title: Transposable Element-Driven Expansion of Enhancer RNA Repertoires Underlies Regulatory Innovation and Polyploid Adaptation in Cereal Crops

city: shanghai

first: yijing

last: zhang

address: 2005 Songhu Road

department: Biochemistry

institute: Fudan University

sample_organism:
Hordeum vulgare
Oryza sativa
Secale cereale
Triticum aestivum
Triticum urartu
Zea mays
Aegilops tauschii


title: Elucidating the impact of chemotherapy on skeletal progenitors

status: Public on Jun 15 2026

city: Toronto

first: Soheil

last: Jahangiri

state: Ontario

address: 610 University Ave

department: Princess Margaret Cancer Centre

country: Canada

institute: University Health Network

type: Expression profiling by high throughput sequencing

type: Genome binding/occupancy profiling by high throughput sequencing

summary: This SuperSeries is composed of the SubSeries listed below.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Refer to individual Series


title: Elucidating the impact of chemotherapy on skeletal progenitors [bulk ATAC-seq]

summary: Mice receiving cyclic doxorubicin (DOX) treatment exhibited long-term skeletal defects. Lineage tracing experiments revealed loss of osteogenesis from bone marrow mesenchymal stem and progenitor cells. We performed molecular characterization on MSPCs to understand the mechanisms underying MSPC dysfunction folloiwng DOX treatment.

overall_design: MSPC specific reporter mice were treated with cyclic DOX treatment. MSPCs were collected 8w post treatment for ATAC-seq analysis.

first: Ximing

last: Li


title: Elucidating the impact of chemotherapy on skeletal progenitors [RNA-seq MSPC]

overall_design: MSPC specific reporter mice were treated with cyclic DOX treatment. MSPCs were collected 8w post treatment for RNA-seq analysis.


title: Elucidating the impact of chemotherapy on skeletal progenitors [RNA-seq Osteoblast]

overall_design: Osteoblast reporter mice were treated with cyclic DOX treatment. Osteoblasts were collected 8w post treatment for RNA-seq.


title: Elucidating the impact of chemotherapy on skeletal progenitors [scRNA-seq]

overall_design: MSPC specific reporter mice were treated with cyclic DOX treatment. Bone marrow non-hematopoietic cells were collected 8w post treatment for scRNA-seq.


title: PRMT1 recruitment and H4R3Me2a modification in control and PRMT1-depleted trophoblast progenitor

city: Kansas City

first: Soumen

last: Paul

state: KS

address: Hemenway Building 3901 Rainbow Boulevard

department: Department of Pathology & Laboratory Medicine

country: USA

institute: University of Kansas Medical Center

summary: To understand PRMT1 recruitment and associated changes in histone H4 arginine3 di-methylation at the chromatin region in trophoblast progenitors, we performed CUT&RUN experiments in CT27 human trophoblast stem cells (CT27 hTSCs) and in primary trophoblast stem and progenitor cells (TSPCs) in mouse embryonic day (E) 7.5 ectoplacental cone region (EPC). For CT27 hTSCs, experiments were done in both control and PRMT1-knockdown CT27 hTSC. We also tested RNA polymerase II recruitment in these cells.

overall_design: For experiments in human TSCs, control and PRMT1KD CT27 hTSCs were used for CUT&RUN experiments. Cells were cultured in human TSC stem state culture condition. CUT&RUN was performed using anti-PRMT1, anti-H4R3Me2a and anti-RNA Pol-II antibodies. IgG was used as control. For experiments with mouse EPC region, pregnant CD1 female mouse was used. EPC were isolated at E7.5 and pulled together. Single cell suspension was prepared using cell strainer and then CUT&RUN analyses were performed. For CUT&RUN experiments, CUT & RUN Assay kit from Cell Signaling technology (#86652) was used. Isolated DNA then used for library preparation and sequencing using Novoseq 6000 platform.

first: Purbasa

last: Dasgupta

first: Rajnish

last: Kumar


title: Discovery and therapeutic exploitation of Master Regulatory miRNAs in Glioblastoma

city: Charlottesville

first: Roger

last: Abounader

state: Virginia

address: 21 Hospital Dr, Room No:4813, PO Box  800733

department: Microbiology, Immunology, Cancer Biology

institute: University of Virginia

summary: Glioblastoma is a fatal primary malignant brain tumor. Despite therapies involving surgical resection, chemotherapy, and radiation therapy, the average survival for glioblastoma patients remains at approximately 15 months. MicroRNAs (miRNAs) are short noncoding RNA molecules that regulate the expression of the majority of human genes. Numerous genes are concurrently deregulated in glioblastoma. Consequently, molecular monotherapies have failed to achieve improvements in clinical outcomes. Several lines of evidence suggest that simultaneous targeting of several deregulated molecules is required to achieve better therapies. However, the simultaneous targeting of several deregulated oncogenic drivers is severely limited by the fact that the drugs needed to target many deregulated molecules do not currently exist, and because combining several drugs in a clinical setting leads to an exponential increase in toxicity. We hypothesized that we can develop and use miRNA to simultaneously inhibit multiple deregulated genes for more efficacious glioblastoma therapies. The goal of this study was therefore to identify master regulatory microRNAs (miRNAs) and use them to simultaneously target multiple deregulated molecules for GBM therapy. We defined master regulatory miRNAs as those that target several deregulated genes in glioblastoma. To find master regulatory miRNAs, we first used PAR-CLIP screenings to identify all targets of all miRNAs in glioblastoma cells. We then analyzed TCGA tumor data to determine which of these targets are deregulated in human tumors. We developed and used an algorithm to rank these targets for significance in glioblastoma malignancy based on their magnitude of deregulation, frequency of deregulation, and correlation with patient survival.  We then ranked the miRNAs for their capacity of targeting multiple glioblastoma-deregulated genes and therefore the potential to exhibit strong anti-tumor effects when delivered as therapy. Using this strategy, we selected two tumor suppressor master regulatory miRNAs, miR-340, miR-382 and an oncogenic master regulatory miRNA, miR-17. We validated the target genes of the miRNAs and showed that they form part of important glioblastoma regulatory pathways. We then showed that the miRNAs (miR-340 and miR-582) or the miR-17 inhibitor have strong inhibitory effects on glioblastoma cell growth, survival, invasion, stemness and in vivo tumor growth. Ultimately, we developed and successfully tested a new therapeutic approach to delivery miR-340 using MRI guided focused ultrasound and microbubbles (FUS-MB) and special brain penetrating nanoparticles (BPN). This approach resulted in a substantial reduction in tumor volume and prolongation of the survival of glioblastoma-bearing mice and can be translated into clinical trials. We therefore developed and successfully tested a novel strategy to discover and deliver miRNAs for glioblastoma and cancer therapy.

overall_design: PAR-CLIP assay with AGO1, AGO2 and AGO3 in U87 glioma cell line


title: SenCat: Redefining human cell senescence through multiomic profiling of multiple senescent cell types [scRNA-seq]

city: Baltimore

first: Supriyo

last: De

state: Maryland

address: 251 Bayview Blvd

department: Laboratory of Genetics and Genomics

institute: NIA-IRP, NIH

summary: There is an urgent need to comprehensively catalog senescence markers across a wide range of cell types in an organism. Here, we profiled the transcriptomes and proteomes in over 30 senescence paradigms employing 14 different primary human cell types. Our results indicate that senescent cells from all tissue types do not share a unique marker, but they do share in the activation of specific metabolic pathways and damage response pathways to elicit tissue repair. Importantly, considering combinations of some of the most widely shared senescence markers validated the presence of senescent-like cells in mice through single-cell RNA-sequencing and immunostaining approaches. The enclosed catalog represents a much-needed resource to identify senescent cells across tissues in the body.

overall_design: Doxorubicin-induced senescence was triggered by a single dose of doxorubicin (10 mg/kg, Selleckchem) in 3 months old mice and studied 8 days later. DMSO or ABT-737 (25 mg/kg, MedChemExpress) were administered to mice treated with doxorubicin for three times from day 5 onwards.

first: Carlos

last: Anerillas

first: Dimitrios

last: Tsitsipatis

first: Krystyna

last: Mazan-Mamczarz

first: Reema

last: Banarjee

first: Ana

middle: S

last: Cunningham

first: Gisela

last: Altés

first: Martin

last: Salamini-Montemurri

first: Jen-Hao

last: Yang

first: Rachel

last: Munk

first: Martina

last: Rossi

first: Yulan

last: Piao

first: Bradley

last: Olinger

first: Quinn

last: Strassheim

first: Jennifer

middle: L

last: Martindale

first: Jinshui

last: Fan

first: Chang-Yi

last: Cui

first: Delaney

middle: V

last: Rutherford

first: Ying

last: Hao

first: Ziyi

first: Jessica

last: Roberts

first: Andy

last: Qi

first: Kotb

last: Abdelmohsen

first: Allison

middle: B

last: Herman

first: Nathan

last: Basisty

first: Myriam

last: Gorospe


title: SenCat: Redefining human cell senescence through multiomic profiling of multiple senescent cell types

first: Supriyo

last: De

overall_design: Transcriptome and proteome analysis of different senescence paradigms in multiple primary human cell types

first: Carlos

last: Anerillas

first: Dimitrios

last: Tsitsipatis

first: Krystyna

last: Mazan-Mamczarz

first: Reema

last: Banarjee

first: Ana

last: Cunningham

first: Gisela

last: Altés

first: Martin

last: Salamini-Montemurri

first: Jen-Hao

last: Yang

first: Rachel

last: Li


title: SenCat: Redefining human cell senescence


title: Global Transcriptome analyses in PRMT1-depleted CT 27 Juman trophoblast stem cells (human TSCs).

first: Soumen

last: Paul

summary: The data presented here represent global gene expression patterns in human TSCs upon knockdown of protein arginine methyla transferase 1 (PRMT1).

overall_design: CT27 human TSCs were cultured with or without PRMT1 knockdown (via shRNA) in stem state culture condition.

first: Purbasa

last: Dasgupta

first: Rajnish

last: Kumar


title: Lonidamine alleviates inflammation and tissue remodeling in a mouse model of eosinophilic chronic sinusitis: A single-cell transcriptomics study

city: Hangzhou

first: Yicheng

last: Xie

address: 3333 Binsheng Rd

country: China

institute: Children’s Hospital Zhejiang University School of Medicine

summary: We performed single-cell sequencing on the mice nasal mucosal tissues of  Control group, ECRS  model group induced by papain (ECRS) and LND treatment group (LND).

overall_design: C57BL/6 mice were obtained from Shanghai SLAC Laboratory Animal Co., Ltd (certificate: SCXK 2022-0004) and housed in individually ventilated cages. All animal experiments were approved by the institutional animal care and use committee at the Zhejiang University Laboratory Animal Center (ethics number: ZJU20220294).Mice were divided into three groups at half male and half female in each group: Control group, intranasal administration of PBS; ECRS group, intranasal administration of 20 μg papain with intragastric administration of PBS; ECRS+LND group, ECRS with intragastric administration of LND 10 mg/kg).The nasal mucosal from a consistent area of the mice was rapidly removed. All mice from each group were sampled and mixed for detection.


title: Single cell RNA sequencing analysis using embryonic day 7.5, 8.5, 10.5, 11.5 and 12.5 placenta from  mice

summary: The placenta establishes a maternal–fetal exchange interface which ensures transportation of nutrients and gases between the mother and the fetus. However, the intricate molecular processes and gene expression dynamics in trophoblast progenitors and in matured trophoblast cells are incopletely understood. Therefor, in this study we performed gene expression analyses during the course of mouse placenta development. We performed single cell RNA-sequencing  analyses with mouse placenta primordium at  embryonic day 7.0 and subsequently at embryonic days 8.5-embryonic day 12.5 to capture gene expression dynamics in trophoblast stem/progenitor compartment as well as in matutered trophoblast cells and other cell types in the placenta.

