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Yin, S.

Publications and source records attributed to Yin, S..

At least 37 records · Page 2Linked to original sources

Inferring Dynamic Information from Protein Structures by Gaussian Integrals and Deep Learning

Protein conformational flexibility underlies a wide range of biological functions, yet experimentally probing dynamics at atomic resolution remains costly and low-throughput. Here, we present a deep learning framework that predicts protein flexibility directly from static structural descriptors, bypassing the need for molecular dynamics (MD) simulations. Using the ATLAS database of standardized all-atom MD trajectories, we encoded 1,374 protein chains as 30-dimensional Gaussian integral (GI) vectors--global shape and topology invariants of the protein backbone. Principal component analysis of GI profiles revealed four structural clusters with distinct secondary structure compositions and flexibility distributions. We trained an attention-based one-dimensional convolutional neural network (1D-CNN) to classify proteins as flexible or non-flexible based on their root-mean-square fluctuation (RMSF) relative to the dataset-wide mean. The classifier achieved an AUC of 0.772 (95% CI: 0.712-0.826) on an independent test set, with balanced sensitivity and specificity, and identified a small subset of GI components as the most predictive. In a regression setting, a recurrent neural network outperformed other architectures, attaining an R2 of 0.537, though high-flexibility values were systematically underestimated. Cluster-specific analyses indicated that coil-rich and {beta}-sheet-dominated proteins were more amenable to flexibility prediction than -helical proteins, likely due to greater structural heterogeneity. Our results demonstrate that compact GI descriptors preserve sufficient information to recover MD-derived flexibility trends, offering a computationally efficient complement to simulation-based approaches. This framework enables large-scale screening of protein dynamics from structural data alone, with potential applications in structural bioinformatics, drug design, and functional annotation.

bioinformatics↗

Single-cell Genomic Copy Number Evolution Reveals Frequent Loss of the Y chromosome in Esophageal Adenocarcinoma

The incidence of esophageal adenocarcinoma (EAC), an aggressive cancer, is rising in Western countries, and incidence is higher in men. To better understand the roles of DNA copy number evolution, tumor heterogeneity, and tumor microenvironment in EAC and its origins, we evaluated EAC, Barretts Esophagus (BE), and normal adjacent tissue using our previously developed ultra-sensitive, single-nucleus DNA copy number analysis (12,186 nuclei, 20 specimens) and single-nucleus RNA-sequencing (snRNA-seq; 87,027 nuclei, 32 specimens). Loss of Y (LOY) chromosome was rare in BE but markedly enriched in EAC. In genome unstable cells, complete LOY chromosome often coincided with X-chromosome duplication. We did not detect X-chromosome inactivation via XIST expression in cells with LOY, suggesting increased expression of X-chromosome genes and potential effects on tumor immune evasion. When considering patients clinical features, we identified distinct differences in tumor microenvironment by sex, age, and obesity status, particularly massively reduced immune cell composition in obese patients. Finally, our cell line models recapitulate LOY, and we identify the first candidate anti-LOY agent. Our findings highlight how LOY affects tumor subpopulations and shapes the tumor microenvironment during EAC progression.

cancer biology↗

Dynamic uterine microenvironment drives endometrial adenocarcinoma carcinogenesis and progression

Endometrial cancer (EC) development is driven by the interaction between the tumor and the microenvironment. However, the immune microenvironment dynamics during this process are not clear. Here, we applied single-cell RNA sequencing (scRNA-seq) to uterine blood samples collected at hysterectomy from 15 individuals encompassing four groups--benign controls, endometrial intraepithelial neoplasia (EIN), the transition from EIN to carcinoma, and EC. Uterine blood, obtained without prior enrichment, provides a liquid biopsy of the local tumor milieu, enabling high-resolution profiling of both immune and stromal cells in a minimally invasive manner. Our analysis revealed simultaneous immune and stromal remodeling in early premalignant lesions. Notably, even in the EIN, we observed significant immune cell reprogramming alongside the emergence of protumorigenic stromal-epithelial interactions. Importantly, we discovered predictive single-cell transcriptomic signatures derived from neutrophils that stratify patients according to disease state, highlighting the potential of tumor-educated innate immune cells as biomarkers. These findings yield candidate cellular and molecular signatures, particularly from neutrophils, that could enhance early EC detection and guide therapeutic strategies. Our work provides a proof-of-concept for leveraging local liquid biopsies in single-cell oncology, offering new insights into EC initiation and paving the way for noninvasive diagnostics on the basis of single-cell transcriptomic profiles.

