GEO 数据集

主题由标题与摘要自动归类；样本量为数据集标注之和，SuperSeries 可能与其 SubSeries 重复计算。

• MORC2A is required for DNA methylation and H3K9me3 at retrotransposons in the male germline
  GSE335170Mus musculus29 个样本2026-10-31

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• MORC2A is required for DNA methylation and H3K9me3 at retrotransposons in the male germline [RNA-seq]
  GSE335166Mus musculus10 个样本2026-10-31

  Transposable elements pose a particular threat to the germline, where their activation can compromise fertility and generate heritable mutations. In male germ cells, transposon silencing depends on repressive epigenetic states, including CpG methylation and H3K9me3. Here, we identify MORC2A as an essential regulator of transposon repression in the mouse male germline. Conditional deletion of Morc2a in primordial germ cells caused complete male infertility, testicular atrophy, germ cell loss and meiotic arrest. MORC2A-deficient testes displayed derepression of evolutionarily young retrotransposons, accompanied by DNA damage and apoptosis. Genome-wide profiling revealed loss of CpG methylation and H3K9me3 at these elements. Small RNA sequencing showed that piRNA biogenesis and ping-pong amplification remain largely intact. Together, these datasets identify MORC2A as a male germline chromatin regulator required for epigenetic silencing of young transposable elements.
• Sarm1 Gates the Transition from Protective to Repair Schwann Cell States Following Nerve Injury [snRNA-Seq]
  GSE332913Mus musculus11 个样本2026-10-31

  Schwann cells (SCs) transition into a Repair state after peripheral nerve injury; however, the early SC injury response preceding this transition remains poorly understood. We demonstrate that Sarm1, a key regulator of axon degeneration, is expressed and upregulated in SCs after nerve injury. Cell-type-specific Sarm1 knockout SCs exhibit enhanced axon protection in vitro, and SC- and glia-specific Sarm1 deletion confers axon protection in mouse sciatic nerve and Drosophila wing injury models. Single-nucleus RNA sequencing revealed that Sarm1-deficient SCs are enriched in a distinct cluster expressing genes with developmental roles in axon and myelin protection, with increased oxidative phosphorylation gene expression across all injured SC states. We propose that Sarm1 gates the transition from a Protection-Associated Schwann Cell (PASC) state to a Repair SC state, establishing Sarm1 as a multi-functional regulator with implications for peripheral neuropathies and neurodegenerative diseases.

  单细胞
• Sarm1 Gates the Transition from Protective to Repair Schwann Cell States Following Nerve Injury [RNA-seq]
  GSE332854Mus musculus12 个样本2026-10-31

  Schwann cells (SCs) transition into a Repair state after peripheral nerve injury; however, the early SC injury response preceding this transition remains poorly understood. We demonstrate that Sarm1, a key regulator of axon degeneration, is expressed and upregulated in SCs after nerve injury. Cell-type-specific Sarm1 knockout SCs exhibit enhanced axon protection in vitro, and SC- and glia-specific Sarm1 deletion confers axon protection in mouse sciatic nerve and Drosophila wing injury models. Single-nucleus RNA sequencing revealed that Sarm1-deficient SCs are enriched in a distinct cluster expressing genes with developmental roles in axon and myelin protection, with increased oxidative phosphorylation gene expression across all injured SC states. We propose that Sarm1 gates the transition from a Protection-Associated Schwann Cell (PASC) state to a Repair SC state, establishing Sarm1 as a multi-functional regulator with implications for peripheral neuropathies and neurodegenerative diseases.

  单细胞
• Single-cell analysis reveals transcriptomic patterns in active macrophage activation syndrome and therapeutic potential of albumin-fused interleukin-10 in a mouse model
  GSE331089Homo sapiens20 个样本2026-10-31

  Hemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS) are life-threatening hyperinflammatory conditions characterized by excessive immune activation and cytokine production. To clarify immune cell characteristics and identify potential therapeutic targets in MAS, we performed single-cell RNA sequencing (scRNA-seq) on bone marrow and peripheral blood samples from patients with newly developed MAS caused by diverse etiologies. To broaden the current knowledge of the immune landscape in the bone marrow, we performed scRNA-Seq of bone marrow cells and isolated blood leukocytes obtained from MAS patients using the Seq-Well.

