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Zhou, Y.

Publications and source records attributed to Zhou, Y..

At least 127 records · Page 7Linked to original sources

eBiota: Designing microbial communities from large seed pools with desired function using rapid optimization and deep learning

Designing microbial communities to generate target products is crucial for biotechnology, agriculture, and disease treatment. However, rationally designing such communities from large seed pools has become a major challenge, as the rapidly expanding number of complete microbial genomes greatly expands the search space and sharply increases the required screening time and computational cost. Here, we introduce eBiota, a platform for ab initio design of microbial communities from a pool of 21,514 strains to generate target products. eBiota not only identifies optimal strain combinations but also simulates community behaviors, including microbial interactions and relative abundances. eBiota integrates three modules: CoreBFS, a graph-based search algorithm that rapidly screens for bacteria with complete metabolic pathways related to the target product; ProdFBA, an extended flux balance analysis that identifies microbial consortia with maximal production efficiency; and DeepCooc, a deep learning model trained on 23,323 microbiome samples across various environments to infer co-occurrence patterns. We validated eBiotas capabilities in microbial community design and production efficiency calculation using public microbiome datasets, ranging from single strains to six-member consortia. Further in vitro experiments involving 94 strains confirmed eBiotas ability to identify species that inhibit pathogen growth and to accurately model the relative abundances within complex microbial communities. As an initial digital twin, eBiota provides a powerful platform for the rational design of functional microbial communities, offering new opportunities for metabolic engineering and synthetic biology.

bioengineering↗

Systematic detection of abnormal samples reveals widespread mislabeling in metagenomic studies

The human microbiome plays a critical role in health and disease, and its dynamic nature has made longitudinal sampling a key strategy for elucidating microbiome-disease relationships. Although the gut microbiome generally stabilizes over time, a subset of samples frequently shows marked deviations from an individuals baseline profile. We refer to these as abnormal samples. To analyze these abnormal samples, we developed a three-stage workflow to identify and classify these abnormal samples to figure out the underlying causes of these abnormal samples. Moreover, we systematically investigated abnormal samples across 16 publicly available metagenomic datasets, comprising a total of 5,171 metagenomes. Our analysis revealed that abnormal samples are often the result of mislabeling during sample collection, processing, or sequencing. Of which, fecal samples from family are more likely mislabeled. We found evidence of mislabeling in 75% of longitudinal datasets, involving up to dozens of samples per study, and in 25% of randomly selected cross-sectional datasets. Additional factors such as disease status (e.g., inflammatory bowel disease), sampling intervals, and sampling density may also contribute to sample abnormalities owing to true biological variations. These findings highlight that mislabeling is a common yet underrecognized issue in microbiome research. Our work underscores the importance of identifying and correcting abnormal samples to ensure data integrity in microbiome studies and provides a practical solution for quality control in large-scale metagenomic datasets.

microbiology↗

Single-cell Landscape of T Cell Heterogeneity in Kawasaki Disease: STAT3/JAK Axis Regulates the Lineage Differentiation Bias of Th17 Cells

BackgroundKawasaki disease (KD) is a pediatric systemic vasculitis in which T-cell-mediated immune responses play a pivotal role. However, the precise dynamic evolution of T-cell subsets during disease progression remains poorly understood. MethodsSingle-cell RNA sequencing (scRNA-seq) was employed to perform high-resolution annotation of peripheral blood mononuclear cells (PBMCs) from healthy controls and KD patients, both pre- and post- IVIG treatment. T-cell developmental trajectories were reconstructed via Monocle3-based pseudotime analysis. Furthermore, the functional significance of the significant pathway was validated in a CAWS-induced KD murine model. ResultsA high-resolution single-cell landscape identified 13 distinct T-cell subtypes. Pseudotime analysis revealed a significant lineage commitment of CD4+ T cells toward a Th17 phenotype during the acute phase of KD, synchronized with the transcriptional upregulation of the STAT3/JAK signaling axis. Animal experiments further demonstrated that pharmacological inhibition of this pathway substantially attenuated inflammatory infiltration in the cardiac vasculature of KD mice. ConclusionThis study identifies the STAT3/JAK-mediated Th17 differentiation bias as a potential regulatory program associated with acute inflammation in Kawasaki disease, thereby highlighting the STAT3/JAK axis as a potential therapeutic target.

