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。

• Bidirectional Plant-Microneedle Responses to Guide Biomaterial Design
  GSE279492Solanum lycopersicum58 个样本2026-10-30

  Designing biomaterials compatible with plants and specific payloads enables new technologies for precision agriculture, including targeted and dose‐controlled agrochemical delivery that overcomes the runoff, drift, and cuticular exclusion limiting conventional methods. However, broader implementation requires a systematic understanding of the complex interactions among payloads, biomaterial properties, and plant responses to establish design principles that support a sustained biotic–abiotic interface. Using microneedles made of different polymers and microstructures, this study investigates plant–biomaterial interactions to develop effective compound delivery strategies. Biodegradation studies show that microneedle biomaterials impart distinct mechanical strength, hydrophilicity, and surface charge, influencing the release of bioactive cargo. Transcriptomic analyses reveal a largely shared acute response to microneedle injection, with some material‐ or structure‐dependent variation in immunity and metabolism. Mid‐term biochemical responses show corresponding differences in membrane integrity and antioxidant activity. Despite these responses, microneedle treatments caused minimal effects on plant growth, chlorophyll content, stomatal conductance, and quantum efficiency of photosystem II. Finally, we demonstrate how biomaterial properties influence agrochemical delivery using hydrophilic plant growth regulator gibberellic acid (GA3) and hydrophobic herbicide pelargonic acid (PA), into tomato and lettuce, respectively. These findings establish principles for engineering plant‐biomaterial interfaces to accommodate payloads with diverse characteristics while ensuring plant safety.
• Gene expression profile and TCR-sequencing at single-cell level of PBMCs responding to EBV after 6 days of in vitro incubation.
  GSE277638Homo sapiens24 个样本2026-10-30

  In this work, we were able to establish a protocol for PBMC infection and sequence, for the first time at a single-cell level, the transcriptome of all cells capable of responding to the Epstein-Barr virus in healthy individuals and in certain patients with Inborn Errors of Immunity. Cells were sorted prior to sequencing based on proliferation (dilution of Cell Trace Violet) or activation (expression of CD69 and/or CD25).

  单细胞
• Species-Dependent WNT/ß-Catenin Signaling Orchestrates Epiblast Morphogenesis during Early Implantation [RNA-Seq]
  GSE273623Homo sapiens15 个样本2026-10-30

  The precise orchestration of epiblast tissue remodeling during implantation is critical for mammalian embryonic development and the regulatory link between cellular signaling and epiblast tissue morphogenesis remains unexplored. We present a fully defined, 3D epiblast-like model derived from human pluripotent stem cells (hPSCs). Functional studies of these in vitro models, alongside in vivo investigations in human and mouse embryos, reveal the pivotal role of canonical WNT signaling in mammalian epiblast morphogenesis. In humans, WNT/β-catenin signaling is crucial for epithelization, rosette formation, and cavitation of epiblast tissue. In mice, inhibition of canonical WNT signaling supports these events. Dual CUT&RUN and RNA sequencing, complemented by multi-study comparative transcriptome profiling, identify a TCF/LEF-mediated mechanism linking WNT signaling to lipid metabolism in human epiblast morphogenesis. This study highlights divergent roles of WNT-mediated mechanisms in early mouse and human development, as well as potential causes of human embryo lethality at implantation.
• Species-Dependent WNT/ß-Catenin Signaling Orchestrates Epiblast Morphogenesis during Early Implantation [Cut & Run]
  GSE273593Homo sapiens4 个样本2026-10-30

  The precise orchestration of epiblast tissue remodeling during implantation is critical for mammalian embryonic development and the regulatory link between cellular signaling and epiblast tissue morphogenesis remains unexplored. We present a fully defined, 3D epiblast-like model derived from human pluripotent stem cells (hPSCs). Functional studies of these in vitro models, alongside in vivo investigations in human and mouse embryos, reveal the pivotal role of canonical WNT signaling in mammalian epiblast morphogenesis. In humans, WNT/β-catenin signaling is crucial for epithelization, rosette formation, and cavitation of epiblast tissue. In mice, inhibition of canonical WNT signaling supports these events. Dual CUT&RUN and RNA sequencing, complemented by multi-study comparative transcriptome profiling, identify a TCF/LEF-mediated mechanism linking WNT signaling to lipid metabolism in human epiblast morphogenesis. This study highlights divergent roles of WNT-mediated mechanisms in early mouse and human development, as well as potential causes of human embryo lethality at implantation.
• Exploration of microRNAs involved in cervical lymph node metastasis of oral squamous cell carcinoma
  GSE246620Homo sapiens12 个样本2026-10-30