  单细胞
• MUC13 enhances IL-17 signaling pathway activity in nasal epithelial cells
  GSE329876Homo sapiens12 个样本2026-10-31

  MUC13 is a membrane-bound mucin involved in epithelial protection and barrier maintenance, but its role in nasal epithelial inflammation remains unclear. This study aimed to investigate the function of MUC13 in nasal epithelial cells (NECs) and its potential involvement in inflammatory signaling. Primary NECs were isolated from patient-derived inferior turbinate mucosa, and MUC13 overexpression was established by direct transfection of human MUC13 mRNA. RNA sequencing and bioinformatics analyses were performed to characterize transcriptomic changes.
• GPR124 upregulation protects AML blasts from lipotoxicity
  GSE329506Mus musculus12 个样本2026-10-31

  GPR124 (ADGRA2), a member of the Adhesion G Protein-Coupled Receptor family, has an established role in the embryonic development of the central nervous system vasculature. However, its function in the context of acute myeloid leukemia (AML) remains unexplored. Transcriptome studies revealed upregulation of GPR124 in AML CD34+ blasts compared to healthy counterparts. Lentiviral overexpression of an GPR124-EGFP fusion protein indicated both plasma membrane and intracellular localization. Immunoprecipitation followed by LC-MS/MS showed strong enrichment of intracellular proteins associated with vesicles and vesicle transport, focal adhesion, actin cytoskeleton, and lipid droplets (LDs). In murine bone marrow mesenchymal stromal cells stimulated towards adipocytic differentiation, CRISPR-Cas9 mediated knockout of Gpr124 (Gpr124KO) reduced LD size, while total neutral lipid accumulation showed an increasing trend. In AML cells, lipidomic studies revealed increased baseline triacylglycerol (TG) levels in GPR124KO cells, suggesting altered LD metabolism. Since TGs are key components of LDs and its accumulation is a known response to lipid peroxidation, we next assessed ferroptosis sensitivity. Indeed, GPR124KO cells were significantly more sensitive to ferroptosis induction by GPX4 inhibition, accompanied by increased reactive oxygen species (ROS) and accumulation of lipid peroxidation. Additionally, GPR124KO cells were more sensitive to DGAT1 inhibition, a key enzyme in LD formation, and combination with the ferroptosis inducer RSL3 was synergistic in GPR124KO cells. Together, our findings indicate that GPR124 is essential for maintaining stable lipid homeostasis in AML and identify GPR124 and LD metabolism as potential therapeutic targets for inducing ferroptosis-mediated cell death.
• Endogenous PD-L1-Blocking Antibodies Drive Potent Anti-Tumor Immunity
  GSE326633Homo sapiens27 个样本2026-10-31

  Checkpoint blockade therapy, though transformative, remains ineffective in 70-80% of patients, with autoimmune adverse effects. Here, we provide the first evidence of a naturally occurring form of immune checkpoint blockade mediated by endogenous antibodies that functionally replicate the effects of therapeutic checkpoint inhibitors, without autoimmune symptoms. Through cloning and reconstructing patient-derived monoclonal antibodies, we show that certain cancer patients produce PD-L1-blocking antibodies that can restore T cell function and induce potent anti-tumor immunity. Broad polyreactive responses to multiple checkpoints confer no survival advantage. However, patients who are selectively positive for PD-L1 antibodies exhibit prolonged survival, tumors enriched with memory T cells, and activated circulating T cells. Mechanistically, these PD-L1 antibodies block PD-1/PD-L1 interactions and restore T cell function, in vitro and in vivo, revealing a naturally regulated form of checkpoint inhibition. Our data reveal that key principles of successful immunotherapy can emerge endogenously in a subset of patients, redefining our understanding of immune competence, tolerance, and therapeutic responsiveness in cancer, offering a mechanistic framework to explain how certain patients mount more effective anti-tumor immunity.
• Small RNA sequencing of fibrotic intestinal tissues from TNBS-induced mice
  GSE326149Mus musculus10 个样本2026-10-31