cancer biology↗

Dorsal Attention Network as a Convergent Hub of Diverse Non-pharmacological Interventions Preserving Functional Gradients and Cognition in Aging

Non-pharmacological interventions (NPIs) in aging neuroscience have largely focused on intervention-specific regional effects, with limited understanding of generalizable network-level mechanisms. Here, adopting a previously unexplored gradient-based perspective of functional brain organization, we analyzed an NPI dataset involving four interventions in older adults (training/control group: n = 112/59). NPIs led to strengthened intra-network functional integration and maintained macroscale gradient architecture. Virtual lesion analyses identified the dorsal attention network (DAN) as a key contributor to gradient maintenance. Critically, enhanced post-intervention DAN connectivity was associated with maintained gradient structure and improved global cognition. These findings establish a unifying framework in which the DAN acts as a convergent hub through which diverse NPIs preserve functional brain organization and attenuate cognitive aging.

neuroscience↗

Exploring non-invasive sexing of early chick embryos in intact eggs using Laser Speckle Contrast Imaging (LSCI) and Deep Neural Network (DNN)

The ability to image blood flow in early-stage avian embryos has significant applications in developmental biology, drug and vaccine testing, as well as determining sex differentiation. In this project, we used our recently developed laser speckle contrast imaging (LSCI) system to non-invasively image extraembryonic blood vessels and used these images to attempt early sex identification of chick embryos. Specifically, we captured images of blood vessels from 1,251 living chicken embryos between day three and day four of incubation. We then applied deep neural network (DNN) models to evaluate whether it is possible to differentiate sex based on vascular patterns. Using ResNetBiT and YOLOv5 models, our results indicate that sex differentiation from extraembryonic blood vessel images was not achievable with sufficiently high accuracy or statistical significance for practical use. Specifically, ResNetBiT had a five-fold cross-validated average accuracy of 59%{+/-}5% (fold-wise p-value, p [≤] 0.3) at day 3 and 61%{+/-}3% (fold-wise, p [≤] 0.04) at day 4. YOLOv5 had a five-fold cross-validated average accuracy of 55%{+/-}3% (fold-wise, p [≤] 0.3) at day 3 and 53%{+/-}3% (fold-wise, p [≤] 0.5) at day 4. Our findings suggest that using vascular pattern imaging alone is inconclusive for reliable early sex identification in chicken embryos.

bioengineering↗

Humpback whales harbor a highly novel and endemic gut microbiome that adapts to periods of fasting during migration

Humpback whales (Megaptera novaeangliae) are cosmopolitan in distribution and most populations migrate between foraging and breeding grounds each year1,2. As capital breeders, many humpbacks reduce foraging behavior and potentially fast for a few months of the year3. Here, we present a comparative genomic analysis of the gut microbiomes from humpbacks on two breeding grounds: Gulf of California, where feeding is common4-6, and Hawai i, where feeding is extremely rare7. The humpback whale gut microbiome shows unexpected taxonomic novelty, high endemism, and coevolutionary signal. These data also suggest an imbalance in the gut community with foraging reduction, supported by the enrichment of several aerobic metabolism genes, potentially indicative of inflammation, and pathogenesis gene sets used to colonize host tissues, modulate the immune system, and lyse tissues. Pathway reconstruction revealed gut communities shared symbiotic functions including the synthesis of essential amino acids, short chain fatty acids (SCFAs), and vitamins, as well as nitrogen salvaging mechanisms and degradation of biogeochemically relevant substrates like cellulose, chitin, and wax esters (including host chitinases). Complementary sequencing and taxonomic annotation revealed that more Clostridiaceae and Oscillospiraceae genera were in foraging whales, whereas fasting samples were enriched in Erysipelotrichaceae genera, associated with gut disease8,9. These data reveal striking changes in humpback whale gut microbiomes between their feeding and breeding grounds, raise the possibility that breeding whales are more susceptible to gut dysfunction or disease, and equally important reveal how humpback whales are likely making varying biogeochemical contributions to upper ocean communities over the course of the year.