  Exploring biomarkers involved in lymph node metastasis in oral cancer
• Epigenomic analysis of the myometrium during late implantation revealed regulatory elements in genes related to the cellular zinc homeostasis pathway in pigs
  GSE246434Sus scrofa24 个样本2026-10-30

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• Epigenomic analysis of the myometrium during late implantation revealed regulatory elements in genes related to the cellular zinc homeostasis pathway in pigs (ChIP-Seq)
  GSE246433Sus scrofa12 个样本2026-10-30

  The myometrium, composed of the inner circular muscle (CM) and outer longitudinal muscle (LM), is crucial in establishing and maintaining early pregnancy. However, the molecular mechanisms involved are not well understood. In this study, we identified the transcriptomic features of the CM and LM collected from the mesometrial (M) and anti-mesometrial (AM) sides of the pig uterus on day 18 of pregnancy during the placentation initiation phase. Some genes in the cellular zinc ion level regulatory pathways (MT-1A, MT-1D, MT-2B, SLC30A2, and SLC39A2) were spatially and highly enriched in uterine CM at the mesometrial side. In addition, the histone modification profiles of H3K27ac and H3K4me3 in uterine CM and LM collected from the mesometrial side were characterized. Genomic regions associated with the expression of genes regulating the cellular zinc ion level were detected. Moreover, six highly linked variants in the H3K27ac-enriched region of the pig SLC30A2 gene were identified and found to be significantly associated with the total number born at the second parity (P < 0.05). In conclusion, the genes in the pathways of cellular zinc homeostasis and their regulatory elements identified have implications for pig reproduction trait improvement and warrant further investigations.

  空间转录组
• Epigenomic analysis of the myometrium during late implantation revealed regulatory elements in genes related to the cellular zinc homeostasis pathway in pigs (RNA-Seq)
  GSE246432Sus scrofa12 个样本2026-10-30

  The myometrium, composed of the inner circular muscle (CM) and outer longitudinal muscle (LM), is crucial in establishing and maintaining early pregnancy. However, the molecular mechanisms involved are not well understood. In this study, we identified the transcriptomic features of the CM and LM collected from the mesometrial (M) and anti-mesometrial (AM) sides of the pig uterus on day 18 of pregnancy during the placentation initiation phase. Some genes in the cellular zinc ion level regulatory pathways (MT-1A, MT-1D, MT-2B, SLC30A2, and SLC39A2) were spatially and highly enriched in uterine CM at the mesometrial side. In addition, the histone modification profiles of H3K27ac and H3K4me3 in uterine CM and LM collected from the mesometrial side were characterized. Genomic regions associated with the expression of genes regulating the cellular zinc ion level were detected. Moreover, six highly linked variants in the H3K27ac-enriched region of the pig SLC30A2 gene were identified and found to be significantly associated with the total number born at the second parity (P < 0.05). In conclusion, the genes in the pathways of cellular zinc homeostasis and their regulatory elements identified have implications for pig reproduction trait improvement and warrant further investigations.