  To investigate miRNA expression changes associated with intestinal fibrosis, we performed small RNA sequencing on colon tissues from TNBS-induced fibrotic mice and control mice. This dataset was generated to identify fibrosis-associated miRNAs and provide a basis for subsequent functional and mechanistic studies of intestinal fibrosis.
• mRNA expression profiling of intestinal fibrosis in TNBS-induced mice
  GSE326147Mus musculus10 个样本2026-10-31

  To characterize transcriptomic alterations associated with intestinal fibrosis, we performed mRNA sequencing on colon tissues from TNBS-induced fibrotic mice and control mice. This dataset was generated to identify differentially expressed genes and signaling pathways involved in intestinal fibrosis.
• Priapulids polarize the recurrent genomic evolution of ecdysozoans
  GSE324316Halicryptus spinulosus; Priapulus caudatus19 个样本2026-10-31

  Priapulids constitute a key lineage for understanding the early ecdysozoan evolution, as their phylogenetic position, slow rates of evolution, and rich Cambrian fossil record contrasts with the highly derived nature of arthropods and nematodes. Here, we report chromosome-scale genomes for two priapulids and show that they did not experience the accelerated genomic evolution prevalent in other ecdysozoans suggesting this acceleration occurred recurrently across multiple branches rather than once. suggesting it did not arise once but occurred recurrently in multiple lineages. This recurrent trend involves the dislocation and rearrangement of ancestral chromosomal units and extensive gene loss, repeatedly affecting essential functions such as ciliary motility and cell division. We further uncover an ancestral whole genome duplication in priapulids; preferential expression of retained paralogues during introvert formation suggests this duplication contributed to priapulid emergence and radiation during the Cambrian. Recurrent loss of ancestral genomic characters during the evolution of Ecdysozoa parallels convergent morphological simplification, such as miniaturisation
• RNA-seq of Mus musculus 2-cell embryos (WT vs Tcl1 KO) with CDCA treatment
  GSE323388Mus musculus14 个样本2026-10-31

  This study includes paired-end bulk RNA-seq data generated from Mus musculus embryos at the 2-cell stage. Samples comprise wild-type (WT) and Tcl1 knockout (KO) embryos, with and without CDCA treatment, with biological replicates. Raw sequencing data are available in SRA and linked here via SRA Run accessions.
• Comparative profiling of SARS-CoV-2 variant infections reveals diverse impacts on host cell RNA and RNA binding protein distribution and regulation
  GSE318110Homo sapiens14 个样本2026-10-31

  RNA viruses perturb cellular RNA metabolism to promote viral transcript expression and genome replication. However, the extent of host cell RNA reprogramming and the consequences on RNA binding protein (RBP) expression and localization remain poorly understood. Here, we utilized an integrated set of transcriptomics, proteomics, and high-content imaging approaches to compare the impact of different SARS-CoV-2 variants, including an early viral isolate and later emerging variants of concern (Alpha, Delta and Omicron) on the host cellular RNA and RBP landscapes. While all variants deeply remodelled the host transcriptome in a subcellular compartment-specific manner, we found that Omicron variants express lower levels of viral RNA products compared to earlier variants, while still driving efficient production of viral proteins. The surge in viral RNA expression correlated with altered subcellular RNA biotype distribution, cytoplasmic mRNA exclusion, the selective disruption of the localization of polyA-tail interacting proteins, and the nuclear accumulation of non-coding transcripts such as RN7SL family members and MALAT-1. Unexpectedly, we found many RBPs that exhibiting altered subcellular localization following abiotic innate immune stimulation with poly(I:C) but remained unaltered in cells infected with SARS-CoV-2 variants, revealing a capacity for these viruses to limit the overall impact on the RBP subcellular distribution. Our results further indicate that Omicron infection sustains higher expression levels of proteins components of the signal recognition particle and translation factors, which may enable a more effective production of immune response and viral components. Altogether, this work highlights the deep impact of SARS-CoV-2 infection on host cell RNA regulatory landscape and provides new insights to explain the differential impact of Omicron compared to early SARS-CoV-2 variants.