overall_design: Single cell RNA sequencing of mouse placenta were generated by deep sequencing using the 10x Genomics Chromium Single Cell Gene Expression Solution (10xgenomics.com).

first: Ananya

last: Ghosh


title: Perturb-seq analysis using genes associated with alcohol consumption and alcohol use disorder

city: Indianapolis

first: Yunlong

last: Liu

state: IN

address: 410 W 10th Street, HS5000

department: Center for Computational Biology and Bioinformatics

institute: Indiana School of Medicine

summary: Although genome-wide association studies (GWAS) have identified loci associated with alcohol consumption and alcohol use disorder (AUD), they do not identify which variants are functional. To approach this, we evaluated the impact of variants in 3’ untranslated regions (3’-UTRs) of genes in loci associated with substance use and neurological disorders using a massively parallel reporter assay (MPRA) in neuroblastoma and microglia cells. We identified genes whose 3’-UTR activities are associated with AUD and alcohol consumption by combining variant effects from MPRA with GWAS results. We examined their effects by evaluating gene expression after CRISPR inhibition of neuronal cells.

overall_design: The Perturb-seq experiment was performed on a modified SH-SY5Y cell line that stably expressed KRAB-dCas9 in one biological replicate and single-cell sequenced across two wells

first: Xuhong

last: Yu

first: Andy

last: Chen

first: Hongyu

last: Gao


title: Massively Parallel Reporter Assay for 3'-UTR Variants Associated with Neurological Disorders in brain tissue cell lines

summary: Although genome-wide association studies (GWAS) have identified loci associated with alcohol consumption and alcohol use disorder (AUD), they do not identify which variants are functional. To approach this, we evaluated the impact of variants in 3’ untranslated regions (3’-UTRs) of genes in loci associated with substance use and neurological disorders using a massively parallel reporter assay (MPRA) in neuroblastoma and microglia cells.

overall_design:
MPRA experiment was performed on two cell lines: SH-SY5Y neuroblastoma (SH) and SV40-immortalized microglia (MG)
For each cell line, six biological replicates were performed, and the DNA and RNA were extracted and sequenced

first: Kriti

last: Thapa

middle: P

last: Tsai


title: Cardiac Fibrosis in Dilated Cardiomyopathy: Transcriptomics Insights, Histological Correlations, and Organoid Model Verifications [RNA-seq I]

city: Kyoto

first: Yoshinori

last: Yoshida

address: 53, Kawahara-cho, Shogoin, Sakyo-ku

country: Japan

institute: Kyoto University

summary: Dilated cardiomyopathy (DCM) represents a leading cause of heart failure among younger adults. Despite endomyocardial biopsy (EMB) transcriptome enriching our understanding of DCM, the link between its gene expression and phenotype remains unclear. RNA-seq analysis of 58 DCM samples and 12 publicly available control samples unveiled about 25,000 transcripts. A principal component analysis highlighted a distinct DCM-control separation. WGCNA revealed four transcriptome modules strongly associated with DCM. The purple module, which is the DCM-related module, was enriched with fibrosis-related genes and showed FSTL3 as a pivotal DCM-associated gene.

overall_design:
Right ventricular septal biopsies were obtained. DCM biopsies transcriptome data were compared with non-failing left ventricular samples (n=12) previously published datasets that are publicly available in the NCBI Gene Expression Omnibus (GEO) database from GSE11625.
Re-analysed Samples PRJNA477855:
Ctrl_1 GSM3219559 SAMN09484150 SRX4297607
Ctrl_2 GSM3219560 SAMN09484149 SRX4297608
Ctrl_3 GSM3219561 SAMN09484148 SRX4297609
Ctrl_4 GSM3219562 SAMN09484147 SRX4297610
Ctrl_5 GSM3219563 SAMN09484145 SRX4297611
Ctrl_6 GSM3219564 SAMN09484144 SRX4297612
Ctrl_7 GSM3219565 SAMN09484143 SRX4297613
Ctrl_8 GSM3219566 SAMN09484142 SRX4297614
Ctrl_9 GSM3219567 SAMN09484141 SRX4297615
Ctrl_10 GSM3219568 SAMN09484139 SRX4297616
Ctrl_11 GSM3219569 SAMN09484138 SRX4297617
Ctrl_12 GSM3219570 SAMN09484137 SRX4297618

first: Reo

last: Hata


title: Basement membrane proteins in extracellular matrix characterize NF1 tumor development and response to MEK inhibitor

city: DALLAS

first: CHUNHUI

last: JIANG

state: TX

address: 6000 HARRY HINES BLVD

department: DERMATOLOGY

institute: UT SOUTHWESTERN

summary: Neurofibromatosis Type 1 (NF1) is one of the most common tumor-predisposing genetic disorders. Neurofibromas are NF1-associated benign tumors. A hallmark feature of neurofibromas is an abundant collagen-rich extracellular matrix (ECM) that constitutes >50% of the tumor dry weight. However, little is known about the mechanism underlying ECM deposition during neurofibroma development and treatment response. We performed a systematic investigation of ECM enrichment during plexiform neurofibroma (pNF) development, and identified basement membrane (BM) proteins, rather than major collagen isoforms, as the most upregulated ECM component. Following MEK inhibitor treatment, the ECM profile displayed an overall down-regulation signature, suggesting ECM reduction as a therapeutic benefit of MEK inhibition. Through these proteomic studies, TGF-β1 signaling was identified as playing a role in ECM dynamics. Indeed, TGF-β1 overexpression promoted pNF progression in vivo. Furthermore, by integrating single-cell RNA-sequencing, we found that immune cells including macrophages and T cells produce TGF-β1 to induce Schwann cells to produce and deposit BM proteins for ECM remodeling. Following Nf1 loss, neoplastic Schwann cells further increased BM protein deposition in response to TGF-β1. Our data delineate the regulation governing ECM dynamics in pNF and suggest that BM proteins could serve as markers for disease diagnosis and treatment response.

overall_design: Cells were isolated from plexiform neurofibroma mouse model Hoxb7cre+Nf1 fl/fl analyzed using scRNAseq.

first: Chunhui

last: Jiang

first: Ashwani

first: Ze

first: Chao

last: Xing

first: Lu

last: Le


title: Profile of micro-RNA in Turmeric-derived nanoparticles

city: Louisville

first: Huang-Ge

last: Zhang

state: KY

address: 505 S Hancock Street

department: James Graham Brown Cancer Center

institute: University of Louisville

type: Non-coding RNA profiling by high throughput sequencing

summary: Analysis of micro-RNA (miRNA) in Turmeric-derived nanoparticles using next-generation sequencing (NGS). The Turmeric-derived nanoparticles were prepared by differential ultracentrifuges. We mapped about 30 to 50 million sequence reads to the plant miRNA database and identified total of 248 miRNAs.

overall_design: High-throughput profiling of miRNA in Turmeric-derived nanoparticles.

first: Yun

last: Teng


title: Differential gene expression in inflamed mucosa of progressed UC patients compared to inflamed mucosa of non-progressed UC patients

city: Lørenskog

first: Hilde

middle: Loge

last: Nilsen

address: Sykehusveien 25

country: Norway

institute: Akershus University Hospital

summary: A small percentage of ulcerative colitis patients may experience disease progression into colitis-associated colorectal cancer (CA-CRC). In the clinic, it is challenging to identify these patients. Consequently, all UC patients are followed closely by e.g. annual colonoscopy from eight years of the UC diagnosis. Although, the progression may still be difficult to discover as the neoplastic mucosa may appear with a flat structure. The need for biomarkers that early in the UC disease course can predict the predisposition to progress into CA-CRC is therefore highly wanted in the clinic. The objective of this gene expression analysis was to identify a set of genes with differential expression in inflamed mucosa of progressed UC patients compared to inflamed mucosa of non-progressed UC patients. The gene expression was examined using Agilent SurePrint G3 human gene expression 60K microarray.

overall_design: Seven UC patients with progressed disease (either having colon lesions of dysplasia or CA-CRC) and 30 UC patients with non-progressed disease were included in the analysis. All patients had had a duration of UC disease of at least eight years at the time of sample collection. In general, three biopsies from each non-progressed patient were included covering histological normal and inflamed tissue and localised to ascending, descending and rectum. In case, a patient had inflamed mucosa at other locations than these, an extra biopsy was included from the inflamed location. In addition to the samples covering the three locations (ascending, descending and rectum), samples from either inflamed, dysplastic or cancerous tissue were included from the progressed UC patients. In total 130 colon biopsies (94 non-progressor samples and 36 progressor samples) were analysed covering histological normal, inflamed, dysplastic and cancerous tissue.

first: Lene

last: Alsoe

first: Anna

last: Wennerstrom

first: Jonas

middle: C

last: Lindstrom

first: Yan

first: Stephan

middle: A

last: Brackmann


title: RNA sequencing of colonic tissues from ulcerative colitis patients and healthy controls

status: Public on Jun 14 2026

city: Jinan

first: Jing

last: Shen

address: Wenhua West Road 44

institute: Shandong University

summary: RNA sequencing was conducted on colonic biopsy tissues obtained from patients with ulcerative colitis and human healthy controls (n = 6 per group).

overall_design: Colonic biopsy tissues were collected from patients with ulcerative colitis and healthy controls, after which the samples were lysed for RNA extraction.

first: Mengqi

last: Zheng

first: Shiyang

last: Li


title: 3' end sequencing of HeLa-NXF1-dTAG cells upon NXF1 degradation to characterize alternative polyadenylation dynamics

city: Beijing

first: Cheng

last: Peng

address: 1 Beichen West Road, Chaoyang District, Beijing, China

institute: China National Center for Bioinformation, Chinese Academy of Sciences

summary: Nuclear export factor 1 (NXF1) is the principal mRNA export receptor in eukaryotes. To characterize the role of NXF1 in regulating alternative polyadenylation (APA) dynamics, we employed the dTAG degradation system in a HeLa-NXF1-dTAG stable cell line. Cells were treated with 500 nM dTAG-13 or DMSO (vehicle control) for 6 hours to induce acute NXF1 depletion. Total RNA was subjected to 3' end sequencing (QuantSeq 3' mRNA-Seq Library Prep Kit V2, Lexogen) for APA analysis. Each condition was performed in biological duplicate.

overall_design: HeLa-NXF1-dTAG cells were treated with 500 nM dTAG-13 (NXF1 degradation) or DMSO (vehicle control) for 6 hours (n=2 biological replicates per condition). Total RNA was subjected to 3' end sequencing (QuantSeq) on the DNBSEQ-T7 platform (150 bp paired-end).


title: Fibroblast-ILC3 crosstalk restrains inflammation in the gut

city: Shanghai

first: Qiang

last: Wang

state: Shanghai

address: 533 Puchi Road

department: Shanghai Immune Therapy Institute

institute: Renji Hospital, Shanghai Jiao Tong University School of Medicine

summary: Fibroblasts exhibit remarkable phenotypic and functional heterogeneity in chronic inflammatory diseases, but how these changes impact immune outcomes remain at early stages of investigation. Here we identify a unique fibroblast population that robustly expresses insulin-like growth factor 1 (IGF1) in the healthy intestine that are reduced in inflammatory bowel disease (IBD) patients and necessary to protect from experimental models of gut inflammation. In silico analyses reveal unexpected cross-talk between IGF1+ fibroblasts and group 3 innate lymphoid cells (ILC3s), which dominantly express the IGF-1 receptor (IGF1R) in the gut to protect from inflammation. Mechanistically, IGF1 limits ILC3 production of CXCL10 in inflammatory contexts to prevent recruitment of plasmacytoid dendritic cells (pDC) and restrain gut inflammation. Finally, IGF1 signaling reduces CXCL10 production in human ILC3s, but this pathway is altered in the inflamed intestine of IBD patients and inversely correlates with a higher frequency of pDC. Our results define an unexpected mechanism by which anti-inflammatory fibroblasts safeguard the gut by IGF1-dependent crosstalk with an innate lymphocyte-pDC axis.

