title: Cortical Alterations in H3K27ac Regulation in Gene Expression  Coincide Associated with Cognitive Decline and Affective Behavior in Mice During Aging: Genome-wide Epigenetic Analysis

city: Chicago

first: Sarah

last: Scheinman

state: Illinois

address: Northwestern Univ 303 E., Ave IL

department: Psychiatry and Behavioral Sciences

institute: Northwestern University

summary: Histone acetylation plays a critical role in the regulation of gene expression in humans and animals, influencing various biological processes, including brain function during aging. Understanding the alterations in histone acetylation during aging could provide insights into the molecular mechanisms underlying age-related cognitive decline. In this study, we investigated the dynamics of histone acetylation and its functional effects in the brain during aging by characterizing and comparing differences in memory and affective behavior, histone H3 levels, expression of histone-modifying enzymes HDACs and HAT, genome-wide H3K27ac abundancy, an active enhancer, and gene expression between young (2-3 months old) and aged (18-20 months old) genetically identical mice. Our results demonstrate that aging induces a variety behavioral phenotypes including a decline in activity/locomotion, increase in anxiety, and memory impairment, that occurs in conjunction with dysregulation of HDAC 1, 2, and 3, HAT p300 and genome-wide differential abundancy of H3K27ac  at a variety of gene promoters. Importantly, we also demonstrated that age-related reductions in H3K27ac at gene promoters were associated with decreased expression levels of genes related to DNA damage and aging including Map3K1, Rev1, and Cdk2ap1. Overall, our study suggests the role of histone acetylation as a regulator of gene expression during brain aging and that changes in histone acetylation are associated with age-related alterations in memory and cognitive decline.

overall_design: Isolated DNA from prefrontal cortical nuclear extracts were prepared for CUT&RUN (Cleavage Under Target and Release Using Nuclease) sequencing according to the manufacturer’s protocol (14-1048, EpiCypher). Cortical nuclei were washed with CUT&RUN wash buffer (200mM HEPES, 150mM NaCl, 0.5mM spermidine), bound to activated ConA beads, permeabilized in wash buffer (wash buffer + 0.002% digitonin), incubated with H3K27ac antibodies (ab4729), washed in wash buffer, incubated with calcium-activated pAG-MNase. CUT&RUN enriched DNA was then purified using a column clean up kit optimized for small fragments. Library preparation was carried out using the NEBNext Ultra II DNA Library Prep Kit (NEB #E7103). Briefly, purified DNA was repaired, ligated to sequencing adapters, and PCR-amplified to generate Next Generation Sequencing (NGS) libraries for each sample. Genome-wide sequencing with 150-bp paired-end reads was carried out by NovoGene Corporation (Sacramento, CA) using the NovaSeq PE150.

middle: B

first: Gemma

last: Carvill

first: Hongxin

last: Dong


title: A virus-free nanoparticle–3D scaffold platform for efficient human iPSC reprogramming and differentiation [WTC0011 RNA-Seq]

status: Public on May 31 2026

city: Seattle

first: YANG

last: Zhou

state: WA

address: 1410 NE Campus Pkwy

country: USA

institute: university of washington

type: Expression profiling by high throughput sequencing

summary: Human induced pluripotent stem cells (hiPSCs) hold substantial promise for regenerative medicine and cell manufacturing, yet their widespread adoption remains limited by reprogramming strategies that are inefficient, costly, unsafe, and difficult to scale, driven by reliance on viral vectors, limited virus-free gene delivery technologies, and two-dimensional (2D) culture systems lacking microenvironmental control.  Here, we present a virus-free, materials-guided reprogramming platform that integrates engineered polymeric nanoparticles with a biomimetic three-dimensional (3D) scaffold to jointly regulate gene delivery and cell-state transitions during fate conversion. A rationally designed fluorocarbon- and heparin-modified polymer nanoparticle enables efficient, low-toxicity episomal delivery of reprogramming factors, while a porous chitosan scaffold provides a permissive 3D microenvironment that accelerates reprogramming kinetics and suppresses somatic cell overgrowth. This integrated strategy concurrently improves reprogramming efficiency, kinetics, and workflow simplicity without the use of viral vectors or manual colony isolation. Scaffold-supported reprogramming yields an approximately eightfold increase in SSEA-4⁺/TRA-1-60⁺ cells by day 25 compared with non-viral 2D conditions, with pluripotent populations emerging as early as day 7, enabling hiPSC generation within weeks rather than the months typically required by conventional workflows. Transcriptomic analyses reveal that the 3D scaffold functions as an active regulatory element, suppressing inflammatory and extracellular matrix–associated programs that stabilize somatic identity while promoting chromatin-remodeling and stem-cell-associated pathways. Importantly, the platform supports a continuous, selection-free workflow, enabling direct differentiation of hiPSCs within the scaffold and further reducing processing time. By coupling delivery chemistry with microenvironmental control, this nanoparticle–scaffold platform provides a safe, efficient, and scalable route for hiPSC generation with direct relevance to regenerative medicine and patient-specific cell manufacturing.