  扰动筛选
• Regenerative macrophages from human iPSCs promoted vascular remodeling in human atherosclerotic organoid model
  GSE317284Homo sapiens26 个样本2026-10-31

  Recent studies have revealed that macrophages exhibit greater phenotypic diversity than the traditional M1/M2 classification, enabling them to display distinct functional properties depending on the surrounding microenvironment. Accordingly, it has become increasingly important to more finely characterize and evaluate macrophage subtypes that may operate within specific disease microenvironments. In this study, we aimed to identify a macrophage phenotype with therapeutic potential for atherosclerosis using an atherosclerosis-induced blood vessel organoid (BVO) model. To assess the effects of diverse macrophage phenotypes on the atherosclerosis, iPSC-derived macrophages (iMac) were generated and polarized into multiple phenotypic states. The polarized iMac populations displayed distinct gene expression profiles and exhibited functional differences in angiogenesis and regeneration related assays. For therapeutic evaluation, iPSC-derived BVOs were established and then induced to develop atherosclerotic features. During co-culture with the atherosclerotic BVO model, iPSC-derived regenerative macrophages (iMac R) showed active interactions with the organoids and produced therapeutic benefits on lipid clearance, anti-inflammatory responses, and regenerative effects. Notably, iMac R demonstrated superior therapeutic efficacy compared with other polarized macrophage phenotypes, highlighting their potential as a novel cell-based therapeutic strategy for atherosclerosis.
• CRISPR screen after venetoclax and azacitidine treatment in AML cells
  GSE314297Homo sapiens12 个样本2026-10-31

  CRISPR screen was performed in three isogenic MOLM-13 acute myeloid leukemia (AML) cell lines (p53 WT/p53 R248Q/p53 KO) to analyze gene dependencies changes after treatment with venetoclax and azacitidine.

  扰动筛选
• Nuclear Argonaute HRDE-1 Maintains Chromatin-Independent Transcriptional Silencing through a Transgenerational Small RNA Feedback Loop [Whole worm CUT&Tag]
  GSE311918Caenorhabditis elegans16 个样本2026-10-31

  Epigenetic inheritance of transcriptional silencing is traditionally attributed to chromatin-based mechanisms in which Argonaute–small RNA complexes recruit histone-modifying enzymes. Here we show that, in Caenorhabditis elegans, the nuclear Argonaute HRDE-1 maintains germline transcriptional repression independently of canonical heterochromatin marks. Using inducible, germline-specific HRDE-1 depletion combined with nuclear sorting, CUT&Tag, and nascent transcription profiling, we identify a functionally defined subset of endogenous genes, pseudogenes, and repetitive elements that become transcriptionally activated upon loss of HRDE-1 despite retaining H3K9me3, H3K23me3, and H3K27me3. HRDE-1 directly restrains RNA polymerase II (Pol II) while simultaneously promoting polyUG-dependent amplification of antisense 22G-RNAs in perinuclear condensates, thereby coupling nuclear transcriptional repression to small RNA biogenesis. HRDE-1 loss causes progressive erosion of 22G-RNAs and delays silencing re-establishment, revealing a transgenerational feedback loop in which small RNAs, and not chromatin modifications, constitute the primary heritable signal. These findings redefine nuclear Argonautes as active drivers of RNA-based epigenetic inheritance and broaden our understanding of how small RNA pathways maintain transcriptional silencing across generations.
• Nuclear Argonaute HRDE-1 Maintains Chromatin-Independent Transcriptional Silencing through a Transgenerational Small RNA Feedback Loop [small RNA-seq]
  GSE311555Caenorhabditis elegans28 个样本2026-10-31