overall_design: ILC3s (CD45+Lineage-CD90.2+ CD127+KLRG1-CD45dim-CD90.2hi) were sort-purified from the small intestine of wild-type mice and cultured in complete RPMI medium. Cells were stimulated with recombinant mouse IFN-γ (20 ng/mL; BioLegend) in the presence or absence of IGF-1 (200 ng/mL; R&D Systems) for 4 h at 37 °C.

first: Qingxia

last: Lin

first: Ruichao

middle: E

last: Liu

first: Lan

last: Kang

first: Gregory

middle: F

last: Sonnenberg

first: Coco

last: Chu

first: Lei

last: Zhou


title: Single cell RNAseq analysis in CT27 human TSC with and without PRMT1 Knockdown

first: Soumen

last: Paul

summary: The study reports single cell RNA seq analyses of gene expression dynamics in human TSCs. Protein Arginine Methyl Transferase 1 (PRMT1) regulates cellular function via methylation of arginine residues on its target proteins. In this study we depleted PRMT1 in CT27 human TSCs via RNAi. Loss of PRMT1 affects human TSC self-renewal process. We performed single cell RNA-seq with control and PRMT1-knocked down CT27 human TSCs to capture gene expression dynamics at a single cell resolution.

overall_design: Control CT27 and PRMT1 knockdown human TSCs were cultured in stem state culture condition followed by single cell RNA preparation using the 10x Genomics Chromium Single Cell Gene Expression Solution (10xgenomics.com).

first: Purbasa

last: Dasgupta

first: Rajnish

last: Kumar


title: Root meristem growth factor (RGF) peptide signaling as a molecular bridge between root development and non-lethal thermal stress adaptation

city: Tainan

first: Joon-Keat

last: Lai

address: No. 100, Sec. 1, Guiren 13th Rd., Guiren Dist.

department: Agricultural Biotechnology Research Center

country: Taiwan

institute: Academia Sinica

summary: Roots adapt to temperature ranges that restrict growth without causing lethality, a largely unexplored physiological state. Although lethal heat shock and moderately high temperatures have been studied in detail, the effects of non-lethal high temperatures on root development remain largely unknown. We defined 31°C as a non-lethal thermal stress in Arabidopsis thaliana and examined its impact on root growth using phenotypic analyses and developmental-zone-specific transcriptomics. Under the non-lethal thermal stress (31°C), primary root growth, meristem size, and superoxide (O₂-) accumulation were all reduced, and the distribution of the meristem master regulator PLETHORA2 (PLT2) became restricted. Transcriptome analysis revealed a strong downregulation of RGFs, RGFRs, and PLT2. Mutants of these genes were more sensitive to the stress, whereas RGF1 treatment restored meristem size, increased O₂- levels, and expanded the distribution of PLT2 protein. RGF peptide also promoted lateral root development, resulting in a more complex root system under the thermal stress. These results indicate that the RGF-RGF receptor-PLT2 pathway plays a central role in root adaptation to the non-lethal heat stress and suggest that manipulating RGF signaling could enhance root thermotolerance and crop resilience under elevated temperatures.

overall_design: RNA-seq profiling of high temperature (31 vs 22 degree celcius) treated wildtype Arabidopsis thaliana root at Day1 and Day2.

first: Yu-Chun

last: Hsiao

first: Shiau-Yu

last: Shiue

first: Masashi

last: Yamada


title: Identification of a set of transcriptional regulators involved in the temporal regulation of neuron subtype differentiation [RNA-Seq 2]

city: Shinjuku-ku

first: Takuya

last: Shimazaki

state: Tokyo

address: 35 Shinanomachi

department: Physiology

institute: Keio University School of Medicine

summary: The sequential generation of various types of neurons and glia from neural stem /progenitor cells (NSPCs) during development is a major part to build complex central nervous system. Here, we identify PHF21b, ZFP7 and ZFP57 as crucial factors that regulate the transition from early-born neuron to late-born neuron generation by NSPCs in the developing mouse cortex. Simultaneous knockdown of these genes suppressed generation of early-born neurons.

overall_design: RNAseq profiling of wildtype mouse NSPCs grown as neurospheres derived from E11.5 cerebral cortex  and their simultaneous knockdown derivatives (shPhf21b, shZfp7, and Zfp57) at Day5 after seeding.

first: Hideyuki

last: Okano


title: XPO1inhibition induces NCOR1-Dependent  oxidative stress to suppress hepatocellular  carcinoma

first: Wei

address: No. 25, Lane 2200, Xietu Road, Xuhui District

institute: Shanghai Cancer Institute

summary: Hepatocellular carcinoma (HCC) remains a therapeutic challenge due to the limited efficacy of current systemic therapies. To identify potential novel therapeutic approaches, computational analysis of HCC datasets and drug screening were integrated, leading to the repurposing of hematological cancer drug selinexor (an XPO1 inhibitor)  for HCC treatment. Functional studies revealed that XPO1 inhibition triggers oxidative stress and cell cycle arrest in HCC cells through nuclear sequestration of NCOR1, disrupting redox homeostasis through FOXK1-dependent transcriptional activation of genes associated with Reactive Oxygen Species (ROS). A genome-wide CRISPR-Cas9 screen further identified the KEAP1-NRF2 axis as a key determinant of sensitivity to XPO1 inhibition. Furthermore, high-throughput compound screening demonstrated that disulfiram, a clinically-used aldehyde dehydrogenase inhibitor, synergizes with XPO1 inhibitor through exacerbation of ROS accumulation. Collectively, these findings demonstrate the therapeutic repurposing of selinexor for HCC while uncovering its novel mechanism of action, establishing a predictive biomarker, and proposing an immediately translatable combination therapy.

overall_design: Examination of the transcriptome changes of liver cancer cells treated with KPT-330 or siNCOR1

first: Linmeng


title: P2X7 receptor promotes non-small cell lung cancer progression through CCL8/CCR5-mediated activation of mTOR and ERK signaling

city: Weifang

first: ronglan

last: zhao

address: No.7166 Bao Tong West Street

institute: Shandong Second Medical University

summary: This study aims to elucidate the role and mechanisms of the P2X7 receptor (P2X7R) in non-small cell lung cancer (NSCLC). By overexpressing or knocking down P2X7R in human A549 and H1703 cells, combined with interventions using BzATP, A438079, and the CCR5 inhibitor Mvc, we systematically evaluated changes in cell proliferation, apoptosis, migration, invasion, and EMT. Results demonstrated that P2X7R activation significantly promoted tumor cell proliferation, migration, and invasion, inhibited apoptosis, and induced EMT, whereas receptor knockdown produced opposite effects. mRNA sequencing and qPCR/ELISA data indicated that P2X7R upregulates CCL8 and its receptor CCR5, further activating ERK and mTOR signaling pathways. Cytoskeletal staining confirmed that P2X7R enhances F-actin remodeling capacity via the CCL8/CCR5 pathway. In tumor-bearing mouse models, P2X7R overexpression promoted tumor growth, whereas knockdown significantly inhibited tumor formation. Collectively, P2X7R drives NSCLC progression by activating the CCL8/CCR5 pathway and its downstream ERK and mTOR signaling, positioning it as a potential therapeutic target.

overall_design: RNA-seg profiling of control A549 cells（transfected with negative control plasmid , GV102‐P2X7R‐scrambled shRNA）and their knockdown derivatives (shP2X7R) （transfected with GV102‐P2X7R‐scrambled shRNA) at 24 hours transfected

first: Ronglan

last: Zhao

first: Xiaoxiang

last: Peng

first: Yahui

last: Cao

first: Yanan

last: Du


title: NMuMG PBRM1 RNA-seq, ATAC-seq, and ChIP-seq

city: West Lafayette

first: Emily

last: Dykhuizen

address: 201 S. University

department: medicinal chemistry and molecular pharmacology

institute: Purdue University

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Analysis of chromosomal structual aberratons in U-937 cell line

city: Mitaka-shi

first: Tetsuko

last: Kobayashi

institute: Kyorin University

summary: This Hi-C experiment was a part of a research which analyzed chromosomal structural aberrations in hematological malignancies. First, the author conducted comprehensive detection of fusion transcripts in RNA-seq data of DSMZ’s 99 cell lines, and then picked up cell lines with characteristic complex karyotype. U-937 cell line is one of them, which shows several characteristic “high-intensity bands” in contact maps. This Hi-C experiment revealed ectopic gene amplifications of cancer-associated genes.

overall_design: in situ Hi-C of DSMZ’s NB-4 cell line with no treatment


title: A Two-Pronged Strategy Eliminates Dissociation Artifacts for High-Fidelity Neuroimmune Single-Cell Transcriptomics

city: Chongqing

first: Yiguo

last: Qiu

state: Chongqing

address: 13 Tianchi Road, Banan District

institute: Chongqing International Institute for Immunology

summary: Single-cell RNA sequencing (scRNA-seq) is revolutionizing neuroimmune research, yet a critical bottleneck persists: the dissociation process introduces pervasive stress-altered transcription (SAT) that obscures genuine in vivo biology. Here, we present a comprehensive two-pronged strategy to eliminate these artifacts in key neuroimmune niches. First, we established a benchmark by applying an optimized experimental protocol that minimizes dissociation stress. Comparative analysis against conventional methods allowed us to map the landscape of SAT artifacts across cell types in the brain and skull bone marrow (SBM), defining distinct, tissue-specific signatures. We then employed random forest-based approach to refine these signatures into powerful SAT gene panels, creating a computational tool for the sensitive detection and removal of artifactual signals. Our experimental approach achieves a ~95% reduction in these artifacts, while computational approach alone also has a 60-64% reduction that enables the retrospective correction of published data. This work provides a robust framework to ensure single-cell transcriptomics faithfully captures biological reality, empowering more precise discoveries in neuroimmunology.

overall_design: These cells were isolated from 3 month old and wild-type male C57 mice. The study analyzed scRNA-seq datasets from enzymatically dissociated murine brain and skull bone marrow (SBM) tissues, comparing cell populations exposed to standard dissociation protocols versus those treated with a transcriptional/translational inhibitor cocktail to suppress stress altered transcription .

first: Yuan

last: Yan

first: Bo

last: Tang

first: Pu

last: Liu

first: Dongmei

last: You

first: Yi

last: Lv

first: Jinmeng

last: Yi

first: Yuzhang

last: Wu


title: Roles of the nuclear receptor corepressor 1 (NCoR1) and the silencing mediator of retinoid and thyroid hormone receptors (SMRT) in the developing brain

city: Maebashi

first: Izuki

last: Amano

state: Gunma

address: 3-9-22 Showa-machi

department: Department of Integrative Physiology, Graduate School of Medicine

institute: Gunma University

summary: The nuclear receptor corepressor 1 (NCoR1) and the silencing mediator of retinoic acid and thyroid hormone (SMRT) are critical coregulators of nuclear receptors, including the thyroid hormone receptor and they mediate transcriptional repression via histone deacetylation. Although they are highly homologous and have similar receptor interacting domains, they have different roles in different tissues. Recently, de novo genetic variants in nuclear corepressors were found in pediatric patients with neurodevelopmental disorders. Thus, we generated novel mouse models to understand the role of NCOR1 and SMRT in the central nervous system. We used the mice with conditional NCoR1 or SMRT (NCoR1lox/lox or SMRTlox/lox) alleles in combination with the mice that express Cre recombinase in a neuronal specific fashion (Snap25-IRES2-cre). First, we performed behavioral tests to assess for any behavioral phenotypes. We found hypoactivity, social deficits, and mild anxiety in neuronal specific deletion of NCoR1 or SMRT KO mice. In addition, NCoR1 KO mice displayed higher learning abilities in a pairwise visual discrimination task. Next, we performed RNA-sequencing analysis with cells from the amygdala taken at postnatal day 21 to investigate gene expression mediated by NCoR1 and SMRT. We found that 449 genes were upregulated by SMRT deletion, whereas only 8 genes were upregulated by NCoR1 deletion. Overall, our data demonstrate that NCoR1 and SMRT have separate functions in the central nervous system.