bioinformatics↗

Gq-pathway activation in hippocampal CA1 astrocytes rescues ischemia-induced memory deficits and synaptic plasticity

More than 30% of stroke survivors develop post-stroke cognitive impairment (PSCI), for which current neuron-centric therapies not only lack cellular specificity but also carry risks of adverse effects such as epilepsy. Here, we explore the therapeutic potential of astrocytes by chemogenetically activating Gq signaling in hippocampal astrocytes, which rescues memory deficits and synaptic plasticity impairments in a mouse model of ischemic stroke. Gq activation restores dendritic complexity, spine density, and long-term potentiation in hippocampal CA1 neurons. Fiber photometry further reveals that astrocytic Ca{superscript 2} signals precede neuronal activity by 600 ms during novel environment exploration, indicating that astrocytes prime memory encoding. In contrast, Gi pathway activation induces pathological neuronal hyperactivity without cognitive improvement. These findings establish that astrocytes regulate post-stroke recovery through pathway-specific calcium signaling and uncover a previously unknown temporal hierarchy in astrocyte-neuron communication during memory processing, offering a new glia-targeted strategy to overcome the limitations of current neuromodulation approaches for PSCI.

neuroscience↗

Nuclear speckle protein SON safeguards efficient splicing of GC-rich genes

Gene architecture in higher eukaryotes exhibits substantial heterogeneity. While most genes follow a canonical pattern of GC-rich exons and AT-rich introns, a subset displays GC-leveled architecture, characterized by uniformly high GC content across both exons and introns. These genes are often associated with nuclear speckles, membraneless compartments enriched in RNA-processing factors, yet the mechanistic basis of this spatial and functional relationship remains unclear. Here, we identify the nuclear speckle protein SON as a critical factor that safeguards the splicing of GC-rich genes. Acute depletion of SON in mouse embryonic stem cells selectively impairs the splicing of short, GC-rich introns. These SON-dependent introns are enriched in highly expressed and functionally essential genes, whose GC-rich architecture contributes to efficient RNA processing and expression. Mechanistically, these introns harbor atypical C-rich, U-poor polypyrimidine tracts at their 3 splice sites, which exhibit reduced affinity for core splicing factors. SON is recruited to these sites via U2 snRNP and further interacts with SR proteins to stabilize the association of U2 snRNP and U2AFs at these C-rich weak splice sites. Notably, the evolutionary expansion of SONs intrinsically disordered region is required to promote efficient splicing of GC-rich genes that emerged during evolution. Together, our study suggests that the evolutionary transition toward GC-rich gene architecture enhances gene expression efficiency, with SON acting to safeguard the splicing of this gene class.

molecular biology↗

ISdetector: precise mapping of insertion sequences and associated structural variations from short-read sequencing data

MotivationInsertion sequences (ISs) are key drivers of genomic plasticity in bacteria and archaea. Determining their exact insertion coordinates is critical for understanding drug resistance, virulence, and pathogen epidemiology. However, accurately mapping ISs from high-throughput short-read sequencing data remains challenging due to the repetitive nature of these elements and accompanying structural variations, which frequently confound standard alignment-based algorithms. As whole-genome sequencing becomes the standard for population-level studies, there is a need for robust, scalable, and specialized pipelines to detect ISs. ResultsWe present ISdetector, a bioinformatics pipeline that detects precise insertion sites of specific ISs using an IS-clean reference strategy combined with clustering of IS-relevant signals from soft-clipped reads. Compared with existing tools, including ISMapper and MGEFinder, ISdetector demonstrates higher accuracy and robustness, achieving high F1 scores in both high-GC-content genomes (e.g., Mycobacterium tuberculosis, F1=0.91) and high-IS-burden genomes (e.g., Shigella sonnei, F1=0.85). Furthermore, ISdetector identifies IS movements accompanied by structural variations, such as large-scale deletions, which are often missed by existing methods. Implemented with multi-threading, ISdetector shows near-linear decreases in running time with increasing thread counts, making it highly scalable and efficient for processing large numbers of samples in population-level studies. AvailabilityISdetector is an open-source pipeline implemented in Python. It integrates standard bioinformatics tools, including BWA, SAMtools, and BLAST+, and uses the Biopython and Pysam libraries for data processing. The source code, documentation, and usage instructions are freely available at https://github.com/carolynzy/ISdetector. CONTACTZHOUYANG@CHINACDC.CN

bioinformatics↗

MRN-ATM Pathway Activation in CD4 T-Cell Senescence during Chronic Hepatitis B Virus Infection