overall_design: Bulk RNA-seq analysis of hiPSC reprogrammed under 2D culture condition and 3D scaffold culture conditions

first: Yang


title: scRNAseq of human intestinal organoids infected with coxsackievirus B1

city: Tampere

first: Hana

middle: Hien

last: LE

state: Pirkanmaa

address: Medisiinarinkatu 3, 33520 Tampere

country: Finland

institute: Tampere University

summary: We applied 10X Genomic scRNAseq to profile cell population within human intestinal organoids infected with coxsackievirus B1. The intestinal epithelium represents the first line of defense in the gastrointestinal tract, forming an essential barrier that, when compromised, renders individuals with celiac disease (CeD) susceptible to mucosal damage. By connecting viral infections and gluten challenges, this study sheds light on a mechanistic bridge between viral infection and gluten peptide modification, a critical step in the onset of CeD.

overall_design: Human intestinal organoids infected with coxsackievirus B1 were dissociated into single-cell suspensions and subsequently analyzed by single-cell RNA sequencing (scRNAseq).

first: Hana Hien

last: Le

first: Veera

last: Räkköläinen

first: Roselia

last: Davidsson

first: Valeriia

last: Dotsenko

first: Laura

last: Martin Diaz

first: Amirbabak

last: Sioofy Khojine

first: Anniina

last: Virtanen

first: Jutta

last: E. Laiho

first: Chaitan

last: Khosla

first: Olli

last: Silvennoinen

first: Heikki

last: Hyöty

first: Keijo

last: Viiri


title: RNA-seq analysis in primary neuroblastoma tumor cells.

city: Wuhan

first: Yingzhe

last: Fang

address: Donghu Road

country: China

institute: Wuhan University

summary: To investigate the transcriptional effects of Paics, we performed RNA-seq on primary tumor cells isolated from Th-MYCN+/+Th-IGF2BP1+/+ mice.

overall_design: Total RNA was extracted from 10 million primary tumor cells of Th-MYCN+/+Th-IGF2BP1+/+ mice following PAICS depletion, with 15% Drosophila S2 cells spiked-in using TRIzol reagent. Additionally total RNA was extracted from 10 million primary tumor cells of Th-MYCN+/+Th-IGF2BP1+/+ mice following treatment with 500 nM prexasertib and 1 μM CHIR-124 using TRIzol reagent. The purified mRNA was used to construct libraries by NEBNext® Ultra™ II RNA Library Prep Kit with Sample Purification Beads (New England Biolabs, #E7775) for Illumina.


title: TT-seq analysis in primary neuroblastoma tumor cells.

summary: To investigated the contribution of PAICS to the progression of MYCN and IGF2BP1 expressing neuroblastoma by identifying its crucial downstream responsive target. TT-seq with 4-thiouridine (4sU) labeling was conducted in Th-MYCN+/+Th-IGF2BP1+/+ primary murine tumor cells to assess RNA transcription elongation.

overall_design: Mouse primary tumor cells were labeled with 400 μM 4-thiouridine for 10 min at 37 °C and were then lysed with TRIzol.


title: Fanconi Anemia Pathway Activation Converts Oncogene-Induced Senescence into a Pro-Tumorigenic State

city: Hangzhou

first: Yue

last: Qiu

state: Zhejiang

address: 600 Dunyu Street

institute: Westlake University

summary: DNA repair pathways are canonically tumor-suppressive, yet emerging evidence suggests their upregulation can promote cancer progression, a paradox whose mechanisms remain poorly understood. Here, we report that activation of the Fanconi Anemia (FA) DNA repair pathway drives malignant tumor progression by reprogramming cellular senescence from a tumor-suppressive to a pro-tumorigenic state. Through an unbiased genetic screen in Drosophila, we identified that loss of Sras (homologous to human RCE1) cooperates with oncogenic RasV12 to induce slow-progressing yet highly malignant tumors. Bioinformatics analysis revealed marked upregulation of the FA pathway and Hippo signaling in these tumors. Genetic manipulation demonstrates that FA pathway activation is required for tumor growth and invasion. Mechanistically, we show that FA pathway upregulation enhances cellular senescence and triggers secretion of senescence-associated secretory phenotype (SASP) factors, particularly the cytokine Unpaired-1 (Upd1; IL-6 homolog), which in turn activates JAK-STAT signaling within tumor cells through an autocrine loop, thereby promoting tumor progression. Notably, p53 activation is dispensable for this pro-tumorigenic senescence program. FA pathway activation and its pro-tumorigenic function are conserved across multiple RasV12-driven malignant tumor models. Our findings reveal a previously unrecognized mechanism by which DNA repair machinery is co-opted to convert oncogene-induced senescence into a tumor-promoting state, with broad implications for understanding cancer progression and developing therapies targeting Ras-driven malignancies.

overall_design: In total 5 groups: 2 Sras mutant groups, WT control group, Ras control group, and scrib mutant group as positive control

first: Jingjie

last: Mu

first: Yifan

last: Guo

first: Jin-Yu

last: Lu

first: Xiaoqin

last: Li

first: Wenahn

last: Liu

first: Wenyan

last: Xu

first: Sha

last: Song

first: Xianjue

last: Ma


title: Salinity induced gene expression profiling in the rice genotypes using Agilent Rice Gene Expression 4x44K Microarray

city: Mymensingh

first: Mohammad

middle: Rashed

last: Hossain

address: Factulty of Agriculture (East Building)

