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Chen, S.

Publications and source records attributed to Chen, S..

At least 271 records · Page 15Linked to original sources

A multi-modal cell-free RNA language model for liquid biopsy applications

Cell-free RNA (cfRNA) profiling has emerged as a powerful tool for non-invasive disease detection, but its application is limited by data sparsity and complexity, especially in settings with constrained sample availability. We introduce Exai-1, a multi-modal, transformer-based generative foundation model that integrates RNA sequence embeddings with cfRNA abundance data to capture biologically meaningful representations of circulating RNAs. By leveraging both sequence and expression modalities, Exai-1 captures a biologically meaningful latent structure of cfRNA profiles. Pre-trained on over 306 billion tokens from 8,339 samples, Exai-1 enhances signal fidelity, reduces technical noise, and improves disease detection by generating synthetic cfRNA profiles. We show that self-attention and variational inference are particularly important for preservation of biological signals and contextual relationships. Additionally, Exai-1 facilitates cross-biofluid translation and assay compatibility through disentangling biological signals from confounders. By uniting sequence-informed embeddings with cfRNA expression patterns, Exai-1 establishes a transfer learning foundation for liquid biopsy, offering a scalable and adaptable framework for next-generation cfRNA-based diagnostics.

bioinformatics↗

Functional landscape of circular RNAs in human cancer cells

Circular RNAs (circRNAs) constitute a novel class of noncoding RNAs showcasing distinct tissue- and cell-specific expression patterns. Despite the extensive profiling of circRNAs, their individual functions remain poorly understood. To fill this gap, we designed a genome-wide library of 65,300 shRNAs, targeting 9,663 clinically relevant circRNAs and 3,981 of their linear parental genes, and conducted functional screening in seven types of human cancer. We identified a total of 1,342 essential circRNAs (13.9% screened) that impact cell proliferation in at least one cell line, and in 96.5% of the cases, the linear counterparts are not essential. While a shared common subset emerges as functional regulators across all examined cell lines, the majority of circRNAs are functional in a cell type-specific manner. For a comprehensive presentation of the functional circRNA landscape in cancer, we introduce FunCirc, an online database encompassing functional circRNAs across cancer cell lines, coupled with circRNA expression profiles from diverse cancer and tissue types. Our work enhances the understanding of circRNA functions in cancer and provides the scientific community with a resource to further investigate their intricate roles.

cancer biology↗

Phase separation of Polycomb-like (PCL) proteins drive PRC2 complex condensates to regulate gene expression

Polycomb group (PcG) proteins function as two major multicomponent protein complexes: Polycomb repressive complex 1 (PRC1) and 2 (PRC2) to repress key developmental genes and maintain epigenetic memory of cell identity during development. Phase-separation has long been implicated in PRC1 mediated gene silencing, but it is still unclear whether PRC2 also utilize a similar mechanism to regulate gene expression. Here we report that Polycomb-like (PCL) proteins, PRC2 accessory factors, can phase-separate in vitro and generate dynamic puncta in vivo. Biochemical and cellular analyses reveal that PCL proteins (hereafter referred to as PCLs) have intramolecular interaction between N- and C-terminal domains, which make PCLs into more compact conformations. The intramolecular interaction not only controls the size of the PCLs phase separation droplets, but also affects the chromatin association of PRC2. Finally, we show that CpG islands, key DNA regulatory elements in mammalian promoters, disrupt the N-C intramolecular interaction of PCLs to expose their middle intrinsically disordered regions (IDRs), which in turn trigger PCLs driven PRC2 condensates formation. Together, this study provides a new perspective on the regulation of PRC2 by PCLs, implicating PCLs read CpG islands to fine-tune their oligomerization to overcome the threshold for PRC2 recruitment to corresponding genomic loci via multivalent interaction with CpG islands chromatin.

