a viable strategy to remodel the tumor microenvironment and improve CAR T cell efficacy in solid tumors.

cancer biology↗

MetaKnogic-Alpha: A Hyper-Relational Knowledge Base for Grounded Metabolic Reasoning

The exponential trajectory of biomedical literature has precipitated a fundamental "synthesis gap" in metabolic research, where critical mechanistic insights remain fragmented across hundreds of thousands of disjointed full-text articles, preventing the consolidation of a global mechanistic view. Here, we present MetaKnogic-Alpha, a foundational mechanistic knowledge substrate designed to bridge this gap by transforming unstructured literature into a navigable, logic-based resource. MetaKnogic-Alpha synthesizes over 100K full-text articles into a hyper-relational hypergraph structure, preserving the n-ary relational logic inherent in complex metabolic pathways. To ensure biological rigor, we implemented a hierarchical discovery protocol: an autonomous reasoning agent first enriches query nomenclature for domain-specific precision, followed by a multi-hop topological expansion within the hypergraph to surface functional neighbors, such as enzymatic co-factors and distal regulators, often lost in traditional search paradigms. Crucially, the system subjects all literature-derived insights to a deterministic biochemical grounding against a curated metabolic reaction network, significantly mitigating the risk of probabilistic hallucinations common in standalone generative models. In rigorous benchmarking, MetaKnogic-Alpha achieved a mechanistic accuracy of 0.98 in scenarios where supporting evidence was present, providing a robustly attributable audit trail back to the primary literature via PubMed Central Identifiers. We designate this primary release as "alpha" to establish the foundational architectural logic for a burgeoning million-scale resource. By compressing the synthesis of thousands of papers from a multi-month manual effort into several hours of automated discovery, MetaKnogic-Alpha serves as a high-fidelity research companion that augments the human experts ability to resolve complex metabolic interactions and identify novel therapeutic drivers in precision oncology.

bioinformatics↗

Transcriptomics-based modeling of methionine metabolism effectively estimates sample-wise DNA methylation activity and epigenetic aging

DNA methylation is a central epigenetic modification that regulates gene expression, maintains genomic stability, and guides cellular differentiation. However, direct measurements of DNA methylation, such as whole-genome bisulfite sequencing or DNA methylation arrays, are costly and require substantial DNA input, limiting their scalability for large cohorts and their applicability to emerging modalities such as single-cell and spatially resolved transcriptomics. In this study, motivated by the fact that DNA methylation is fundamentally a metabolic process, we investigate whether sample-wise DNA methylation activity can be inferred directly from transcriptomic profiles of genes involved in methionine and one-carbon metabolism. We show that a compact metabolic model comprising seven core reaction steps and 98 genes accurately predicts total DNA methylation activity across matched transcriptomic and methylation datasets from CCLE, TCGA, GTEx, and an independent single-cell multi-omics data set. Building on this framework, we develop Total DNA Methylation Activity (TDMA), a physics-informed neural network-based score that enables robust estimation of DNA methylation activity from bulk, single-cell, and spatial transcriptomics data. We demonstrate that TDMA captures methylation-dependent transcriptional regulation and identifies genes and pathways under epigenetic control. Applying TDMA to GTEx, we further reveal strong associations between the predicted total methylation activity, chronological aging, and established epigenetic clocks. We also demonstrated that TDMA can serve as a transcriptomics-derived epigenetic clock and highlights age-dependent roles of folate and glutathione metabolism in epigenetic aging. Applying TDMA to single cell and spatial transcriptomics data collected from pancreatic adenocarcinoma (PDAC), we identified that methionine metabolism and DNA methylation regulates T cell cytotoxicity in the tumor microenvironment of PDAC. Together, this work establishes a scalable, modality-agnostic framework for estimating DNA methylation activity from transcriptomics and provides new insights into the metabolic regulation of epigenetic aging.

bioinformatics↗

Causality-oriented regulatory inference and rational transcriptomic reprogramming design with CASCADE