department: Genetics and Plant Breeding

country: Bangladesh

institute: Bangladesh Agricultural University

summary: Whole genome transcriptional responses is profiled in the 0 & 120 mM NaCl (salinity) stressed whole seedlings of the rice genotypes FL478, Hassawi, Nonabokra and IR29 using Agilent Rice Microarrays. Stress was imposed on 14 day old seedlings and total RNA from the whole seedlings was collected after 48 h of stressed period (i.e., from 16 day old seedlings). The transcriptomic data of these genotypes (submitted now) along with the previously submitted dataset (GSE79043) were used to develop traditional and orthogonal signal correction filtered partial least square discriminant analysis (OSC-PLSDA) models using the differential transcriptomic fingerprints in tolerant vs susceptible rice genotypes. These models are then used to test the transcriptomic fingerprints of stressed and unstressed samples of several genetically diverse rice genotypes in a way to predict their salinity tolerance status. The accuracy of the prediction using OSC-PLSDA model was higher compared to that of the traditional PLSDA model. Besides, the accuracy of the prediction of salinity tolerance of the salt stressed samples was higher than that of the unstressed samples indicating that the stress induced transcriptomic fingerprints can better discriminate the tolerance and susceptible genotypes.The minimum number of genes (109 genes) that highly contributed to the classification and model prediction of salinity tolerance status was identified using the Variable Importance vector in OSC-PLSDA model.This study provides an example of prediction model building using whole genome transcriptomic data. The fingerprints of such transcriptomic profiles could be used as possible markers for the overall prediction of tolerance or resistance to abiotic and biotic stresses, respectively.

overall_design: Fourteen day old whole seedlings of the rice genotypes were treated with 0 & 120 mM NaCl stress for 48 hours with three replications and the microarray based gene expressions were measured using Agilent Rice Gene Expression 4x44K Microarray.

last: Rashed Hossain


title: HBcAg-Induced IL-17F Drives Liver Fibrosis in Occult HBV Infection

status: Public on Jun 21 2026

city: 广州市

first: Bochao

address: 广州市越秀区麓苑路31号

institute: GUangzhou Blood Center

summary: While occult hepatitis B virus infection is a known risk factor for progressive liver diseases, the mechanistic basis for this association is poorly understood. To investigate this, we conducted a comparative study involving 40 OBI blood donors and 100 healthy blood donors to assess clinical parameters of liver fibrosis, including serum biomarkers, the FIB-4 index, and liver stiffness measurement. Transcriptome sequencing of peripheral blood mononuclear cells from these donors identified IL-17F as significantly upregulated in the OBI group. Mechanistically, we found that IL-17F was chiefly secreted by CD4+ T cells upon HBcAg stimulation and functionally promoted the expression of key fibrosis-related cytokines and markers. Collectively,  our study unveils a novel pathway wherein HBcAg induces CD4+ T cells to secrete IL-17F, which in turn accelerates liver fibrogenesis, providing a mechanistic basis for OBI-associated liver disease.

overall_design: In light of the increased liver fibrosis susceptibility observed in OBI blood donors, we performed transcriptome sequencing of their PBMCs to identify potential molecular drivers. Samples were obtained from five OBI blood donors with concurrent abnormalities in liver fibrosis markers (≥ 2 indices), LSM values (≥ 6.8 kPa), and also moderate-risk FIB-4 index (≥ 1.3), which were further confirmed the presence of liver injury through ultrasound detection (Figure 1), alongside five matched healthy donors as negative controls. These samples were subsequently subjected to transcriptome sequencing.


title: Spatial transcriptomics reveals C10 tumor transcriptomic changes generated by Smarta cell transfer

status: Public on Jun 22 2026

city: Bethesda

first: Jia

last: Nie

state: Maryland

address: Building 37, Room 3016

department: Center for Cancer Research

institute: National Cancer Institute

summary: To elucidate how antigen-specific CD4 T cells indirectly repress tumor growth independently of other lymphocytes, we first sought to gain insight into the changes they induced in the tumor micro-environment (TME) using the 10x Genomics Visium technology

overall_design: C10 tumors from Rag1–/– mice, treated with either PBS or Smarta on day 4 post-tumor transplant, were dissected at day 10 and subjected to formalin-fixed and paraffin-embedded (FFPE) processing. Two 5 μm FFPE tissue sections were prepared for each condition and were conducted for spatial transcriptomics analysis.


title: Identification of potential targets of FTO in GIST via transcriptome-wide RNA-seq

status: Public on Jun 10 2026

city: Changsha

first: Zhi

address: NO. 87 Xiangya Road, Kaifu District

institute: Xiangya hospital, Central South University

summary: Tyrosine kinase inhibitor (TKIs) resistance remains the leading obstacle for treating gastrointestinal stromal tumor (GIST), in which the secondary mutations within KIT causes escape of TKI inhibition and KIT reactivation. Here we found FTO was highly expressed in GIST and positively correlated with the high-grade and recurrence liability. m6A-seq and RNA-seq analyses of GIST cells treated with FTO inhibitor CS1 demonstrated that FTO demethylated the m6A modification in the 3’UTR of KIT mRNA, which in turn partially blocked recognition by m6A reader YTHDF2, thus enhanced KIT mRNA stability. Pharmacological inhibition or genetic knockdown of FTO led to decreased KIT expression, mitigated malignant phenotypes and increased imatinib sensitivity in vitro, while genetic knockout of FTO or entacapone treatment combined with imatinib evoked regression of tumor in KIT-Asp818Tyr/+ heterozygote GIST mouse model. Phase I trial in five TKIs-refractory GIST patients with a combination of entacapone and imatinib (NCT 04006769) demonstrated that two of three assessable participants (66.7%) achieved partial remission. Our results suggest that targeting FTO is a feasible therapeutic strategy for clinical management of TKI resistance and recurrence of GIST.

