title: Sexually Dimorphic Sail Feathers in the Mandarin Duck: A Model for Lifelong Developmental Modulation [ChIP-seq]

status: Public on Oct 15 2025

city: Los Angeles

first: Ya-Chen

last: Liang

address: 2011 Zonal Ave., HMR 304A

department: Department of Pathology

institute: University of Southern California

summary: Developmental processes extend beyond embryogenesis to support lifelong tissue adaptations. Avian feather follicles, with their resident stem cells and capacity for cyclic regeneration, provide a dynamic model for postnatal tissue remodeling. Here, we propose the Mandarin duck (Aix galericulata) as an ideal model to study lifelong developmental modulation, focusing on the sexually dimorphic “sail feather”—a secondary flight feather in males that undergoes seasonal transformation into a strikingly asymmetric, ornamented phenotype during the breeding season. We identified asymmetric morphogen expression in regenerating male sail feathers and used transcriptome and H3K27ac ChIP-seq to uncover male and female signaling pathways and regulatory elements. Comparative epigenomic profiling reveals enriched estrogen receptor binding motifs in females. Hormone profiling shows seasonal variation, with a marked rise in female estrogen levels preceding the mating season. These results imply Mandarin duck sail feathers integrate local morphogenetic programs, epigenetic regulation, and systemic hormonal cues to orchestrate sexually dimorphic and seasonally dynamic feather morphogenesis. This work establishes a framework for further mechanistic study of the interplay between regeneration, regional identity, and hormonal plasticity in a vertebrate integumentary system.

overall_design: We profiled active regulatory elements in Mandarin duck (Aix galericulata) feather follicles using H3K27ac ChIP-seq during early regenerative growth in the breeding season (“in season”). Two body regions were compared: the sexually dimorphic sail feather (remex 12) and the adjacent secondary flight feather (remex 11). For males, we collected regenerating sail feathers that contain lateral blue and medial brown vanes (“blue+brown sail feather”; 2 biological replicates) and regenerating flight feathers with the same vane composition (“blue+brown flight feather”; 2 biological replicates). For females, we collected regenerating sail feathers characterized by dark/black pigmentation (“black sail feather”; 2 biological replicates) and regenerating flight feathers with blue and black pigmentation (“blue+black flight feather”; 2 biological replicates). In total, eight H3K27ac ChIP libraries (2 reps × 4 conditions) were generated; samples were processed in parallel with identical protocols to enable differential analyses by sex and by region (sail vs. flight).

first: Pin-Chi

last: Tang

first: Hsu-Chen

last: Cheng

first: Gee-Way

last: Lin

first: Yung-Chih

last: Lai

first: Ping

last: Wu

first: Tzu-Chiao

first: Chen Siang

last: Ng

first: Isheng

last: Tsai

first: Ang

first: Wen Hsiung

first: Chih-Feng

last: Chen

first: Cheng-Ming

last: Chuong

first: Randall

last: Widelitz


title: Single-cell spatiotemporal transcriptomic and chromatin accessibility profiling in developing postnatal human and macaque PFC

status: Public on Oct 19 2025

city: Beijing

first: Suijuan

last: Zhong

state: Haidian

address: No.19 Xinjiekouwai Street

country: China

institute: Beijing Normal University

type: Expression profiling by high throughput sequencing

summary: Unraveling the cellular and molecular characteristics of human prefrontal cortex (PFC) development is crucial for understanding human cognitive abilities and vulnerability to neurological and neuropsychiatric disorders. Here, we have created a comparative repository for gene expression, chromatin accessibility, and spatial transcriptomics of human and macaque postnatal PFC development at single-cell resolution. Integrative analyses outlined species-specific dynamic trajectories of different cell types, highlighting key windows and gene regulatory networks for processes such as synaptogenesis, synaptic pruning, and gliogenesis. We identified regulatory correlates of the prolonged development of human PFC relative to macaques. Glial progenitors showed higher proliferation capability in humans compared to macaques, which was associated with distinct gene expression profiles. Furthermore, we uncovered cell types and lineages most susceptible to neurodevelopmental and neuropsychiatric disorders, focusing on transcription factors (TFs) with human-specific expression features. In summary, our discoveries shed light on human-specific regulatory programs extending postnatal cortical maturation through coordinated neuronal and glial development, with implications for cognition and neurodevelopmental disorders.

overall_design: we sampled and performed snRNA-seq on macaque prefrontal samples  with biological replicates

first: Qian


title: Time course analysis of the effect of reseeding on laminin-411 vs fibronectin on gene expression in in vitro differentiated pancreatic progenitor cells.

city: København N

first: Adam Kappel

last: Rump

address: Blegdamsvej 3

department: DanStem

country: Denmark

institute: University of Copenhagen

summary: The extracellular matrix has recently emerged as a key regulator of endocrine fate choice in the pancreas via integrins and YAP signaling. To elucidate the intermediate mechanism between exposure to specific ECM components and induction of a proendocrine transcriptional program, we performed bulk RNA sequencing of in vitro differentiated HUES4-derived pancreatic progenitor cells. Cells were reseeded on either fibronectin (FN, non-endocrinogenic) or laminin-411 (LN411, highly endocrinogenic) and RNA was collected after 3, 6, or 24 hours. The dataset revealed a progressive induction of an endocrinogenic program, but with significant upregulation of endocrine genes only at the 24 hour time point. Interestingly, other YAP target genes were strongly and significantly downregulated already at 6 hours. Additionally, the dataset revealed novel potential intermediate regulators between LN411-exposure, YAP inhibition and endocrine specification.

overall_design: To investigate the intermediate effects between exposure to laminin-411 and endocrine fate choice, ESC-derived pancreatic progenitor cells were reseeded on either laminin-411 or fibronectin and harvested after 3, 6, or 24 hours. Triplicates were collected and sequenced for each condition.

first: Christine

last: Ebeid

first: Adam


title: High rate triggers increased atrial release of BMP10, a biomarker for atrial fibrillation and stroke, and BMP10 affects ventricular cardiomyocytes

status: Public on Oct 14 2025

city: Hamburg

first: Laura

last: Sommerfeld

address: Martinistr. 52

country: Germany

institute: UKE Hamburg

summary:
Background
Bone morphogenetic protein 10 (BMP10) is a ligand of the TGFβ superfamily secreted mainly by atrial cardiomyocytes. Elevated BMP10 blood concentrations predict atrial fibrillation (AF), AF recurrence after ablation and AF-related cardiovascular complications like stroke. The conditions increasing BMP10 secretion and downstream effects of BMP10 in cardiomyocytes are poorly understood. We assessed BMP10 secretion dynamics and BMP10 effects in a human 3D model of atrial and ventricular engineered heart tissue (EHT).
Methods
Cardiomyocytes differentiated from human induced pluripotent stem cells (atrial and ventricular) were cast into a fibrin-matrix to generate EHT. Atrial EHTs were optogenetically paced (3-5 Hz) or maintained at intrinsic beating rate for 24 h up to 15 days. Release of BMP10 and other cardiac biomarkers from EHT were quantified. BMP10 plasma concentrations were compared between 1370 patients in different atrial rhythm at blood draw. Additionally, ventricular EHTs were exposed to BMP10 for 10 days.
Results
Atrial but not ventricular EHT released BMP10 within 48 h of culture. High rate optogenetic pacing increased atrial EHT BMP10 release by ~3-fold after a latency of at least 24 h post pacing initiation. BMP10 plasma concentrations were elevated in patients with documented AF compared to sinus rhythm and even higher in patients with current AF. BMP10 induced upregulation of TGFβ pathway transcripts, increased expression of genes related to AF and heart failure, including PITX2 and NPPB, and increased relative contraction times in ventricular EHTs.
Conclusions
High atrial rates elevate BMP10 expression and release, and higher plasma concentrations of BMP10 are observed in patients with active AF. BMP10 exposure induces transcriptomic changes linked to AF and heart failure in ventricular EHT. These findings support BMP10 as a biomarker and potential mediator of AF-related remodeling and tachycardiomyopathy.

overall_design: Effects of BMP10 on ventricular EHT (vEHT) were assessed by longer-term (10 days) exposure of vEHT to recombinant human BMP10 (rhBMP10, 2926-BP-025, R&D Systems, Minneapolis, USA) dissolved in water containing 0.1% bovine serum albumin and 4 mM HCl (vehicle). RNA was harvested and subjected to RNAseq.

middle: C

first: Jessica

last: Schrapers

first: Justus

last: Stenzig

first: Larissa

last: Fabritz


title: 4-Vinylcyclohexene diepoxide induces ovarian toxicity and oocyte damage in mice: mechanisms involving m6A/IGF2BP3-mediated meiotic mRNA stability regulation

status: Public on Oct 18 2025

city: Guangzhou

first: yang

middle: li

last: Li

state: guangdong

address: No. 111, Dade Road, Guangzhou City, Guangdong Province

institute: The Second Clinical College, Guangzhou University of Chinese Medicine

summary: This study investigates the role of m6A RNA methylation and IGF2BP3 in VCD-induced ovarian toxicity in mice. VCD exposure caused follicular depletion, oxidative stress, DNA damage, and meiotic defects in oocytes. Mechanistically, VCD altered m6A modifiers (METTL3, FTO, ALKBH5) and destabilized key meiotic mRNAs (e.g., Cenpa, Bub1, Polq) via IGF2BP3 downregulation, leading to spindle defects and chromosomal missegregation. Our findings reveal an m6A/IGF2BP3 axis as a critical mediator of environmental ovotoxicity.

first: Yang

first: Yu

middle: L

last: Zhou

first: Jian

last: Liu

first: Hong

middle: Y

last: Yang

first: Guang

middle: N

last: Nie

first: Fang

middle: P


title: Multimodal Single-Cell Integration Across Time, Individuals, and Batches

status: Public on Oct 23 2025

city: Somerville

first: Mauricio

last: Cortes

state: MA

address: 101 South Street

country: USA

institute: Cellarity

type: Genome binding/occupancy profiling by high throughput sequencing

summary: In the past decade, the advent of single-cell genomics has enabled the measurement of DNA, RNA, and proteins in single cells. These technologies allow the study of biology at an unprecedented scale and resolution. Among the outcomes have been detailed maps of early human embryonic development, the discovery of new disease-associated cell types, and cell-targeted therapeutic interventions. Moreover, with recent advances in experimental techniques it is now possible to measure multiple genomic modalities in the same cell.  While multimodal single-cell data is increasingly available, data analysis methods are still scarce. Due to the small volume of a single cell, measurements are sparse and noisy. Differences in molecular sampling depths between cells (sequencing depth) and technical effects from handling cells in batches (batch effects) can often overwhelm biological differences. When analyzing multimodal data, one must account for different feature spaces, as well as shared and unique variation between modalities and between batches. Furthermore, current pipelines for single-cell data analysis treat cells as static snapshots, even when there is an underlying dynamical biological process. Accounting for temporal dynamics alongside state changes over time is an open challenge in single-cell data science.  Generally, genetic information flows from DNA to RNA to proteins. DNA must be accessible (ATAC data) to produce RNA (GEX data), and RNA in turn is used as a template to produce protein (ADT data). These processes are regulated by feedback: for example, a protein may bind DNA to prevent the production of more RNA. This genetic regulation is the foundation for dynamic cellular processes that allow organisms to develop and adapt to changing environments. In single-cell data science, dynamic processes have been modeled by so-called pseudotime algorithms that capture the progression of the biological process. Yet, generalizing these algorithms to account for both pseudotime and real time is still an open problem.