  Epigenetic inheritance of transcriptional silencing is traditionally attributed to chromatin-based mechanisms in which Argonaute–small RNA complexes recruit histone-modifying enzymes. Here we show that, in Caenorhabditis elegans, the nuclear Argonaute HRDE-1 maintains germline transcriptional repression independently of canonical heterochromatin marks. Using inducible, germline-specific HRDE-1 depletion combined with nuclear sorting, CUT&Tag, and nascent transcription profiling, we identify a functionally defined subset of endogenous genes, pseudogenes, and repetitive elements that become transcriptionally activated upon loss of HRDE-1 despite retaining H3K9me3, H3K23me3, and H3K27me3. HRDE-1 directly restrains RNA polymerase II (Pol II) while simultaneously promoting polyUG-dependent amplification of antisense 22G-RNAs in perinuclear condensates, thereby coupling nuclear transcriptional repression to small RNA biogenesis. HRDE-1 loss causes progressive erosion of 22G-RNAs and delays silencing re-establishment, revealing a transgenerational feedback loop in which small RNAs, and not chromatin modifications, constitute the primary heritable signal. These findings redefine nuclear Argonautes as active drivers of RNA-based epigenetic inheritance and broaden our understanding of how small RNA pathways maintain transcriptional silencing across generations.
• Nuclear Argonaute HRDE-1 Maintains Chromatin-Independent Transcriptional Silencing through a Transgenerational Small RNA Feedback Loop [nuclear RNA-seq]
  GSE311553Caenorhabditis elegans20 个样本2026-10-31

  Epigenetic inheritance of transcriptional silencing is traditionally attributed to chromatin-based mechanisms in which Argonaute–small RNA complexes recruit histone-modifying enzymes. Here we show that, in Caenorhabditis elegans, the nuclear Argonaute HRDE-1 maintains germline transcriptional repression independently of canonical heterochromatin marks. Using inducible, germline-specific HRDE-1 depletion combined with nuclear sorting, CUT&Tag, and nascent transcription profiling, we identify a functionally defined subset of endogenous genes, pseudogenes, and repetitive elements that become transcriptionally activated upon loss of HRDE-1 despite retaining H3K9me3, H3K23me3, and H3K27me3. HRDE-1 directly restrains RNA polymerase II (Pol II) while simultaneously promoting polyUG-dependent amplification of antisense 22G-RNAs in perinuclear condensates, thereby coupling nuclear transcriptional repression to small RNA biogenesis. HRDE-1 loss causes progressive erosion of 22G-RNAs and delays silencing re-establishment, revealing a transgenerational feedback loop in which small RNAs, and not chromatin modifications, constitute the primary heritable signal. These findings redefine nuclear Argonautes as active drivers of RNA-based epigenetic inheritance and broaden our understanding of how small RNA pathways maintain transcriptional silencing across generations.
• Nuclear Argonaute HRDE-1 Maintains Chromatin-Independent Transcriptional Silencing through a Transgenerational Small RNA Feedback Loop [bulk RNA-seq]
  GSE311522Caenorhabditis elegans12 个样本2026-10-31

  Epigenetic inheritance of transcriptional silencing is traditionally attributed to chromatin-based mechanisms in which Argonaute–small RNA complexes recruit histone-modifying enzymes. Here we show that, in Caenorhabditis elegans, the nuclear Argonaute HRDE-1 maintains germline transcriptional repression independently of canonical heterochromatin marks. Using inducible, germline-specific HRDE-1 depletion combined with nuclear sorting, CUT&Tag, and nascent transcription profiling, we identify a functionally defined subset of endogenous genes, pseudogenes, and repetitive elements that become transcriptionally activated upon loss of HRDE-1 despite retaining H3K9me3, H3K23me3, and H3K27me3. HRDE-1 directly restrains RNA polymerase II (Pol II) while simultaneously promoting polyUG-dependent amplification of antisense 22G-RNAs in perinuclear condensates, thereby coupling nuclear transcriptional repression to small RNA biogenesis. HRDE-1 loss causes progressive erosion of 22G-RNAs and delays silencing re-establishment, revealing a transgenerational feedback loop in which small RNAs, and not chromatin modifications, constitute the primary heritable signal. These findings redefine nuclear Argonautes as active drivers of RNA-based epigenetic inheritance and broaden our understanding of how small RNA pathways maintain transcriptional silencing across generations.
• Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2 induced gene expression
  GSE311192Mus musculus27 个样本2026-10-31