overall_design: To elucidate the molecular mechanism by which FTO promotes GIST progression and imatinib resistance, we treated GIST-T1, GIST-882, GIST-48, and GIST-430 cells with the FTO inhibitor CS1 for 48 hours (at a concentration of 100nM) and subsequently extracted RNA from the cells for RNA-seq.

first: Junju

last: He

first: Lunquan

last: Sun


title: A yolk sac-derived hepatic γδ T cell subpopulation develops in a hematopoietic stem cell- and thymus-independent manner

city: Beijing

first: Guoju

last: You

state: Beijing

address: Shuangqing Road

institute: Tsinghua University

summary: γδ T cells are a highly heterogeneous T cell lineage with diverse immunological functions; however, the developmental origins underlying this heterogeneity, particularly the existence and physiological relevance of extrathymic pathways, remain incompletely defined. Our previously generated transcriptomic datasets indicate that Stab2 is specifically expressed in the yolk sac but not the aortic endothelial cells. Leveraging this spatially restricted expression pattern, we generated a Stab2-CrexERT2 inducible genetic lineage tracing mouse model and demonstrated its ability to label yolk sac–derived hematopoietic cells in vivo. Importantly, we detected the contribution of the yolk sac endothelial cells labeled at embryonic day 9.5 to a subset of Vγ1 γδ T cells in the adult liver but hardly to any hematopoietic progenitors in the thymus and bone marrow. Single-cell transcriptomic profiling revealed that the Stab2-labeled yolk sac endothelial cell-derived hepatic γδ T cells follow a developmental trajectory distinct from other hepatic γδ T cells, that the labeled hepatic naïve γδ T cells exhibited a bias toward differentiation into IFN-γ–producing γδ T1 cells and an enhanced granzyme-mediated activity by comparison. Collectively, our findings provide direct in vivo evidence for the existence of a bone marrow hematopoietic stem cell-independent and thymus-independent developmental pathway of liver γδ T cells originating from yolk sac endothelial cells.

overall_design: To delineate the molecular features of E9.5-labeled γδ T cells, we performed single‑cell RNA sequencing on flow cytometry‑isolated CD45⁺tdTomato⁺ cells and  CD45⁺tdTomato- from the liver of 2‑month‑old mice.For 10X Genomics-based scRNA-seq, we implemented the Chromium Single Cell 5’ PE v3 libraries according to the manufacturer’s instructions (https://cdn.10xgenomics.com/image/upload/v1710231087/support-documents/CG000733_ChromiumGEM-X_SingleCell5_ReagentKitsv3_UserGuide_RevA.pdf). Sequencing was performed on the NovaSeq X PLUS pe150 platform.

first: Yuzhe

last: Chen

first: Kangyu

last: Huang

first: Chaojie

last: Wang

first: Bing

first: Yu

last: Lan


title: DNP63 regulates epithelial stratification and differentiation in the murine ureter

city: Hannover

first: Florian

last: Bergmann

address: Carl-Neuberg-Straße 1

department: Institut für Molekularbiologie

country: Germany

institute: Hannover Medical School

summary: The urothelium is a stratified epithelium that lines the inner surface of the organs of the urinary drainage system. The urothelium consists of a layer of basal cells, one to several layers of intermediate cells, and an apical layer of large superficial cells. How this patterned arrangement of differentiated cell types arises from uncommitted precursor cells is insufficiently understood. Here, we analyzed the cellular and molecular function of the transcription factor DNP63. DNP63 expression begins in epithelial progenitors at embryonic day (E)14.5, and is confined to basal and intermediate cells from late fetal stages onwards. We show that in mice with a conditional loss of DNp63 in the ureter, the urothelium presents around birth as a monolayered but folded epithelium, consisting predominantly of partially differentiated superficial cells. At E15.5, i.e. shortly after the onset of DNP63 expression in the ureter, epithelial proliferation and cell division planes were unaffected. Transcriptional profiling revealed that DNp63 is required for the expression of genes that regulate epithelial stratification, cell adhesion and division. DNP63 is also responsible for repression of Ihh, precluding premature formation of the lamina propria. Analysis of mutant ureters at postnatal stages revealed a progressive reconstitution of the normal urothelial cytoarchitecture, suggesting that DNP63+ epithelial progenitors that have escaped recombination, undergo rapid proliferative expansion and differentiation into I and B cells. Our results suggest that a conserved DNP63 gene regulatory module is responsible for epithelial stratification, expansion of basal and intermediate cells, and correct differentiation of superficial cells in the murine ureter.

overall_design: snRNAseq of DNp63cKO and controll mouse ureters collected at P0

first: Carsten

last: Rudat

first: Andreas

last: Kispert


title: Diverse infection models demonstrate robust resistance of Mycobacterium tuberculosis to innate immunity

city: Berkeley

first: Marian

last: Fairgrieve

state: CA

address: 415 Weill Hall, University of California

institute: University of California

summary: We employeed 10X genomics single cell sequencing to examine the influence of innate immune system priming on the response of macrophages to M. tuberculosis (Mtb) infection during the innate immune response phase of infection.