  空间转录组
• Nuclear corepressors NCOR1 and NCOR2 entrain thymocyte signaling, selection, and emigration
  GSE246149Mus musculus3 个样本2026-10-30

  T cell development proceeds via discrete stages that require both gene induction and gene repression. Transcription factors direct gene repression by associating with corepressor complexes containing chromatin-remodeling enzymes; the corepressors NCOR1 and NCOR2 recruit histone deacetylases to these complexes to silence transcription of target genes. Earlier work identified the importance of NCOR1 in promoting the survival of positively-selected thymocytes. Here, we used flow cytometry and single cell RNA sequencing to identify a broader role for NCOR1 and NCOR2 in regulating thymocyte development. Using Cd4-cre mice, we found that conditional deletion of NCOR2 had no effect on thymocyte development, whereas conditional deletion of NCOR1 had a modest effect. In contrast, Cd4-cre x Ncor1f/f x Ncor2f/f mice exhibited a significant block in thymocyte development at the DP to SP transition. Combined NCOR1/2 deletion resulted in increased signaling through the T cell receptor, ultimately resulting in elevated BIM expression and increased negative selection. The NF-κB, NUR77, and MAPK signaling pathways were also upregulated in the absence of NCOR1/2, contributing to altered CD4/CD8 lineage commitment, TCR rearrangement, and thymocyte emigration. Taken together, our data identify multiple critical roles for NCOR1/2 throughout thymocyte development.

  单细胞
• Identification of 2’-O-methylation sites on mRNA and pre-mRNA
  GSE188194Homo sapiens6 个样本2026-10-30

  There have been reports suggesting that there may be thousands of Nm-modified mRNA or pre-mRNA transcripts in mammalian cells, there have been no studies that validate the proposed sites or determine the molecular mechanism responsible for their placement. In this study, we have refined a method for transcriptome-wide mapping of Nm sites and identified numerous high-confidence sites in mature mRNA
• H3K27me3 and total H3 ChIP-seq in stage 9, 11, and 12 Drosophila melanogaster embryos
  GSE352458Drosophila melanogaster12 个样本2026-10-29

  In an associated manuscript, we measured by ChIP-seq the genome-wide distribution of Histone H3 trimethylated at Lysine 27 (H3K27me3) and total Histone H3 in Drosophila embryos at three developmental stages following the maternal-to-zygotic transition: stage 9 (~NC14 + 2h), stage 11 (~NC14 + 4h), and stage 12 (~NC14 + 6h). These measurements extend a prior time course of H3K27me3 establishment during nuclear cycle 14 (NC14; GSE299311) and show that, after H3K27me3 appears local to Polycomb Response Elements (PREs) in mid-NC14, the modification continues to spread outward from these nucleation sites over the following ~6 hours. In the associated manuscript, these data are used to quantify the in vivo rate of H3K27me3 spreading and to benchmark a reaction-diffusion model of de novo Polycomb domain establishment by PRC2.
• Metabolic trapping of arachidonic acid by Treg cells shapes CD8+ T cell anti-tumor immunity
  GSE352441Mus musculus7 个样本2026-10-29

  Regulatory T (Treg) cells rely on lipid metabolism to thrive in the lipid-rich tumor microenvironment (TME), but whether this metabolism shapes the extracellular metabolite landscape that acts on effector T cells remains unknown. Here, we identify epoxide hydrolase 1 (Ephx1), highly expressed in tumor-infiltrating Treg cells, as a cell-intrinsic determinant of arachidonic acid (AA) availability in the TME. Treg-specific deletion of Ephx1 induced compensatory, ACSL4-dependent incorporation of exogenous AA, converting Treg cells into a metabolic trap for tumor-derived AA and lowering its extracellular abundance. The resulting AA scarcity restored the mitochondrial fitness of CD8⁺ T cells, rewired their metabolism away from fatty acid oxidation toward more efficient energy generation, and skewed exhaustion trajectories toward effector-like intermediate states while preserving the stem-like progenitor pool, collectively restraining tumor progression. In patients with hepatocellular carcinoma, TME AA levels tracked with tumor burden and inversely with the mitochondrial fitness of infiltrating CD8⁺ T cells. Accordingly, intratumoral delivery of the AA-release inhibitor Methyl Arachidonyl Fluorophosphonate (MAFP) reinvigorated CD8⁺ T cell immunity and acted synergistically with anti-PD-1 therapy. Targeting Treg cell lipid metabolism thus offers a route to reprogram the TME metabolome and potentiate cancer immunotherapy.
• Trisomy 21 Perturbs Oligodendrocyte Developmental States and Oligo-Neuron Communication in Human Forebrain Assembloids
  GSE352389Homo sapiens12 个样本2026-10-29