T-cell senescence is a hallmark of immune dysfunction in persistent viral infections, characterized by DNA damage accumulation and telomere erosion. However, the mechanisms driving CD4 T-cell senescence in the context of chronic hepatitis B virus (HBV) infection remain poorly defined. In this study, we demonstrated that people with chronic HBV infection exhibited CD4 T-cell senescence, marked by elevated KLRG1, along with increased DNA damage and telomere shortening, compared to HS. Notably, activation of the MRN-ATM (MRE11/RAD50/NBS1-Ataxia Telangiectasia Mutated Protein) pathway was prominent in CD4 T cells from HBV patients. Importantly, suppression of MRN attenuated ATM phosphorylation and its downstream signaling molecules, and inhibition of ATM reduced the production of proinflammatory cytokines in CD4 T cells derived from both HBV patients and HS. These results suggest that in chronic HBV infection, the virus induced CD4 T-cell senescence, telomere erosion, and DNA damage, while concurrent activation of the MRN-ATM pathway may serve as a compensatory mechanism to preserve CD4 T-cell function. Elucidating this relationship between T-cell senescence and DNA damage repair helps to understanding the mechanisms underlying HBV persistence and providing potential therapeutic targets against chronic HBV infection.

immunology↗

Indazolone-Based Molecular Glue Degraders as a Tunable Platform for Reprogramming Cereblon Substrate Specificity

Molecular glue degraders (MGDs) represent a transformative modality in drug discovery, with the cereblon (CRBN)-MGD axis offering a strategic gateway to systematically address the historically undruggable proteome. However, the limited chemical diversity of existing CRBN-mediated MGDs has constrained the full exploration of the degradable landscape. Here, we introduce an innovative indazolone-based platform that extends beyond canonical isoindolinone-glutarimide scaffolds, significantly expanding the accessible chemical space for CRBN modulation. Guided by mechanistic insights into CRBN-MGD complex conformational plasticity, we rationally designed indazolone architectures as novel CRBN ligands, developing diverse MGDs with potent ligase binding and exceptional substrate programmability. This platform enables fine-tuned control over neo-substrate recognition, supporting diverse degradation profiles ranging from the broad targeting of critical proteins (IKZF1/3, ZFP91, and LIMD1) to the exquisitely selective degradation of CK1 and IKZF2. Beyond expanding the chemical landscape for intractable targets, our indazolone-based MGDs exhibit favorable pharmacokinetic properties, offering robust promise for therapeutic development. Collectively, the remarkable tunability and exceptional neo-substrate programmability of the indazolone-based platform provide a highly transformative blueprint for next-generation MGD discovery, enabling systematic exploration of the vast CRBN-accessible proteome. Furthermore, as superior CRBN ligands, this platform holds immense potential for PROTAC discovery to systematically address previously intractable targets.

biochemistry↗

Zhi-Shi-Huang-Wu slows Parkinson's disease progression in transgenic C. elegans models