overall_design: In this study, we infected C57BL/6 mice with Mtb and in parallel, we primed the lungs of C57BL/6 mice with Legionella pneumophila (Lp) infection for three days, followed by infection with fluorescent Mtb. After 14 days of Mtb infection, we harvested the lungs, enriched for CD64+ cells, and sorted cells, further excluding neutrophils. This data set represents uninfected (bystander) cells from infected mice.

middle: R

first: Ella

middle: C

last: Brydon

first: Roberto

middle: A

last: Chavez

first: Dmitri

middle: I

last: Kotov

first: Russell

middle: E

last: Vance


title: Trichoderma reesei Nsd3 transcription factor: pleiotropic roles in development, stress response, secondary metabolism, and cellulase production [ATAC-seq]

city: Ribeirão Preto

middle: N

last: Silva

state: São Paulo

address: Bandeirantes Avenue

department: Biochemistry and Immunology

country: Brazil

institute: University of São Paulo

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Trichoderma reesei is widely known for its ability to secrete high amounts of cellulases, enzymes of fundamental importance in generating products from lignocellulosic biomass. Diverse signaling pathways and transcription factors (TFs) control the cellulolytic repertoire in T. reesei to ensure correct adaptation to the environment and consumption of the most favorable carbon source. Here, we analyzed RNA-Seq data and identified a new potential regulator of cellulase production in T. reesei: a novel zinc finger TF named Nsd3, homolog of NsdC from Aspergilli. Deletion of nsd3 reduced vegetative growth and conidiation on solid medium. Phenotypic characterization of the Δnsd3 strain showed that it is more sensitive to osmotic stress but more resistant to cell wall and oxidative stresses. Our results showed that Nsd3 acts as a repressor of cellulase expression, an unreported role for this TF in fungi. Loss of nsd3 leads to a faster and more robust induction of cellulolytic genes and higher cellulase and hemicellulase activities. Transcriptional profiling by RNA-Seq and chromatin accessibility profiling by ATAC-Seq showed that sugar transporters are important targets of Nsd3 during cellulase expression regulation. Combined with microscopy and gene expression analyses, the ATAC-Seq data also highlighted Nsd3 as a central regulator of cell wall remodeling and organization. Furthermore, the transcriptomics also showed that Nsd3 regulates genes involved in secondary metabolism. These results showed that Nsd3 regulates several physiological processes and provide novel insights into the regulatory system of cellulases in T. reesei that can be used in the design of high-performance strains for biorefinery.

overall_design: ATAC-Seq profiling of T. reesei WT and Δnsd3 strains grown in glucose (24 h)

first: David

last: Maués

first: Lucas

last: Pereira

first: Andrei

last: Steindorff

first: Amanda

last: Antoniêto

first: Rafael

last: Silva-Rocha

first: Marcelo

last: Gomes

first: Zachary

last: Lewis


title: Endocardial HAND2 orchestrates hypoxic and TGFbeta signaling to modulate coronary artery formation

city: Nanjing

first: Huijuan

last: Wang

address: 163 Xianlin Road

institute: Nanjing University

summary: The endocardium is a major source of coronary angiogenesis and arterialization, through coordinated cell fate transition and migration. However, the transcriptional regulatory network synchronizing cell fate determination and movement remains unclear. Here, we identified transcription factor HAND2 as a key candidate for coronary vascular formation. Endocardial deletion of Hand2 in mice disrupted arterial-venous networks and stunted coronary arteries, paralleling a ventricular noncompaction phenotype. Moreover, deletion of Hand2 produced excessive tip cells with defective movement. RNA-seq analysis revealed enhanced hypoxic metabolic activation but declined TGF-β/p38MAPK-dependent Endo-MT. In consistence, genetic inhibition of the core hypoxic regulators or pharmaceutical administration of TGFβ2 partially recovered the coronary arterial defects in Hand2 mutants. Furthermore, HAND2 was found directly bound to promoters of the target genes, harmonizing cell migration and cell fate transition. These findings pinpoint HAND2 as an essential regulator to regulate endocardial transcriptional regulatory network for coronary arterialization and provide potential therapeutic targets for coronary artery diseases.

overall_design: The GSE311984 superseries consists of three independent sub-datasets: GSE311981 (CUT&Tag), GSE311982 (RNA-seq), and GSE311983 (scRNA-seq).


title: Cell‑type‑specific gene expression profiling in Stevia rebaudiana leaves by single‑nucleus RNA sequencing

city: Yokohama

first: Keiko

last: Sugimoto

state: Kanagawa

address: 1-7-22 Suehiro, Tsurumi

department: CSRS

country: Japan

institute: RIKEN

summary: Stevia rebaudiana (stevia) is a plant that accumulates high levels of steviol glycosides (SGs) in its leaves, which provide strong sweetness. In this study, we used single‑nucleus RNA sequencing (snRNA‑seq) to resolve the expression landscape of SG‑biosynthetic genes across individual cell types in stevia leaves. We identified distinct nuclear clusters corresponding to different cell types such as mesophyll, epidermis, trichomes and vascular bundle sheath. Notably, UGT76G‑family and UGT91D4 sugar‑transferase genes showed high expression in mesophyll and epidermal nuclei, suggesting spatial division of SG production within leaf tissues.