overall_design: The dataset for this competition comprises single-cell multiomics data collected from mobilized peripheral CD34+ hematopoietic stem and progenitor cells (HSPCs) isolated from four healthy human donors. More information about the cells can be found on the vendor website.  Measurements were taken at five time points over a ten-day period. During this time, cells were cultured with StemSpan SFEM media supplemented with CC100 and thrombopoietin (TPO) and incubated at 37ºC. Media was changed every 2-3 days. No additional media supplements were added to the cell culture conditions.  From each culture plate at each sampling time point, cells were collected for measurement with two single-cell assays. The first is the 10x Chromium Single Cell Multiome ATAC + Gene Expression technology (Multiome) and the second is the 10x Genomics Single Cell Gene Expression with Feature Barcoding technology technology using the TotalSeq™-B Human Universal Cocktail, V1.0 (CITEseq).

first: Allegra

last: Lord

first: Samuel

last: Miller

first: Sunil

last: Kuppasani

first: Aakash

last: Kabbin

first: Benjamin

last: DeMeo

first: Jonathan

last: Bloom

first: Peter

last: Holderrieth

first: Hiyab

last: Stefanos

first: Qing

first: Kaylie

last: Scheneider

first: Cameron

last: Reilly

first: Aquib

last: Hasnain

first: Ethan

last: French

first: Karen

last: Gaffney

first: Aishwarya

last: Chandler

first: Mrunali

last: Manjrekar

first: Sophie

last: Guo

first: Yash

last: Raj

first: Sakina

last: Saif

last: Issaco

first: Scott

last: Steelman

first: Daniel

last: Burkhardt

first: Malte

last: Lücken

first: Christopher

last: Lance


title: Sexually Dimorphic Sail Feathers in the Mandarin Duck: A Model for Lifelong Developmental Modulation [RNA-seq]

first: Ya-Chen

last: Liang

state: CA

overall_design: We performed bulk RNA-seq to profile gene expression in regenerating Mandarin duck (Aix galericulata) sail feather follicles during early growth in the breeding season (“in season”). Feathers were dissected to separate pulp (mesenchymal) and epithelium (epidermal) compartments from the lateral blue and medial brown vanes of male sail feathers. In total, eight libraries were generated: blue sail feather pulp (Chuong-152, Rep 1; Chuong-251, Rep 2), brown sail feather pulp (Chuong-151, Rep 1; Chuong-248, Rep 2), blue sail feather epithelium (Chuong-150, Rep 1; Chuong-250, Rep 2), and brown sail feather epithelium (Chuong-149, Rep 1; Chuong-247, Rep 2). Each sample represents an independent biological replicate, enabling differential expression analysis between tissue compartments (pulp vs. epithelium) and feather vane identities (blue vs. brown). This design allowed us to identify gene expression programs associated with asymmetry and pigmentation in sexually dimorphic sail feather morphogenesis.

first: Pin-Chi

last: Tang

first: Hsu-Chen

last: Cheng

first: Gee-Way

last: Lin

first: Yung-Chih

last: Lai

first: Ping

last: Wu

first: Tzu-Chiao

first: Chen Siang

last: Ng

first: Isheng

last: Tsai

first: Ang

last: Li

first: Wen Hsiung

first: Chih-Feng

last: Chen

first: Cheng-Ming

last: Chuong

first: Randall

last: Widelitz


title: Interferon Dependent Immune Memory during HSV-1 Neuronal Latency via Increased H3K9me3 and Restriction by ATRX

city: Charlottesville

first: Abigail

last: Whitford

state: Virginia

address: 1340 Jefferson Park Ave, Apt 305

department: Microbiology

institute: University of Virginia

summary: Herpes simplex virus-1 (HSV-1) establishes a latent infection in neurons, periodically reactivating to cause disease. Neuronal conditions, including immune signaling, during initial HSV-1 infection, impact later reactivation. Type I interferon (IFNα) exposure during initial infection results in promyelocytic leukemia nuclear-body (PML-NB) formation and subsequent restriction of reactivation, via mechanisms that were unknown. Here we find that PML-NB formation results in the recruitment of histone chaperones to the viral genome and increased enrichment of the repressive heterochromatin mark, histone H3 lysine 9 tri-methylation (H3K9me3), and its reader, ATRX (alpha-thalassemia/mental retardation, X-linked). ATRX is highly abundant in neurons and prevents reactivation from H3K9me3-bound latent genomes by remaining associated with viral chromatin. Therefore, we demonstrate how immune signaling during initial infection results in an epigenetic memory on HSV-1 genomes and identify ATRX as a neuronal restriction factor against HSV-1 reactivation, elucidating a new potential target for inhibiting HSV-1 reactivation and subsequent human disease.

overall_design: CUT&Tag of H3K9me3 in primary murine neurons latently infected with HSV-1. Neurons were either treated or untreated with Interferon alpha at the time of infection with HSV-1.

first: Gaelle

last: Auguste

first: Alison

last: Francois

first: Chris

last: Boutell

first: Clint

last: Miller

first: Sarah

last: Dremel

first: Anna

middle: R

last: Cliffe


title: Single-cell RNA Sequencing Analysis Reveals Cell Landscape and Gene Signatures Associated with Granulomatous Lobular Mastitis

first: Junyue

last: Wang

address: No. 23, Art Museum Back Street, Dongcheng District.

department: Department of Breast

institute: Beijing Hospital of Traditional Chinese Medicine Affiliated to Capital Medical University

summary: We have employed a single cell sequencing approach using 10x Genomics scRNAseq to study granulomatous lobular mastitis (GLM), a chronic inflammatory breast disease characterized by granuloma formation and recurrent abscesses. GLM is considered an immune-mediated disorder, yet its underlying pathogenesis remains poorly defined. This study is the first to perform single-cell transcriptomic profiling of GLM tissue and provides new insights into the cellular landscape and immune dysregulation associated with GLM.

overall_design: Fresh breast tissue samples from 3 patients with granulomatous lobular mastitis (GLM) and 3 healthy controls were surgically obtained.  Single-cell suspensions were prepared and subjected to single-cell RNA sequencing (scRNA-seq) using the 10x Genomics Chromium Single Cell 3′ v3 platform.

first: Yifei

last: Zeng

first: Mengjie

first: Dongxiao

last: Zhang

first: Xulong


title: single cell chromatin accessiblity profiling in formlin fixed paraffin embedded samples

city: Uppsala

first: Xingqi

address: Husargata

department: Immunology, Genetics and Pathology

country: Sweden

institute: uppsala university

summary: We evaluated the performance of ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) on formalin-fixed paraffin-embedded (FFPE) spleen samples from C57BL/6J mice. Nuclei were isolated from FFPE mouse spleen tissue, and ATAC-seq was performed at both the bulk and single-cell levels, with and without reverse crosslinking. The resulting datasets were compared to ATAC-seq and scATAC-seq profiles obtained from fresh spleen samples. Our analysis revealed a markedly reduced library complexity in FFPE-derived samples compared to fresh tissue, across both bulk and single-cell experiments. These findings highlight the technical limitations of applying standard ATAC-seq protocols to FFPE samples. Based on our results, we conclude that conventional ATAC-seq approaches are not well-suited for chromatin accessibility profiling in FFPE-preserved tissues.

overall_design: Nuclei were isolated from snap-frozen FFPE spleen tissues of C57BL/6J mice following the Omni-ATAC-seq protocol. A total of 20,000 to 100,000 DAPI-positive nuclei were counted and collected. The nuclei were pelleted and resuspended in 1 mL of ATAC-Resuspension Buffer (ATAC-RSB) supplemented with 0.1% Tween-20. Transposition was performed using Tn5 transposase. The tagmented DNA was purified under both reverse crosslinking and non-crosslinking conditions, and subsequently PCR-amplified for 8–15 cycles using indexed primers to introduce sample-specific barcodes. For single-cell ATAC-seq, a combinatorial indexing (split-pool) strategy was employed to profile chromatin accessibility in individual nuclei isolated from FFPE mouse spleen samples. Nuclei were first isolated using a modified Omni-ATAC protocol optimized for FFPE tissue. After DAPI staining and counting, the nuclei were subjected to a three-level barcoding scheme. In the first round, transposition was performed using indexed Tn5 transposase. The nuclei were then split across multiple wells and underwent successive rounds of PCR with unique barcoded primers at each step. This split-pool barcoding enabled the unique indexing of individual nuclei. Libraries were pooled, purified under both reverse crosslinking and non-crosslinking conditions, and sequenced to generate single-nucleus ATAC-seq data.

first: Ram

last: Yadav

first: Pengwei

last: Xing


title: Identification of a novel minor-groove DNA binder that represses mitochondrial genes expression and induces apoptosis in highly aggressive leiomyosarcoma cells

city: Udine

first: Raffaella

last: Picco

address: P.le Kolbe 4

department: Department of Medicine

country: Italy

institute: University of Udine

summary: The induction of cellular stress is a common strategy in cancer therapy. Leiomyosarcomas (LMS) are aggressive tumors for which there are few effective therapeutic options. Through a combination of in silico and in vitro screens, the compound NSC-260594/XMH95 was identified as a promising molecule that selectively induces apoptosis in aggressive LMS cells. This apoptotic response is associated with the upregulation of the BH3-only genes PMAP1/NOXA, BIK, HRK and BBC3/PUMA. XMH95 binds DNA and possibly the minor groove, similar to Hoechst 33258. Unlike Hoechst, XMH95 is not fluorescent but can be photoactivated by UV irradiation when bound to DNA. Also, unlike Hoechst, XMH95 suppresses mitochondrial gene expression and is a more effective inducer of apoptosis. Apart from suppressing mitochondrial genes, XMH95 has many effects on gene expression that are common to Hoechst. Using an inhibitor of mitochondrial RNA polymerase (POLRMT), we show that XMH95 triggers apoptosis by perturbing both nuclear and mitochondrial transcription. Our results propose a new compound and a novel stress that can trigger apoptosis in aggressive cancer cells by upregulating multiple BH3-only genes.

overall_design: RNA-seq profiling of HUtSMC and SK-UT-1 cells treated with by two double strand DNA binders: Hoechst 33 and NSC26954/XMH95.

first: Eleonora

last: Malavasi

first: Raffaellla

first: Martina

last: Minisini

first: Alessio

last: Bertozzo

first: Claudio

last: Brancolini


title: Acute Arrhythmias in a Long-chain 3-Hydroxyacyl-CoA Dehydrogenase Deficiency (LCHADD) Mouse Model

city: Portland

first: Gabriela

last: Elizondo

state: OR

address: 3222 SW Research Drive

institute: OHSU

summary: Patients with LCHADD, a mitochondrial fatty acid oxidation (FAO) disorder, frequently present with cardiomyopathy and can suffer life-threatening arrhythmias and heart failure. While these remain the leading causes of death, the pathophysiology remains unknown. We used an LCHADD mouse model to examine the mechanisms of impaired cardiac function. Methods: We previously determined that LCHADD mice (Hadha c.1528G>C homozygotes) recapitulate human disease and develop cardiomyopathy. We performed electrophysiological tests on LCHADD and WT mice, followed by cardiac tissue and molecular expression analysis. Results: LCHADD mice showed significantly increased frequency of atrial premature beats, premature ventricular contractions, atrial flutter, and atrial and ventricular fibrillation after b-agonist stimulation compared to WT mice. Long QRS and long QT intervals were also observed. LCHADD heart sections demonstrated increased cardiomyocyte cross-sectional area, increased lipid and collagen deposition, and decreased glycogen deposits. There was global sympathetic denervation in LCHADD hearts compared to WT. Differentially expressed gene analysis showed increased expression of glycolytic and glutathione synthesis enzymes, decreased gene expression of TCA cycle enzymes, Ca++ signaling, and cardiac muscle contraction proteins. Conclusions: LCHADD cardiomyopathy has a hypertrophic phenotype with diffuse fibrosis, accumulation of lipids, and lower glycogen storage in the absence of obesity. LCHADD cardiomyocyte metabolism suggests a shift from FAO toward glycolysis with chronic oxidative stress. Energy deficiency and lipotoxicity likely influence Ca++ signaling and cardiac contraction. Long QRS and QT intervals with global sympathetic denervation may predispose the heart to repolarization abnormalities susceptible to arrhythmias and increased risk of sudden cardiac arrest and death.