Parkinsons disease (PD) is the second most progressive degenerative disorder of the brain due to dopaminergic (DA) neuron degenerations and alpha-synuclein (-Syn) accumulations. At present, the disease has no effective treatment. Therefore, the current study objective is to identify a novel anti-PD formula (Zhi-Shi-Huang-Wu Formula, F-2) computed at 8:4:2:1 ratio from HSP 70 promoter activators Valeriana jatamansi (V), Acori talarinowii (A), Scutellaria baicalensis (S), Fructus Schisandrae (F). Traditionally, V is used to cure memory impairments, A treats mental disorders, and chronic mild stress, S for neuroprotection, and F showed multiple therapeutic actions to treat insomnia. This study investigated the neuroprotective potential of the V, A, S, F, formula F-2 and its underlying molecular mechanisms in transgenic Caenorhabditis elegans models. A, S, F, and F-2 successfully restored 6-hydroxydopamine intoxicated DA neuron degenerations, reduced food-sensing behavior disabilities, and attenuated -Syn aggregations. Moreover, activates the lipid deposition and proteasome expressions to confirm -Syn degradations at the cellular level. Reactive oxygen species (ROS) cause oxidative stress, and A, S, F, and F-2 repressed ROS and raised SOD-3 expressions. Overall, these data indicate that V, A, S, F combined into F-2 (22.3%) are more effective against PD progression-like symptom than individual drugs V (0.7%), A (11.4%), S (9.6%), and F (12.6%). These improved neuroprotective actions of F-2 possibly due to following the antioxidative pathway. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=144 SRC="FIGDIR/small/709540v1_ufig1.gif" ALT="Figure 1"> View larger version (47K): org.highwire.dtl.DTLVardef@1a6f1f7org.highwire.dtl.DTLVardef@157a270org.highwire.dtl.DTLVardef@69a238org.highwire.dtl.DTLVardef@1194b5e_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

Strigolactone signaling regulates corm development through SPL15-mediated hormonal crosstalk in banana

Strigolactones (SLs) are an important class of plant hormones that play crucial roles in regulating plant branching, root architecture, and organ development. However, the regulatory mechanisms underlying the crosstalk between SLs and other plant hormones remain largely unclear, particularly regarding the key regulatory genes that integrate and coordinate multiple hormonal signaling pathways. In this study, secondary cup seedlings of the Pisang Awak banana cultivar Yufen 6 at the eight-leaf stage were used as experimental materials. The roots were treated with a nutrient solution containing 30 mol/L exogenous SLs, while a nutrient solution supplemented with water served as the control. Tissues near the corm growth point were collected at 0, 15, 30, 60, 90, and 120 days after treatment to measure corm weight, height, and diameter, and transcriptome sequencing was performed using the collected tissues. Differentially expressed genes (DEGs) at different treatment stages were identified, followed by Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses to systematically investigate the crosstalk between SLs and endogenous hormone metabolism and signaling during corm development in Pisang Awak banana. The results showed that SL treatment significantly inhibited the weight, height, and diameter of the corm. The regulatory effect of SLs on Pisang Awak banana corm development exhibited a clear temporal dynamic pattern, representing a gradual accumulation process that ultimately triggers key developmental transitions. The highest number of DEGs was detected at 15 days after treatment, including 3943 upregulated genes and 3704 downregulated genes, indicating that this stage represents a critical phase for SL response initiation. GO enrichment analysis revealed that the DEGs were mainly involved in metabolic processes, biological regulation, response to stimulus, and regulation of biological processes. KEGG pathway analysis indicated that these DEGs were significantly enriched in pathways related to plant hormone signal transduction, starch and sucrose metabolism, and secondary metabolite biosynthesis. Further analysis revealed that the crosstalk between SLs and multiple hormone metabolic and signaling pathways is mediated by the SPL15 gene, involving auxin (IAA), cytokinin (CTK), abscisic acid (ABA), brassinosteroids (BRs), gibberellins (GA), and jasmonic acid (JA) pathways. This study reveals the molecular mechanism by which SLs regulate Pisang Awak banana corm development through SPL15-mediated integration of multiple hormonal signals, providing new insights into the role of SLs in regulating the development of underground organs in banana.

bioinformatics↗

Interactome mapping in human excitatory neurons reveals novel risk genes and pathways in Alzheimer's disease