overall_design: To determine the role of NCoR1 and/or SMRT in neurons, pan-neuronal Snap25-IRES2-cre mice (RRID: IMSR_JAX:023525) were crossed to NCoR1 floxed and/or SMRT floxed mice. Total RNA was extracted from postnatal day 21 hippocampus or amygdala.

first: Ayane

last: Ninomiya

first: Reika

last: Kawabata-Iwakawa

first: Megan

middle: J

last: Ritter

first: Anthony

middle: N

last: Hollenberg

first: Noriyuki

last: Koibuchi


title: Hyperactive BMP and Mechanosignaling Remodel Chromatin to Drive Aberrant Osteogenesis in Fibrodysplasia Ossificans Progressiva (ATAC-Seq)

status: Public on Jun 13 2026

city: Philadelphia

first: Ellen

last: Zhang

state: PA

address: 36th Street and Hamilton Walk

department: Orthopaedic Surgery

institute: University of Pennsylvania

summary: Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disorder in which a recurrent ACVR1 (R206H) mutation drives progressive heterotopic ossification (HO). We combined super-resolution stochastic optical reconstruction microscopy (STORM), transposase-accessible chromatin with sequencing (ATAC-Seq), and RNA sequencing (RNA-Seq) to investigate how Acvr1R206H remodels chromatin to promote osteogenic transcriptional programs. Mutant mouse embryonic fibroblasts (MEFs) exhibited globally decondensed chromatin and increased accessibility at developmental and osteogenic loci enriched for HOX, TEAD, and RUNX motifs. Integration of ATAC-Seq and RNA-Seq data identified transcriptional networks primed for osteochondrogenic gene expression, including ossification, extracellular matrix organization, and cell adhesion pathways, consistent with enhanced BMP-SMAD and mechanotransduction activity. Pharmacological modulation showed that chromatin alterations were dynamic and reversible: activation of Rho/ROCK in wild-type cells reproduced the mutant chromatin state, while inhibition of Rho/ROCK or BMP-SMAD signaling restored condensation to wild-type levels in mutant cells. These findings establish that Acvr1R206H enforces a pro-osteogenic chromatin landscape through convergent BMP-SMAD and Rho/ROCK signaling.

overall_design: ATAC-seq profiling of wild-type (Acvr1+/+) and FOP mutant (Acvr1R206H/+) mouse embryonic fibroblasts (MEFs) isolated from E13.5 embryos to characterize chromatin accessibility differences driven by the Acvr1R206H mutation, with 3 biological replicates per genotype.

first: Sang Hyun

last: Lee

first: Inkyung

last: Jung

first: Su Chin

last: Heo


title: Host infection selects for sRNA variants that drive bacterial social cheating

city: Jena

first: Marcel

last: Sprenger

address: Winzerlaer Straße 2

department: Institute of Microbiology

country: Germany

institute: Friedrich Schiller University

summary: Single-nucleotide mutations in regulatory small RNAs (sRNAs) represent a largely unexplored route to social cheating during bacterial infection. Here we show that arcZ, encoding a conserved Hfq-dependent sRNA in the plant pathogen Dickeya solani, undergoes recurrent single-nucleotide mutations during potato tuber infection. Five distinct arcZ alleles define a graded series of ArcZ functional impairment in which antifungal and protease activities are progressively reduced while virulence is compromised only in a subset of alleles. All five variants gain a fitness advantage exclusively during co-infection with wild-type arcZ1 cells, an advantage that is strongest when variants are rare, declines as cheater frequency increases, and correlates with declining total bacterial productivity, the canonical signature of social cheating and a tragedy of the commons.[kp1.1] No fitness benefit is detected in vitro. Transcriptomic profiling of five arcZ variants identifies a conserved core of 132 downregulated genes enriched in secreted and diffusible functions. Systematic genetic dissection, supported by quantitative proteomics, establishes BudAB-dependent acetoin production as the dominant cooperative public good exploited during co-infection. Wild-type arcZ1 cells divert pyruvate flux toward acetoin via the BudAB pathway, maintaining a less acidic tissue environment that sustains disease progression; arcZ variants, which repress this pathway, exploit the resulting pH buffering without contributing to it. These results establish pleiotropic regulatory sRNAs as a previously unrecognized class of mutational targets for the emergence of social cheaters during host infection.

overall_design: RNA profile of D. solani strains DS624 (arcZ1), DS623 (arcZ2), DS625 (arcZ3), DS931 (arcZ4), DS944 (arcZ5), and DS945 (arcZpmut) were cultivated in triplicate in LB medium at 30°C with shaking to OD 0.5. Three independent biological replicates for each are provided.

first: Quentin

last: Dubois

first: Typhaine

last: Brual

first: Kai

last: Papenfort

first: Laetitia

last: Attaiech

first: Erwan

last: Gueguen


title: Hyperactive BMP and Mechanosignaling Remodel Chromatin to Drive Aberrant Osteogenesis in Fibrodysplasia Ossificans Progressiva (RNA-Seq)

overall_design: RNA-seq profiling of wild-type (Acvr1+/+) and FOP mutant (Acvr1R206H/+) mouse embryonic fibroblasts (MEFs) isolated from E13.5 embryos to characterize transcriptional differences driven by the Acvr1R206H mutation, with 3 biological replicates per genotype.


title: NF1 loss in estrogen receptor-positive breast cancer induces osteoclast formation and immunosuppression to promote bone metastasis

city: Missouri City

first: Zifan

last: Zhao

address: 34 Chapparal Ct

department: Breast Center

institute: Baylor College of Medicine

summary: Estrogen receptor-positive (ER⁺) breast cancer exhibits a marked propensity for skeletal metastasis; however, the molecular drivers of bone colonization remain incompletely defined. We investigated the tumor suppressor neurofibromin (NF1), a dual repressor for RAS and ER signaling, whose inactivation promotes endocrine therapy (ET) resistance and is associated with inferior relapse-free survival.  NF1 copy number loss was detected in 62% of ER+ patients who subsequently developed metastases and was associated with an increased likelihood of bone metastases at initial diagnosis. In mouse xenograft models, NF1-depleted ER+ breast cancer cells demonstrated enhanced dissemination to skeletal sites following surgical resection of primary tumors. Furthermore, after intra-iliac injection, NF1-depleted cells generated significantly greater tumor burden in bone. Transcriptomic profiling revealed enrichment of bone-related gene signatures in NF1-depleted ER+ breast cancer cells, which more potently induced osteoclast differentiation and bone loss in co-culture systems. In parallel, low NF1 expression correlated with repressed T cell functional states in primary breast tumors and bone metastases.  Consistent with these clinical observations, NF1-depleted ER+ breast cancer cells more effectively inhibited proliferation, interferon-γ secretion, and cytotoxicity of human primary CD8+ T cells. Collectively, these findings identify NF1 inactivation as a key driver of bone metastasis in a substantial subset of ER+ breast cancers.  By amplifying the osteolytic “vicious cycle” and promoting immune evasion, NF1 loss remodels the microenvironment to favor tumor expansion.  These results further suggest that NF1 loss functionally links therapy resistance with increased skeletal metastatic potential.

overall_design: Gene expression of NF1+ and NF1KO MCF7 cells were compared to access NF1 KO induced change.

first: Ze-Yi

last: Zheng

first: Jonathan

middle: T

last: Lei

first: Matthew

last: Baik

first: Yi-Hsuan

last: Wu

first: Lauren

middle: K

last: Somes

first: Andres

last: Mosquera Paternina

first: Omar

last: Harb

first: Owen

last: Chang

first: Fengshuo

last: Liu

last: Holt

first: Junkai

last: Wang

first: Igor

last: Bado

first: Hai

first: George

last: Miles

first: Zbigniew

last: Gugala

first: Meenakshi

last: Anurag

first: Ahmed

last: Elkhanany

first: Yi

last: Li

first: Valentina

last: Hoyos

first: Xiang

middle: H

first: Eric


title: The alteration of BA metabolism during development and inflammatory challenge

first: Jing

last: Shen

summary: To characterize alterations in bile acid metabolism under inflammatory conditions, RNA sequencing was conducted on proximal and distal colonic tissues from WT mice following 3 days of treatment with water or 3% DSS (n = 5 per group). To profile changes in bile acid metabolism during development, RNA sequencing was performed on proximal colonic tissues collected from WT mice at postnatal day 1, day 7 and day 21 under physiological conditions (n = 3 per group).

overall_design: C57BL/6J mice received H2O or DSS via drinking water for 3 days, after which proximal and distal colon tissues were isolated and lysed for RNA extraction. C57BL/6J mice were maintained under physiological conditions, and colonic proximal tissues were isolated at day 1, day 7 and day 21, followed by lysis for RNA extraction.

first: Mengqi

last: Zheng

first: Shiyang


title: ATAC-seq for proximal and distal colonic epithelial cells sorted from newborn and adult WT mice

summary: ATAC‑seq was conducted on sorted proximal and distal colonic epithelial cells derived from newborn and adult WT mice (n = 2 per group).

overall_design: This study was designed to investigate regional differences in chromatin accessibility of colonic epithelial cells between neonatal and adult wild-type (WT) mice. Proximal and distal colon tissues were collected from two age groups of WT mice (neonatal and adult) for subsequent epithelial cell purification and ATAC-seq sequencing. To ensure consistent sampling, tissue collection sizes were standardized: 1 cm colon segments for neonatal mice and 2 cm segments for adult mice. Fluorescence-activated cell sorting (FACS) was applied to obtain pure viable colonic epithelial cells for chromatin accessibility profiling, eliminating non-epithelial cell interference and ensuring the accuracy of regional and age-related chromatin difference analysis.


title: Whole-transcriptome-scale isoform-resolved spatial imaging of single cells in tissues

city: Cambridge

first: Limor

last: Cohen

state: MA

address: 38 Oxford Street

institute: Harvard University

summary: Cell and tissue functions arise from complex interactions among numerous genes, and a systematic understanding of these functions requires isoform-resolved transcriptomic analysis of single cells with high spatial resolution. Here, we introduce an in situ RNA amplification method and its integration with multiplexed error-robust fluorescence in situ hybridization (MERFISH) to detect short RNA sequences and enable isoform-resolved spatial transcriptomics of individual cells in intact tissues. Using this approach, we imaged ~33,000 distinct RNAs—including ~23,000 genes and ~10,000 isoforms—in the mouse brain. Our data enabled systematic analyses of region- and cell-type-specific gene programs and ligand-receptor-based cell-cell communications. These data further revealed rich spatial diversity and cell-type specificity in isoform usage across numerous genes, as well as brain structures particularly rich in specific isoform usage. We anticipate broad application of this method for characterizing molecular and cellular basis of tissue functions, unlocking previously inaccessible discoveries in cell and organismal biology.

overall_design: RNA-seq of mouse brain tissue in C57BL/6J, Male, 14 weeks


title: Engineering Human PEG10-based Nanoparticles for RNA Self-packaging, Delivery and Cancer Therapy

city: Hsinchu

first: Pin-Yan

last: Chen

address: No. 101, Section 2, Kuang-Fu Road

department: Chemical Engineering

institute: National Tsing Hua University

summary: Engineered protein-based protein nanoparticles (PBNPs) were developed for RNA self-packaging and delivery. To characterize the RNA cargo composition preferentially encapsulated within PEG10 PBNPs, RNA sequencing was performed on purified nanoparticle samples and producer cells. This dataset provides transcriptomic profiling of packaged RNAs associated with PEG10-mediated RNA delivery systems.