Systematically elucidating the causal structure of gene expression regulation is the foundation for identifying key regulators of cellular function and designing rational interventions thereof. While advances in high-content perturbation screens enables experimental probing of causal regulatory effects, the massive genomic scale, measurement noise and confounding factors pose significant challenges for existing causal discovery and inference algorithms. Here, we present CASCADE, an end-to-end framework that integrates de novo causal discovery with prior regulatory knowledge for genome-wide causal discovery and inference. In addition to its superior performance on causal regulatory structure discovery and counterfactual inference for unseen perturbation effects, CASCADE enables, for the first time, causality-oriented rational intervention design for transcriptomic programming towards various targeted cells within a unified framework.

bioinformatics↗

A spatially-resolved human brain proteome atlas for understanding function and disease

While the brain performs specialized functions across distinct regions, the spatial organization of the human brain proteome remains largely uncharted. Here we present a comprehensive spatially-resolved proteome atlas of the human brain, analyzing over two thousand MRI- guided locations across four individuals. Proteome analysis integrated with transcriptomics reveals extensive post-transcriptional regulation, with cortical regions showing markedly higher protein diversity than transcript. Unsupervised molecular clustering defines distinct brain territories that transcend anatomical boundaries, instead reflecting metabolic demands and functional specialization patterns. Application to epilepsy brain tissue uncovered disrupted astrocyte metabolism, protein homeostasis and therapeutic targets including the seizure-associated purinergic receptor P2RX7. This resource bridges molecular and systems neuroscience to accelerate neurological drug discovery.

neuroscience↗

Pancreatic Cancer Induces Population-Specific Switching of Myosin Isoforms and Discrete Activation of Cachexia Genes in Skeletal Muscle Myocytes

Skeletal muscle loss in pancreatic cancer is a significant cause of morbidity and mortality for patients. In order to understand myocytes changes we examined myonuclei- and myofiber-specific dynamics during pancreatic cancer cachexia progression. Single-nucleus RNA-seq was used to interrogate myonuclear gene expression, and RNAscope and immunofluorescence characterized myofiber-specific changes. Bulk RNA-seq of skeletal muscle provided a whole-muscle transcriptomic profile. Cachexia induces a progressive loss of muscle differentiation factor Maf and its target Myh4, accompanied by increased expression of Myh1 and Myh2. This myofiber dedifferentiation occurs without evidence for fiber type shifting, regeneration, or proliferation. Single-nuclei analysis reveals global shifts in myofiber gene expression identity including the identification of a cachexia only myonuclear subpopulation. Cachexia gene expression was not restricted solely to this PDAC-specific myonuclear subpopulation and did not overlap with Myh1 and Myh2 expressing myonuclei early in cachexia. Altogether, PDAC cachexia elicits distinct transcriptional responses across different myonuclear populations. These results reveal population-specific heterogeneity in cachexia gene activation, rather than a uniform upregulation of cachexia mediators across muscle tissue. Our data suggest that myonuclei fate occurs prior to overt muscle wasting when cachexia gene expression only modestly overlaps with differentiation factors, with a strong association after irreversible muscle wasting. These findings explain the challenge of effectively targeting skeletal muscle wasting in cancer cachexia requires addressing the changing cell population induced through non overlapping mechanisms.

cancer biology↗

LAMP2A-dependent chaperone-mediated autophagy enhances oxidative stress resistance in gastric cancer cells through selective degradation of accumulated oxidized DJ-1

Reactive oxygen species (ROS) function as potent activators of chaperone-mediated autophagy (CMA). While previous investigations have demonstrated that CMA facilitates cancer cell survival through selective degradation of oxidatively damaged proteins, the precise molecular mechanisms remain poorly defined. Hence, it is important to investigate the correlation between CMA and the antioxidative stress within tumor cells and elucidate its specific mechanism. LAMP2A expression profiles in gastric carcinoma cell lines and clinical specimens were quantified via qPCR, WB and immunohistochemical analysis. An in vitro oxidative stress model was established through 24-hour hydrogen peroxide (H2O2) exposure. Gastric cancer cell models with knockdown and overexpression of LAMP2A were established. Apoptotic indices and proliferative capacity were assessed through high-throughput flow cytometry and CCK-8 viability assays. The interaction between LAMP2A and DJ-1 was investigated via co-immunoprecipitation and confocal microscopy. This study demonstrates that LAMP2A is upregulated in gastric cancer and further induced by oxidative stress. Down-regulated LAMP2A impaired CMA functionality, sensitizing gastric cancer cells to oxidative cytotoxicity and significantly augmenting apoptosis rates. Elevated DJ-1 levels in gastric cancer cells are further amplified by oxidative stress, with severe stress enhancing LAMP2A-DJ-1 colocalization. Mechanistically, CMA inhibition precipitated accumulation of hyperoxidized DJ-1 isoforms, concomitant with pro-apoptotic BAX upregulation and anti-apoptotic BCL-2 downregulation. We found hyperoxidized DJ-1 as a novel CMA substrate. The LAMP2A-DJ-1 regulatory axis represents a critical adaptive mechanism whereby CMA activation maintains redox homeostasis in gastric malignancies. Specifically, CMA-mediated clearance of oxidized DJ-1 prevents pro-apoptotic protein cascade activation, thereby conferring oxidative stress resistance and promoting tumor cell survival.