genomics↗

Morphogenesis and morphometry of brain folding patterns across species

Evolutionary adaptations associated with the formation of a folded cortex in many mammalian brains are thought to be a critical specialization associated with higher cognitive function. The dramatic surface expansion and highly convoluted folding of the cortex during early development is a theme with variations that suggest the need for a comparative study of cortical gyrification. Here, we use a combination of physical experiments using gels, computational morphogenesis, and geometric morphometrics to study the folding of brains across different species. Starting with magnetic resonance images of brains of a newborn ferret, a fetal macaque, and a fetal human, we construct two-layer physical gel brain models that swell superficially in a solvent, leading to folding patterns similar to those seen in vivo. We then adopt a three-dimensional continuum model based on differential growth to simulate cortical folding in silico. Finally, we deploy a comparative morphometric analysis of the in vivo, in vitro, and in silico surface buckling patterns across species. Our study shows that a simple mechanical instability driven by differential growth suffices to explain cortical folding and suggests that variations in the tangential growth and different initial geometries are sufficient to explain the differences in cortical folding across species.

neuroscience↗

Biophysical basis for brain folding and misfolding patterns in ferrets and humans

A mechanistic understanding of neurodevelopment requires us to follow the multiscale processes that connect molecular genetic processes to macroscopic cerebral cortical formations and thence to neurological function. Using magnetic resonance imaging of the brain of the ferret, a model organism for studying cortical morphogenesis, we create in vitro physical gel models and in silico numerical simulations of normal brain gyrification. Using observations of genetically manipulated animal models, we identify cerebral cortical thickness and cortical expansion rate as the primary drivers of dysmorphogenesis and demonstrate that in silico models allow us to examine the causes of aberrations in morphology and developmental processes at various stages of cortical ontogenesis. Finally, we explain analogous cortical malformations in human brains, with comparisons with human phenotypes induced by the same genetic defects, providing a unified perspective on brain morphogenesis that is driven proximally by genetic causes and affected mechanically via variations in the geometry of the brain and differential growth of the cortex. Impact statementPhysical gel models and numerical simulations are created to study ferret brain gyrification and cortical malformations, and comparisons with human phenotypes are presented to link genetics and brain morphogenesis.

neuroscience↗

Stress-driven emergence of heritable non-genetic drug resistance

Drug resistance is the chief cause of treatment failure for therapies targeting chronic and infectious diseases. Whether the emergence of resistance is accelerated by environmental exposure to low levels of therapeutics remains controversial. Here, we report a non-genetic mechanism of stress adaptation that promotes heritable resistance to the widely used antifungal drug fluconazole. In the human fungal pathogen Candida albicans, transient exposure to subtherapeutic fluconazole doses induces a protective response that we term para-resistance. Like conventional resistance mechanisms, para-resistance is heritable. However, it does not arise from genetic mutations and can revert spontaneously. Systematic analyses of para-resistant isolates suggest that its key regulators include the stress-activated MAP kinase Hog1, the histone deacetylase subunit Snt1, the chromatin regulator Rap1, and the Sko1 transcriptional factor. Notably, molecules that disrupt biomolecular condensation and prion propagation - crucial for the inheritance of protein assemblies - block the induction of para-resistance, whereas inhibiting histone deacetylases facilitates its induction. We find that para-resistance is common in clinical isolates and, remarkably, passage through the mammalian gut triggers its acquisition, compromising fluconazoles therapeutic efficacy. Our work defines a pervasive, prion-like epigenetic mechanism of stress adaptation and highlights potential strategies to mitigate the rapid emergence of drug resistance.

microbiology↗

How much is 'enough'? Considerations for functional connectivity reliability in pediatric naturalistic fMRI