overall_design: Mature leaves from the stevia cultivar SF2‑1355 were harvested, and nuclei were isolated using a standard protocol. Libraries were prepared on the 10x Genomics Chromium platform, sequenced, and processed for quality control. After filtering, 5,700 high‑quality nuclei were retained and subjected to Leiden clustering, yielding 13 distinct clusters. Cell type annotation was performed based on marker genes from Arabidopsis thaliana homologs and over‑representation analysis. The clusters included mesophyll cells, epidermal cells, vascular bundle sheath, trichomes, and others. Trichome nuclei exhibited elevated expression of genes associated with the MEP pathway and terpenoid biosynthesis, whereas SG‑specific genes (e.g., UGT76G4, UGT91D4) were predominantly expressed in mesophyll and epidermal nuclei, revealing a cell‑type specialization in SG biosynthesis.

first: Hatsune

last: Morinaka

first: Ayako

last: Kawamura

first: Dongbo

last: Shi

first: Kotaro

last: Torii

first: Akira

last: Iwase

first: Tsubasa

last: Shoji


title: Endocardial HAND2 orchestrates hypoxic and TGFbeta signaling to modulate coronary artery formation [scRNA-seq]

overall_design: The endothelial cells were sorted from E14.5 hearts of Hand2f/f;VE-cad-CreERT2; iSure-Cre(HD-ko) mice(HD-ko) and VE-cad-CreERT2; iSure-Cre(HD-wt) mice, Tamoxifen (8 mg) was administered via gavage at E11.5 and E12.5 to induce the expression of VE-cad-CreERT2; iSure-Cre. Each sample was analyzed using a 10x Genomics Chromium single-cell controller. The Single Cell 3’ Library and Gel Bead Kit V3.1 were used for single-cell cDNA library construction, and sequencing was conducted on an Illumina Novaseq 6000 sequencer.

first: Haosheng

last: Zhang

first: Yinlei

last: Zheng

first: Peihan

first: Yuqian

first: Sijia

last: Ding

first: Wenping

last: Liu

first: Zhongzhou

last: Yang

first: Wen

last: Luo


title: Multi-omics Analysis of Immune Cells Induced by Artificial Adjuvant Vector Cell (aAVC) Therapy in HPV-Positive Tumor-Bearing Mice [scRNA-seq]

city: Yokohama City

first: Takuya

last: Ishibashi

address: 1-7-22 Suehiro-cho, Tsurumi-ku

institute: RIKEN Center for Integrative Medical Sciences

summary: Immune evasion by tumors highlights the need to activate both CTLs and NK cells against “immune-desert” type of tumor, yet the synergistic potential of dual activation in immune-desert tumors remains unclear. Here, we uncover a spatiotemporal synergy between NK cells and CTLs that drives functional antitumor effects in an immune-desert tumor model.  Using a multi-omics imaging approach integrating spatial transcriptomics, scRNA-seq re-clustering, and multicolor flow cytometry, we show that vaccination rapidly reshapes lymphocyte localization and function in the tumor microenvironment (TME). Early activated IRF8+Klrg1+NK cell infiltration establishes a niche that guides subsequent antigen-primed CXCR3+CTL influx, accompanied by dendritic cell activation and inflammatory monocyte recruitment. This coordinated response relies on structural and chemotactic remodeling of the TME, facilitating NK-CTL interactions at the tumor margin. Our findings demonstrate how integrated multi-omics analyses can uncover previously inaccessible interactions and provide a framework for designing next-generation immunotherapies.

overall_design: Mice were inoculated with HPV-E6 and E7 expressing lung cancer (TC-1) cells and treated with cancer vaccine,  artificial Adjuvant Vector Cells (aAVC) on day7. We collected tumor samples on day3 and day7 after aAVC treatment. Then, we performed sc-RNA-seq and spatial transcriptomic analysis. For spatial transcriptomic analyis, Xenium in situ technology platform (10x Genomics) was employed.

first: Hiroshi

last: Nakazato

first: Kanako

last: Shimizu

first: An

last: Sampei

first: Yan

first: Marin

last: Yanagawa

first: Satoru

last: Yamasaki

first: Jun

last: Shinga

first: Shin-ichiro

last: Fujii


title: Swi-Snf and Tup1-Cyc8 directly cooperate to antagonistically regulate gene transcription in yeast.[MNase]

city: Dublin 2

first: Alastair

last: Fleming

address: College Green

department: Microbiology Dept.

country: Ireland

institute: Trinity College Dublin

summary: The Saccharomyces cerevisiae Swi-Snf co-activator complex was the first ATP-dependent chromatin remodelling complex discovered which functions by altering promoter chromatin structure to enable gene transcription. Conversely, the yeast Tup1-Cyc8 complex was identified as the first global co-repressor which can repress transcription by establishing ordered arrays of hypoacetylated nucleosomes across gene promoters. Although studies have indicated potential cooperation between these archetypal complexes upon transcription regulation, the precise mechanism and global extent of this antagonistic interplay remains unclear. We have identified all of the genes subject to repression by Tup1-Cyc8 and activation by Swi-Snf in glucose-grown yeast. These antagonistically regulated genes are enriched for those involved in cell wall structure and sugar metabolism. The data reveals that some co-regulated genes are kept inactive by Tup1-Cyc8 in wt and are de-repressed in the absence of CYC8 in a SNF2-dependent manner. Conversely, other co-regulated genes are actively transcribed in wt at levels mediated by the net negative influence of CYC8 and the positive influence of SNF2. In all cases, co-regulated genes located nearest to telomeres are subject to the most robust regulation by Swi-Snf and Tup1-Cyc8. ChIP analysis suggests that Snf2p and Cyc8p are present at both the active and inactive co-regulated genes in wt, where SNF2 is required for full Tup1p occupancy. We show that Snf2p and Cyc8p can directly interact with each other, most likely in the context of their respective complexes, suggesting that Swi-Snf and Tup1-Cyc8 are present together at co-regulated genes. We demonstrate that the nucleosome remodelling activities by Swi-Snf and Tup1-Cyc8 are specific to each target gene and extend over the available upstream intergenic region, the length of which is dependent upon the genes chromosomal context. Together, these data/ provide a deeper insight into the interplay between Tup1-Cyc8 and Swi-Snf upon transcription regulation and /suggest their occupancy and activity are intimately intertwined to yield the target gene transcriptional outcome via chromosomal location-dependent chromatin remodelling covering the available upstream gene regions.