overall_design: RNA-seq was performed on purified PEG10-based protein nanoparticles and corresponding producer HEK293T cells. Libraries were prepared from extracted RNA and sequenced to evaluate the enrichment and composition of packaged transcripts within PBNPs.

first: Ting-Lun

last: Tien

first: Vy Anh

last: Truong

first: Quyen Thuc

last: Dang

first: Nuong Thi Kieu

last: Nguyen

first: Pin-Hsin

first: Yu-Chen

last: Hu


title: Oncogenic Ras signaling disrupts PRC2 via EED downregulation to drive oncogenic reprogramming and niche remodeling in squamous cell carcinoma

city: New York

first: Elena

last: Ezhkova

state: NY

address: 1428 Maidson Avenue 702

department: Cell, Developmental, and Regenerative Biology

institute: Icahn School of Medicine at Mount Sinai

summary: Squamous cell carcinoma (SCC) is a common epithelial malignancy, yet its epigenetic underpinnings remain poorly defined. Here, we identify the Polycomb Repressive Complex 2 (PRC2) as a key epigenetic barrier of SCC tumorigenesis. Despite high EZH2 levels, the PRC2-dependent H3K27me3 is depleted in human and murine SCCs, indicating complex destabilization rather than enzymatic failure. Mechanistically, oncogenic Ras signaling downregulates the PRC2 scaffolding subunit EED, disrupting PRC2 and H3K27me3 and activating oncogenic loci. Depletion of Eed in epidermal progenitors disrupts the proliferation–differentiation balance and, upon carcinogen exposure, drives invasive SCC. Single-cell RNA-seq of Eed-deficient tumors reveals an expansion of tumor-specific keratinocytes and a remodeled pro-tumorigenic microenvironment. Notably, reintroducing EED in SCC cells restores PRC2 integrity and H3K27me3 levels, suppressing tumor growth and mitigating the pro-tumorigenic niche. Our findings establish PRC2 as an essential epigenetic gatekeeper in SCC and suggest restoring PRC2-mediated repression may offer a novel therapeutic strategy.

overall_design: SCC tumors  from the back skin of Ctrl-D and Eed iKO-D mice. SCC cells  from the whle tumors was analyzed by scRNA-seq.

first: Meng-Yen

first: Aubrey

last: Houser

first: Paula

last: Restrepo

first: Andrew

last: Ji


title: Targeting the STING-NFκB Pathway via BTK Inhibition: A Dual-Mechanism Therapeutic Strategy Mitigating Neuronal and Microglial Dysfunction in Amyotrophic Lateral Sclerosis [RNA-seq]

city: 北京-Beijing

first: QING

last: Liu

state: 北京市

address: Department of Neurology, Peking Union Medical College Hospital (PUMCH), Peking Union Medical College (PUMC) & Chinese Academy of Medical Science (CAMS), Beijing, China

summary: Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder with limited therapeutic interventions. We identified the cGAS-STING-NFκB pathway as a dual therapeutic target that combats both neuronal degeneration and neurotoxic glial activity in ALS. Utilizing SOD1-mutant human iPSC-differentiated motor neurons(hiPSC-MNs) and microglia(hiPSC-MGs), we demonstrated that ALS hiPSC-MGs displayed a pronounced proinflammatory phenotype, characterized by significant inflammatory marker elevation (NLRP3 increased 0.66-fold, secreted IL-1β elevated 2.85-fold compared to controls) and compromised phagocytic capacity (48% reduction in bioparticle uptake). Concurrently, ALS hiPSC-MNs exhibit DNA damage, activating STING-NFκB signaling and triggering caspase-3-mediated apoptosis. Notably, co-culture experiments revealed that inflammatory hiPSC-MGs substantially increased neuronal apoptosis, indicating a toxic intercellular communication mechanism mediated through STING-NFκB signaling. Pharmacological inhibition of Bruton's tyrosine kinase (BTK) - a critical upstream regulator of STING activation - effectively suppressed this inflammatory cascade. This intervention reduced DNA damage in ALS hiPSC-MNs by 61.4% and restored microglial phagocytic function to approximately 87.2% of normal levels. In vivo studies with SOD1-G93A ALS mice demonstrated that BTK inhibitor treatment significantly improved motor performance, extended median survival (183 days versus 158 days in untreated controls), and mitigated neuropathological progression. The treatment enhanced motor neuron survival, reduced microgliosis and astrogliosis, and modulated the PI3K-AKT-mTOR pathway without disrupting autophagy-lysosome dynamics. Our study presents a translational therapeutic strategy that simultaneously addresses neuron-intrinsic and glial-mediated mechanisms in ALS, providing a compelling rationale for repurposing BTK inhibitors in future ALS clinical trials.

overall_design: The study utilized motor neurons derived from human induced pluripotent stem cells (iPSCs), dividing them into a control group and an ALS disease group. Each group comprised three biological replicates, with the experimental group consisting of samples from three ALS patients carrying SOD1 mutations (G42D, G11A, and D101K), and the control group comprising samples from three age- and sex-matched healthy controls, ensuring the reliability of the data and the validity of statistical analysis.


title: Establishment of a human inner ear model for evaluating diminished ototoxicity of gentamicin subtype C2b

city: Palo Alto

first: Konstantina

last: Stankovic

state: CA

address: Cooper Lane

institute: Stanford University

summary: Clinically used gentamicin, a widely used aminoglycoside antibiotic, is a mixture of 5 major subtypes and potentially differential contributions to the drug’s known ototoxicity. The gentamicin subtype C2b has been previously associated with reduced ototoxicity in animal models, but its effects in humans remain uncertain due to the lack of appropriate in vitro models of the human inner ear. To address this gap, we generated otic progenitor cells (OPCs) from human induced pluripotent stem cells and rigorously characterized them using transcriptomic and immunocytochemical analyses to confirm their otic lineage identity and validate their relevance as a model for ototoxicity studies. We then compared the effects of gentamicin C2b and clinical gentamicin on cell viability and cytotoxicity in human OPCs. In parallel, we examined auditory function in mice following exposure to each formulation using auditory brainstem response and distortion product otoacoustic emissions. Gentamicin C2b exposure resulted in substantially lower cytotoxicity—via reduced mitochondria-dependent apoptosis—and higher cell viability in human OPCs, as well as dramatically attenuated hearing loss across all frequencies in mice. Together, these findings indicate that gentamicin C2b has reduced ototoxicity compared to clinically used preparations, supporting the need for further investigations in clinical settings.

overall_design: During OPC differentiation from hiPSCs (SK8-A and UCSD lines), cells were collected on days 14 and 20 for scRNA-seq.

first: Jeong

last: Minjin

first: Stankovic

last: Konstantina


title: Targeting the STING-NFκB Pathway via BTK Inhibition: A Dual-Mechanism Therapeutic Strategy Mitigating Neuronal and Microglial Dysfunction in Amyotrophic Lateral Sclerosis [scRNA-seq]

institute: Peking Union Medical College Hospital (PUMCH), Peking Union Medical College (PUMC) & Chinese Academy of Medical Science (CAMS)

overall_design: The study utilized microglia derived from human induced pluripotent stem cells (iPSCs), dividing them into a control group and an ALS disease group. Each group comprised three biological replicates, with the experimental group consisting of samples from three ALS patients carrying SOD1 mutations (G42D, G11A, and D101K), and the control group comprising samples from three age- and sex-matched healthy controls, ensuring the reliability of the data and the validity of statistical analysis.


title: Single Cell Gene Expression Profiling of CD45+ Cells in Mouse Liver with or without MCD diet

city: Guangzhou

first: Huizhen

last: Lin

address: Shatai Nan Road

institute: Southern medical university

summary: Single-Cell Sequencing Reveals Immune Cell Subtype Differences in Mouse Liver Between ND and MCD Treatment.

overall_design: CD45+ cells from NASH mouse models were isolated using Fluorescence-Activated Cell Sorting (FACS) and subsequently analyzed through scRNA-seq.Mice were fed with ND or MCD-diet.

first: Xiaojun


title: Integrated miRNA-mRNA Analysis Reveals Regulatory Mechanisms of Muscle Fiber Transformation Underlying Meat Quality Variation in Chicken

city: chengdu

first: donghao

last: zhang

address: No. 211, Huimin Road, Wenjiang District, Chengdu City

institute: sichuan agricultural university

summary: Chicken muscle fibers are classified as oxidative or glycolytic, with distinct metabolic properties that influence meat quality. However, the molecular mechanisms linking fiber type to quality traits remain unclear. This study compared the pectoralis major (PEM) and soleus (SOL) muscles of Guangyuan Grey chickens, revealing significant differences in fiber characteristics and meat quality. Transcriptome analysis identified key pathways—MAPK, PPAR, and calcium signaling—associated with fiber-type variation. The transcription factor HOXC10, enriched in SOL, showed inverse expression to its predicted regulator, miR-6701-3p. Dual-luciferase assays confirmed HOXC10 as a direct target of miR-6701-3p. Functional studies in skeletal muscle satellite cells demonstrated that miR-6701-3p promotes proliferation, inhibits differentiation, and induces fast-twitch fiber formation, while HOXC10 facilitates slow-twitch fiber development. These findings reveal a novel miR-6701-3p/HOXC10 axis that modulates muscle fiber types and provides molecular targets for improving poultry meat quality.

overall_design: Samples of the pectoralis major muscles (PEM) and soleus muscles (SOL) on both sides of 180-day-old broilers were collected immediately after slaughter. A portion of each sample was rapidly frozen in liquid nitrogen for subsequent sectioning, biochemical analysis and RNA sequencing. The remaining tissue was stored at 4 °C for meat quality assessment. The distribution and proportion of muscle fiber types in these two muscle samples are vastly different. Sequencing is used to evaluate the characteristics of genetic material differences under huge phenotypic differences and screen out the key regulatory factors of muscle fiber types.


title: Somatic Mutations in MCOLN3 Are Associated with Aldosterone-Producing Adenomas

city: Ann Arbor

first: Antonio

middle: Marcondes

last: Lerario

state: MI

address: 109 Zina Pitcher Place, 1528 BSRB

department: MEND

institute: University of Michigan

summary: Background: Primary aldosteronism is a common but underdiagnosed cause of endocrine hypertension that contributes to global cardiovascular morbidity and mortality. It is characterized by renin-independent hyperaldosteronism that originates from adrenal lesions — the majority of which are found to harbor aldosterone-driver somatic mutations in genes encoding ion-transporting proteins. These mutations disrupt intracellular calcium homeostasis, facilitating pathologic increase in aldosterone synthase (CYP11B2) expression and aldosterone production. Elucidating the exact mechanisms causing aldosterone excess in primary aldosteronism would further the development of targeted treatments and alleviate the global hypertension burden.Methods: Next-generation sequencing analysis of formalin-fixed paraffin-embedded aldosterone-producing adenomas identified novel somatic variants in MCOLN3 (encoding the cation-permeable channel, TRPML3). Electrophysiologic, fura-2 calcium measurements, gene expression and steroid quantification studies were performed in adrenal HAC15 cells to characterize the functional effects of the novel MCOLN3 mutations. Results: Three somatic MCOLN3 variants (p.Y391D, p.F415I and p.N411_V412delinsI) were identified in four aldosterone-producing adenomas from male primary aldosteronism patients. Mutated MCOLN3 expressed in HAC15 cells resulted in a gain-of-function phenotype, which induced cell membrane depolarization and calcium influx and, in turn, triggered a significant increase in aldosterone synthase expression and aldosterone production. Conclusions: This is the first report of disease-causing MCOLN3 mutations in humans and first to implicate mutated MCOLN3 as a driver of dysregulated aldosterone production in primary aldosteronism.