functional connectivity (FC) measurements are important for robust and reproducible findings, yet pediatric functional magnetic resonance imaging (fMRI) faces unique challenges due to head motion and bias toward shorter scans. Passive viewing conditions during fMRI offer advantages for scanning pediatric populations, but FC reliability under these conditions remains underexplored. Here, we used precision fMRI data collected across three passive viewing conditions to directly compare FC reliability profiles between 25 pre-adolescent children and 25 adults, with each participant providing over 2.8 hours of data over four sessions. We found that FC test-retest correlations increased asymptotically with scan length, with children requiring nearly twice the post-censored scan time (24.6 minutes) compared to adults (14.4 minutes) to achieve comparable reliability, and that this effect was only partly attributable to head motion. Reliability differences between lower-motion adults and higher-motion children were spatially non-uniform and largest in ventral anterior temporal and frontal regions. While averaging features within functional networks improved intraclass correlation coefficient (ICC) reliability, values for higher-motion children remained in the poor-to-fair ICC range even with 48 minutes of total scan time. Viewing conditions with greater engagement reduced head motion in children but had lower FC reliability compared to less engaging low-demand videos, suggesting complex state- or condition-related trade-offs. These findings have important implications for developmental neuroimaging study design, particularly for higher motion pediatric populations.

neuroscience↗

Rationalize the Functional Roles of Protein-Protein Interactions in Targeted Protein Degradation by Kinetic Monte-Carlo Simulations

Targeted protein degradation is a promising therapeutic strategy to tackle disease-causing proteins that lack binding pockets for traditional small-molecule inhibitors. Its first step is to trigger the proximity between a ubiquitin ligase complex and a target protein through a heterobifunctional molecule, such as proteolysis targeting chimeras (PROTACs), leading to the formation of a ternary complex. The properties of protein-protein interactions play an important regulatory role during this process, which can be reflected by binding cooperativity. Unfortunately, although computer-aided drug design has become a cornerstone of modern drug development, the endeavor to model targeted protein degradation is still in its infancy. The development of computational tools to understand the impacts of protein-protein interactions on targeted protein degradation, therefore, is highly demanded. To reach this goal, we constructed a non-redundant structural benchmark of the most updated ternary complexes and applied a kinetic Monte-Carlo method to simulate the association between ligases and PROTAC-targeted proteins in the benchmark. Our results show that proteins in most complexes with positive cooperativity tend to associate into native-like configurations more often. In contrast, proteins very likely failed to associate into native-like configurations in complexes with negative cooperativity. Moreover, we compared the protein-protein association through different interfaces generated from molecular docking. The native-like binding interface shows a higher association probability than all the other alternative interfaces only in the complex with positive cooperativity. These observations support the idea that the formation of ternary complexes is closely regulated by the binary interactions between proteins. Finally, we applied our method to cyclin-dependent kinases 4 and 6 (CDK4/6). We found that their interactions with the ligase are not as similar as their structures. Altogether, our study paves the way for understanding the role of protein-protein interactions in PROTACE-induced ternary complex formation. It can potentially help in searching for degraders that selectively target specific proteins.

biophysics↗

Interpretable high-resolution dimension reduction of spatial transcriptomics data by DeepFuseNMF

Spatial transcriptomics (ST) technologies have revolutionized tissue architecture studies by capturing gene expression with spatial context. However, high-dimensional ST data often have limited spatial resolution and exhibit considerable noise and sparsity, posing significant challenges in deciphering subtle spatial structures and underlying biological activities. Here, we introduce SpaHDmap, an interpretable dimension reduction framework that enhances spatial resolution by integrating ST gene expression with high-resolution histology images. SpaHDmap incorporates non-negative matrix factorization into a multimodal fusion encoder-decoder architecture, enabling the identification of interpretable, high-resolution embeddings. Furthermore, SpaHDmap can simultaneously analyze multiple samples and is compatible with various types of histology images. Extensive evaluations on synthetic and real ST datasets from various technologies and tissue types demonstrate that SpaHDmap can effectively produce highly interpretable, high-resolution embeddings, and detects refined spatial structures. SpaHDmap represents a powerful approach for integrating ST data and histology images, offering deeper insights into complex tissue structures and functions.

bioinformatics↗

Torsional Twist of the SARS-CoV and SARS-CoV-2 SUD-N and SUD-M domains

Coronavirus non-structural protein 3 (nsp3) forms hexameric crowns of pores in the double membrane vacuole that houses the replication-transcription complex. Nsp3 in SARS-like viruses has three unique domains absent in other coronavirus nsp3 proteins. Two of these, SUD-N (Macrodomain 2) and SUD-M (Macrodomain 3), form two lobes connected by a peptide linker and an interdomain disulfide bridge. We resolve the first complete x-ray structure of SARS-CoV SUD-N/M as well as a mutant variant of SARS-CoV-2 SUD-N/M modified to restore cysteines for interdomain disulfide bond naturally lost by evolution. Comparative analysis of all structures revealed SUD-N and SUD-M are not rigidly associated, but rather, have significant rotational flexibility. Phylogenetic analysis supports that the disulfide bond cysteines are also absent in pangolin-SARS and closely related viruses, consistent with pangolins being the presumed intermediate host in the emergence of SARS-CoV-2. The absence of these cysteines does not impact viral replication or protein translation.