overall_design: Mnase-seq

first: Xuyuan

last: Guo

first: Mohamed

last: Al Hussain

first: Brenda

last: Lee

first: Nicole

last: Byrne

first: Hadel

last: Aljaeed

first: Reham

last: Alnajjar

first: Karsten

last: Hokamp

first: Nicholas A

last: Kent

first: Alastair B


title: Swi-Snf and Tup1-Cyc8 directly cooperate to antagonistically regulate gene transcription in yeast

overall_design: RNA-seq profiling of wild-type, Cyc8 mutant, Snf2 mutant and Cyc8 and Snf2 double mutant of Saccharomyces cerevisiae S288C-derived strains.


title: Growth hormone (GH) suppresses DNA damage repair in human prostate epithelial cells

city: Los Angeles

first: Vera

last: Chesnokova

address: 8700 Beverly Blvd

institute: Cedars Sinai Medical Center

summary: In normal prostate, DNA damage accumulates with age, resulting in local GH induction. Age-associated local GH abundance enables further DNA damage accumulation. Employing RNA sequencing, we report here that genes related to DNA damage repair were found to be significantly suppressed in primary human prostate epithelial cells (HPrEC) line 1 and in line 2, in 3 independent experiments after treatment with 100 ng/mL GH for 24 h. BRCC3, TAF5, H4C16, NUDT16L1, and TADA3 , all pivotal in DNA damage repair were significantly downregulated. The data revealed mechanisms underlying GH-induced unrepaired DNA damage accumulation in prostate epithelial cells.

overall_design: RNA-seq profiling of HPrEC cells line 1 and line 2 treated with 100 ng/ml GH, in 3 independent expreiments.

first: Masaki

last: Ryuzaki

first: Svetlana

last: Zonis

first: Sandrine

last: Billet

first: Stephen

middle: J

last: Freedland

first: Hyung

last: Kim

first: Neil

last: Bhowmick

first: Shlomo

last: Melmed

first: Saravana Kumar

last: Kailasam Mani


title: Molecular Characterization of Meningioma

city: Baltimore

first: Eli

last: Yazigi

address: 1550 Orleans St

institute: Johns Hopkins

summary: Meningiomas are the most common primary tumors of the central nervous system. A majority of meningiomas have a relatively benign clinical course. However, even benign meningiomas can manifest with focal neurological symptoms or mass effect depending on the size and location of the tumor. Current standard of care for symptomatic tumors remains maximal safe surgical resection followed by radiological surveillance, with additional radiation therapy for high-grade tumors or tumors where complete resection is not feasible. To date, there is limited evidence demonstrating definitive efficacy of systemic therapies for meningiomas. Here, we perform full-transcriptome spot-resolution spatial transcriptomics using the 10X Visium platform on 19 low-grade meningiomas. We use bulk methylation profiling to classify these meningiomas into three previously described methylation classes corresponding to the Merlin-intact, immune-enriched, and hypermitotic molecular phenotypes.

overall_design: We perform full-transcriptome spot-resolution spatial transcriptomics using the 10X Visium platform on 19 surgicall resected low-grade meningiomas (WHO I and II). We use bulk methylation profiling to classify these meningiomas into three previously described methylation classes corresponding to the Merlin-intact, immune-enriched, and hypermitotic molecular phenotypes.

first: Lyla

last: Atta

first: A. Karim

last: Ahmed

first: Landon

last: Hansen

first: Calixto-Hope

last: Lucas

first: Christoper

middle: M

last: Jackson

first: Jean

last: Fan


title: A Biodegradable Piezoelectric Vertebral Implant for Programmable Electro-neuromodulation in Spinal Cord Injury

first: Yanchun

last: Liu

address: No. 45, Changchun Street

institute: Xuanwu Hospital

summary: Spinal cord stimulation is a promising strategy for functional recovery after spinal cord injury (SCI), but conventional electronic implants pose surgical and long-term risks. Here, we report a biodegradable piezoelectric cryogel (Piezo Gel) that enables programmable electro-neuromodulation without implanted electronics. Mimicking spinal biomechanics, Piezo Gel converts physiological movement into localized endogenous electric fields, while externally applied ultrasound (US) amplifies its electrical output, enabling on-demand in situ programming. In a rat model of acute severe SCI, US-activated Piezo Gel significantly enhanced locomotor recovery, improved Basso–Beattie–Bresnahan (BBB) scores, and promoted bladder functional remodeling. In a mild contusion model, we further implemented a phase-adaptive neuromodulation strategy, shifting from US-driven stimulation during acute immobility to movement-driven stimulation during subacute rehabilitation, aligning with the evolving spinal microenvironment. This sequential programming resulted in substantial restoration of coordinated gait. Together, this work establishes an electronic-free, programmable electro-neuromodulation paradigm that integrates US and physiological motion, offering a clinically translatable approach for SCI repair.