  Intellectual disability is a hallmark of Down syndrome (DS), caused by the triplication of human chromosome 21. Abnormal neuronal connectivity and impaired myelination are consistently observed in DS, yet the underlying mechanisms remain poorly understood. Here, we used DS-derived isogenic induced pluripotent stem cell-derived forebrain assembloids (FAs) to investigate oligodendrocyte lineage cell (OLLC) development and neuron-glia interactions. Trisomic FAs exhibited an expansion of BCAS1+ pre-myelinating OLLCs, without a corresponding increase in myelin basic protein (MBP) expression. Transcriptomic analyses identified a euploid-enriched, trophic and maturation-supportive state (OLLC_2-TMS) and a trisomy-enriched state, characterized by enhanced neuronal interactions and restricted progression beyond the pre-myelinating stage (OLLC_3-NID). These transcriptional signatures were also present in OLLCs from early postnatal human cortex. Increased excitatory neuronal contacts with pre-myelinating OLLCs accompanied ultrastructural myelin abnormalities in trisomic assembloids. Our findings suggest that trisomy redirects OLLC development toward a pre-myelinating state, uncoupling oligodendrocyte differentiation from productive myelination.

  扰动筛选
• BAP1 safeguards double-strand DNA break repair by limiting DNA end resection [ChIP-Seq]
  GSE352106Homo sapiens5 个样本2026-10-29

  The tumor suppressor BAP1 is frequently mutated in uveal melanoma and has been linked to homologous recombination (HR), yet how it influences DNA double-strand break (DSB) repair pathway choice remains unclear. Here, we identify BAP1 as a critical regulator that restricts DNA end resection to preserve non-homologous end-joining (NHEJ) capacity. Loss of BAP1 leads to aberrant accumulation of H2AK119 ubiquitination at DSBs, driving unscheduled resection in G1-phase cells and impairing recruitment of the anti-resection factor 53BP1. Co-depletion of the resection initiator CtIP restores NHEJ efficiency in BAP1-depleted cells, and pharmacological suppression of H2AK119 ubiquitination reverses these defects, placing unscheduled resection causally upstream of the end-joining failure. RNA sequencing and genome-wide H2AK119ub profiling show that neither the expression of NHEJ and HR genes nor the H2AK119ub landscape at their promoters is appreciably altered by BAP1 loss, supporting a role of altered H2AK119ub at the DSBs. These findings indicate that BAP1 safeguards DSB repair fidelity by preventing hyper-resection, thereby maintaining NHEJ competence. Consistent with this role, BAP1-depleted cells accumulate micronuclei, and BAP1 loss is associated with genomic instability in human uveal melanoma. Together, our results uncover a mechanism by which chromatin regulation constrains resection to coordinate repair pathway utilization.
• SH2 Domain Protein E sustains perivascular fibroblasts to maintain arterial stability
  GSE352057Danio rerio8 个样本2026-10-29

  Developing arteries must withstand pulsatile blood flow while remaining sufficiently flexible to accommodate changing hemodynamic demands. Endothelial interactions with perivascular cells and extracellular matrix are essential for this balance, but the signaling mechanisms that coordinate them remain incompletely understood. We previously showed that SH2 domain protein E (She), an endothelial adaptor protein implicated in ABL signaling, limits the size of the dorsal aorta (DA) in zebrafish embryos. Here, we investigated why zebrafish she mutants subsequently develop DA collapse and circulatory failure at 4–5 days post-fertilization. Before circulatory failure, the mutant DA retained an approximately circular cross-section and showed no detectable changes in the endothelial cell geometry, but exhibited increased distensibility during the cardiac cycle. Mutants had fewer perivascular stromal cells between the DA and posterior cardinal vein, smaller perivascular col1a1 and col5a1 expression domains, and reduced col1a1 transcript level. Single-cell RNA sequencing independently identified a reduced relative abundance of perivascular fibroblast subpopulation. In contrast, DA-associated mural cell numbers, laminin immunoreactivity, and local col4a1 transcript levels were not detectably altered. Ablation of pdgfrb-positive cells largely prevented DA narrowing and circulatory failure, while the nitric oxide donor sodium nitroprusside provided partial rescue. These findings support a contribution of mural cell-dependent vascular tone to collapse of the mechanically vulnerable DA. Mutants also exhibited cardiac chamber enlargement, increased atrial and bulbus arteriosus deformation, atrioventricular regurgitation, and increased Elastin B accumulation in the enlarged bulbus arteriosus. However, endocardial-specific She expression failed to rescue circulatory failure, supporting its requirement in vascular endothelium. Together, these findings link She function to perivascular fibroblast abundance, fibrillar collagen-gene expression, and arterial stability. They support a model in which impaired perivascular support renders the developing DA susceptible to mural cell-associated collapse, extending the role of She from early vessel-size regulation to maintenance of vascular function.