biochemistry↗

N-Glycans Modulate HIV-1 Env Conformational Plasticity

Human immunodeficiency virus-1 (HIV-1) remains a global health crisis, with over 39 million people living with the virus and no effective vaccine available. Central to HIV infection and immune evasion is the envelope glycoprotein (Env), a heavily glycosylated class I fusion protein that mediates viral entry and is the sole immunogenic target. Despite the recent advancements provided by imaging techniques, the characterization of Envs structure and dynamics within its native membrane environment remains incomplete. Here, we present microsecond-long, all-atom molecular dynamics simulations of the full-length Env glycoprotein embedded in a biologically relevant lipid bilayer with a complete glycosylation profile. Our simulations reveal a pronounced tilting motion of Env relative to the membrane, with supporting evidence from cryo-electron tomography, which also captures Env tilting within the native membrane. Importantly, we identify a critical role for N-linked glycans at N88 and N611 in modulating the tilting transition. These findings highlight the dual role of Envs glycan shield as both a protective barrier against neutralizing antibodies and a structural modulator of conformational plasticity. While providing an atomically detailed view of Env in a native membrane environment and advancing the general understanding of its glycan shield and its vulnerabilities, this work also suggests a possible strategy to modulate Envs conformational plasticity.

biophysics↗

Caterpillar counter-adaptations to hooked trichomes: does the coevolutionary arms race continue?

Plants protect themselves against herbivory with diverse chemical and physical defences, and many herbivores have evolved counter-adaptations against these defences. So far, little is known about herbivore counter-adaptations to physical plant defences and their underlying mechanisms. Here, we investigated how specialised Heliconiini caterpillars are able to cope with the hooked trichomes of Passiflora adenopoda vines. P. adenopoda trichomes have sharp tips reinforced with silica, in contrast to simpler trichomes of other Passiflora that do not deter Heliconiini larvae. While Heliconius melpomene and H. erato caterpillars placed on P. adenopoda leaves were arrested and their soft cuticle was pierced by the sharp hooked trichomes, H. charithonia and Dryas iulia caterpillars of all sizes could move easily over the leaves without any injury. The superior performance of these two species on trichome-bearing leaves can be explained by their thicker and more puncture-resistant cuticle. Morphological and penetrometry measurements showed that the relevant cuticle regions in H. charithonia and D. iulia caterpillars are significantly thicker and more puncture-resistant than in H. melpomene and H. erato. When we tested the ability of the caterpillars to feed on P. adenopoda leaves with hooked trichomes, only H. charithonia survived, indicating the existence of further, previously unknown post-ingestive adaptations. Understanding insect counter-adaptations to physical plant defences is essential for studying the evolutionary arms-race between plants and insect herbivores.

evolutionary biology↗

Human Body Single-Cell Atlas of 3D Genome Organization and DNA Methylation

Higher-order chromatin structure and DNA methylation are critical for gene regulation, but how these vary across the human body remains unclear. We performed multi-omic profiling of 3D genome structure and DNA methylation for 86,689 single nuclei across 16 human tissues, identifying 35 major and 206 cell subtypes. We revealed extensive changes in CG and non-CG methylation across almost all cell types and characterized 3D chromatin structure at an unprecedented cellular resolution. Intriguingly, extensive discrepancies exist between cell types delineated by DNA methylation and genome structure, indicating that the role of distinct epigenomic features in maintaining cell identity may vary by lineage. This study expands our understanding of the diversity of DNA methylation and chromatin structure and offers an extensive reference for exploring gene regulation in human health and disease.

genomics↗

Scale drop disease virus (SDDV) triggering ferroptosis both in vivo and in vitro facilitates virus infection via targeting transferrin receptor 1 (TfR1)

Scale drop disease virus (SDDV) is a distinct member in genus Megalocytivirus of family Iridoviridae, garnering increasing attention due to its significant threat to teleost. Ferroptosis is a new type of cell death discovered recently and involved in various viral infections. Knowledges on SDDV induced ferroptosis remains unclear. Here, we demonstrated that SDDV infection triggers ferroptosis, as evidenced by hallmark features such as iron overload, massive lipid peroxides accumulation, glutathione depletion and glutathione peroxidase 4 downregulation. SDDV-infected MFF-1 cells exhibited increased reactive oxygen species production and mitochondrial shrinkage. Treatment with Ferrostatin-1, a potent ferroptosis inhibitor, significantly attenuated SDDV replication in MFF-1 cells and could improve the survival of mandarin fish upon SDDV challenge. Treatment with an iron chelator mitigated ferroptosis and reduced the mortality of mandarin fish following SDDV infection, suggesting that SDDV-induced ferroptosis is iron-dependent. Finally, we demonstrated that SDDV infection could upregulate the expression of transferrin receptor protein 1 (TfR1), a critical iron transporter, to disrupt cellular iron homeostasis, induce ferroptosis, and then facilitate viral infection. Collectively, our findings provide compelling evidence that SDDV infection induces ferroptosis by targeting TfR1 to facilitate virus infection. Inhibiting ferroptosis represents a promising immunotherapeutic strategy for combating SDDV infection in aquaculture.