overall_design: RNAseq profiling of mice heart ventricles with LCHADD vs WT in males and females.

first: Arianna

last: Scalco

first: Ayah

last: Asal

first: Hak

last: Chung

first: Garen

last: Gaston

first: Beth

middle: A

last: Habecker

first: Melanie

middle: B

last: Gillingham


title: RNA-sequencing transcriptomic analysis of scrapie-exposed ovine mesenchymal stem cells

status: Public on Oct 16 2025

city: Zaragoza

first: Inmaculada

last: Martín Burriel

state: Zaragoza

address: Miguel Servet, 177

department: Anatomy, Embriology and Animal Genetics

country: Spain

institute: University of Zaragoza

summary: In neurodegenerative diseases, including prion diseases, cellular models arise as useful tools to study the pathogenic mechanisms occurring in these diseases and to assess the efficacy of potential therapeutic compounds. In the present study, a RNA-sequencing analysis of bone marrow-derived ovine mesenchymal stem cells (oBM-MSCs) exposed to scrapie brain homogenate was performed to try to unravel genes and pathways potentially involved in prion diseases and MSC response mechanisms to prions. The oBM-MSCs were cultured in three different conditions (inoculated with brain homogenate of scrapie-infected sheep, with brain homogenate of healthy sheep and in standard growth conditions without inoculum) that were analysed at two exposure times: 2 and 4 days post-inoculation (dpi). Differentially expressed genes (DEGs) in scrapie-treated oBM-MSCs were found in the two exposure times finding the higher number at 2 dpi, which coincided with the inoculum removal time. Pathways enriched in DEGs were related to biological functions involved in prion toxicity and MSC response to the inflammatory environment of scrapie brain homogenate. Moreover, RNA-sequencing analysis was validated amplifying by RT-qPCR a set of 11 DEGs with functions related with prion propagation and its associated toxicity. Seven of these genes displayed significant expression changes in scrapie-treated cells. These results contribute to the knowledge of the molecular mechanisms behind the early toxicity observed in these cells after prion exposure and to elucidate the response of MSCs to neuroinflammation.

overall_design: To discover genes and pathways potentially involved with prion disease mechanisms and to evaluate the potential of ovine mesenchymal stem cells as in vitro models of prion toxicity, we performed a RNA-sequencing analysis of oBM-MSCs. Two infection times (2 days and 4 days post-inoculation) and three conditions were studied (cells inoculated with scrapie-infected brain homogenate, cells inoculated with negative brain inoculum and non-inoculated controls) with 3 technical replicates per condition and time.

first: Adelaida

last: Hernaiz

first: Belén

last: Marín

first: Francisco

middle: J

last: Vázquez

first: Juan

last: Badiola

first: Pilar

last: Zaragoza

first: Rosa

last: Bolea

last: Martín-Burriel


title: A cis-regulatory element of the PHYTOCHROME A gene confers the submergence escape capacity for amphibious plants

city: Shanghai

first: Chuanwei

last: Yang

address: 2005 Songhu Road, Yangpu District

department: school of life sciences

institute: Fudan university

summary: Submergence is a type of abiotic stress that can severely impact the survival of plants and the yield of crops. Plants not only sense the hypoxic conditions during submergence but also exposed to a range of low-light intensities, depending on the submergence depth and turbidity. However, how light availability affects submergence tolerance remains largely unknown. To clarify the functions of light receptor AtPHYA and transcription factor AtEIN3/EIL1 in the transcriptional response to submergence, we conducted RNA-seq analysis on the wild type Col-0, the atphyA-211 mutant, and the atein3eil1 double mutant. Following a 6-hour submergence stress treatment, we identified 7325 differentially expressed genes (DEGs) in the Col-0 seedlings. The expression of 3748 submergence-induced genes was notably reduced in the atein3eil1 double mutant, while it was significantly enhanced in the atphyA-211 mutant. This suggests that AtPHYA exerts a negative regulatory effect on the expression of genes induced by submergence. The absence of AtPHYA leads to an upregulation of these submergence-induced genes, confirming that AtPHYA negatively modulates their expression.

overall_design: Terrestrial-grown plants were either maintained under terrestrial conditions or subjected to submergence for 6 h and leaves tissue was collected. Three replicates were prepared for each condition and each line.


title: Genome-wide identification of AphEIN3-targeted genes in A. philoxeroides

summary: Ethylene play a key role in submergence stress. The invasive plant Alternanthera philoxeroides has strong resistance to submergence stress, but the related mechanisms are not clear. We found that the ethylene signaling component AphEIN3 may be involved. To investigate the genome-wide AphEIN3 binding sites, we performed a DNA affinity purification sequencing (DAP-seq) as described by (Bartlett et al., 2017). In two replicates, approximately 22,604 peaks (for 6,831 genes) and 29,912 peaks (for 8,547 genes) were identified as high-confidence AphEIN3 binding peaks. Combined with RNA-seq analysis, we found that submergence can induce AphEIN3 binds to a cluster of elongation genes to regulate theses gene expression.

overall_design:
A DNA affinity purification sequencing (DAP-seq) for transcription factor AphEIN3 in Alternanthera philoxeroides.
To capture the HaloTag fusion proteins, we used magnetic beads containing Halo antibodies (Magne HaloTag Beads, Promega, G728A).

first: Ji


title: Single-nuclei RNA-seq and ATAC-seq for Human Retina from Diverse Ancestry Backgrounds

city: Palo Alto

first: Lattice

last: Data Coordination

address: 3165 Porter Drive

department: Genetics

institute: Stanford University

summary: The Human Retina Cell Atlas (HRCA) integrates data from a wide range of ancestry backgrounds, making it a highly valuable resource for understanding retinal cell types and their molecular profiles. By collecting data from 60 donors with diverse ancestry backgrounds, the atlas enabled the investigation of how ancestry affects gene expression patterns and chromatin accessibility across retinal cell types. The project's findings on gene expression and chromatin openness provide critical insights into how genetic heritage influences retinal function and susceptibility to certain eye conditions. The ancestry-related data can also help identify population-specific variations in retinal biology, potentially paving the way for more personalized diagnosis and treatment of eye disorders across different ethnic groups.

overall_design: snRNA-seq and snATAC-seq of peripheral region of retina tissue, fovea centralis tissue, macula lutea tissue from 59 human donors

first: Rui

last: Chen

first: Jin

last: Li

first: Jun

last: Wang

first: Ignacio

last: Ibarra

first: Xuesen

last: Cheng

first: Malte

middle: D

last: Luecken

first: Jiaxiong

last: Lu

first: Aboozar

last: Monavarfeshani

first: Wenjun

last: Yan

first: Yiqiao

last: Zheng

first: Zhen

last: Zuo

first: Samantha Lynn

last: Zayas Colborn

first: Berenice Sarahi

last: Cortez

first: Leah

last: Owen

first: Nicholas

middle: M

last: Tran

first: Karthik

last: Shekhar

first: Joshua

last: Sanes

first: J

middle: T

last: Stout

first: Shiming

first: Yumei

first: Margaret

last: DeAngelis

first: Fabian

last: Theis


title: Unlocking single cell chromatin accessibility in formalin-fixed paraffin-embedded tissues by scFFPE-ATAC

first: Xingqi

last: Chen

summary: Formalin-fixed paraffin-embedded (FFPE) samples are the gold standard for clinical tissue preservation. However, single-cell chromatin accessibility profiling technology, a powerful tool to understand epigenetic regulation in human disease, is not available for FFPE samples due to extensive DNA damage. To solve this technical challenge, we introduce scFFPE-ATAC by integrating uniquely designed DNA oligos on Tn5 transposase, split-and-pool ligation DNA barcoding, T7 promoter-mediated DNA damage rescue, and in vitro transcription—the first high-throughput single-cell chromatin accessibility assay for FFPE samples. scFFPE-ATAC enables the simultaneous profiling of up to 64 FFPE samples or spatial regions, with 884,736 cell barcodes in a single run. We successfully applied scFFPE-ATAC to clinical FFPE human lymph nodes stored for 8–15 years and identified distinct epigenetic regulators between tumor centers and invasive edge epithelial cells in human lung cancer. Additionally, we analyzed paired primary and relapsed follicular lymphoma (FL), as well as FL transformed into diffuse large B-cell lymphoma, from clinical samples archived for 2–7 years, revealing key epigenetic drivers of tumor progression. Overall, scFFPE-ATAC enables high-throughput, high-sensitivity chromatin accessibility profiling in long-term archived clinical specimens, paving the way for retrospective epigenetic studies and spatial epigenetic analysis. This technology provides a powerful tool for understanding tumor relapse and metastasis, with broad applications in basic research and personalized medicine.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

first: xingqi

last: chen

first: Ram

last: Yadav

first: Pengwei

last: Xing


title: con7 regulates the development of Penicillium oxalicum fungi and the expression of chitinase and cellulolytic genes

status: Public on Oct 13 2025

city: Qingdao 266237

first: Kexuan

last: Ma

state: China

address: No. 72 Binhai Road

department: State Key Laboratory of Microbial Technology

institute: Shandong University

summary: The goals of this study are to compare different gene expressions for Penicillium oxalicum wild type strain (WT) and Con7 destruction strain (con7-A) under conditions of 2% glucose，2% glycerol or 1% bran + 1% microcrystalline cellulose as carbon source. The results of correlation analysis between each sample showed that the gene expression level of con7-A  was significantly different from that of the WT strain. The destruction of con7 significantly affect the expression levels of sporulation process genes and the expression of chitinase and cellulase-encoding genes.

overall_design: Examination of differential gene expressions by digital gene expression tag profiling in Penicillium oxalicum wild type strain, con7 destruction mutant strains in 24h in modifeid Mendal’s medium with 2% glucose，2% glycerol or 1% bran + 1% microcrystalline cellulose as carbon sources. Three replicates were included for each samples.

first: Yuqi

last: Qin


title: Role of Wnt signalling in the self-renewal and differentiation capacities of primary hepatoblast organoids.

city: Cambridge

first: Irina

last: Mohorianu

address: Puddicombe Way

department: Wellcome-MRC Cambridge Stem Cell Institute

country: United Kingdom

institute: University of Cambridge

summary: Primary hepatoblast organoids (HBOs) are grown and passaged in medium that contains both Wnt3a and R-spondin conditioned media (HBO complete medium). It is hypothesised that these molecules that are part of the WNT signalling pathway may be contributing to the HBOs self-renewal properties.

overall_design: To investigate the function of Wnt3a and R-spondin on the self-renewal as well as differentiation capacity of the HBOs the removal of the signalling molecules from the HBO complete medium was tested, separately as well as combined.

first: Ekaterini

last: Zacharis

first: Arash

last: Shahsavari

first: Ludovic

last: Vallier


title: A Global View of Cell Type Homology and Transcriptomic Divergence in the Mammalian Brain

city: San Francisco

first: Alex

last: Pollen

address: 35 Medical Center Way

department: Neurology

institute: UCSF

summary: This study is a high-level comparison of the embryonic brains of Homo sapiens, Macaca mulatta, and Mus musculus using scRNA-seq. This submission includes the novel Macaca mulatta scRNA-seq generated for this study between PCD40 and 100. The supplementary h5ad file contains the meta-atlas including processed data from all 3 species, with annotations from the publication.