  单细胞
• RNA-seq of human meningioma samples
  GSE351918Homo sapiens59 个样本2026-10-29

  Meningiomas are frequently diagnosed tumors of intracranial location. In the WHO classification, tumor aggressiveness is assessed by assigning increasing grades, with WHO grade I tumors considered benign and WHO grade III tumors the most aggressive. In our study, we aimed to identify biological features associated with meningioma aggressiveness by profiling gene expression in FFPE tumor samples of different WHO grades (I, II, and III).
• LAMA2-related muscular dystrophy alters Schwann cell calcium homeostasis and increases peripheral nerve inflammation
  GSE351764Mus musculus43 个样本2026-10-29

  LAMA2-related muscular dystrophy (LAMA2-RD) affects skeletal muscle and peripheral nerves, yet the consequences of LAMA2 deficiency for peripheral nerve integrity beyond early postnatal development remain incompletely understood. We investigated sciatic nerve architecture and molecular alterations across postnatal life in hypomorphic Lama2dy2J/dy2J mice. LAMA2 localizes around the abaxonal surface of myelinating Schwann cells in control nerves. LAMA2-deficient nerves exhibited patchy regions lacking myelinated axons from early postnatal stages into adulthood, including expanded Remak bundles along with axons completely lacking normal Schwann cell ensheathment. In adult nerves, myelin infolding and reduced myelin circularity revealed abnormalities in the architecture of myelin that had formed. Bulk sciatic nerve RNA sequencing identified altered calcium-signaling and immune-related transcriptional signatures. Complementary Fura Red measurements in primary nerve-derived Schwann cell cultures demonstrated decreased intracellular calcium in LAMA2-deficient samples, while ATP-evoked responses were preserved. Older LAMA2-deficient nerves also exhibited increased CD45+CD11b+ myeloid-cell infiltration. Together, these observations extend the characterization of LAMA2-associated neuropathy into adulthood and identify calcium homeostasis and neuroimmune responses as candidate processes relevant to persistent peripheral nerve pathology.
• Cancer-Associated Transcriptional Readthrough Reveals Distinct Stress- and Proliferation-Related Programs
  GSE349075Homo sapiens47 个样本2026-10-29

  Transcriptional readthrough generates downstream-of-gene (DoG) RNAs through transcription beyond canonical termination sites. Although DoGs have been implicated in cellular stress and cancer, their biological and clinical significance remains poorly understood. We analyzed DoG transcripts in 787 experimental and 3,066 public RNA-seq profiles encompassing colorectal, lung, pancreatic, stomach, and thyroid cancers. RNA-seq library design strongly influenced DoG detection, with rRNA-depleted and paired-end libraries providing greater sensitivity than poly(A)-selected and single-end approaches. DoG abundance and expression were increased in most cancer types, whereas DoG length was largely unchanged. Joint analysis of DoG and parental gene expression identified two distinct classes of cancer-associated readthrough. DoGs upregulated independently of parental genes, consistent with dysregulated transcription termination, included 31 transcripts recurrently increased across all five cancer types and were associated with stress-related functions. In contrast, DoGs co-upregulated with their parental genes were enriched for proliferation-related processes. In an experimental cohort of 95 lung cancer patients receiving PD-(L)1 immune checkpoint therapy, higher abundance and expression of recurrent DoG signatures were associated with shorter progression-free survival (HR 2.53–3.24). These findings reveal distinct biological components of cancer-associated transcriptional readthrough and identify recurrent DoG signatures as candidate prognostic biomarkers.
• Transcriptional response of primary human pancreatic cancer-associated fibroblasts to IFN-γ and lipopolysaccharide stimulation
  GSE348821Homo sapiens9 个样本2026-10-29