overall_design: RNAseq profiling of HAC15-MCOLN3WT and HAC15-MCOLN3Y391D cells. Human adrenocortical HAC15 cells (2x106 live cells) were transfected with empty pIRES-CD8 plasmid DNA, or with pIRES-CD8 plasmids containing MCOLN3WT  or MCOLN3Y391D  via electroporation using  the  Amaxa™ Cell Line Nucleofector Kit R following the manufacturer’s recommendation (Lonza). Cells were subjected to electroporation using the T20 Nucleofector® program. Immediately post-electroporation, 500 µL warm growth medium was added to the cells for recovery. Using a plastic pipette, the transfected cells were gently divided, in a dropwise-manner, between 3 wells of a 12-well plate containing 600 µL pre-warmed growth media. Cells were incubated for 48 h after which the plates were stored at -80 °C for RNA isolation.

first: Juilee

last: Rege

first: Desmaré

last: van Rooyen

first: William

last: Rainey


title: CircRAPGEF5 acts as a modulator of RAS/RAF/MEK/ERK signaling during colorectal carcinogenesis

city: Hefei

first: yu

middle: xiang

last: dai

address: No.81 Meishan Road Hefei China

institute: Anhui Medical University

summary: Mutations in oncogenes such as KRAS, NRAS and BRAF promote cancer cell survival and proliferation, while excessive RAS/RAF/MEK/ERK signaling instead exerts an inhibitory effect on tumor growth. The precise regulatory mechanism of moderate RAS/RAF/MEK/ERK pathway activation during tumorigenesis remains elusive. Here, we discovered that a circular RNA, circRAPGEF5, was significantly upregulated in KRAS mutant colorectal cancer (CRC) cells. CircRAPGEF5 suppressed mutant and constitutively activated KRAS and the expression of the death receptor TNFRSF10A. Silencing of circRAPGEF5 induced RAS/RAF/MEK/ERK signaling hyperactivation and apoptosis in CRC cells. Moreover, the circularization of circRAPGEF5 was promoted by EIF4A3, whose expression was also elevated in tumor tissues. Taken together, our findings reveal a mechanism of accurate regulation of RAS/RAF/MEK/ERK signaling during CRC progression and provide potential targets for cancer therapy.

overall_design: HCT116 cells were transfected with an sh-RNA knockdown

first: Zaibiao

last: Wang

first: Zhipeng

last: Yin

first: Hao

last: Li

first: Heng

last: Zhao


title: Whole-exome sequencing reveals mutational signature of hypertrophic cardiomyopathy

city: Shijiazhuang City

first: Xiqin

state: Hebei Province

address: Yuhua District

department: Department of Internal Medicine

institute: Yuhua Yunfang Integrated Traditional Chinese and Western Medicine Clinic

summary: Hypertrophic cardiomyopathy (HCM) is an extremely insidious, lethal disease caused by genetic variation and characterized by cardiac hypertrophy. It has been studied for nearly 70 years since its discovery, but its cause of the disease remains a mystery.  Here, aiming to identify pathogenic genes that causes HCM, 14 patients with HCM were collected and whole exome sequencing (WES) of peripheral blood DNA was performed.

overall_design: A total of 14 patients with HCM were collected in this study. Peripheral blood of these patients was collected for whole exome sequencing.

first: Xi-qin

first: Fang

last: Yuan

first: Bao-rui

last: Yu


title: Omental support of ovarian tumor cell growth is unabated in the absence of mature adipocytes

city: Saint Louis

first: Gwendalyn

last: Randolph

state: Missouri

address: 660 South Euclid Ave

department: Immunolgoy

institute: Washington University in St. Louis

summary: The omentum, a specialized adipose tissue arising off the stomach, is a key premetastatic niche for ovarian cancer metastasis and growth within the peritoneum. Why the omentum promotes optimal ovarian cancer growth remains unclear, but the prevailing concept is that omental adipocytes and the accompanying metabolic exchange of FABP4-binding fatty acids are critical. Here, we generated mice lacking mature adipocytes in all peritoneum tissues, including the omentum. ID8p53–/–Brca2–/– tumors retained a propensity to seed at regions typically associated with adipose depots, even without mature adipocytes. However, the lack of mature adipocytes did not suppress tumor expansion in the peritoneum, whereas removing the adipocyte-free omentum did. Single-cell RNA sequencing analysis revealed that endothelial FABP4 was especially high in the omentum, potentially accounting for the role of FABP4 in tumor growth rather than adipocyte FABP4, as previously thought. Thus, whether and how tumor cell-adjacent adipocytes impact tumor progression needs re-evaluation

overall_design: Mesenteries and omenta from lipoatrophic mice that received fat transplant surgeries in their scruff, rendering the peritoneal cavity free of mature adipocytes, or littermate controls with standard fat depots who received sham surgery were divided into mesothelial sheet regions or adipose regions and submitted separately for single-cell RNA sequencing. Thus, mesenteric sheet (MS), mesenteric fat region (MSR), omentum sheet (OS), and omentum fat region (OFR) were collected from eight lipoatrophic and eight control mice weeks after surgery. The tissues were labeled with antibody-derived hashtags to separate the biological replicates in each sample.

first: Rachel

last: Mintz

first: Emily

middle: G

last: Butka

first: Alexandre

last: Gallerand

first: Jichang

last: Han

first: Ayoung

last: Kim

first: Sarah

last: Ning

first: Nicole

last: Yiew

first: Mary

last: Wohltmann

first: Wei

last: Zou

first: Samantha

last: Morris

first: Bernd

last: Zinselmeyer


title: 10X Visium spatial transcriptomics of mouse thoracic spine intervertebral disc, IVD2 (area D1)

status: Public on Jun 12 2026

city: Austin

first: Ryan

last: Gray

address: 1400 Barbara Jordan Ave

department: Nutritional Sciences

institute: University of Texas at Austin

summary: Spatial gene expression profiling of mouse thoracic spine tissue using the 10x Genomics Visium platform (FFPE, probe-based chemistry). Library IVD2 was profiled on Visium slide V11A19-364 capture area D1. This capture area contains both mutant and control tissue regions. Raw FASTQs comprise two sequencing lanes (L001 and L002) of the same IVD2 library (8 files total).

overall_design: One Visium spatial RNA-seq library (IVD2, slide V11A19-364 area D1) was generated from mouse thoracic spine tissue containing both mutant and control regions on the same capture area. The library was sequenced on an Illumina NovaSeq 6000 (run 220311_A00842_0226_BH5FJYDRX2) across two lanes. All 8 raw FASTQ files are included: IVD2_S2_L001_I1/I2/R1/R2_001.fastq.gz and IVD2_S2_L002_I1/I2/R1/R2_001.fastq.gz. Processed Space Ranger outputs match the original IVD2 count using both lanes. Manual Loupe ROI outputs for mutant vs control are on GitHub. Raw sequencing data will be deposited to SRA by GEO staff.

first: Valeria

last: Aceves

first: Ziyi

last: Xu

first: Zhaoyang

last: Liu

middle: S


title: EphA4 Mediates Pro- and Anti- Tumoral Effects Through Upstream Negative Regulation of AKT in Head and Neck Squamous Cell Carcinoma- The effect of EphA4 knockout on RNA expression in HNSCC cell line.

city: Aurora

first: Sophia

last: Corbo

state: CO

address: 12801 E 17th ave, L18-4402E RC1 South/4th Floor

institute: University of Colorado-Denver (UCDenver) (Anschutz Medical Campus)

summary: Head and Neck Head and Neck Squamous Cell Carcinoma (HNSCC) is driven by an immunosuppressive tumor microenvironment (TME). We examined the immune-modulatory role of EphA4 in HNSCC using spatial analysis, multi-compartment RNA-sequencing from Oral Cavity Squamous Cell Carcinoma (OCSCC), and three genetically engineered mouse models. Within the HNSCC TME, EphA4 is primarily expressed in Tregs, macrophages, CD8+ T cells, and HNSCC cancer cells. EphA4 in Tregs promotes tumor growth, whereas EphA4 in myeloid cells, CD8+ T cells, and cancer cells limits it. EphA4 mediates these differential effects through shared negative regulation of AKT signaling where its knockout increases AKT activation, leading to reduced Treg immunosuppression, increased M2 macrophage polarization, impaired CD8+ T cell memory differentiation, and enhanced cancer cell proliferation. APY-d3-PEG4, EphA4 inhibitor, reduced tumor growth primarily by targeting Tregs. EphA4 expression on CD8+ T cells correlates with treatment response, representing a potential biomarker, and cell-type-specific targeting via cis-bispecific antibodies offers a promising therapeutic strategy. Interrogating human data shows that EphA4 expression on CD8 correlates to response to treatment, posing it as a potential biomarker for future studies. Mechanistically, our data show EphA4 inhibits AKT signaling, and its inhibition enhances AKT functionality across cell types, yielding opposing effects in cancer.

overall_design: Comparison of gene expression using bulk RNA-sequencing of MOC2 EphA4 knockout cells and MOC2 control knockout cells.

first: Corbo

last: Sophia

first: Karam

last: Sana


title: Mapping the spatial architecture of glioblastoma from core to edge delineates niche-specific tumor cell states and intercellular interactions [xenium_cohort3]

city: Boston

first: Allegra

last: Petti

state: Massachusetts

address: 185 Cambridge St.

department: Department of Neurosurgery

institute: Massachusetts General Hospital

summary: Treatment resistance in glioblastoma (GBM) is largely driven by the extensive multi-level heterogeneity that typifies this disease. Despite significant progress toward elucidating GBM’s genomic and transcriptional heterogeneity, a critical knowledge gap remains in defining this heterogeneity at the spatial level. To address this, we employed spatial transcriptomics to map the architecture of the GBM ecosystem. This revealed tumor cell states that are jointly defined by gene expression and spatial localization, and multicellular niches whose composition varies along the tumor core-edge axis. Ligand-receptor interaction analysis uncovered a complex network of intercellular communication, including niche- and region-specific interactions. Finally, we found that CD8 +ve GZMK +ve T cells colocalize with LYVE1 positive CD163 positive myeloid cells in vascular regions, suggesting a potential mechanism for immune evasion. These findings provide novel insights into the GBM tumor microenvironment, highlighting previously unrecognized patterns of spatial organization and intercellular interactions, and novel therapeutic avenues to disrupt tumor-promoting interactions and overcome immune resistance.

overall_design:
We designed a panel of oligonucleotides targeting transcripts from 362 genes, comprising 266 genes from the predesigned 10X Genomics human brain-and-glioblastoma panel and 96 custom genes indicated by our scRNA-seq analyses (Table S4). Together, this customized panel captures diverse neurons, glia, endothelial cells, microglia, immune cells, GBM cells (including both spatial GBM cell states derived from our Visium data and published scRNA-seq-derived GBM cell states), and ligand-receptor pairs that putatively mediate tumor/neuron, tumor/T cell, and tumor/macrophage interactions.
Sample Preparation - Primary Cohort
Formalin-fixed, paraffin-embedded (FFPE) tumor samples were sectioned into 5-um sections using a microtome onto Xenium slides according to Protocol CG000578 published by 10X Genomics. The Xenium slides were then deparaffinized and decrosslinked according to the Protocol CG000580. Both a pre-designed gene expression panel (Human Brain Probe set) and a custom probe set were used during probe hybridization, ligation, and amplification according to Protocol CG000749, which also contained cell segmentation staining. The Xenium slide was then loaded into the Xenium Analyzer using Protocol CG000584 and regions of interest (ROIs) were initially selected using the on-instrument software.
Sample Preparation - Secondary Cohort
Samples were processed similarly as previously published20. In brief, formalin-fixed, paraffin-embedded (FFPE) tumor samples were sectioned into 5-um sections using a microtome onto Xenium slides according to Protocol CG000578 published by 10X Genomics. The Xenium slides were then deparaffinized and decrosslinked according to the Protocol CG000580. Both a pre-designed gene expression panel (Human Brain Probe set) and a custom probe set were used during probe hybridization, ligation, and amplification according to Protocol CG000582. The Xenium slide was then loaded into the Xenium Analyzer using Protocol CG000584 and regions of interest (ROIs) were initially selected using the on-instrument software.