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2 induced gene expression [Cut & Run]
  GSE311187Mus musculus15 个样本2026-10-31

  Transcription factor Foxp3, with its singular role in differentiation and function of regulatory T (Treg) cells in physiologic and inflammatory settings, is thought to act by modulating transcriptional responses to activatory extracellular cues including pro-inflammatory cytokines. However, the underlying mechanisms remain largely unknown. After Foxp3 is induced during Treg differentiation upon STAT5 activation downstream of interleukin-2 receptor (IL-2R), sustained STAT5 signaling facilitates fitness and suppressive capacity of mature Treg cells. We found that Foxp3 and phospho-STAT5 (pSTAT5) form a stable transcriptional complex. Upon IL-2 sensing, Foxp3 is recruited in a pSTAT5-dependent manner to GAS-motif-enriched cis-regulatory elements that are developmentally primed by STAT5 in Treg precursors prior to Foxp3 expression. Using chemogenetically and pharmacologically induced protein degradation, we demonstrate that Foxp3 modulates STAT5 signaling in activated Treg cells to selectively modulate their transcriptional response to IL-2, most prominently involving a Myc-dependent gene module. Our studies suggest that direct Foxp3-STAT5 cooperativity fine-tunes STAT5 signaling downstream of IL-2 receptor activation to support functionality of differentiated Treg cells.
• Cooperative interaction of Foxp3 and STAT5 confers regulatory T cell fitness by tuning IL-2 induced gene expression [RNA-Seq]
  GSE311182Mus musculus12 个样本2026-10-31

  Transcription factor Foxp3, with its singular role in differentiation and function of regulatory T (Treg) cells in physiologic and inflammatory settings, is thought to act by modulating transcriptional responses to activatory extracellular cues including pro-inflammatory cytokines. However, the underlying mechanisms remain largely unknown. After Foxp3 is induced during Treg differentiation upon STAT5 activation downstream of interleukin-2 receptor (IL-2R), sustained STAT5 signaling facilitates fitness and suppressive capacity of mature Treg cells. We found that Foxp3 and phospho-STAT5 (pSTAT5) form a stable transcriptional complex. Upon IL-2 sensing, Foxp3 is recruited in a pSTAT5-dependent manner to GAS-motif-enriched cis-regulatory elements that are developmentally primed by STAT5 in Treg precursors prior to Foxp3 expression. Using chemogenetically and pharmacologically induced protein degradation, we demonstrate that Foxp3 modulates STAT5 signaling in activated Treg cells to selectively modulate their transcriptional response to IL-2, most prominently involving a Myc-dependent gene module. Our studies suggest that direct Foxp3-STAT5 cooperativity fine-tunes STAT5 signaling downstream of IL-2 receptor activation to support functionality of differentiated Treg cells.
• Accurate In Vitro Recapitulation of Bile and Blood Partitioning of Drug Metabolites Using a hepatocyte culture system with induced open-form bile canaliculus icHep
  GSE307757Homo sapiens16 个样本2026-10-31