  Single-cell analysis of a pan-cancer tumor microenvironment atlas identified transcriptionally distinct inflammatory cancer-associated fibroblast (iCAF) subpopulations, including an ISG15+ iCAF population predicted to arise downstream of interferon-γ signaling from CD8+/GZMB+ T cells, and a CXCL8+ iCAF population. To test these predictions experimentally, primary cancer-associated fibroblasts (CAFs) were isolated from a fresh human pancreatic ductal adenocarcinoma (PDAC) surgical specimen, expanded in culture, and treated for 24 hours with control media, recombinant human interferon-γ, or lipopolysaccharide (LPS). Bulk RNA-sequencing of the resulting nine libraries was used to compare the induced transcriptional programs against gene signatures derived from the ISG15+ iCAF and CXCL8+ iCAF subpopulations of the atlas. Results are reported in the associated publication.

  单细胞细胞图谱
• Mitochondrial Complex III Drives Skeletal Muscle Metabolic Reprogramming and Alters Glucose Utilization
  GSE347652Mus musculus12 个样本2026-10-29

  Mitochondrial dysfunction is closely associated with metabolic disease, yet how mitochondrial respiratory capacity influences skeletal muscle glucose handling remains poorly understood. Here, we investigate the role of mitochondrial Complex III in skeletal muscle using a muscle-specific Rieske iron-sulfur protein (RISP) knockout model. Loss of RISP did not impair basal Complex III respiratory capacity, but reduced skeletal muscle endurance while preserving muscle contractility and overall muscle structure. Importantly, Complex III deficiency was accompanied by alterations in systemic glucose metabolism. RISP-deficient mice exhibited lower basal glucose levels in fed and fasted states and improved glucose tolerance. Together, these findings suggest that impaired Complex III function triggers metabolic adaptations that extend beyond mitochondrial respiration and influence whole-body glucose handling. These findings identify mitochondrial Complex III as a potential metabolic checkpoint linking skeletal muscle oxidative capacity with glucose utilization and systemic glucose homeostasis. This work raises the possibility that enhancing skeletal muscle glucose utilization could represent a strategy to reduce glucose stress in metabolic disease, including diabetes.
• Lamin B1 physically regulates neuronal migration by modulating nuclear deformability in the developing cortex
  GSE347519Mus musculus18 个样本2026-10-29

  Neuronal migration positions billions of neurons to form a functional brain. Effective navigation through the cortex requires precise regulation of nuclear mechanics in migrating neurons. We demonstrate that Lamin B1 (LB1) regulates neuronal migration by modulating nuclear deformability. Elevated LB1 in neurons halted migration in vivo, without affecting laminar identity or pre-migratory gene expression. Mispositioned neurons subsequently caused electrophysiological defects in the brain. In vitro, increased LB1 raised nuclear stiffness, as measured by atomic force microscopy, and reduced neuronal motility in confined environments reconstituted with microchambers. Computational modeling predicted a temporal link between nuclear deformation and increased migration velocity, which was validated experimentally through live imaging. Notably, cerebral organoid assays using induced pluripotent stem cells established from patients with LMNB1 duplication exhibited impaired neuronal migration in a human model. Collectively, these findings establish LB1 as a critical regulator of nuclear mechanics, ensuring accurate spatiotemporal positioning of neurons.