first: Saad

middle: M

last: Khan

first: Anthony

middle: Z

last: Wang

first: Rupen

middle: R

last: Desai

first: Colin

last: McCornack

first: Rui

last: Sun

first: Sonika

last: Dahiya

first: Jennifer

last: Foltz

first: Ngima

middle: D

last: Sherpa

first: Lydia

last: Leavitt

first: Timothy

last: West

first: Alexander

first: Aleksandar

last: Krbanjevic

first: Bryan

last: Choi

first: Eric

last: Leuthardt

first: Bhuvic

last: Patel

first: Albert

first: Gavin

last: Dunn


title: Oxidative stress triggers RNAPII arrest through PARylation and DNA damage [ELCAP-seq]

city: København

first: Lea

middle: Haarup

last: Gregersen

address: Blegdamsvej 3B,

department: ICMM

country: Denmark

institute: University of Copenhagen

summary: UV or gamma irradiation, as well as certain chemicals, generate DNA damage that disrupts transcription through a variety of well-characterised mechanisms. In contrast, the transcriptional response to oxidative stress remains poorly understood. Here, we describe a rapid and widespread shutdown of transcription following oxidative DNA base damage. By monitoring RNAPII occupancy and elongation dynamics, we demonstrate that oxidative stress temporarily halts RNAPII pause release and arrests the progression of elongation complexes within the gene body. We present evidence that this occurs in a unique and transient manner, characterised by abrupt arrest of elongating RNAPII dead in its tracks, followed by rapid transcriptional recovery as DNA lesions are repaired. We find that the restriction of initiation and early elongation complexes is regulated by PARylation, whereas recovery of RNAPII arrested within the gene body requires DNA repair mediated by the base excision repair (BER) and single-strand break repair (SSBR) pathways.

overall_design: ELCAP-Seq or sequencing of small RNA bound to either RPB3-FLAG RNAPII, 4H8 Ab (phospho RNAPII) and 8WG16 Ab (unphospho RNAPII) upon 1mM H2O2 15min stress and recovery.

first: Quentin

last: Thomas

first: Liyang

last: Wu

first: Emma

last: Lesage

first: Henriette

last: Iversen

first: David

last: Lopez-Martinez

first: Haiyue

last: Liu

first: Nicolas

last: Nieto-Moreno


title: Oxidative stress triggers RNAPII arrest through PARylation and DNA damage [TTchem-seq]

overall_design: TTchemSeq data upon a brief 15min H2O2 stress and recovery timepoints. With various inhibitors (DRB, Olaparib, OGG1i) and KnockOut cell line XRCC1.

middle: A


title: Oxidative stress triggers RNAPII arrest through PARylation and DNA damage [ChIP-seq]

overall_design: ChIP-seq analysis of NELFE and total RNAPII (with D8L4Y Ab) upon 1mM h2o2 15min stress and 1hour recovery of H2O2 stress


title: Genomic hallmarks of depot medroxyprogesterone acetate-associated meningiomas

city: Pittsburgh

first: Sakibul

last: Huq

address: 200 Lothrop St, Suite B-400

department: Neurological Surgery

institute: University of Pittsburgh Medical Center

type: Methylation profiling by genome tiling array

summary: This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: RNA-seq and ONT full-length transcriptome profiling of HCT116 and WiDr cells treated with DMSO, GSK025, or GSK715

city: Nanjing

first: Mu

last: Xu

address: No.32, Gongqingtuan Road,

department: Nanjing First Hospital

institute: Nanjing Medical University

summary: This study profiles transcript abundance and full-length transcript isoforms in colorectal cancer cell lines after PRMT inhibitor treatment.

overall_design: Bulk short-read RNA-seq was performed on HCT116 cells treated with DMSO, 10 uM GSK025 (GSK3235025, PRMT5 inhibitor), or 5 uM GSK715 (GSK3368715, PRMT1 inhibitor) for 96 h (n=3 each), and on WiDr cells treated with DMSO or 5 uM GSK715 for 96 h (n=3 each). ONT full-length cDNA sequencing was performed on WiDr cells treated with DMSO or 5 uM GSK715 for 96 h (n=2 each).


title: Genomic hallmarks of depot medroxyprogesterone acetate-associated meningiomas [methylation]

summary: Integrated genomic characterization of meningiomas from 10 women with long-term exposure to depot medroxyprogesterone acetate (DMPA), a commonly used injectable progestin contraceptive. All tumors were newly diagnosed WHO grade 1 meningiomas. We profiled genome-wide DNA methylation (Illumina Infinium MethylationEPIC v2.0) and performed bulk RNA sequencing on all 10 tumors, and integrated these data with public reference meningioma cohorts (Baylor, GSE189521; Heidelberg, GSE109381) for methylation classifier assignment, consensus clustering, copy-number analysis, and differential methylation testing.

overall_design: Genome-wide DNA methylation profiling (Illumina Infinium MethylationEPIC v2.0) of 10 FFPE WHO grade 1 meningiomas from women with long-term DMPA exposure, analyzed against Baylor (GSE189521) and Heidelberg (GSE109381) reference cohorts.

first: Taylor

last: Gatesman

first: Hussam

last: Abou-Al-Shaar

last: Raleigh

first: Constantinos

last: Hadjipanayis

first: James

middle: C

last: Bayley

first: Georgios

last: Zenonos

first: Thomas

last: Pearce

first: Daniel

last: Marker

first: Sameer

last: Agnihotri

first: Paul

last: Gardner


title: Genomic hallmarks of depot medroxyprogesterone acetate-associated meningiomas [RNA-seq]

overall_design: Bulk RNA sequencing of 10 FFPE WHO grade 1 meningiomas from women with long-term DMPA exposure. RNA exome-capture libraries were sequenced paired-end on an Illumina NextSeq 2000. Exploratory comparison of TRAF7-mutant (n=5) vs TRAF7-wildtype (n=5) tumors.

middle: F


title: Transcriptome analysis of neutrophils from recurrent vulvovaginal candidiasis patients and IL-17A-treated healthy controls

city: Kunming

first: xiang

middle: wen

last: lan

address: 300 Bailong Temple, Panlong District, Kunming, Yunnan 650224, China

institute: Southwest Forestry University

summary: Recurrent vulvovaginal candidiasis (RVVC) is a common mucosal infectious disease characterized by recurrent episodes of vulvovaginal inflammation caused by Candida albicans. Neutrophils are critical innate immune cells in antifungal defense, and IL-17A plays an important regulatory role in neutrophil function. To explore the mechanism by which IL-17A regulates neutrophils in RVVC, we collected vaginal lavage fluid from 3 healthy women and 3 RVVC patients, isolated neutrophils, and treated healthy neutrophils with IL-17A. Total RNA was extracted from three groups (healthy control group A, healthy+IL-17A group B, and RVVC patient group C), followed by transcriptome sequencing. Through quality control, library construction, sequencing, alignment, gene expression quantification, and differential expression analysis, we aim to identify differentially expressed genes and key pathways related to RVVC pathogenesis and IL-17A regulation of neutrophils.

overall_design: Neutrophils were isolated from vaginal lavage fluid of 3 healthy volunteers and 3 patients with recurrent vulvovaginal candidiasis (RVVC). Neutrophils from healthy controls were treated with IL-17A in vitro. Three groups were included: healthy control neutrophils (Group A, n=3), healthy neutrophils treated with IL-17A (Group B, n=3), and neutrophils from RVVC patients (Group C, n=3). Total RNA was extracted and subjected to RNA-seq transcriptome analysis to compare gene expression profiles across groups.


title: Human keratinocytes and fibroblasts coordinate early cutaneous innate defense against Candida auris

city: Vienna

first: Trinh

last: Phan-Canh

state: Vienna

address: Dr.-Bohr-Gasse 9

department: Max Perutz Labs Vienna, Campus Vienna Biocenter

country: Austria

institute: Medical University of Vienna

summary: Candida auris (C. auris) is an emerging fungal pathogen with a remarkable ability to persist on human skin, but how structural skin cells respond to colonization is unclear. We used ex vivo human skin models, primary keratinocytes and fibroblasts to characterize epithelial and stromal responses to C. auris compared with Candida albicans (C. albicans). C. auris formed biofilms and induced a wound-model-dependent pattern of cytokine secretion dominated by IL-1β and IL-6, yet caused minimal epithelial damage and modest reductions in leukocyte viability.  RNA sequencing revealed complementary but cell-type-specific responses. Keratinocytes and fibroblasts both amplified a pro-inflammatory IL-6/CXCL8 response, while keratinocytes additionally upregulated antimicrobial genes such as RNASE7, TSLP, DEFB103A, and the neutrophil-recruiting chemokines CXCL2 and CXCL3. Fibroblasts further induced CCL28, supporting T-cell recruitment, alongside transcriptional programs associated with tissue remodeling. Recombinant RNase 7 and short form TSLP directly inhibited C. auris growth in vitro in a dose-dependent manner. Together, these findings identify keratinocytes as epithelial sentinels that integrate inflammatory and antimicrobial defenses against skin-tropic C. auris and suggest that fibroblast-driven cytokine amplification and especially antimicrobial peptides from within the skin barrier may provide therapeutic targets to limit C. auris skin colonization.

overall_design:
Bulk RNA-seq of human primary keratinocytes and fibroblasts of four skin donations infected with four different Candida auris isolates ("47", "48", "255", "304") versus uninfected controls ("PBS").