overall_design: 10X Genomics Chromium single cell 3’ capture RNA-sequencing of macaque embryos between embryonic day 40 and 100

first: Matthew

last: Schmitz


title: Fosl1 is a transcriptional effector of BRAFV600E-driven intestinal tumorigenesis

city: Geelong

first: Laurence

middle: James

last: Croft

state: Victoria

address: 75 Pigdons Road

department: School of Medicine

country: Australia

institute: Deakin University

summary: The serrated neoplasia pathway in an alternate route to colorectal cancer (CRC) development where BRAFV600E is the most common initiating genetic alteration. BRAFV600E-driven tumorigenesisrequires gene expression changes mediated by activation of the ERK MAPK signalling pathway. However, the key effectors of this process are elusive. Here, we identify the ERK-regulated transcription factor Fosl1 one such effector. We show that Fosl1 is dispensable for the initiation ofBRAFV600E-driven serrated neoplasia in mice but promotes progression of the disease by regulatingthe expression of genes involved in inflammation, immunity, cell cycle control, fetal-likeprogramming, and gastric metaplasia. Notably, transgenic Fosl1 expression alone was sufficient to induce tumours with a BRAFV600E-like serrated morphology and transcriptional profile. Thesefindings reveal a mechanism through which oncogenic BRAF-driven ERK signalling reprograms transcription to drive serrated neoplasia.

overall_design: RNA-seq using Illumina paired-ends of polyA transcriptomes comparing mouse normal intestinal epithelium to BRAF mutant and FLAG-Fosl1 transgene tumours and to BRAF mutant with or without Fosl1

first: Zakia

last: Alam

first: Rebecca

last: Nightingale

first: Analia

last: Lesmana

first: Cheng

last: Liu

first: Laura

last: Jenkins

first: Mark

middle: F

last: Richardson

first: Larry

first: Ian

last: Luk

first: Camilla

last: Reehorst

first: Fiona

last: Chionh

first: Natalia

last: Vukelic

first: Faiza

last: Basheer

first: Eugene

last: Tulchinsky

first: Joshua

last: Badshah

first: Troy

last: Dumenil

first: Latifa

last: Bakiri

first: Erwin

last: Wagner

first: Niall

last: Tebutt

first: Vicki

last: Whitehall

first: John

last: Mariadason

first: Amardeep

middle: S

last: Dhillon


title: Unlocking single cell chromatin accessibility in formalin-fixed paraffin-embedded tissues by scFFPE-ATAC [mouse]

first: Xingqi

last: Chen

overall_design: Tagmentation and combinatorial indexing via ligation Before tagmentation, 50,000 purified FFPE single-cell nuclei were centrifuged at 2,000 g for 5 minutes at 4°C and resuspended in 0.1% lysis buffer (10 mM Tris-Cl, pH 7.4, 10 mM NaCl, 3 mM MgCl₂, 0.1% IGEPAL CA-630). The nuclei were then centrifuged again at 2,000 g for 5–10 minutes at 4°C. The nuclei pellet was resuspended in 95 μl of 1× tagmentation buffer (10 mM Tris-HCl, pH 7.5, 5 mM MgCl₂, 10% dimethylformamide, and dH₂O), and 5 μl of barcoded FFPE-Tn5 transposase (2 mM) was added per sample. The reaction mix was gently mixed and incubated at 37°C for 30 minutes at 400 rpm. The reaction was stopped by directly adding EDTA to a final concentration of 30 mM to each sample. All samples were then pooled and centrifuged to obtain a nuclei pellet. Next, three rounds of ligation were performed using the split-and-pool technique in a 96-well plate, with each well containing a ramped specific linker and ligation barcode. Detailed DNA sequences are provided in Supplementary Table 1. In brief, the ligation process was performed as follows: the pooled nuclei were resuspended in 1 mL of 1× NEBuffer 3.1 and mixed with the ligation mix (100 μL of 10× NEBuffer 3.1, 22 μL of 50 mg/mL BSA, 500 μL of 10× T4 DNA ligase buffer, 2,278 μL of ultrapure water, and 100 μL of T4 DNA ligase). A total of 40 μL of this mix was transferred per well, containing 10 μL of the ramped Ligation1 mixture, and incubated at 37°C for 30 minutes at 400 rpm. Then, 10 μL of Blocker-Ligation1 solution (2.64 μL of 100 μM Blocker-Ligation1, 2.50 μL of 10× T4 ligation buffer, and 4.86 μL of ultrapure water) was added per well, and the reactions were incubated at 37°C for 20 minutes at 400 rpm. The samples were then pooled into a 15 mL tube pre-coated with 0.5% BSA, followed by centrifugation at 1,500 g for 10 minutes at 4°C. The second and third ligation reactions were performed identically to the first. After the second and third ligations, blocking reactions were carried out using: 10 μL of Blocker-Ligation2 solution per well (2.64 μL of 100 μM Blocker-Ligation2, 2.50 μL of 10× T4 ligation buffer, and 4.86 μL of ultrapure water); 7.5 μL of Terminator_Ligation3 solution per well (2.64 μL of 100 μM Terminator_Ligation3, 2.50 μL of 0.5 M EDTA, and 2.36 μL of ultrapure water) for reaction termination. After gently mixing, the samples were pooled again into a 15 mL tube pre-coated with 0.5% BSA, followed by centrifugation at 1,500 g for 10 minutes at 4°C. After the third ligation, each nucleus acquired a unique combination of barcodes. Finally, the pellet was resuspended in PBS, nuclei were counted, and the sample was split into tubes containing 30,000–80,000 nuclei for reverse crosslinking.  Reverse-crosslinking, gap filling and in vitro transcription After the third ligation, reverse cross-linking buffer (50 mM Tris-HCl, pH 8, 250 mM NaCl, 1 mM EDTA, and 1% SDS) and 0.22 mg/mL proteinase K were added to each tube, following previous publications 42, 43. The reaction mixture was incubated in a thermomixer at 1,200 rpm overnight at 65°C. The next day, a second proteinase K digestion was performed at 37°C for 2 hours at 850 rpm to ensure complete protein digestion. DNA was then purified using the Zymo ChIP DNA Clean & Concentrator Kit, following the manufacturer’s instructions. For gap filling, an equal volume of NEBNext High-Fidelity 2X PCR Master Mix was added to the eluted DNA, and the reaction mixture was incubated at 72°C for 8 minutes in a thermal cycler. The sample was then purified using the Qiagen MinElute PCR Purification Kit, following the manufacturer’s instructions. Further DNA purification was carried out using the 1X SPRI beads method to remove fragments shorter than 150 bp. Finally, the DNA was eluted in nuclease-free water. For in vitro transcription (IVT), a T7 RNA synthesis kit (New England Biolabs) was used. The following reagents were mixed: • 12.4 μL of template DNA • 2.5 μL of 10X T7 buffer • 1 μL of DTT • 2 μL each of ATP, CTP, UTP, and GTP • 1 μL of T7 mix • μL of RNase inhibitor (Thermo Fisher Scientific)  The IVT mixture was incubated at 37°C overnight (16 hours), followed by DNase treatment and RNA purification using the ZYMO RNA Purification Kit (RNA Clean & Concentrator-5), according to the manufacturer’s instructions. Finally, RNA was eluted in 20 μL of nuclease-free water. The RNA concentration was measured using NanoDrop, and the sample was either immediately used for DNA library preparation or stored at −80°C for future use.  Single cell FFPE-ATAC DNA library preparation Single-stranded cDNAs are prepared from 0.5–1 μg of purified IVT transcripts using the FirstStrand_cDNA oligo (DNA oligo sequences are provided in Supplementary Table 1). The reaction mixture (11.25 μL), containing 500ng-1 μg of RNA, 1 μL of 100 μM random octamer primer stock, and 0.25 μL of RNase Inhibitor (20 U/μL), is heated at 70°C for 3 minutes, then immediately cooled on ice. Next, the master mix is added, which consists of: • 4 μL of 5× First-Strand Buffer • 2 μL of dNTP Mix • 2 μL of 100 mM DTT • 0.25 μL of RNase Inhibitor (20 U/μL) • 0.5 μL SMART MMLV RT The reaction is gently mixed and incubated at 42°C for 60 minutes and then at 70°C for 15 minutes. Next, 2.2 μL of 10× RNase H buffer and 0.2 μL of RNase H (5 U/μL) are added to each reaction and incubated at 37°C for 20 minutes. The RNAClean XP beads (1.8X) are used to purify the cDNA reaction mixture, and the cDNA is eluted in Qiagen Elution Buffer. A sequencing library mix is prepared using purified cDNA, NEBNext high-fidelity 2× PCR master mix, and a unique forward (i5) and reverse (i7) primer combination (DNA oligo sequences are provided in Supplementary Table 1). PCR amplification is run with the following cycling program: • 98°C for 30 seconds • 12 cycles of: • 98°C for 20 seconds • 63°C for 20 seconds • 72°C for 1 minute The sample is purified using the Qiagen MinElute PCR Purification Kit and run on a 6% PAGE gel. The gel region corresponding to 250–800 bp is cut, and the gel is made into fine pieces, which are incubated overnight at 55°C in crush-soak buffer (500 mM NaCl, 1 mM EDTA, 0.5% SDS) at 1,200 rpm. The DNA is purified from the gel using Costar spin-X centrifuge tubes and the Zymo ChIP DNA Clean & Concentrator Kit, following the manufacturer's instructions. A high-sensitivity DNA bioanalyzer chip is used to check the DNA size distribution and quantify the DNA concentration of the DNA library. Finally, deep sequencing is performed with NovaSeq  6000 on the mouse and human scFFPE-ATAC samples for single-cell analysis.

first: xingqi

last: chen

first: Ram

last: Yadav

first: Pengwei

last: Xing


title: Sensitive and unbiased genome-wide profiling of base-editor-induced off-target activity with CHANGE-seq-BE

status: Public on Oct 20 2025

city: Memphis

first: Shengdar

last: Tsai

state: TN

address: 262 Danny Thomas Pl

department: Department of Hematology

institute: St Jude Children's Research Hospital

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

sample_organism:
Homo sapiens
synthetic construct

platform_organism:
Homo sapiens
synthetic construct

overall_design: Refer to individual Series


title: 3S-DB: SBP2-Bound RNA Sequencing for the Discovery of Novel Functional SECIS Elements

status: Public on Oct 12 2025

first: Chenfang

last: Si

address: Haike Road 100

institute: Chinese Academy of Sciences

summary: Selenoproteins are defined as proteins that contain selenocysteine (Sec, U), playing crucial roles in living organisms. The incorporation of Sec involves a unique mechanism that primarily includes the UGA codon, the SECIS element, and its binding protein SBP2. Currently, the 25 known human selenoproteins were largely discovered through predictions of stem-looped SECIS structures. However, the exploration of yet-to-be-defined selenoproteins and SECIS elements has been hindered by the accuracy and depth of these predictions. In this study, we focus on SBP2, the core SECIS-binding protein, to analyze all its binding RNAs using RNA immunoprecipitation sequencing (RIP-Seq) technology. Based on this data, we have constructed a robust selenoprotein repository known as the 3S-DB (SBP2-bound RNA sequencing-supported selenoprotein database, SSS-DB or 3S-DB). This 3S-DB contains 1,333 RNA sequences, including all those known selenoprotein RNAs, that can bind to SBP2 with potential SECIS function. Importantly, we validate that the 3' UTRs of PDF and ATP5MJ exhibit SECIS activity. In summary, the established 3S-DB highlights the mRNA that SBP2 can directly bind to, potentially recruiting the entire Sec insertion machinery to generate new selenoproteins. Our results provide a crucial resource for uncovering novel selenoproteins and previously unidentified SECIS elements.

overall_design: RNA immunoprecipitation sequencing (RIP-Seq) was performed using Flag antibody in HEK 293T cell lysates overexpressing the Flag vector, Flag-SBP2, and Flag-SBP2 with concomitant sodium selenite treatment. The experimental design included three groups, each with three biological replicates, and each group comprised input and IP samples.