Alzheimers disease (AD) is an irreversible neurodegenerative disease defined by its molecular hallmarks - amyloid beta peptide plaques and neurofibrillary Tau tangles. Despite significant progress that has been made in uncovering a large number of genetic risk factors through extensive genomic sequencing and genetic studies, the molecular mechanisms driving AD-associated pathology and cognitive decline remain poorly understood. Therefore, alongside the identification of more risk genes, it is also paramount to study how these genes function and influence each other within the cellular pathways and overall molecular networks in AD-relevant brain cell types. However, current human protein-protein interactome datasets were all generated in either yeast or generic human cell lines. Consequently, many important neuronal interactions, especially neuron-specific ones, have yet been discovered. To address this critical gap, we developed a highly scalable, high-quality interactome mapping pipeline in human excitatory neurons derived from induced pluripotent stem cells (iPSC), and generated a comprehensive, neuron-specific interactome map, named ADNeuronNet, for key AD risk genes. ADNeuronNet consists of 1,767 high-confidence interactions among 1,189 proteins and is the only dataset enriched with neuron-specific genes when compared to known protein interactions, including previous large-scale interactome maps, for the same baits in the literature. Within ADNeuronNet, we identified 1,375 novel interactions, many of which are likely neuron specific. For example, we identified a neuron-specific interactor, RIN2, for major AD risk factor BIN1 and confirmed RIN2s function in recruiting BIN1 to RAB5 positive early endosomes, a process that has been well-associated with AD etiology. Additionally, we performed quantitative interaction perturbation analyses on AD risk genes with AD-associated mutations or isoforms and identified significant changes in 99 protein interactions among 11 different protein variants. Finally, we found that subunits from the anaphase-promoting complex/cyclosome (APC/C), another novel BIN1 interactors identified by ADNeuronNet, mediated modulation of Tau-aggregation in neurons via regulation of APOE expression, uncovering a previously unrecognized BIN1-APC/C-APOE regulatory axis in AD pathobiology. In summary, these findings illustrate how our neuron-specific ADNeuronNet can be leveraged to uncover new risk gene candidates and cellular pathways that help advance our understanding of molecular mechanisms underlying AD etiology.

systems biology↗

Human claustrum neurons encode uncertainty and prediction errors during aversive learning

Flexible behavior depends on continuous updating of internal models, yet the neural circuits coordinating this process remain poorly understood [1]. The claustrum -- reciprocally connected to nearly the entire neocortex -- is uniquely positioned to influence cortical processing. Here we report single-neuron recordings from the human claustrum during aversive learning [2], with anterior cingulate cortex and amygdala recordings for comparison. Claustrum and anterior cingulate neurons displayed structured, task-related responses. Distinct subpopulations encoded stimulus onset and action-contingent outcomes, with outcome representations diverging between regions. Critically, both regions encoded model-derived latent variables -- uncertainty and prediction error -- but with different temporal profiles: only the anterior cingulate carried uncertainty signals during the intertrial period, while both regions encoded uncertainty and prediction error during the active-avoidance period. The amygdala, by contrast, showed minimal latent-variable modulation. These findings provide evidence that human claustrum neurons track higher-order cognitive variables not directly observable from sensory input, and reveal dissociable roles for the claustrum and anterior cingulate cortex in tracking latent task states.

neuroscience↗

A Genetic Tool for Specific Tracking of Mature Neutrophils

Tracking mature neutrophils remains challenging due to the lack of reliable cell surface markers. Although CD101 is a promising candidate for mature neutrophils, its stability under pathological conditions is unclear. Using a CD101-tdTomato reporter mouse model, we confirmed that the reporting system does not alter CD101 expression, and tdTomato fluorescence is predominantly expressed in mature neutrophils across peripheral tissues. Further analysis revealed that CD101+ and tdTomato+ neutrophils display identical characteristics of mature neutrophil, including poly-segmented nuclei, cell size, and key functions under homeostasis. By comparing tdTomato fluorescence with CD101 protein levels, we demonstrate that reduced CD101 expression under pathological states was not attributed to shedding or degradation. Our finding enhances CD101 as a robust and reliable marker of neutrophil maturity, providing a foundation for future applications in spatial transcriptomics and lineage tracing studies to dissect neutrophil heterogeneity and function. Highlights of the studyO_LIIn CD101-tdTomato homozygous mice, tdTomato is predominantly expressed in neutrophils and labels nearly 100% of mature neutrophils, aligning with the phenotype of CD101+ mature neutrophils; C_LIO_LIThe CD101-tdTomato reporting system does not interrupt CD101 expression or neutrophil functions; C_LIO_LICD101 remains a stable and reliable cell surface marker for labeling mature neutrophils, even under pathological conditions. C_LI

immunology↗

A Novel Glycoproteomics Platform for High-Throughput Identification of Disease-Associated Glycoforms