microbiology↗

Homoharringtonine Promotes FTO Degradation to Suppress LILRB4-Mediated Immune Evasion in Acute Monocytic Leukemia

Acute monocytic leukemia (AML-M5), a subtype of acute myeloid leukemia, is a highly aggressive malignancy characterized by a poor prognosis, primarily due to the ability of leukemic cells to evade immune surveillance. In this study, we demonstrate that homoharringtonine (HHT), an FDA-approved therapeutic agent for chronic myeloid leukemia (CML), inhibits this immune evasion by targeting the FTO/m6A/LILRB4 signaling pathway in monocytic AML. Utilizing RNA sequencing (RNA-seq) and various functional assays, we reveal that HHT treatment significantly reduces LILRB4 expression at both the RNA and protein levels, suggesting that the effects of HHT on LILRB4 are distinct from its well-established role as a protein synthesis inhibitor. Mechanistically, HHT treatment markedly increases global levels of RNA m6A in THP-1 cells by promoting the degradation of FTO, which subsequently diminishes the expression of its downstream targets, MLL1 and LILRB4. Furthermore, in vitro and in vivo analyses employing monocytic AML cell lines, mouse-derived AML xenograft models, and patient samples collectively support the conclusion that HHT suppresses immune evasion in monocytic AML by reducing LILRB4 expression. Importantly, the downregulation of LILRB4 resulting from HHT treatment enhances the susceptibility of THP-1 cells to CD8+ T cell cytotoxicity, accompanied by increased markers of immune activation. Overall, our findings position HHT as a promising clinical agent for enhancing CD8+ T cell-based cancer immunotherapy by mitigating immune evasion in monocytic AML. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=147 HEIGHT=200 SRC="FIGDIR/small/643466v1_ufig1.gif" ALT="Figure 1"> View larger version (20K): org.highwire.dtl.DTLVardef@e72e5dorg.highwire.dtl.DTLVardef@19519aeorg.highwire.dtl.DTLVardef@1c8f786org.highwire.dtl.DTLVardef@f2a963_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

Manganese suppresses tumor growth through hyper-activating IRE1α

IRE1 and its downstream XBP1 signal is the most conserved unfolded protein response pathway that cells utilize to combat endoplasmic reticulum stress, also known to be utilized by tumor cells to adapt to harsh environment, leading to tumor progression. Several inhibitors against IRE1 have been developed, some of which show promising effect in clinical trial for cancer therapy, but none of them have been used in practice. Considering that hyper-activation of IRE1 induces cell death, we hypothesize that activation of IRE1 could be an alternative way for tumor suppression. Here, we identified divalent manganese ion as a potent activator to IRE1, which interacts with the cytosolic part of IRE1 directly, augmenting the downstream pro-apoptotic pathway but not the pro-survival outcome. Mn2+ limits tumor growth in xenograft model in an IRE1-dependent way. Our finding suggests pharmacological activation of IRE1 as an underestimated but promising way in cancer therapy. HighlightsO_LIMn2+ binds to cytosolic segment of IRE1 and promotes its oligomerization C_LIO_LIMn2+ hyper-activates IRE1 and induces downstream terminal UPR under ER stress C_LIO_LIMn2+ does not elevate XBP1s expression C_LIO_LIMn2+ as an IRE1 activator impairs tumor growth in xenograft model C_LI

cancer biology↗

Molecular Insights into Cell Wall Architecture and Xylan-Bound Cellulose Fibrils in the Wheat Straw