first: Bing

last: Shan

first: Yaoyang

last: Zhang


title: Blocking Nuclear Receptor Nr4a3 Unlocks the Senescence Barrier to Promote Direct Cardiac Reprogramming

status: Public on Oct 11 2025

city: wuhan

first: yu

middle: zhang

last: yi

state: hubei

address: donghu street

department: wuhan

institute: wuhan university


summary: Direct cardiac reprogramming of fibroblast to cardiomyocytes represents a potential means of restoring cardiac function following injury.   However, aged and adult fibroblast are less efficient for reprogramming compared with neonatal fibroblast. In this study, through the joint analysis of RNAseq and ATACseq, we found that compared with Neo-iCM, cardiac related features were down-regulated with aging, while fibrosis and SASP related genes were significantly up-regulated with aging. Single-cell transcriptomics reveals a bifurcated trajectory of aged iCM reprogramming. Then, we screened 51 transcriptomic and epigenomic regulators of the barriers to aged-iCM reprogramming and found that Nuclear receptor subfamily 4 group A member 3 (Nr4a3), an pro-inflammatory transcription factor, induced cellular senescence to inhibit direct reprogramming during aging. Mechanistically, knockdown of Nr4a3 enhanced direct cardiac reprogramming by promoting cardiac gene programs and inhibiting fibrosis pathway and secretes SASP. In addition, knockdown of Nr4a3 promoted human reprogramming in primary ventricular human cardiac fibroblasts (HCFs) and improved heart function after MI.

overall_design: To comprehensively decipher why iCM reprogramming is dramatically hindered in adult and aged CFs, we investigated the global transcriptomic changes of iCMs from neonatal to advanced age.

first: Li

last: Wang

first: Mengxin

last: Liu

first: Zhangyi

last: Yu


city: Wuhan

address: 115 Donghu Road

overall_design: To determine the molecular basis by which overexpression of Nr4a3 inhibits iCM reprogramming, we conducted RNA-seq using OENr4a3-CFs and OECtrl-CFs collected at reprogramming day 7.


overall_design: To comprehensively decipher why iCM reprogramming is dramatically hindered in adult and aged CFs, we investigated the global transcriptomic changes of CFs from neonatal to advanced age.


title: Blocking Nuclear Receptor Nr4a3 Unlocks the Senescence Barrier to Promote Direct Cardiac Reprogramming [neonatal scRNA-seq]

summary: Direct cardiac reprogramming of fibroblast to cardiomyocytes represents a potential means of restoring cardiac function following injury. However, aged and adult fibroblast are less efficient for reprogramming compared with neonatal fibroblast. In this study, through the joint analysis of RNAseq and ATACseq, we found that compared with Neo-iCM, cardiac related features were down-regulated with aging, while fibrosis and SASP related genes were significantly up-regulated with aging. Single-cell transcriptomics reveals a bifurcated trajectory of aged iCM reprogramming. Then, we screened 51 transcriptomic and epigenomic regulators of the barriers to aged-iCM reprogramming and found that Nuclear receptor subfamily 4 group A member 3 (Nr4a3), an pro-inflammatory transcription factor, induced cellular senescence to inhibit direct reprogramming during aging. Mechanistically, knockdown of Nr4a3 enhanced direct cardiac reprogramming by promoting cardiac gene programs and inhibiting fibrosis pathway and secretes SASP. In addition, knockdown of Nr4a3 promoted human reprogramming in primary ventricular human cardiac fibroblasts (HCFs) and improved heart function after MI.

overall_design: Single cell RNA-seq profiles of MGT-transduced neonatal FBs cultured at reprogramming day 14 by 10x Genomics Chromium System.


overall_design:
To comprehensively decipher why iCM reprogramming is dramatically hindered in adult and aged CFs, we investigated the global epigenetic changes of iCMs from neonatal to advanced age.
To determine the molecular basis by which knockdown Nr4a3 enhances iCM reprogramming, we conducted ATAC-seq using shNr4a3-iCMs and shNT-iCMs collected at reprogramming day 7.


overall_design: To determine the molecular basis by which knockdown Nr4a3 enhances iCM reprogramming, we conducted CUT&Tag profiling of two histone modifications including histone H3 acetylation on lysine 27 (H3K27ac, a mark for active enhancers and promoters) and histone H3 trimethylation on lysine 27 (H3K27me3, a repressive epigenetic mark) using shNr4a3-iCMs and shNT-iCMs collected at reprogramming day 7


title: Prospective isolation of mouse and human hematopoietic stem cells using PLXDC2

city: Minato

first: Yosuke

last: Tanaka

state: Tokyo

address: Shirokanedai

country: Japan

institute: IMS, The University of Tokyo

summary: Numerous strategies exist to isolate hematopoietic stem cells (HSCs) using complex combinations of markers and flow cytometry. However, robust identification of HSCs using imaging techniques is substantially more challenging which has prompted the recent development of HSC reporter mice. To date, very few molecules used in these reporters have been useful for human HSC identification. Here we report that PLXDC2 is a useful marker for both mouse and human cord blood HSCs. Using a green fluorescent protein (GFP) knock-in at the Plxdc2 locus in mice (hereafter denoted as Plxdc2-GFP), we showed that Plxdc2-GFP is highly expressed in HSCs with 1 in 2.8 Plxdc2-GFP+CD150+ cells giving long-term multi-lineage reconstitution in transplantation. Moreover, we developed a novel human PLXDC2 antibody and showed that human PLXDC2+ HSCs have higher long-term multilineage reconstitution ability compared with PLXDC2- HSCs in a xenograft model. This study identifies PLXDC2 as a highly relevant molecule in HSC identification.

overall_design: 100 cells each of PLXDC2⁺ and PLXDC2⁻ human hematopoietic stem cells (CD34⁺CD38⁻CD90⁺CD45RA⁻CD49f⁺), isolated from cord blood-derived CD34⁺ cells, were sorted and subjected to RamDA-seq.

first: Yasushi

last: Kubota


title: Effect of palmitate on breast cancer cells according to CD36 expression

status: Public on Oct 10 2025

city: Paris

first: Michèle

last: SABBAH

address: Hôpital Saint-Antoine, 34 rue Crozatier, Bâtiment Kourilsky, 1er étage

country: France

institute: INSERM U938

summary: Breast tumors develop in a complex microenvironment whose main component is adipose tissue and gain aggressiveness through increased fatty acid uptake.  Here, we demonstrated that palmitic acid (PA) induced ferroptosis in triple negative breast cancers (TNBC). We found that PA increases the protein expression levels of the long-chain fatty acid transporter CD36 leading to increased lipid uptake. Mechanistically, overexpression of CD36 increases lipid peroxidation, mitochondrial ROS production, the labile iron pool and especially Fe2+ content. Additionally, we found increased expression of ferroptotic target genes (HMOX1, ACSL1, SAT1) and decreased of anti-ferroptotic genes (GPX4 and FSP1) in TNBC following PA exposure. Overexpression of CD36 did not induce ferroptosis in estrogen receptor positive breast cancer. Clinically, higher CD36 expression correlated with the luminal androgen receptor (LAR) subtype of TNBC, known to exhibit a higher sensitivity to ferroptosis. Altogether, these data provide evidence for an essential role of the CD36 protein in the ferroptotic process induced by the saturated fatty acid PA, opening potential new therapeutic approaches promoting ferroptosis in the most aggressive breast cancers.

overall_design: RNA-seq profiling of wildtype MCF-7 and SUM-159 and their CD36-overexpressed derivatives (MCF-7-CD36 and SUM-159-CD36) treated or not with palmitate.

first: Lara

last: Closset

first: Jean-Philippe

last: Foy

first: Lila

last: Louadj

first: Elodie

last: Pramil

first: Elisabetta

last: Marangoni

first: Ivan

last: Bieche

last: Sabbah


title: CD8+ T cell stemness precedes post-intervention control of HIV viremia

first: Jonathan

middle: Morris

last: Urbach

state: Massachusetts

address: 400 Technology Sq Rm 851

institute: Ragon Institute of MGH, MIT and Harvard

summary: Interventions to induce lasting HIV remission are needed to obviate the requirement for lifelong antiretroviral therapy (ART). Durable post-intervention control (PIC) of viremia has been achieved in a subset of individuals following broadly neutralizing anti-HIV-1 antibody (bNAb) administration and analytical treatment interruption (ATI)1-4. Prior studies support a role for CD8+ T cells5-9 but the precise features of CD8+ T cells involved in PIC remain unclear. Here we mapped and functionally profiled CD8+ T cell responses to autologous HIV epitopes using longitudinal samples from four ATI trials in bNAb recipients. PIC was associated with superior pre-intervention HIV-specific CD8+ T cell proliferative capacity, stem cell-like memory phenotype, and recall cytotoxicity against autologous HIV peptide-pulsed CD4+ T cells. CD8+ T cell stemness was further increased following bNAb administration without emergence of new clonotypes targeting defined HLA-optimal epitopes. Multimodal single-cell analyses revealed molecular features associated with PIC and HIV-specific CD8+ T cell stemness, including signatures of metabolic fitness and reduced T cell exhaustion. These results identify immune features that precede subsequent PIC to inform the development of combination immunotherapies that will elicit durable HIV remission.

overall_design:
HIV and CMV epitope-specific CD8+ T cells were isolated from participant PBMCs by FACS using combinations of barcoded fluorescent peptide-HLA tetramers among longitudinal samples collected before (pre) and/or following (post) infusion of broadly-neutralizing antibodies against HIV-1 and analytical treatment interruption. Each sample was also stained with a unique barcoded hashing antibody (HTO) and a panel of commercially available library of barcoded surface antibodies prior to isolation. Gene expression (GEX), antibody-derived tags (ADT), and T cell receptor (VDJ) sequencing libraries were prepared using 10X GEM-X 5’ single-cell RNA-sequencing with feature barcode technology before sequencing via the Illumina NextSeq 2000 platform.

Funding by Howard Hughes Medical Institute.

first: Zahra

last: Kiani

first: Hannah

last: Wisner

first: Mpho

last: Olatotse

first: Daniel

last: Chang

first: Joshua

last: Acklin

first: Alicja

last: Piechocka-Trocha

first: Nathalie

last: Bonheur

first: Ashok

last: Khatri

first: Mathias

last: Lichterfeld

first: Jesper

last: Gunst

first: Ole

last: Sogaard

first: Marina

last: Caskey

first: Michel

middle: C

last: Nussenzweig

first: Bruce

last: Walker

first: David

last: Collins


title: Effect of Alpelisib treatment and MAEA knockout on gene expression of the EBV+ gastric cancer cell line YCCEL1

status: Public on Oct 08 2025

city: Boston

first: Yin

last: Wang

address: 181 Longwood Ave

institute: Brigham and Women's Hospital

summary: EBV+ gastric cancer cell line was reported with PI3K pathway activated. Alpelisib is the PIK3CA specific inhibitor. To study the MAEA knockout and alpelisib treatment, RNAseq was conducted to study the gene expression changes in YCCEL1.

overall_design: YCCEL1 cells expressing MAEA or control sgRNAs were treated with 0.5 uM alpelisib or DMSO for 30 hours.

first: Rui

last: Guo

first: Benjamin

middle: E

last: Gewurz


title: Effect of Alpelisib treatment and PIK3CA knockout on gene expression of the EBV+ gastric cancer cell line YCCEL1

summary: EBV+ gastric cancer cell line was reported with PI3K pathway activated. Alpelisib is the PIK3CA specific inhibitor. To compare the drug treatment against the gene knockout, RNAseq was conducted to study the gene expression changes in YCCEL1.

overall_design: Two conditions were included for RNAseq analysis: (1) YCCEL1 treated with 5 uM alpelisib for 6 hours or DMSO, and (2) YCCEL1 cells expressing PIK3CA or control sgRNAs.