  Systemically circulating drug metabolites can cause organ damage, and there are species differences in the both the types of metabolites formed and their partitioning into bile and blood. Thus, it is necessary to evaluate the formation and biliary excretion of hepatic drug metabolites using in vitro evaluation system using human hepatocytes. Conventional sandwich-cultured hepatocytes (SCHs), however, form closed bile canaliculi that preclude direct collection of biliary excreted metabolites. Here, we assessed whether primary cultured hepatocytes with induced open-form bile canaliculus (icHep) provide a suitable system for evaluating the partitioning of drug metabolites produced in hepatocytes between bile and blood. Human hepatocytes derived from human liver–chimeric mice were cultured on claudin-1–coated plates, which facilitated the formation of open bile canalicular lumina, confirmed by co-immunostaining for MRP2 and ZO-1. RNA-seq analysis revealed that the expression levels of representative pharmacokinetics-related genes in icHep were comparable to those in SCHs. Following the addition of parent drugs to the blood-side chamber, metabolites were successfully collected from both blood- and bile-side chambers. Ziprasidone sulfoxide and mycophenolic acid glucuronide were predominantly recovered on the blood side, whereas celecoxib carboxylic acid and SN-38 glucuronide were preferentially excreted into bile. The metabolite partitioning observed in icHep was consistent with human in vivo data. In conclusion, icHep enables a quantitative evaluation of the hepatic disposition of drug metabolites including partitioning into bile and blood in human and represents a physiologically relevant in vitro system for human pharmacokinetic studies.
• Geometric inference of cross-species transcriptome correspondence
  GSE307647Gorilla gorilla; Pan troglodytes; Homo sapiens; Macaca fascicularis; Pongo abelii; Mus musculus28 个样本2026-10-31

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• Geometric inference of cross-species transcriptome correspondence [RNA-Seq]
  GSE307646Macaca fascicularis; Homo sapiens22 个样本2026-10-31

  Sequence homology underpins cross-species analysis but cannot identify evolutionarily distinct genes that play analogous regulatory roles. Furthermore, ethical restrictions on human experiments necessitate analytical frameworks that translate insights from other animals to humans. To address these challenges, we develop Species-OT, a cross-species transcriptome analysis framework based on Gromov-Wasserstein optimal transport, which quantitatively compares the geometry of transcriptome distributions. Given a pair of bulk or single-cell RNA-sequencing datasets, Species-OT returns a gene-to-gene correspondence capturing probabilistic alignments of regulatory roles, and a transcriptomic distance quantifying overall divergence. Applied pair wise, Species-OT yields a transcriptomic discrepancy array and a hierarchical clustering tree analogous to a phylogenetic tree. We validate Species-OT using bulk RNA-seq data from human, mouse, and macaque germ cell specification as well as scRNA-seq data from pluripotent stem cells of six mammalian species. Species-OT identifies evolutionarily related and distinct gene correspondences including biologically unexplored candidates, while transcriptomic discrepancies recapitulate expected species relationships.

  单细胞
• Transcriptomic changes from resulting from treatment of SVG-A with drugs of abuse
  GSE306251Homo sapiens21 个样本2026-10-31

  SVG-A cells were treated with drugs of abuse (ethanol, cocaine, morphine, THC, and psilocin) prior to RNA sequencing. A bioinformatics pipeline of Trim Galore, Kallisto, DESeq2 and Qiagen Ingenuity Pathway Analysis was used for pathway analysis.
• Disruption of nucleolar integrity triggers cellular quiescence through organelle rewiring and secretion
  GSE305361Homo sapiens27 个样本2026-10-31

  Intrinsic cellular stress responses are often mis regulated in complex human diseases such as cancer and neurodegeneration. To investigate how cellular homeostasis is balanced upon loss of key membraneless organelle – Nucleolus, we performed unbiased systems approach including cellular and temporal characterization of activated cellular stress signaling, associated sub-cellular changes and changes in cellular states and behavior. We report that transient loss of nucleolar architecture and defective ribosome biogenesis is well tolerated by cells as they undergo prolonged cell cycle arrest and rely on buffering capacity of cytoplasmic translation machinery. Cells immediately mount a comprehensive stress response predominantly mediated by TP53 and its downstream effector proteins. This mounted stress response is distinct from other acute stresses altering nucleolar morphology or function such as Pol I inhibition by ActD, heat shock or chemicals like Arsenate and CPT. Cells show a robust transcriptional reprogramming showing upregulation of structural and signaling genes of organelles such as Golgi apparatus and Endo-lysosomal vesicles. This leads to translation and microscopically evident tubular-vesicular expansion of Golgi and increase in number and size of endo-lysosomes. Cells become secretory, pro-metastatic and alter their cell-to-cell communication behavior. Taken together, these stress response pathways show an adaptive quiescent program and acquired partial EMT, allowing cells to resist loss of ribosome biogenesis, nucleolar architecture and ensure survival and restore homeostasis upon recovery. Correlatively, similar stress adaptions are seen to be contributing to progression of different cancer types especially in breast cancer and AML originating in the later stages of ribosomopathies.
• Determination of transcriptomic changes associated with salt stress in ethanol-treated control plants and TRB3-SRDX mutants.
  GSE302039Arabidopsis thaliana32 个样本2026-10-31