cancer biology↗

The neuroimaging correlates of depression established across six large-scale datasets

Neuroimaging data offers noninvasive insights into the structural and functional organization of the brain and is therefore commonly used to study the neuroimaging correlates of depression. To date, a substantial body of literature has suggested reduced size of subcortical regions and abnormal functional connectivity in frontal and default mode networks linked to depression. However, recent meta analyses have failed to identify significant converging correlates of depression across the literature such that a conclusive mapping of the neuroimaging correlates of depression remains elusive. Here we leveraged 23,417 participants across six datasets to comprehensively establish the neuroimaging correlates of depression. We found reductions in gray matter volume/ cortical surface area associated with depression in the frontal cortex, anterior cingulate, and insula, confirming prior studies showing the importance of prefrontal and default mode regions in depression. Our findings demonstrate multiple surprising results, including a lack of depression correlates in subcortical brain regions, significant depression correlates in somatomotor and visual regions, and limited functional connectivity findings. Overall, these results shed new light on key brain regions involved in the pathophysiology of depression, updating our understanding of the neuroimaging correlates of depression. We anticipate that these insights will inform further research into the role of sensorimotor and visual regions in depression and into the impact of heterogeneity on functional connectivity correlates of depression.

neuroscience↗

MassNet: billion-scale AI-friendly mass spectral corpus enables robust de novo peptide sequencing

Breakthroughs in artificial intelligence (AI) for natural language processing and computer vision have been largely driven by high-quality, large-scale datasets such as OpenWebText and ImageNet. Inspired by this, we present MassNet, a foundational resource for proteomics designed to accelerate deep learning applications. MassNet is the largest known corpus of data-dependent acquisition (DDA) mass spectrometry (MS) data, derived from ~30 TB of raw files and comprising 1.54 billion MS/MS spectra, resulting in 558 million peptide-spectrum matches (PSMs) across 35 species, including animals, plants, and microbes. Within the human subset, MassNet includes more than 1.7 million precursors and 19,966 proteins, covering 98% of annotated human proteins. To enable efficient AI training, we developed the Mass Spectrometry Data Tensor (MSDT), a structured format based on Parquet that enables standardized, high-performance batch access and seamless integration with GPU and TPU platforms for distributed training. We further extended MassNet to support de novo peptide sequencing, which infers peptide sequences directly from MS/MS spectra without reference databases, and is critical for discovering novel proteins, characterizing non-model organisms, and identifying post-translational modifications (PTMs). We introduce XuanjiNovo, a non-autoregressive Transformer model that leverages a curriculum learning strategy to enhance training stability. By dynamically adjusting learning difficulty based on model performance, XuanjiNovo achieves smooth convergence on complex, multi-distributional data without manual hyperparameter tuning. Trained on 100 million PSMs from the MassNet, it consistently outperforms state-of-the-art methods across diverse benchmarking tasks. Peptide recall exceeds 0.8 on the Bacteroides thetaiotaomicron and Zea mays datasets. On human data acquired using the Orbitrap Astral platform, XuanjiNovo achieves achieves 38.8% to 144.3% improvement over existing models. MassNet represents the first large-scale, standardized foundational dataset in proteomics, marking a critical milestone in the integration of artificial intelligence into proteomics research.

bioinformatics↗