***************************************************************
Raw files for human/patient samples were not submitted to GEO due to concerns about submitting personally identifiable sequence data for open access.
***************************************************************

first: Saskia

last: Seiser

first: Philipp

last: Penninger

first: Karl

last: Kuchler

first: Adelheid

last: Elbe-Bürger


title: Mapping immune cellular landscapes and vaccine responses across a spectrum of health and immunodeficiency [CITE-seq]

city: Parkville

first: Davide

last: Vespasiani

state: VIC

address: 1G Royal Parade

country: Australia

institute: The Walter and Eliza Hall Institute

summary: Immune responses to infection and vaccination exhibit diversity between individuals that can be shaped by differences in their immune cell landscapes and the signalling, transcriptional, and genetic mechanisms that coordinate immune cell function. Specific antibody deficiency (SAD) and common variable immunodeficiency (CVID) are common forms of predominantly antibody deficiencies that result in poor responses to vaccination. While molecular and cellular causes of the immune dysfunction and poor vaccination responses for individuals with CVID have been reported, immune cell or molecular defects have not yet been identified in SAD. Here, we have used single-cell multi-omics to define the cellular landscapes, transcriptional states, adaptive immune repertoires and protein expression of patients with SAD and CVID before and after polysaccharide vaccination. We discovered that while SAD and CVID exhibit overlapping immune defects, including accumulation of exhausted NK memory cells and dysregulated expression of genes that mediate lipopolysaccharide sensing and clearance by monocytes, individuals with SAD have a unique expansion of cytotoxic CD4+ T cells that correlates with reduced regulatory T cells. In response to vaccination, we observed rapid changes in gene expression associated with lipopolysaccharide responses by monocytes and NF-kB pathway activation in B cells, and an apparent expansion of a CD95+ class-switched memory B cell population that does not occur in patients with lower antigen-specific responses. Together, our findings reveal cellular and molecular factors that underpin variability in vaccine responses and define SAD in a broader spectrum of immune dysfunction.

overall_design: This project contains data from CITE-seq and VDJ-seq of peripheral mononuclear blood cells (PBMC) collected from 10 patients with CVID, 10 SAD and 10 healthy controls before and after vaccination. All 60 PBMC samples were stained with Hash Tag Oligonucleotides (HTOs) and a panel of 130 Antibody-Derived Tags (ADTs) using TotalSeqTM antibodies before pooling and split them into 5 batches (12 samples each). For each batch, GEX, ADT and HTO and VDJ libraries were generated using the 10X Genomics Chromium single-cell 5′ reagent kit v3 and then sequenced on a NovaSeq X Plus (PE150). The resulting dataset includes single-cell expression data (GEX) and single-cell protein expression data (ADT, antibody-derived tags library) for 454,025 human PBMCs (322,174 after quality filtering) and single-cell B/T cell receptor repertoire data for 157,108 human T and 26,873 B cells after quality filtering.

last: Lancaster

first: Hamish

middle: W

last: King


title: Transcriptomic profiling of jejunal tissues from ETEC-challenged yak calves supplemented with Pediococcus pentosaceus NQ0729

city: Lanzhou City, Gansu Province

first: Yanbin

last: Zhu

address: No.1 Yingmen Village, Anning District

institute: Gansu Agricultural University

summary: This study generated transcriptomic data to investigate gene expression changes in the jejunum of yak calves following enterotoxigenic Escherichia coli (ETEC) challenge and Pediococcus pentosaceus NQ0729 supplementation.

overall_design: Yak calves were divided into three groups: a control group (CON), an ETEC-challenged group (ETEC), and a P. pentosaceus NQ0729-pretreated group followed by ETEC challenge (PET). Jejunal tissue samples were collected at the end of the animal trial and subjected to RNA sequencing. The dataset was used to compare transcriptomic profiles among the three groups and to identify differentially expressed genes and enriched biological pathways associated with ETEC challenge and probiotic intervention in yak calves.

first: Jiang

last: Hu


title: Differences in serum microRNA expression in rat  following single- and combination drug  administration of caffeine and dextromethorphan

city: hirakata

first: Yuko

last: Emoto

institute: Kansai Medical University

summary: Caffeine and dextromethorphan are among the most commonly abused substances by young people in Japan. However, reports on interactions between caffeine and dextromethorphan and comprehensive miRNA analyses following the administration of these drugs are limited. We aimed to determine whether miRNA expression differs in rats administered caffeine and dextromethorphan alone or in combination. We performed a comprehensive analysis of miRNAs in the livers of rats treated with caffeine, dextromethorphan, or both drugs at toxic dose in a single dose

overall_design: Six-week-old male Sprague-Dawley rats (Jcl:SD).After the acclimatization period, the 7-week-old rats were divided into four groups: control, caffeine, dextromethorphan, and caffeine plus dextromethorphan (n = 5 per group). The rats were orally administered the drugs in a single dose. The caffeine group (CAF) received 180 mg/kg caffeine, the dextromethorphan group (DEX) received 200 mg/kg dextromethorphan hydrobromide monohydrate, and the combination group (CAF + DEX) received 180 mg/kg caffeine and 200 mg/kg dextromethorphan hydrobromide monohydrate.Dextromethorphan was administered one hour after caffeine administration.  All drugs were dissolved in sterile distilled water. Age-matched control groups (control) were treated with vehicle (sterile distilled water) only. One hour after dextromethorphan administration, blood samples were collected under anesthesia, and serum was isolated.


title: Transcriptomic determinants of humoral immunity for heterogeneously antigenic PL45 cells

city: Baltimore

first: Elana

last: Shaw

address: 855 N Wolfe St

institute: Johns Hopkins University

summary: Ascitic fluid from patients with pancreatic ductal adenocarcinoma (PDAC) contains IgG antibodies that bind to allogeneic PDAC cell lines, including the commercially available PDAC cell line PL45. PL45 cells exhibited heterogeneous binding by IgG from patients with PDAC (A1 and A14). We hypothesized that transcriptomic heterogeneity within the cell line contributes to the observed antigenic heterogeneity. To investigate potential transcriptomic determinants of humoral antigenicity, PL45 cells were stained with ascitic IgG from patients A1 or A14 and flow-cytometrically sorted using a fluorescently labeled anti-human IgG detection antibody. RNA was isolated from the IgG-positive and IgG-negative PL45 subpopulations and subjected to bulk RNA sequencing followed by DESeq2 differential expression analysis.

first: Alexei

last: Hernandez

first: Linda

last: Huang

first: Bryan

last: Szeglin

first: Yuqian

last: Wang

first: Carolyn

last: Merwanji

first: Rosela

last: Golloshi

first: Matthew

last: Dunworth

first: Shannon

middle: N

last: Radomski

first: Charles

last: Lim

first: David

last: Lichtman

first: Patrick

last: Balao

first: John

last: Texter III

last: Woller

first: Christopher

middle: J

last: VandenBussche

first: Patrizio

last: Caturegli

first: Luann

last: Rezavi

first: Conlan

last: Tran

last: Thoburn

first: Joel

last: Bader

first: Felipe

last: Andrade

first: Maximilian

last: Konig

first: Won Jin

last: Ho

first: Andrew

last: Ewald


title: iAstrocytes model cytokine influences on complement expression and neuronal network synchronization.

first: Beth

last: Stevens

address: 300 Longwood Ave

institute: Boston Children's Hospital

summary: Astrocytes play essential roles in neuronal development, function, and disease, yet existing methods to derive astrocytes from human pluripotent stem cells (hPSCs) are complex and can involve months of in vitro maturation. We developed a genomic safe-harbor knock-in system for inducible expression of the astrogenic transcription factors NFIA, NFIB, and SOX9, enabling rapid and robust generation of functional induced astrocytes (iAstrocytes). Across five hPSC lines, NFIB-SOX9 and NFIA-NFIB-SOX9 combinations efficiently generated highly pure populations expressing astrocyte-specific and synaptogenic genes. iAstrocytes displayed cytokine-induced expression of complement factors C3 and C4 and were amenable to CRISPR interference (CRISPRi) gene expression knockdown. Optimization of culture conditions enabled survival of NFIB-SOX9 iAstrocytes in co-culture with human induced neurons (iNeurons). Through pharmacological and genetic perturbations, we uncovered a previously undescribed phenomenon in which co-culture with iAstrocytes promoted the development of synchronized iNeuron network calcium activity mediated by specific gap junction proteins. This rapid and genetically tractable iAstrocyte platform provides a robust model to dissect human genetic and environmental effects on astrocyte-neuron interactions.

overall_design: 7 differentiated iAstrocyte lines and 1 undifferentiated hPSC line were sequenced with 3 replicates per condition.

first: Nader

last: Morshed

last: Demers

first: Ana

last: Gonzalez-Ramos

first: Henna

last: Jäntti

first: Jordan

last: Doman

first: Shreyas

last: D’Souza

first: Letian

last: Li

first: Adam

last: Granger

middle: B

last: Johnson


title: Methylation profiling of brain metastasis tissue, cerebrospinal spinal (CSF) and plasma from patients with non-small cell lung cancer (NSCLC)

city: New Haven

first: Darin

last: Dolezal

address: 310 Cedar Street

department: Pathology

institute: Yale School of Medicine

type: Methylation profiling by high throughput sequencing

summary: This project investigates genome-wide DNA methylation patterns in tumor, cerebrospinal fluid (CSF), and blood from patients with non-small cell lung cancer (NSCLC) brain metastasis. Brain metastasis tumor tissues obtained at the time of neurosurgical resection performed as part of routine clinical care were profiled alongside time-matched cell-free DNA (cfDNA) derived from CSF and plasma collected from the same patients. Additional longitudinal CSF and plasma cfDNA samples collected at the time of clinically suspected leptomeningeal metastasis were also analyzed. All samples were assessed using the PredicineEPIC whole-genome methylation analysis platform to identify CpG sites covered by differentially methylated fragments (DMFs). These data support the development of liquid biopsy approaches for the detection, monitoring, and risk stratification of central nervous system disease in patients with NSCLC brain metastases.

overall_design: This study evaluated biospecimens collected from patients with non-small cell lung cancer (NSCLC) brain metastasis including 102 brain metastasis tumor tissue, 35 cerebrospinal fluid (CSF), and 60 plasma samples. Samples were collected at time of neurosurgical intervention (craniotomy [CRANI1, CRANI2]) performed as part of routine clinical care or in the clinical setting of leptomeningeal metastasis [LMD1, LMD2, LMD3]. The PredicineEPIC whole-genome methylation analysis platform was applied to tumor tissue-derived genomic DNA and cell-free DNA (cfDNA) extracted from CSF and plasma. Using this platform, samples were tested against a background model generated from healthy donors in order to identify CpG sites covered by differentially methylated DNA fragments (DMFs). Processed data are provided as DMF matrices, in which the rows correspond to DMF counts and columns correspond to individual samples, and as DMF annotation tables that include the genomic location, mean methylation beta-values, human gene symbol annotations, region annotation and other parameters corresponding to abnormally-methylated fragments. Separate matrices and corresponding feature annotation tables are provided for each sample types (TUMOR, CSF, PLASMA). Raw sequencing data are available in the Sequence Read Archive (SRA) under the associated BioProject accession.

first: Sampada

last: Chande

first: Giancarlo

last: Bonora

first: Yong

last: Huang

first: Myles

last: Walsh

first: Savannah

last: Kandigian

first: Wei

last: Wei

first: Anna

last: Arnal-Estape

first: Kurt

last: Shalper

first: Sarah

last: Goldberg

first: Darren

last: Cross

first: Massimo

last: Squatrito

first: Nicholas

last: Blondin

first: Pan

last: Du

first: Shidong

last: Jia

first: Veronica

last: Chiang

first: Don

last: Nguyen


title: CDK8 Inhibition Releases the Muscle Differentiation Blockade in Fusion-driven Alveolar Rhabdomyosarcoma [ChIP-Seq]

first: Susu

last: Zhang

address: 360 Longwood Ave, LC6102

department: Pediatric Oncology

institute: Dana-Farber Cancer Institute

summary: Alveolar rhabdomyosarcoma (aRMS) is a fusion-driven pediatric cancer with poor survival and limited therapeutic options. To uncover novel vulnerabilities, we employed complex-based analysis of the functional genomic dataset (Depmap), identifying CDK8 as a novel dependency in aRMS. Both CDK8 knockout or pharmacologic inhibition impaired tumor cell growth and induced myogenic differentiation in vitro and in vivo. Compared to genetic loss, CDK8 inhibition induced more dynamic transcriptional changes, suggesting a distinct gain-of-function mechanism of the CDK8 inhibitor. With a genome-scale CRISPR-Cas9 drug modifier screen, we determined that the maximal anti-tumor activity of the CDK8 inhibitor requires the presence of the Mediator kinase module and transcriptional cooperation with the SAGA complex. We further identified SIX4 as a key transcription factor mediating CDK8 inhibitor-induced transcriptional activation of myogenic differentiation genes and tumor cell proliferation. These findings establish a strong rationale for CDK8 inhibition as a differentiation-inducing therapeutic strategy in aRMS.

overall_design: Rh30 cells were treated with DMSO or BI1347 from 24 hr to 72hr.

first: Clare

last: Malone

first: Kenneth

last: Ross

first: Diyana

last: Granum

first: Kristianne

last: Oristian

first: Assil

last: Fahs

first: Corinne M

last: Linardic

first: Kimberly

last: Stegmaier