  Soil salinization severely threatens crop productivity. We previously revealed that ethanol treatment enhances abiotic stress tolerance, including salt stress, in plants. Ethanol up-regulated the transcription and activity of ascorbate peroxidase (APX1/2), key ROS detoxifing enzymes, thereby reducing ROS accumulation and improving salt stress tolerance. However, the transcriptional regulation underlying ethanol-mediated stress tolerance remains unclear. In this study, we identified Telomere repeat binding (TRB) proteins as transcription factors involved in ethanol-mediated salt stress tolerance. Transcriptome analysis revealed that copper/zinc superoxide dismutase (CSD) genes were down-regulated in TRB3-SRDX mutant. We further demonstrated that SOD activity was reduced in trb1/2/3 mutantm and csd mutant showed salt stress sensitivity even presence with ethanol, indicating that CSD are essential for ethanol-mediated salt stress tolerance. ChIP assays confirmed that TRB3 directly binds to CSD genes. Furthermore, ethanol treatment promoted H4K5 acetylation at CSD loci. These findings suggests that ethanol metabolism contributes to histone acetylation, and TRB3 facilitates its deposition at CSD loci, leading to enhanced CSD activation and improved salt stress tolerance.
• scRNA-seq of skin and PBMC samples of systemic sclerosis patients and healthy controls
  GSE299141Homo sapiens20 个样本2026-10-31

  Skin and blood samples from systemic sclerosis (SSc) patients and healthy donors were analyzed using single-cell transcriptomics (scRNA-seq). CCL19+ fibroblast was upregulated in the dermis of patients with SSc, and exhibited high expression of immuno-regulatory genes, including CCL19. CCL19 expression correlated with the severity of dermal fibrosis in SSc. The most significant ligand-receptor interaction from CCL19+ fibroblast to T cells in SSc skin was CCL19-CCR7. Furthermore, CCR7+ T cells in the fibrotic skin, particularly CCR7+CD8+ T cells, displayed enhanced stemness and cytotoxicity, actively interacting with extracellular matrix (ECM)-producing fibroblasts in SSc.

  单细胞
• Transcriptomic responses of zebrafish following dietary exposure to the short chain PFAS perfluorohexanoic acid (PFHxA)
  GSE291637Danio rerio19 个样本2026-10-31

  Per- and polyfluoroalkyl substances (PFAS) have garnered tremendous concern due to the widespread contamination and environmental persistence as PFAS and their heavy use in commercial products. While the properties of PFAS are useful for various consumer goods, the same properties result in high persistence of PFAS in the environment as well as an increased risk of exposure and deleterious effects for humans and ecosystems. To address data gaps for less studied PFAS, the use of molecular tools is essential to identify novel toxicity pathways that help to reduce additional animal testing for this large chemical class. In our current study, we exposed a model species (zebrafish) to a short chain PFAS, perfluorohexanoic acid (PFHxA), via the diet, which is an understudied exposure route in fish. Fish were exposed over 28 days to a measured low dietary dose (57.6 ng/g) as well as a higher dose (60.7 ng/g). At the end of the exposure, liver tissues were processed for mRNA and libraries were prepared for RNA-seq analysis. In addition to the transcriptome, qPCR will be performed to further assess changes in gene expression due to PFHxA dietary exposure. This study will be the first to examine sub-chronic dietary exposures to PFHxA and the resulting impacts on the transcriptome.