The plant cell wall, a highly abundant renewable resource, remains insufficiently understood in terms of its structure, particularly the architecture of cellulose microfibrils and their interactions with hemicellulose and lignin, which impede the development of efficient downstream conversion. Here we present an alternative model of xylan-bound cellulose microfibril architecture in the cell wall of intact wheat straw, using solid-state nuclear magnetic resonance (ssNMR) coupled with X-ray scattering techniques. We show that the spectroscopic and scattering data can be fit to a simple elementary microfibril consisting of 18 glucan chains, with additional contributions from 0 to 4 tightly bound flat-ribbon xylan chains across the cellulose fibril axis. These xylan-bound cellulose microfibrils are found to serve as the secondary interaction site with lignin, following the non-flat xylan domains. The loose packing of these xylan-bound cellulose fibrils results in a heterogenous hydration landscape within the cell wall, allowing water penetration while maintaining structural integrity through numerous physical contacts between the polymers. This study provides a potential framework to reconcile the mounting biochemical evidence supporting the 18-chain elementary cellulose microfibril model and cellulose synthase complex with the oversized observations from characterization techniques, which report averaged structures influenced by microfibril coalescence and hemicellulose binding. The structural insights also offer valuable information regarding recalcitrance and the potential applications of biomass in biorefinery operations.

biochemistry↗

A functional anatomical shift from the lateral frontal pole to dorsolateral prefrontal cortex in emotion action control underpins elevated levels of anxiety: partial replication and generalization of Bramson et al., 2023

Flexible control over emotional behavior represents a promising target for novel interventions for mental disorders. Accumulating evidence has indicated a key role of the lateral frontal pole (FPl) and its connections with other cortical and subcortical systems in emotional action regulation. A recent study from Bramson et al., (2023) employed a multi-modal neuroimaging approach to demonstrate a functional-anatomical shift from FPI to dorsolateral prefrontal cortex (DLPFC) in a sample of anxious individuals during emotional action control. While these findings might represent a venue for interventions in anxiety disorders, conventional neuroimaging strategies are often limited with respect to generalizability and reproducibility. Against this background we capitalized previous large-scale fMRI data in n = 250 participants using an affective linguistic Go/NoGo paradigm to examine the robustness of the reported associations with trait social anxiety across samples, cultures and paradigms. Additionally, context-dependent functional connectivity patterns were explored to examine action control in different emotional contexts. In line with previous study, we found no difference between high- and non-anxious group on the behavioral congruency-effect. The neural results showed that non-social anxious group engaged the left FPl while the high-social anxious group specifically recruited the DLPFC, however in the absence of significant between-group differences. Importantly, the level of trait social anxiety was significantly positively related with DLPFC activity and negatively with left FPl activation across groups. Furthermore, context-dependent functional connectivity analyses revealed a negative context-specific neural shift from the sgACC-FPl to sgACC-DLPFC specifically in the high anxiety group. Together, the present study employed a different task paradigm, population and analytic methods, partially replicated the findings described by Bramson et al., (2023) and additionally determined context-specific changes in the communication with the sgACC in high anxiety. The findings provide further evidence for target-based interventions of persistent emotional control deficits in anxiety disorders.

neuroscience↗

High throughput identification of genetic regulators of microglial inflammatory processes in Alzheimer's disease

Genome-wide association studies (GWAS) have identified over a hundred genetic risk factors for Alzheimers disease (AD), many of which are predominantly expressed in microglia. However, the pathogenic role for most of them remains unclear. To systematically investigate how AD GWAS variants influence human microglial inflammatory responses, we conducted CRISPR inhibition (CRISPRi) screens targeting 119 AD GWAS hits in hiPSC-derived microglia (iMGLs) and used the production of reactive oxygen species (ROS) in response to the viral mimic poly(I:C) as a functional readout. Top hits whose knockdown either increased or decreased ROS levels in response to poly(I:C) were further analyzed using CROP-seq to integrate CRISPRi with single-cell RNA sequencing (scRNA-seq). This analysis identified 9 unique microglial clusters, including a poly(I:C)-driven inflammatory cluster 2. Emerging evidence supports a pathogenic role of viral infections in AD and cross comparison of our scRNA-seq data with iMGLs xenotransplanted into an AD mouse model shows significant overlap between our clusters and AD-relevant microglial clusters. Knockdown of MS4A6A and EED, which resulted in elevated ROS production in the presence of poly(I:C), increased the proportion of cluster 2 cells and induced functionally related changes in gene expression. In addition, KD of MS4A6 led to a reduction in the proportion of iMGLs in the DAM (disease associated microglia) cluster under all conditions, suggesting that this gene may modulate the DAM response. In contrast, KD of INPP5D or RAPEP1 which lead to low levels of ROS in the presence of poly(I:C), did not significantly affect the proportion of cells in cluster 2 but rather shaped the inflammatory response. This included the upregulation of an HLA-associated inflammatory cluster (cluster 6) by INPP5D knockdown under all conditions, independent of poly(I:C) stimulation. Importantly, KD of INPP5D or RAPEP1 had many shared differentially expressed genes (DEGs) under both vehicle and poly(I:C) treated conditions. Overall, our findings demonstrate that despite the diverse biological functions of AD GWAS variants, they converge functionally to regulate human microglial states and shape inflammatory responses relevant to AD pathology.