Glycosylation is a critical post-translational modification, and its aberrant forms are potent disease biomarkers; however, the comprehensive, site-specific identification of all glycosites and glycoforms across an entire proteome remains prohibitively slow and computationally demanding. To address this bottleneck and accelerate biomarker discovery, we introduce the Glycoproteomics Data Analysis Software (GDAS), a novel, high-throughput platform designed to provide confident, proteome-scale identification of disease-specific glycoforms. GDAS streamlines the analysis through a core, multi-step workflow: it initially employs an ultrafast open search (e.g., MSFragger-Glyco) on mass spectrometry data to rapidly screen and statistically reduce the vast proteome database to a manageable subset of significantly regulated glycoproteins, conserving computational resources for subsequent, in-depth, targeted N- and O-glycosylation analysis using specialized tools (e.g., GlycReSoft and O-Pair). Furthermore, a unique Final Analysis Module utilizes an advanced statistical and machine learning pipeline (incorporating Bootstrap/Bayesian methods, XGBoost, and Random Forest) to integrate quantitative results and generate a robust, comprehensive glycosylation score. We demonstrate GDASs power to recognize biologically relevant glycosylation changes in targeted proteins by validating it using published Alzheimers disease data. GDAS can be downloaded from https://github.com/yang-lab/GDAS. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=92 SRC="FIGDIR/small/708406v1_ufig1.gif" ALT="Figure 1"> View larger version (19K): org.highwire.dtl.DTLVardef@189b270org.highwire.dtl.DTLVardef@1221045org.highwire.dtl.DTLVardef@15a3f50org.highwire.dtl.DTLVardef@1f2d43f_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioinformatics↗

AAV-Mediated Dual-Gene Therapy Restores Metabolic Function in Mice with Propionic Acidemi

Background and AimsPropionic acidemia (PA) is a rare autosomal recessive disorder caused by mutations in PCCA or PCCB, which encode the two subunits of propionyl-CoA carboxylase (PCC). PCC deficiency causes toxic metabolite accumulation and multi-organ damage. Current management, including dietary restriction, pharmacological support, and liver transplantation, does not restore enzymatic activity. We developed a dual-gene adeno-associated virus (AAV) therapy that delivers both PCC subunits to treat both PA subtypes. MethodsWe generated a clinically relevant PCCA-R73W knock-in mouse model and administered AAV8 vectors encoding native human PCCA and PCCB under the control of a liver-specific thyroxine-binding globulin promoter (AAV8-TBG-hPCCA-P2A-hPCCB). Metabolite levels and organ safety were longitudinally assessed. ResultsDual-gene therapy produced dose-dependent reductions in plasma C3/C2 ratio, 3-hydroxypropionic acid, 2-methylcitric acid, and propionylglycine, and significantly outperformed single-gene (PCCA-only) therapy. Neonatal facial-vein injection achieved metabolic correction comparable to or better than adult treatment. The longitudinal follow-up revealed sustained efficacy over a 16-week period, with no signs of hepatotoxicity or adverse effects. ConclusionsSingle-dose, dual-gene AAV therapy achieves sustained metabolic correction and demonstrates long-term safety in a clinically relevant PA model, supporting its translational potential for both type I and type II propionic acidemia.

genetics↗

Subthreshold membrane depolarization powerfully engages intracellular calcium dynamics in the brain

Membrane voltage (Vm) regulates spike timing and intracellular signaling. While Vm is extensively modulated by behavior, it is unclear how subthreshold Vm dynamics engage intracellular signaling in the awake mammalian brain. We developed a bicistronic viral vector to express genetically encoded and color compatible voltage and calcium (Ca2+) indicators in the same neuron, and simultaneously recorded cellular Vm and Ca2+ dynamics in awake mice. We report that prolonged subthreshold Vm depolarization is closely accompanied by prominent large amplitude Ca2+ elevation, whereas isolated spikes are coupled with weak Ca2+ rise. Additionally, individual spikes differentially engage intracellular Ca2+ dynamics depending on post-spiking Vm depolarization, consistent with a prominent role of slow Vm depolarization in regulating cellular signaling. While brief intracranial electrical stimulation consistently leads to Vm depolarization and Ca2+ increase, longer stimulation disrupts Vm and Ca2+ coupling, highlighting a tightly regulated cellular mechanism that relays slow Vm depolarization to intracellular signaling.