microbiology↗

FADS and semi-rational design modified T7 RNA polymerase reduced dsRNA production, with lower terminal transferase and RDRP activities

T7 RNA polymerase (T7 RNAP) is the preferred tool for in vitro transcription (IVT), it synthesizes mRNA while accompanied by the generation of dsRNA by-products. This undesirable dsRNA triggers immune stress responses, compromises therapeutic efficacy, and raises safety concerns. To evolve T7 RNAP for reduced dsRNA, we pursued two complementary strategies. Firstly, the FADS (fluorescence-activated droplet sorting) based on molecular beacons was used to screen random libraries with diversity exceeding 105. Secondly, we constructed several single-site saturated libraries to facilitate the transition of T7 RNAP from the initiation to the elongation conformation. These libraries were screened using the traditional microplate-based dual-probe screening technique. Both approaches identified two dominant variants: Mut1 (V214A) and Mut7 (F162S/A247T) from FADS, Mut11 (K180E) and Mut14 (A70Q) from saturated libraries. Furthermore, the combinatorial mutant Mut17 (A70Q/F162S/K180E), generated via DNA shuffling, exhibited significantly reduced dsRNA production compared to the wild-type under various conditions, ranging from 0.18% to 1.80%, with a minimum value of 0.5 pg/g. Cell experiments confirmed that variants generated capped-mRNA with similar quality and quantity to the wild-type, while significantly reducing immune stress response in cells. These results indicate the compatibility and broad potential applications of these mutations. We then observed a close correlation between the production of dsRNA and the activities of T7 RNAP in terminal transferase and RDRP. Particularly, the terminal transferase activity appears to play a critical role in dsRNA generation. These findings align with the mechanism of dsRNA formation during IVT and provide new screening criteria for further evolution of T7 RNAP.

molecular biology↗

Maternal obesity may disrupt offspring metabolism by inducing oocyte genome hyper-methylation via increased DNMTs

Maternal obesity has deleterious effects on the process of establishing oocyte DNA methylation; yet the underlying mechanisms remain unclear. In the present study, we found that maternal obesity induced by high-fat diet (HFD) disrupted the genomic methylation of oocytes, and that at least a part of the altered DNA methylation was transmitted to the F2 oocytes and the livers via females. We further examined the metabolome of serum and found that the altered metabolites such as melatonin may play a key role in the disrupted genomic methylation in the oocytes of obese mice. We further found that exogenous melatonin treatment significantly reduced the hyper-methylation of HFD oocytes, and the increased expression of DNMT3a and DNMT1 in HFD oocytes was also decreased. To address how melatonin regulates the expression of DNMTs, the function of melatonin was inhibited or activated upon oocytes. Results revealed that melatonin may regulate the expression of DNMTs via the cAMP/PKA/CREB pathway. These results suggest that maternal obesity induces genomic methylation alterations in oocytes, which can be partly transmitted to F2 in females, and that melatonin is involved in regulating the hyper-methylation of HFD oocytes by increasing the expression of DNMTs via the cAMP/PKA/CREB pathway.

developmental biology↗

Glutamate as a co-agonist for acid-sensing ion channels to aggravate ischemic brain damage