neuroscience↗

DORA AI Scientist: Multi-agent Virtual Research Team for Scientific Exploration Discovery and Automated Report Generation

Modern goal-oriented scientific research process involves hierarchical teams of researchers of diverse backgrounds performing generalist and domain-specific tasks. Many of these tasks include hypothesis generation, literature review, data collection, cleanup, processing and analysis, experimental design, virtual and physical experiments, research report and academic paper writing, reference management, bibliography and quality control. Most of these tasks can be performed automatically or in a co-pilot mode by the generative reinforcement learning systems. In this paper, we introduce a versatile multi-agent scientific exploration and draft outline research assistant (DORA), which provides multiple templates and workflows for automated or semi-automated research studies and report generation. Under user guidance, it employs hierarchical teams of AI agents based on the plug-and-play generalist and domain-specific large language models (LLMs) exploiting a variety of specialized research tools and open data repositories and generates high-quality research outputs publication drafts with maximally-accurate references. DORA is designed to minimize the time and effort required for manuscript preparation, thereby enabling researchers to devote more attention to high-value discovery tasks. The system is constantly evolving with user feedback with regular feature and resource updates. The platform is available at https://dora.insilico.com.

bioinformatics↗

Speed-accuracy trade-offs in Roulette betting

To investigate real-time decision-making in a simplified context, we analyze the trade-offs individuals make using a game of Roulette. In this game, players observe a ball that gradually decelerates as it moves around a circular track, and the participants must predict where the ball will ultimately stop. Players are rewarded for making rapid, accurate predictions, while slower but accurate predictions, or fast yet inaccurate ones, result in lower rewards. In this speed-accuracy trade-off setup we can calculate the optimal timing for placing a bet based on the balls initial speed and the deceleration rate, given the capacity of an individuals tracking abilities. We find that the participants improve their performance by accruing more reward with each trial and saturates close to the optimal performance, indicating that individuals learn the parameters of the physical model as well as a representation of the form of the reward under constrained time. Looking at the correlation between the bet time of the participant and the optimal betting time, the response delay and reward accrued, we find that the participant can be classified on a novice-expert spectrum. Our study offers ways to quantify human adaptation in competitive and dynamic environments such as sports, which may be helpful in enhancing participant performance.

animal behavior and cognition↗

Fast, accurate parsing of antibody structures and antibody-antigen interactions enables a comprehensive structural antibody database

Antibody (Ab) structures and antibody-antigen interactions (AAIs) are essential for understanding immune recognition and designing Ab therapeutics. While existing structural Ab databases provide valuable insights, they still have notable limitations. Here, we present SAAINT-parser, an computational workflow for rapid, accurate, and robust extraction of Ab and AAI information from the Protein Data Bank (PDB). SAAINT-parser features precise detection of Ab chains, accurate pairing of Ab chains, and reliable identification of AAIs. The resulting SAAINT-DB contains 18,031 data entries from 9,373 PDB structures, offering a comprehensive and up-to-date resource. Detailed analyses of SAAINT-DB reveals its advantages over the most widely used SAbDab database, particularly in terms of data accuracy and completeness. Furthermore, SAAINT-DB provides nearly twice as many nonredundant, manually curated Ab-Ag binding affinity data compared to SAbDab. Both SAAINT-parser and SAAINT-DB are available as open-source resources, aimed at advancing Ab-related research and benefiting the broader scientific community.