  计算与 AI
• Acquired resistance to anti-PD-1 therapy is associated with tumor intrinsic macrophage reprogramming.
  GSE344292Mus musculus19 个样本2026-10-29

  Immune checkpoint inhibitors targeting the PD-1/PD-L1 axis can produce durable tumor responses, but acquired resistance remains a major clinical problem. To define tumor-intrinsic transcriptional changes associated with acquired resistance, we generated independently derived anti-PD-1-resistant MC-38 colon adenocarcinoma cell lines (MC38-PR) by serial in vivo selection in immunocompetent C57BL/6 mice. Isotype-control-passaged MC38-ISO lines and the parental MC-38 line served as controls. Bulk RNA sequencing was performed to compare parental, isotype-control-passaged, and acquired anti-PD-1-resistant cell lines. These data support a multi-omic investigation of resistance in which independently derived resistant tumors converged on an immunosuppressive, macrophage-skewing tumor program despite retaining antigen-presentation machinery, interferon-gamma responsiveness, and most predicted neoantigens.

  多组学
• Multi-omics analysis reveals an EXOSC10-lncRNA-dependent checkpoint in nucleolar proteostasis recovery
  GSE329077Homo sapiens12 个样本2026-10-29

  Proteotoxic stress induced by heat shock drives the formation of nucleolar aggresomes. However, the mechanisms governing their resolution during recovery remain poorly understood. Here, we combine temporal quantitative proteomics, transcriptomics and live imaging to define the dynamics of the detergent-insoluble fraction during heat shock and recovery. We find that nucleolar aggresome recovery follows a multiphasic lag–burst–resolution kinetic program that tightly couples the recruitment of protein quality-control factors and remobilization of ribosomal proteins. We identify stress-induced long non-coding RNA IGS16 as a critical regulator of this process. IGS16 accumulates in the nucleolus upon heat shock where it restrains chaperone engagement. Clearance of IGS16 by the nucleolar exonuclease EXOSC10 is required to initiate nucleolar remodeling and enable HSP70-dependent restoration of ribosomal protein mobility. Notably, IGS16 degradation occurs independently of HSP70 ATPase activity, indicating that RNA turnover precedes and licenses chaperone-mediated aggregate resolution. Together, our findings uncover an RNA-dependent regulatory checkpoint that coordinates RNA metabolism and protein quality control to regulate nucleolar proteostasis recovery. This work also reveals a previously unknown function for EXOSC10 in stress-induced condensate dynamics control potentially through long non-coding RNA degradation.

  多组学
• Prenatal maternal cold stress exposure drives sex-specific neurodevelopmental disruptions in the fetal hypothalamus
  GSE328919Mus musculus3 个样本2026-10-29

  The prevalence of neurodevelopmental disorders (NDDs) is increasing, with growing evidence implicating the intrauterine environment as a critical regulator of fetal brain development. Gestational perturbations such as maternal stress can increase NDD risk; however, the mechanism(s) by which prenatal maternal stress reshape fetal neurodevelopment remain unclear. Accordingly, the objective of my project was to characterize how maternal cold stress exposure during pregnancy disrupts neural stem and progenitor cell (NSPC) developmental programs in the fetus and the impact this has on neurodevelopment in the hypothalamus. Pregnant mice were exposed to 4°C for 30 minutes daily from embryonic day 11.5 (E11.5) to E15.5—a critical period of neurodevelopment in the hypothalamus. To assess how maternal cold stress impacts neural stem cell (NSC) behaviours, we employed the neurosphere assay, quantifying the number and size of primary and secondary neurospheres as a measure of NSC proliferation and self-renewal, respectively. Our findings revealed no change in NSC proliferation or self-renewal when comparing control and maternal cold stress male and female neurospheres. However, differentiation of dissociated NSCs revealed that neurons from both sexes had longer axons following maternal cold stress exposure. Interestingly, only male-derived cultures exhibited a significant increase in the number TUJ1+ neurons in response to maternal cold stress exposure, whereas only female-derived maternal cold stress cultures showed enhanced dendritic arborization. To explore the molecular basis of these changes, we performed single-cell RNA sequencing on E15.5 fetal hypothalamic NSPCs. Analysis of differentially expressed genes uncovered basal sex differences between the transcriptional signatures of control male and female Cycling NSPCs and suggested that maternal cold stress shifts female Cycling NSPCs toward a more male-like transcriptional profile. Gene ontology analysis revealed that maternal cold stress upregulates pathways linked to neuronal growth, development, and GABAergic neuron differentiation, but only in females. Importantly, ligand-receptor analysis suggested that maternal cold stress exposure disrupts neurodevelopmental programs through altered cell-cell signalling within Cycling NSPCs predominantly in females. These findings demonstrate that prenatal maternal cold stress exposure drives sex-specific effects on fetal neurodevelopment and uncover distinct cellular pathways that may contribute to sex differences seen in the presentation and risk of many NDDs.