Glutamate is traditionally viewed as the first messenger to activate N-methyl-D-aspartate receptors (NMDARs) and downstream cell death pathways in stroke1,2, but unsuccessful clinical trials with NMDAR antagonists implicate the engagement of other NMDAR-independent mechanisms3-7. Here we show that glutamate and its structural analogs, including NMDAR antagonist L-AP5 (or APV), robustly potentiated currents mediated by acid-sensing ion channels (ASICs) which are known for driving acidosis-induced neurotoxicity in stroke4. Glutamate increased the proton affinity and open probability of ASICs, aggravating ischemic neurotoxicity in both in vitro and in vivo models. Site-directed mutagenesis and structure-based in silico molecular docking and simulations uncovered a novel glutamate binding cavity in the extracellular domain of ASIC1a. Computational drug screening of NMDAR competitive antagonist analogs identified a small molecule, LK-2, that binds to this cavity and abolishes glutamate-dependent potentiation of ASIC currents but spares NMDARs, providing strong neuroprotection efficacy comparable to that in ASIC1a or other cation ion channel knockout mouse models4-7. We conclude that glutamate serves as the first messenger for ASICs to exacerbate neurotoxicity, and that selective blockage of glutamate binding sites on ASICs without affecting NMDARs may be of strategic importance for developing effective stroke therapeutics devoid of the psychotic side effects of NMDAR antagonists.

neuroscience↗

Unveiling neoadjuvant chemotherapy-induced immune landscape remodeling and metabolic reprogramming in lung adenocarcinoma by scRNA-sequencing

BackgroundChemotherapy is widely used to treat lung adenocarcinoma (LUAD) patients comprehensively. Considering the limitations of chemotherapy due to drug resistance and other issues, it is crucial to explore the impact of chemotherapy and immunotherapy on these aspects. Methods and MaterialsTumor samples from nine LUAD patients, of which four only received surgery and five received neoadjuvant chemotherapy, were subjected to scRNA-seq analysis. In vitro and in vivo assays, including flow cytometry, immunofluorescence, Seahorse assay, and tumor xenograft models, were carried out to validate our findings. ResultsA total of 83,622 cells were enrolled for subsequent analyses. The composition of cell types exhibited high heterogeneity across different groups. Functional enrichment analysis revealed that chemotherapy drove significant metabolic reprogramming in tumor cells and macrophages. We identified two subtypes of macrophages: Anti-mac cells (CD45+CD11b+CD86+) and Pro-mac cells (CD45+CD11b+ARG+) and sorted them by flow cytometry. The proportion of Pro-mac cells in lung adenocarcinoma tissues increased significantly after neoadjuvant chemotherapy. Pro-mac cells promote tumor growth and angiogenesis and also suppress tumor immunity. Moreover, through analyzing the remodeling of T and B cells induced by neoadjuvant therapy, we noted that chemotherapy ignited a relatively more robust immune cytotoxic response towards tumor cells. ConclusionOur study demonstrates that chemotherapy induces metabolic reprogramming within the TME of LUAD, particularly affecting the function and composition of immune cells such as macrophages and T cells. We believe our findings will offer insight into the mechanisms of drug resistance and provide novel therapeutic targets for LUAD in the future.

cancer biology↗

Investigating 3D microbial community dynamics in the rhizosphere using complex-field and fluorescence microscopy

Microbial interactions in the rhizosphere contribute to soil health. Understanding these interactions thus has the potential to advance sustainable agriculture, ecosystem management, and environmental stewardship. Yet it is difficult to understand what we cannot see; amongst the limitations in rhizosphere imaging are challenges associated with rapidly and non-invasively imaging microbial cells over field depths relevant to plant roots. Here, we present a novel bimodal imaging technique called Complex-field and Fluorescence microscopy using the Aperture Scanning Technique (CFAST) that begins to address these limitations by integrating quantitative phase and 3D fluorescence imaging. We showcase CFASTs practicality and versatility in two ways. First, by harnessing its depth of field of more than 100 microns, we significantly reduce the number of captures required for 3D imaging of plant roots and bacteria in the rhizoplane, thereby minimizing potential photobleaching and phototoxicity. Second, by leveraging CFASTs phase sensitivity and fluorescence specificity, we track early bacterial aggregate development, bacterial competition, and gene expression under varying environmental conditions. Specifically, we resolve bacterial growth dynamics of mixed populations at the early stages of colonization without the need for genetically labeling environmental isolates. Moreover, we find that the expression of genes of interest to rhizosphere chemistry (e.g. representative genes involved in phosphorus-sensing and antibiotic production) varies spatiotemporally within microbial populations that are surface-attached and appears distinct from their expression in planktonic cultures. Together, CFASTs attributes overcome commercial imaging platform limitations and enable new insights to be gained into microbial behavioral dynamics in experimental systems of relevance to the rhizosphere.

microbiology↗