title: MeRIP-seq and RNA-seq Reveals RNA m6A Methylation Patterns and Gene Expression Profile of Arabidopsis Plants in Response to CMV Infection [MeRIP-Seq]

city: Shenzhen

first: yujing

last: lin

address: No. 1088 Xueyuan Avenue, Nanshan District, Shenzhen City, Guangdong Province

institute: Southern University of Science and Technology

type: Methylation profiling by high throughput sequencing

summary: We reported that m6A plays a positive role in plant defense against virus pathogen Cucumber mosaic virus (CMV). CMV genomic RNAs can be m6A modified during plant infection, leading to reduced stability of viral RNAs. Dysfunctions of m6A writers and some readers led to increased susceptibility to CMV. Intriguingly, the increased susceptibility was only observed in the absence of 2b protein encoded by CMV. Our data demonstrated that CMV-2b can inhibit the deposition of m6A at viral RNAs through interfering with the assembly of m6A catalytic complexes. Expression of 2b protein can also antagonize plant m6A deposition. Moreover, CMV-2b was also found to interact with m6A reader proteins to disrupt its recognition of m6A-marked viral RNAs. Our findings unraveled an antagonistic mechanism of m6A-mediated plant antiviral defense.

overall_design: The Arabidopsis Col-0 plants were inoculated by wild-type cucumber mosaic virus (CMV) and the mutated virus deficient in 2b protein (CMVΔ2b). At 14 days post infection, CMV and CMVΔ2b-infected plants as well as uninfected mock plants were subjected to MeRIP-seq and RNA-seq analysis.

first: Jiahui

last: Liu

first: Yujing

last: Lin

first: Chengguo

last: Duan


title: Blocking Nuclear Receptor Nr4a3 Unlocks the Senescence Barrier to Promote Direct Cardiac Reprogramming [aged scRNA-seq]

first: Mengxin

overall_design: Single cell RNA-seq profiles of MGT-transduced aged FBs cultured at reprogramming day 14 by 10x Genomics Chromium System.

first: Li

first: Zhangyi

last: Yu


title: Prostaglandin D2 Synthase: A novel Player in the Pathological Signaling Mechanism of the Aldosterone–Mineralocorticoid Receptor Pathway in the Heart

city: Hannover

first: Maximilian

last: Fuchs

address: Carl-Neuberg-Str. 1

department: IMTTS

institute: Hanover Medical School

summary: A deregulated aldosterone (Aldo)–mineralocorticoid receptor (MR) pathway is linked to cardiovascular disease, including hypertension and heart failure. Despite the association of elevated plasma Aldo levels with cardiac stress, inflammation, myocardial fibrosis, and cardiac remodeling, the underlying mechanisms remain elusive. To study the impact of Aldo–MR pathway overactivation on cardiac health, a novel mouse model with AAV9-mediated MR overexpression and Aldo administration via subcutaneous osmotic pumps was generated. Echocardiographic analyses, transcriptome sequencing, and loss-of-function experiments of an identified lead candidate gene were performed. Additionally, cardiac tissue samples from human patients with end-stage heart failure were analyzed in the study. Mice with an overactivated Aldo–MR pathway exhibited increased neutrophil gelatinase-associated lipocalin (NGAL) expression, cardiac dysfunction, hypertrophy, and fibrosis. Transcriptomics identified prostaglandin D2 synthase (Ptgds) as a novel downstream effector of the cardiac Aldo–MR pathway. SiRNA-mediated inhibition of Ptgds in primary cardiomyocytes reduced NGAL levels and the hypertrophic impact of Aldo, suggesting a role in mediating Aldo-induced cardiac pathologies. Elevated expression of PTGDS was observed in hiPSC-CMs treated with the pro-hypertrophic cytokine leukemia inhibitory factor (LIF) and in end-stage heart failure patients, ascertaining its importance in cardiac disease settings. PTGDS is a newly identified mediator of Aldo–MR-induced cardiac remodeling and may represent a potential therapeutic target for CVD.

overall_design: RNA-seq profiling of C57BL/6N mouse heart tissue after AAV9-Empty control treatment, or AAV9-mineralocorticoid receptor (MR) overexpression with aldosterone treatment.

first: Ankita

last: Garg

first: Malte

last: Juchem

first: Sinje

last: Biss

first: Carla

last: Borisch

first: Julia

last: Leonardy

first: Christian

last: Baer

first: Shashi

middle: K

last: Gupta

first: Thomas

last: Thum


title: Single-cell Transcriptome Analysis Reveals Mechanical Properties of Leukemic Stem Cells in AML.

city: Hefei

first: Mingming

last: Zhu

state: Anhui

address: No.96, JinZhai Road Baohe District,

department: life sciences and medicine

institute: University of Science and Technology of China

summary: Leukemic stem cells (LSCs) are crucial drivers of leukemia, yet the mechanisms underlying their function remain poorly understood. Here, we investigated the physical properties of LSCs and their potential role in LSCs function. single-cell RNA-sequencing analysis has revealed that small-sized LSCs aberrantly overexpress ALDH1A1, a crucial regulator of stem cell function. Lastly, ALDH1A1 inhibition increases cell stiffness and suppresses leukaemogenesis in patient-derived xenograft models. Our findings establish a novel link between the biomechanics of LSCs and their function in leukemia, providing a compelling rationale for targeting therapy-resistant LSCs by inhibiting G3BP. Overall, our study provides valuable insights into the mechanisms of LSCs function and has significant implications for the development of more effective therapies for this devastating disease.

overall_design: In order to explore the mechanism of the function in mechanical properties of LSCs, we isolated small cells and large cells derived from bone marrow lin- cells of 4 AML patients.For the scRNA-seq analysis of human lin- small and large cells ,we pooled 4 sample from the small group in one tube and 4 sample from the large group in another tube. We then counted and resuspended the pooled cells at a concentration of 1000 cells/µL, targeting an estimated 6000 cells per library, following the instructions of the Single Cell 3ʹ Solution v3 Kit (10X Genomics). Single-cell libraries were constructed strictly according to the manufacturer's standard protocol. Libraries were sequenced on the Illumina NovaSeq 6000 System.

first: Haoxiang

last: Yang

first: Tingting

last: Liang

first: Beibei

last: Huang

first: Hongyuan

last: Jiang

first: Fang

last: Ni


title: Expression profiling of human foetal and adult aortic valves

status: Public on Oct 09 2025

city: Marseille

first: Stéphane

last: ZAFFRAN

address: 27 Bd JEan Moulin

institute: Aix Marseille Université

summary: Bicuspid aortic valve (BAV) is a frequent congenital heart defect with a high heritability. Identification of genes associated with the disease and the molecular mechanisms required genetic studies including genome-wide association studies (GWAS) meta-analysis. To prioritize genes identified through such meta-analysis several additional data are required including transcriptomic of aortic valve at early fetal and adult stages. RNA-sequencing was carried out on human fœtal aortic valves at 9, 13, and 22 post conceptional week (PCW) and adult controls. These data were used to compare gene expression profile of several genes identified in a GWAS meta-analysis. Comparing the expression of these genes in valve RNA-sequencing dataset we identified several genes with higher expression in fœtal tissues suggesting their involvement in aortic valve development. In conclusion, we performed integrative analyses taking advantage of human aortic valve transcriptome data to prioritize candidate causal gene of BAV.

overall_design: To prioritize BAV causal genes, we compared the expression profile of these genes in fœtal and adult stages using RNAseq data performed on fœtal and adult aortic valve tissues.

last: Zaffran

first: Sébastien

last: Theriault

first: Simon

last: Bosdy


title: Chromatine structure in Female and Male mice subcutaneous WAT depot

status: Public on Oct 07 2025

city: Nice

first: Jean-Francois

last: Louet

address: C3M 151 route Saint Antoine de Ginestière 151 route Saint Antoine de Ginestière

institute: INSERM

summary: To determine  chromatine structure differences in Female and Male mice subcutaneous WAT depot, we performed ATAC-seq experiment.

overall_design: ATAC-seq in Female and Male mice subcutaneous WAT depot

first: Jean-François

first: Mounia

last: Tannour-louet


title: Placental transcriptome profiles in late-onset preeclampsia: a cross-sectional observational analysis stratified by fetal sex

city: Bedford Park

first: Claire

middle: Trelford

last: Roberts

state: South Australia

address: HMRB Building, Loading Bay via Sports Road

department: College of Medicine and Public Health

institute: Flinders University

summary: Background Preeclampsia is a hypertensive disorder of pregnancy with significant maternal and fetal health implications. While the molecular mechanisms underlying early-onset preeclampsia have been studied extensively, less is known about late-onset preeclampsia, particularly with regard to fetal sex-specific effects. Understanding transcriptional changes in the placenta may provide insight into persistent mechanisms or downstream consequences of the disease, thereby contributing to our understanding of its pathophysiology. While the initiating events of late-onset preeclampsia occur earlier in gestation, analysis of term placental tissue can reveal cumulative effects of disease processes and identify biological pathways that remain altered at delivery. Methods We conducted a cross-sectional observational analysis of placental gene expression using RNA sequencing in a subset of 58 term placentas (21 male-bearing and 37 female-bearing pregnancies) drawn from two large prospective birth cohorts. Pregnancies were classified based on clinical diagnosis of late-onset preeclampsia (diagnosed ≥20 weeks’ gestation according to ISSHP criteria) or uncomplicated and assessed for differential gene expression. Cell type proportions were estimated using CIBERSORTx from a placenta-specific reference single-cell dataset. Weighted gene co-expression network analysis identified modules of co-expressed genes associated with late-onset preeclampsia and fetal sex. Results Differential gene expression analysis identified 150 genes with altered expression in male-bearing placentas from pregnancies with late-onset preeclampsia compared to those from uncomplicated pregnancies. No differentially expressed genes were identified in female-bearing placentas. Cell type deconvolution revealed increased abundance of CD14+ monocytes and CD8+ activated T cells (log odds of 1.42 and 1.44 respectively) and reduced fetal GZMK natural killer cells (log odds of 0.60) in male-bearing placentas from affected pregnancies. In female-bearing placentas, late-onset preeclampsia was associated with increased fetal nucleated red blood cells and maternal plasma cells (log odds of 1.33 and 1.40 respectively). Male-specific co-expression analysis identified gene modules enriched for biological processes including RNA processing, immune regulation, and metabolism. Conclusions Placental transcription and cellular responses to late-onset preeclampsia differ by fetal sex. Evidence of altered immune cell composition and gene co-expression in male-bearing placentas suggests a sex-specific vulnerability. These findings highlight the importance of considering fetal sex in molecular investigation and clinical management of preeclampsia.

overall_design: RNA-seq profiling of placental chorionic villous tissue from male- and female-bearing pregnancies complicated by late-onset preeclampsia or uncomplicated outcomes at term.

first: Melanie

last: Smith

first: Seema

last: Plaisier

first: James

last: Breen

first: Konstantinos

last: Bogias

first: Tanja

last: Jankovic-Karasoulos

first: Dylan

last: McCullough

first: Dale

last: McAninch

first: Anya

middle: L

last: Arthurs

first: Melissa

last: Wilson

first: Katherine

last: Pillman


title: Effect of butyrate stimulation on CD19 CAR-T cells for the treatment of Non-Hodgkin Lymphoma

city: Madrid

first: Roberto

last: Garcia-Vicente

address: Avd Cordoba s/n

department: Translational Hematology

institute: Instituto de Investigacion Hospital 12 de Octubre

summary: Gut microbiota plays a pivotal role in the development and function of the immune system, therefore it has been described as an important factor for the efficacy and safety of immunotherapy, including CAR-T. The mechanisms by which this occurs are not well understood. Short Chain Fatty Acids (SCFAs) are metabolites derived from the microbial fermentation that are involved in the regulation of metabolic, endocrine and immune function. In this study we analyze the transcriptomic changes that SCFA butyrate generates in CAR-T cells.