  单细胞扰动筛选
• AP-1 Family Member Transcription Factors Play a Critical Role in Human Beta Cell Replication and Differentiation
  GSE327169Homo sapiens21 个样本2026-10-29

  This SuperSeries is composed of the SubSeries listed below.

  SuperSeries
• AP-1 Family Member Transcription Factors Play a Critical Role in Human Beta Cell Replication and Differentiation [scATAC-seq]
  GSE326466Homo sapiens3 个样本2026-10-29

  Insulinomas are a rare and benign type of pancreatic neuroendocrine tumor. They consist of pancreatic beta cells that are able to replicate as opposed to their human islet counterparts. They are also able to secrete insulin. Although we know epigenetics is a critical factor, it is unclear which exact pathways play a role in the control of replication and differentiation. Here we performed snATAC-seq to gain further insight into the open accessible chromatin regions in various insulinoma cell types.

  单细胞
• AP-1 Family Member Transcription Factors Play a Critical Role in Human Beta Cell Replication and Differentiation [Multiome]
  GSE326458Homo sapiens2 个样本2026-10-29

  Insulinomas are a rare and benign type of pancreatic neuroendocrine tumor. They consist of pancreatic beta cells that are able to replicate as opposed to their human islet counterparts. They are also able to secrete insulin. Although we know epigenetics is a critical factor, it is unclear which exact pathways play a role in the control of replication and differentiation. Here we performed multiome assay to delineate open accessible chromatin regions and single cell transcriptomic profiles in various insulinoma cell types.

  单细胞多组学
• AP-1 Family Member Transcription Factors Play a Critical Role in Human Beta Cell Replication and Differentiation [snRNA-seq]
  GSE326455Homo sapiens2 个样本2026-10-29

  Insulinomas are a rare and benign type of pancreatic neuroendocrine tumor. They consist of pancreatic beta cells that are able to replicate as opposed to their human islet counterparts. They are also able to secrete insulin. Although we know epigenetics is a critical factor, it is unclear which exact pathways play a role in the control of replication and differentiation in insulinomas. Here we performed snRNAseq to gain further insight into the transcriptomic profiles of various insulinoma cell types.

  单细胞
• AP-1 Family Member Transcription Factors Play a Critical Role in Human Beta Cell Replication and Differentiation [ChIP-seq]
  GSE326450Homo sapiens7 个样本2026-10-29

  Insulinomas are a rare and benign type of pancreatic neuroendocrine tumor. They consist of pancreatic beta cells that are able to replicate as opposed to their human islet counterparts. They are also able to secrete insulin. Although we know epigenetics is a critical factor, it is unclear which exact pathways play a role in the control of replication and differentiation in insulinomas. Here we performed bulk RNA-seq to gain further insight into the transriptomic profiles of insulinomas and FACS-sorted beta cells.
• AP-1 Family Member Transcription Factors Play a Critical Role in Human Beta Cell Replication and Differentiation [ATAC-seq]
  GSE326447Homo sapiens7 个样本2026-10-29

  Insulinomas are a rare and benign type of pancreatic neuroendocrine tumor. They consist of pancreatic beta cells that are able to replicate as opposed to their human islet counterparts. They are also able to secrete insulin. Although we know epigenetics is a critical factor, it is unclear which exact pathways play a role in the control of replication and differentiation in insulinomas. Here we performed bulk ATAC-seq to gain further insight into the open accessible chromatin regions in insulinomas and FACS-sorted beta cells.