bioinformatics↗

ETP-Specific Knockout Mice Reveal Endotrophin as a Key Regulator of Kidney Fibrosis in Ischemia-Reperfusion Injury Models

Endotrophin (ETP), a cleavage product of the C5 domain of collagen VI 3 (COL6A3), plays a crucial role in extracellular matrix remodeling. Previously established Col6a3 knockout (KO) mouse models primarily reflect the consequences of COL6A3 loss rather than the specific effects of ETP depletion, making it challenging to directly assess ETPs function. These models either disrupt COL6A3 along with ETP production or express functionally defective COL6A3 while maintaining ETP production. To address this limitation, we developed and validated a novel ETP knockout (ETPKO) mouse model that selectively ablates ETP while preserving Col6a3 expression. To generate the ETPKO model, we introduced lox2272 sites and a fluorescent mCherry-CAAX reporter into the Col6a3 locus, ensuring that ETP expression is turned off and reporter expression is turned on upon Cre-mediated recombination. Crossing the Col6a3-Etp+mCherry-CAAX mouse line with CMV-Cre mice yielded ETPKO mice, in which successful ETP deletion was confirmed by genomic DNA sequencing and mCherry expression. Using this model, we investigated ETPs role in kidney fibrosis. ETPKO mice subjected to unilateral or bilateral renal ischemia-reperfusion injury (IRI) exhibited complete Etp mRNA ablation with only a partial reduction in Col6a3 mRNA. Notably, ETP depletion significantly attenuated fibrosis progression, demonstrating its critical role in the pathogenesis of kidney fibrosis. The ETPKO mouse model provides a targeted and specific approach for studying ETP function independently of Col6a3 expression. These findings establish ETP as a key driver of fibrosis and position ETPKO mice as a valuable tool for elucidating ETP-mediated mechanisms in preclinical disease models.

genetics↗

Derivation and analysis of human somatic sensory neuron subtypes facilitated through fluorescent hPSC reporters

Peripheral sensory neuropathy (PSN) is associated with several devastating neurological conditions, yet effective strategies to prevent or alleviate the consequences of PSN are nearly non-existent. A major challenge in the development of better therapeutic interventions is the lack of appropriate human model systems. Human induced pluripotent stem cell (hiPSC)-derived somatosensory neurons present a promising strategy to overcome this issue but remain of limited translational utility, in part due to the low efficiency and lack of sensory subtype selectivity of the existing sensory neuron derivation protocols. To improve upon iPSC-based somatosensory disease models, we here describe the generation and validation of a genetic toolset to fluorescently label all or distinct (nociceptor, low threshold mechanoreceptor, and proprioceptor) somatosensory subtypes. These new resources will be transformative for hPSC-based approaches in PSN disease modeling - a critical step towards translating new findings into clinically relevant therapeutic strategies.

neuroscience↗

MuFIX - Enabling Combinations of Concurrent Optogenetics and Lock-in Amplification Fiber Photometry via Removal of Optogenetic Stimulation Crosstalk

Simultaneous fiber photometry and optogenetics is a powerful emerging technique for precisely studying the interactions of neuronal brain networks. However, spectral overlap between photometry and optogenetic components has severely limited the application of an all-optical approach. Due to spectral overlap, light from optogenetic stimulation saturates the photosensor and occludes photometry fluorescence, which is especially problematic in physically smaller model organism brains like mice. Here, we demonstrate the Multi-Frequency Interpolation X- talk removal algorithm (MuFIX, or {micro}FIX) for recovering crosstalk-contaminated photometry responses recorded with lock-in amplification. {micro}FIX exploits multi-frequency lock-in amplification by modeling the remaining uncontaminated data to interpolate across crosstalk- affected segments (R2 [~] 1.0); we found that this approach accurately recovers the original photometry response after demodulation (Pearsons r [~] 1.0). When applied to crosstalk- contaminated data, {micro}FIX recovered a photometry response closely resembling the dynamics of non-crosstalk photometry recorded simultaneously. Upon further verification using simulated and empirical data, we demonstrated that {micro}FIX reproduces any signal that underwent simulated crosstalk contamination (r [~] 1.0). We believe adopting {micro}FIX will enable experimental designs using simultaneous fiber photometry and optogenetics that were previously not feasible due to crosstalk.

neuroscience↗