overall_design: T cells were isolated from peripheral blood of four healthy donors and activated on anti-CD3/28-coated plates. After that, they were transduced with a CD19CAR lentiviral vector and separated into two conditions. One was exposed to SCFA butyrate and the other to the control medium. Comparative gene expression profiling analysis of RNA-seq data for both conditions was performed

first: Andrés

last: Arroyo-Barea

first: Joaquín

last: Martínez-López

first: María

last: Linares


title: CDK12/13 inhibition in NSCLC cell lines with acquired resistance to sotorasib

city: Tampa

first: Eric

last: Haura

state: FL

address: 12902 Magnolia Drive

institute: H. Lee Moffitt Cancer Center and Research Institute, Inc

summary: The efficacy of KRAS-G12C inhibitors in lung cancer is limited by the rapid onset of acquired resistance. While divergent mechanisms of resistance across patients and preclinical models have complicated efforts to identify therapeutic strategies for sotorasib-resistant cancers, we found that sotorasib-resistant H358 and LU65 cell lines, which have distinct mechanisms of resistance and drug sensitivity profiles, both exhibited increased vulnerability to treatment with SR-4835, an inhibitor of the transcriptional kinases CDK12 and CDK13. To identify CDK12/13-dependent genes linked to the increased sensitivity we observed in sotorasib-resistant over parental cells, we treated parental and sotorasib-resistant H358 and LU65 cells with SR-4835 and performed RNA sequencing.

overall_design: Whole-transcriptome RNA sequencing was performed in three independent biological replicates of parental and sotorasib-resistant H358 and LU65 cell lines after 24-hour treatment with 0.1% DMSO or 100 nM SR-4835.

first: Yaakov

last: Stern

first: Andrii

last: Monastyrskyi

first: Derek

middle: R

last: Duckett


title: Tumor-Initiating Stem Cells Fine-tune the Cell States of Neutrophils to Drive Cancer Relapse from Immunotherapy [Parse scRNAseq]

city: Chicago

first: weijie

last: guo

state: IL

address: 929 East 57th Street, GCIS W423N

institute: university of Chicago

summary: The highly heterogeneous and plastic nature of tumor-associated neutrophils (TANs) has been recognized, but how different cell states of TANs emerge, evolve, distribute, and impact cancer immunotherapy efficacy remains elusive. Using single-cell RNA sequencing, spatial transcriptomic analysis, and genetic manipulations, we show that, while anti-PDL1/CD40 agonist immunotherapy can reprogram TANs to gain strong anti-tumor activities in squamous cell carcinomas (SCCs), a subset of neutrophils residing at the tumor-stroma interface can preserve their immune-suppressive state. Importantly, we identified a group of Sox2Hi tumor-initiating stem cells (tSCs) at the tumor-stroma interface that can activate Fatty Acid Desaturase 1 (Fads1) and produce arachidonic acid (AA) to induce autocrine prostaglandin E2 signaling which can disrupt the interferon responses in neutrophils. Thus, through this interaction, tSCs fine-tunes the cell states of neutrophils, shapes neutrophil heterogeneity, and sculpts a protective micro-niche to drive cancer relapse following immunotherapy.

overall_design: To define how immunotherapy treatments impact TANs, we sought to employ a highly immunogenetic mouse cancer model that is induced by exposing the mouse skin epithelium to chemical mutagen 7,12-dimethylbenz[a]anthracene (DMBA) followed by repeated applications of phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA). With this ideal model, we next treated the mice bearing spontaneous skin SCCs with PDL1 blocking and CD40 agonist antibodies which were recently demonstrated to induce anti-tumor activities in neutrophil. Immediately after the treatment (e.g. day two after the last dose), we collected these tumors, isolated total CD45+ immune cells, and subjected them, together with immune cells isolated from untreated naïve tumors, to single cell RNA-sequencing.

first: Weijie

last: Guo

first: Yuxuan

last: Miao


title: Tumor-Initiating Stem Cells Fine-tune the Cell States of Neutrophils to Drive Cancer Relapse from Immunotherapy [GeoMx]

overall_design: To profile the neutrophils at different regions in the TME and their responses to immunotherapies, we employed spatial transcriptomics analysis to determine the distribution patterns of neutrophil responses in the spontaneous mouse SCCs.


title: Tumor-Initiating Stem Cells Fine-tune the Cell States of Neutrophils to Drive Cancer Relapse from Immunotherapy [SCC bulk RNA-Seq]

overall_design: To investigate the mechanisms by which tSCs modulate neutrophils, we isolated Itga6hi CD80+ tumor stem-like cells and Itga6low CD80⁻ differentiated cancer cells from DMBA/TPA-induced skin squamous cell carcinoma (SCC), and performed bulk RNA sequencing on these populations.


title: Tumor-Initiating Stem Cells Fine-tune the Cell States of Neutrophils to Drive Cancer Relapse from Immunotherapy [neutrophil bulk RNAseq]

overall_design: To test whether Sox2 is responsible for endowing tSCs with the capacity in modulating neutrophils and suppressing their ability to respond to interferons, we grafted either parental Sox2low control or Sox2Hi SCC cells on the ‘CatchupIVM-red’ mice. When the SCC tumors are established, we treated the mice bearing these two groups of tumors with anti-PDL1/CD40 agonist. We then isolated Tomato+ neutrophils from both untreated naïve or treated Sox2low control or Sox2Hi SCC tumors and subjected them to bulk-RNA-seq.


title: Sex Differences in WAT Thermogenesis of NCOA1 Knockout Mice

first: Jean-Francois

last: Louet

summary: To elucidate the sex-specific role of the transcriptional coregulator NCOA1 on thermogenic adipocytes in subcutaneous white adipose tissue (SAT), we performed RNA-seq analysis on  male and female NCOA1 knockout mice after ß3-receptor agonist stimulation(CL316,243)

overall_design: RNA-seq profiling of female and male SAT after administration of CL316,243 (0.5 mg/kg body weight) during seven days

first: Jean-François

first: Mounia

last: Tannour-louet


title: High-throughput characterization of transcription factors that modulate UV damage formation and repair at single-nucleotide resolution

status: Public on Oct 06 2025

city: Durham

first: Hana

middle: Isadora

last: Wasserman

state: NC

address: 3308 Old Chapel Hill Road

institute: Duke University

summary: Genomic studies have revealed elevated damage and mutation rates in active transcription factor (TF) binding sites of UV-linked cancers. Previous research investigating the relationship between TF activity and UV DNA damage have primarily focused on select TFs or been done in aggregate across large cohorts of TFs at kilobase resolution. While collectively, there is evidence that TFs contribute to UV-induced mutagenesis by both enhancing initial damage formation and attenuating repair, no method exists to comprehensively characterize these mechanisms driving downstream mutation enrichment on a per-TF basis. Using genome-wide maps of UV damage from human skin fibroblasts, we developed a scalable statistical framework to identify and deconvolve TF-mediated mutagenic mechanisms across hundreds of TFs. We show that numerous previously unidentified TFs significantly modulate damage formation in their binding sites. Our systematic survey of TF-DNA complexes reveals that TF-induced structural distortions predispose DNA to specific photodimer types and coincide with UV damage enrichment, highlighting the role of structure in UV damage formation. Additionally, we analyzed repair efficiency in TF binding sites with unprecedented resolution, identifying specific TFs and binding site positions likely driving competition with repair factors. By comparing these results with skin cancer sample mutations, we can distinguish mutation peaks driven by increased damage susceptibility versus attenuated repair, illustrating that the mechanisms of TF-mediated mutagenesis are both TF- and position-specific. Our approach provides a robust statistical framework to elucidate the mechanisms of mutagenic TF-binding and offers novel insights into the complex interplay between protein interactions with DNA damage and repair.

overall_design: ATAC-seq performed using four biological replicates to define open chromatin regions for the human skin fibroblast cell line, CS1AN/CSBWT

middle: I

first: Alexias

last: Safi

first: Gregory

last: Crawford

first: Raluca

last: Gordân

first: Peng

last: Mao


title: Tumor-Initiating Stem Cells Fine-tune the Cell States of Neutrophils to Drive Cancer Relapse from Immunotherapy [Cut and Run]

overall_design: We performed a Cut & Run assay in the PDV cell lines to profile the direct binding of Sox2 to the target genes.


title: Tumor-Initiating Stem Cells Fine-tune the Cell States of Neutrophils to Drive Cancer Relapse from Immunotherapy [tumor cell bulk RNAseq]

overall_design: To explore the underlying mechanisms activated by Sox2 in tSCs that is responsible for modulating neutrophils, we isolated Sox2low and Sox2Hi SCC cells from grafted tumors and then subjected these cells for bulk RNA-seq.


title: Expression profiling of THP-1 cells with and without infection by Francisella tularensis and with or without treatment with Dillapiole

city: Huntington

first: James

last: Denvir

state: WV

address: One John Marshall Drive

department: Biochemistry and Microbiology

institute: Marshall University School of Medicine

summary: In order to assess the effect of treatment by Dillapiole on human monocyte THP-1 cells infected by Francisella tulerensis, we performed expression profiling by RNA sequencing on THP-1 cells with and without infection and with or without treatment. Differential expression analysis revealed 1174 genes whose expression was affected by the Dillapiole treatment differently in the infected cells when compared to the treatment effect in the uninfected cells. These genes identified 45 biological pathways, including an inhibitory effect on the TNF-receptor pathway.

overall_design: THP-1 cells were either infected by Francisella tularensis or grown without infection. Infected and uninfected cells were treated by either Dillapiole or a control vehicle. Five biological replicates for each of the resulting four experimental groups were utilized for expression profiling by RNA-Seq.

first: Elliot

last: Collins

first: Anthony

last: Sako

first: Kristen

last: Sikorsky

first: Jun

last: Fan

first: Donald

middle: A

last: Primerano

first: Deanna

last: Schmitt

first: Stuart

last: Cantlay

first: Roger

last: Seeber

first: Francisco

last: León

first: Joseph

last: Horzempa


title: Palmitate suppresses CD8+ T cell antitumoral response by disrupting mitochondrial metabolism [RNA-seq]

city: Milano

first: Teresa

last: Manzo

state: Milano

address: Via Adamello 16

department: Department of Experimental Oncology

institute: IEO

summary: Accumulation of lipids in the tumor microenvironment (TME) is a feature of several solid tumors and increased palmitate (PA) availability fosters tumor progression and metastases. The intrinsic effects of PA on cancer cells are well understood, but its role in modulating CD8+ T cells (CTL) functional performances remains elusive. Here, we found that PA alters the mitochondrial metabolism of CTL and prevents their effector functions in an irreversible manner, resulting in impaired antitumoral immunity. Mechanistically, PA-induced mitochondrial blocking demotes histone acetylation and chromatin accessibility and decreases the transcription of genes promoting DNA replication and production of effector molecule production. We identified the metabolic enzyme Sphingosine Kinase 2 (SPHK2) as a molecular target of PA in establishing CTL dysfunction. Consistently, pharmacological inhibition of SPHK2 restored CTL mitochondrial fitness, effector functions and anti-tumor potential. Thus, we reveal that PA fosters tumor progression by impairing CTL antitumor immunity and highlight the therapeutic potential of inhibiting SPHK2 activity to optimize T cellfunctionality.