neuroscience↗

A Resolution-Agnostic Geometric Transformer for Chromosome Modeling Using Inertial Frame

AO_SCPLOWBSTRACTC_SCPLOWChromosomes are the carriers of genetic information. Further understanding their 3D structure can help reveal gene-regulatory mechanisms and cellular functions. However, high-resolution 3D structures are often missing due to the high cost and inherent noise of experimental screening. A standard pipeline for reconstructing the chromosome 3D structure first applies the single-cell Hi-C high-throughput screening method to measure pairwise interactions between DNA fragments at different resolutions; then it adopts computational methods to reconstruct the 3D structures from these contacts. These include traditional numerical methods and deep learning models, which struggle with limited model expressiveness and poor generalization across resolutions. To handle this issue, we propose InertialGenome, a novel transformer-based framework for robust and resolution-agnostic chromosome reconstruction. InertialGenome first adopts the inertial frame for the pose canonicalization. Then, based on such an invariant pose, it proposes a Transformer with geometry-aware positional encoding, leveraging Nystrom estimation. To verify the effectiveness of InertialGenome, we conduct experiments on two single-cell 3D reconstruction datasets with four resolutions, reaching superior performance over all four computational baselines. Additionally, we observe that the 3D structure reconstructed by InertialGenome is more in line with the results of real experimental results on two functional verification tasks. Finally, we leverage InertialGenome for cross-resolution transfer learning, yielding up to a 5% improvement from low to high resolution. The source code is available at https://github.com/yize1203/InertialGenome.

bioinformatics↗

Metabolic compensation via gluconeogenesis explains the non-essentiality of glycogen phosphorylase as an insecticidal target in Plutella xylostella

Glycogen phosphorylase (GP) catalyzes the rate-limiting step of glycogenolysis and occupies a central position in insect carbohydrate metabolism, supplying precursors for chitin biosynthesis. Acyl urea compounds structurally related to benzoylphenylurea (BPU) insecticides are potent inhibitors of mammalian GP, raising the question of whether insect GP could serve as an independent insecticidal target. Here, we systematically evaluate this possibility in the diamondback moth Plutella xylostella. We show that a mammalian GP inhibitor (GPI) potently inhibits recombinant PxGP (IC50 = 2.96 nM), while the BPU insecticide diflubenzuron (DFB) does not. Molecular docking and MM/GBSA analysis predict that this selectivity reflects differential side-chain engagement: GPI is predicted to occupy the allosteric site at the dimer interface via contacts with seven residues spanning both subunits ({Delta}G = -34.63 kcal/mol), whereas DFB's difluorobenzoyl moiety is predicted to remain solvent exposed without productive protein contacts ({Delta}G = -29.29 kcal/mol). Despite potent in vitro inhibition, GPI exhibits no insecticidal activity, and RNAi-mediated knockdown of PxGP (confirmed by enzyme activity measurements showing ~29% reduction in per-larva GP-a activity) does not impair development or survival. We provide evidence that insects compensate through a multi-layered metabolic response: upregulation of gluconeogenic enzymes (PEPCK, G-6-Pase), selective upregulation of glycogen branching enzyme (GBE) but not -amylase, and changes in protein content suggestive of catabolic substrate mobilization. Fitness assessment reveals transient larval weight loss (24-48 h) with complete recovery of pupal weight, adult wing morphology, and female fecundity, indicating that the metabolic compensation response is ultimately effective in sustaining development. These findings suggest that GP is functionally non-essential under these conditions, likely through a combination of gluconeogenic compensation and the availability of alternative carbon sources, and highlight the importance of considering metabolic network redundancy in target-based insecticide design.

biochemistry↗