overall_design: To investigate the effects of Palmitate on CD8+ T cell function, RNA Sequencing of Palmitate-treated vs control cells was carried out after 48 hours of treatment

first: Silvia

last: Tiberti

first: Sara

last: Gennari

first: Martina

last: Romeo

first: Ilir

last: Sheraj

first: Mohamed

last: Kassir

first: Juan

last: Fernández-García

first: Carina

middle: B

last: Nava Lauson

first: Roberta

last: Noberini

first: Carlotta

last: Catozzi

first: Tiziano

last: Dallavilla

first: Mattia

last: Ballerini

first: Alessia

last: Loffreda

first: Simona

middle: G

last: Codreanu

first: Stacy

middle: D

last: Sherrod

first: Katrina

last: Leaptrot

first: Alexandra

last: Schrimpe-Rutledge

first: John

last: McLean

first: Martin

middle: H

last: Schaefer

last: Rodighiero

first: Tiziana

last: Bonaldi

first: Sarah-Maria

last: Fendt

first: Besim

last: Ogretmen

last: Sdelci

first: Luigi

last: Nezi


title: Integrated multi-omics single cell atlas of the human retina

city: Palo Alto

first: Lattice

last: Data Coordination

state: CA

address: 3165 Porter Drive

institute: Stanford University

summary: Single-cell sequencing has revolutionized the scale and resolution of molecular profiling of tissues and organs. Here, we present an integrated multimodal reference atlas of the most accessible portion of the mammalian central nervous system, the retina. We compiled around 2.4 million cells from 55 donors, including 1.4 million unpublished data points, to create a comprehensive human retina cell atlas (HRCA) of transcriptome and chromatin accessibility, unveiling over 110 types. Engaging the retina community, we annotated each cluster, refined the Cell Ontology for the retina, identified distinct marker genes, and characterized cis-regulatory elements and gene regulatory networks (GRNs) for these cell types. Our analysis uncovered intriguing differences in transcriptome, chromatin, and GRNs across cell types. In addition, we modeled changes in gene expression and chromatin openness across gender and age. This integrated atlas also enabled the fine-mapping of GWAS and eQTL variants. Accessible through interactive browsers, this multimodal cross-donor and cross-lab HRCA, can facilitate a better understanding of retinal function and pathology.

relation:
Reanalysis of: GSM7064213
Reanalysis of: GSM7064214
Reanalysis of: GSM7064215
Reanalysis of: GSM7064216
Reanalysis of: GSM7064217
Reanalysis of: GSM7064218
Reanalysis of: GSM7064219
Reanalysis of: GSM7064220
Reanalysis of: GSM7064221
Reanalysis of: GSM7064222
Reanalysis of: GSM7064223
Reanalysis of: GSM7064224
Reanalysis of: GSM7064225
Reanalysis of: GSM7064226
Reanalysis of: GSM7064227
Reanalysis of: GSM7064228
Reanalysis of: GSM7064229
Reanalysis of: GSM7064230
Reanalysis of: GSM7064231
Reanalysis of: GSM7064232
Reanalysis of: GSM7064233
Reanalysis of: GSM7064234
Reanalysis of: GSM7064235
Reanalysis of: GSM7064236
Reanalysis of: GSM7064237
Reanalysis of: GSM7064238
Reanalysis of: GSM7064239
Reanalysis of: GSM7064240
Reanalysis of: GSM7064241
Reanalysis of: GSM7064242
Reanalysis of: GSM7064243
Reanalysis of: GSM7064244
Reanalysis of: GSM7064245
Reanalysis of: GSM7064246
Reanalysis of: GSM7064247
Reanalysis of: GSM7064248
Reanalysis of: GSM7064249
Reanalysis of: GSM7064250
Reanalysis of: GSM7064251
Reanalysis of: GSM7064252
SubSeries of: GSE265801

overall_design:
snRNA-seq and snATAC-seq of adult human retina, peripheral lobe region tissue and macula region tissue, 22 adult human donors

Please note that all the samples from GSE226108/PRJNA938514were re-analyzed for this dataset (as listed below).
The original processed data files were processed on the hg19 assembly using the GENCODE19 genome annotation.
The reprocessed samples were processed on the GRCh38 assembly using the GENCODE32 genome annotation in order to standardize their processing with the new samples and the resulting data files are linked as Series supplementary files.

Sample title BioSample SRA Experiment
=====================================================
GSM7064213: 17D013_NeuNT_lib SAMN33441072  SRX19501854
GSM7064214: 19_D003_atac_lib SAMN33441071  SRX19501852
GSM7064215: 19_D005_atac_lib SAMN33441070  SRX19501853
GSM7064216: 19_D006_atac_lib SAMN33441069  SRX19501855
GSM7064217: 19_D007_atac_lib SAMN33441068  SRX19501856
GSM7064218: 19_D008_atac_lib SAMN33441067  SRX19501857
GSM7064219: 19_D009_atac_lib SAMN33441066  SRX19501861
GSM7064220: 19_D010_atac_lib SAMN33441065  SRX19501858
GSM7064221: 19_D011_atac_lib SAMN33441064  SRX19501859
GSM7064222: 19_D019_atac_lib SAMN33441063  SRX19501860
GSM7064223: 19D013_fovea_atac_lib  SAMN33441062  SRX19501862
GSM7064224: 19D013_fovea_lib SAMN33441061  SRX19501863
GSM7064225: 19D013_foveaR_lib SAMN33441060  SRX19501864
GSM7064226: 19D013_mac_lib  SAMN33441059  SRX19501873
GSM7064227: 19D013_macular_atac_lib  SAMN33441058  SRX19501874
GSM7064228: 19D013_NeuNT_lib SAMN33441057  SRX19501875
GSM7064229: 19D014_fovea_atac_lib  SAMN33441056  SRX19501876
GSM7064230: 19D014_fovea_lib SAMN33441055  SRX19501879
GSM7064231: 19D014_foveaR_lib SAMN33441054  SRX19501877
GSM7064232: 19D014_mac_lib  SAMN33441053  SRX19501878
GSM7064233: 19D014_NeuNT_2_lib SAMN33441052  SRX19501880
GSM7064234: 19D015_fovea_lib SAMN33441051  SRX19501884
GSM7064235: 19D015_mac_lib  SAMN33441050  SRX19501885
GSM7064236: 19D015_NeuNM_lib SAMN33441049  SRX19501886
GSM7064237: 19D015_NeuNT_lib SAMN33441048  SRX19501887
GSM7064238: 19D015_per_lib  SAMN33441047  SRX19501888
GSM7064239: 19D016_atac_lib  SAMN33441046  SRX19501889
GSM7064240: 19D016_mac_lib  SAMN33441045  SRX19501890
GSM7064241: D001-12_NeuNM_lib SAMN33441044  SRX19501891
GSM7064242: D001-12_NeuNT_lib SAMN33441043  SRX19501865
GSM7064243: D005_13_atac_lib SAMN33441042  SRX19501866
GSM7064244: D009_13_atac_lib SAMN33441041  SRX19501867
GSM7064245: D013_13_atac_lib SAMN33441040  SRX19501868
GSM7064246: D017_13_atac_lib SAMN33441039  SRX19501869
GSM7064247: D018_13_atac_lib SAMN33441038  SRX19501870
GSM7064248: D019_13_atac_lib SAMN33441037  SRX19501871
GSM7064249: D021_13_atac_lib SAMN33441036  SRX19501872
GSM7064250: D026_13_atac_lib SAMN33441035  SRX19501881
GSM7064251: D027_13_atac_lib SAMN33441034  SRX19501882
GSM7064252: D028_13_atac_lib SAMN33441033  SRX19501883

first: Rui

last: Chen

first: Jin

last: Li

first: Jun

last: Wang

first: Ignacio

last: Ibarra

first: Xuesen

last: Cheng

first: Malte

last: Luecken

first: Jiaxiong

last: Lu

first: Aboozar

last: Monavarfeshani

first: Wenjun

last: Yan

first: Yiqiao

last: Zheng

first: Zhen

last: Zuo

first: Samantha

last: Colborn

first: Berenice

last: Cortez

first: Leah

last: Owen

first: Nicholas

middle: M

last: Tran

first: Karthik

last: Shekhar

first: Joshua

last: Sanes

first: J

middle: T

last: Stout

first: Shiming

first: Yumei

first: Margaret

last: DeAngelis

first: Fabian

middle: J

last: Theis


title: The Function of Tetrameric MADS-box Transcription Factors in Floral Fate Determination

city: Berlin

first: Manuel

last: Neumann

address: Philippstr. 13

institute: HU Berlin

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

overall_design: Refer to individual Series

first: Xiaocai

last: Xu

first: Frederic

last: Carew

first: Cezary

last: Smaczniak

first: Kerstin

last: Kaufmann


title: Tumour-associated tissue-resident memory T (TRM) cells and exhausted T cells are clonally and developmentally distinct populations

city: Parkville

first: Jan

last: Schroeder

address: Peter Doherty Institute Melbourne

department: DMI

institute: University of Melbourne

summary: CD8+ T cells serve as a key weapon in the therapeutic armamentarium against cancer. While CD8+ CD103+ T cells with a tissue-resident memory (TRM) phenotype have been favourably correlated with patient prognoses1-6, the tumour microenvironment comprises dysfunctional exhausted T (TEX) cells that exhibit a myriad of TRM-like features, leading to conflation of these cell types. Here, we deconvolute TRM and TEX cells within the intratumoural CD8+ CD103+ T cell pool across human cancers, ascribing markers and gene signatures that distinguish these CD8+ populations and enable their functional distinction. We found that while TRM cells exhibit superior functionality and are associated with long-term survival post tumour resection, TEX cells are associated with responsiveness to immune checkpoint blockade. Importantly, we show that tumour-associated TEX and TRM cells are clonally and developmentally distinct populations, with the latter predominantly comprised of low affinity and tumour-independent bystanders. Tumour-specific TRM cells may form in circumstances where specific tumour antigens are lost or inaccessible, and these TRM cells can be pushed towards exhaustion when cognate antigen is re-encountered. Thus, chronic T cell receptor signalling within tumours is the key distinction between tumour-associated TRM and TEX cells. Therefore, the most fruitful approaches to utilise TRM cells in anti-tumour therapies are likely embedded in the repurposing of tumour-independent TRM cells already present within tumours.

overall_design: Breast tissue from women with breast cancer and blood from healthy women was sampled and CD3+ cells sequenced.

first: Thomas

last: Burn

first: Laura

last: Mackay


title: Interferons inhibit Ebola virus infection of human keratinocytes

status: Public on Oct 04 2025

city: Iowa City

first: Jonah

last: Elliff

state: Iowa

address: 51 Newton Rd

institute: University of iowa

summary: Orthoebolavirus zairense, or Zaire Ebola virus (EBOV) is a species within the virus family Filoviridae, a group of viruses that can cause severe disease in humans characterized by hemorrhagic shock, coagulation abnormalities, and severe inflammation. While tissue macrophages are critical targets early during EBOV infection, other cell types support viral replication as disease progresses. At late stages of infection, infectious EBOV is found on the surface of the skin, which may be a critical source of infectious virus transmitted be-tween individuals during outbreaks. Human skin contains a number of cellular targets of EBOV, including keratinocytes. Here, we demonstrate EBOV infection of telomer-ase-immortalized normal human skin keratinocytes (NHSK-1) as well as EBOVΔVP30 in-fection of NHSK-1 cells that were stably complemented with the EBOV transcription factor VP30. Infection with EBOVΔVP30 did not elicit detectable endogenous interferon re-sponses, however, exogenous pre-treatment of NHSK-1 cells with type I, II, and III inter-feron (IFN) inhibited EBOVΔVP30 infection and infection of an additional low contain-ment model of EBOV, rVSV/EBOV GP, in a dose-dependent manner. Analysis of the transcriptome of IFN-treated keratinocytes identified multiple genes unique to each IFN and a subset of ISGs upregulated by each IFN. Our results indicate that ISGs induced by IFN pre-treatment of keratinocytes can reduce infection, underlining possible anti-EBOV ISGs for development of EBOV-targeting therapeutics.

overall_design: RNA-seq profiling of the transcriptome of telomerase-immortalized human keratinocytes at 6 or 24 hours following treatment with IFN-β, IFN-γ, IFN-α, or IFN-λ.

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