overall_design: Bulk RNA-seq was performed on spinal cord lesion-core tissues (~5 mm3) collected from the lesion epicenter (T9 segment) of rats subjected to a T9 spinal cord contusion injury model. Samples were obtained from two treatment groups, Gel+US and Piezo Gel+US. Total RNA was extracted from injured spinal cord cores, followed by paired-end sequencing and differential gene expression analysis to identify molecular changes associated with Piezo Gel-mediated programmable electro-neuromodulation.

first: Wanru

last: Duan

first: Qing

last: Cai

first: Yingjie

last: Yu

first: Penghao

first: Xinyu

last: Wang


title: Splice-altering TP53 missense mutations: Drivers of functional loss and therapeutic targets via RNA modulation

city: Daejeon

first: Su-Jin

last: Baek

address: 1672, Yuseong-daero

country: South Korea

institute: KOREA INSTITUTE of ORIENTAL MEDICINE

summary: Using bacterial artificial chromosome DNA-mediated targeting, we developed knock-in TP53 mutant cell models including c.182A>G, c.318C>G, c.356C>G and c.362C>A. These missense mutations can function as frameshift or hypomorphic mutations due to aberrant splicing, significantly compromising TP53 mRNA integrity.

overall_design: To investigate the molecular functions of the four TP53-mutants and their changes induced by AMO treatment, we profiled gene expression signatures between AMO-untreated (Control) and AMO-treated (AMO) TP53 mutant cells. In particular, we compared gene expression between TP53 mutants treated with doxorubicin reagent and untreated TP53 mutants in the control and AMO groups, respectively.


title: DNMT3A mutation coordinates epigenetic and translational regulation through orchestrating BCAA metabolism in acute myeloid leukemia (WGBS)

first: Yongjia

last: Wei

address: No. 1 Shuaifuyuan

department: Department of Hematology

institute: Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College

type: Methylation profiling by high throughput sequencing

summary: Acute myeloid leukemia (AML) harboring DNMT3A mutation exhibits epigenetic dysregulation, chemoresistance and poor outcome, but the underlining mechanism remains elusive. Here, inspired by the unexpected finding that DNMT3A-mutated AML patients exhibit a unique translatome landscape, we connected this epigenetic mutation to translational dysregulation through reprogrammed branched-chain amino acid (BCAA) metabolism. Particularly, DNMT3A mutation induces DNA hypomethylation-dependent activation of BCAT1, a rate-limiting aminotransferase gene for BCAA metabolism. Thereafter, the accumulation of intracellular BCAA more profoundly alters translation of a select subset of transcripts with higher BCAA codon ratios. Accordingly, deficiency in BCAA availability reduces the translation of target genes and attenuated the proliferative advantages of DNMT3A-mutated AML cells. More importantly, the pharmacological inhibition of BCAT1 with Gabapentin normalized BCAA levels, reversed target genes translation and repressed leukemia cell growth specifically in DNMT3A-mutated AML cells. Collectively, these findings uncovered a novel epigenetics-metabolism axis, in which DNMT3A mutation boosts BCAA metabolism thereby not only forming a positive feedback loop to enhance DNA hypomethylation through alpha ketoglutarate (α-KG)-dependent ten-eleven translocation (TET) activation, but also affecting gene translation in a BCAA codon-biased manner. Moreover, the efficacy of Gabapentin in suppressing AML cell proliferation highlights the clinical relevance of targeting BCAA metabolism to improve outcomes of DNMT3A-mutated AML.

overall_design: WGBS performed on DNMT3A WT- and DNMT3A R882H-transduced THP-1 cells

first: Chengyang

last: Xu

first: Chenxi

last: Han

first: Jian

last: Li

first: Jia

first: Fang


title: DNMT3A mutation coordinates epigenetic and translational regulation through orchestrating BCAA metabolism in acute myeloid leukemia

overall_design: RNA-seq and Ribo-seq performed on DNMT3A WT- and DNMT3A R882H-transduced THP-1 cells


title: Modulation of non-canonical WNT5B-NFATc2 pathway-dependent MMP14 expression in astrocytes ameliorates neuropathology and motor behaviors in Huntington's disease mice

city: Seoul

first: Hoon

last: Ryu

state: Seoul

address: Seoul

department: Brain Science Institute

institute: Korea Institute of Science and Technology

summary: Huntington’s disease (HD) is a fatal neurodegenerative disorder characterized by a triad of behavioral symptoms, including involuntary movement, emotional change, and cognitive dysfunction. Although alterations in the WNT signaling pathway have been reported in HD, its precise role in disease pathogenesis remains unclear. In this study, we found that astrocytic WNT5B mRNA and protein levels were elevated in the striatum of both HD patients and HD mouse models. WNT5B induced prolonged expression of matrix metallopeptidase 14 (MMP14), an extracellular matrix (ECM)-degrading enzyme, through NFATc2 transcription factor activation via the non-canonical WNT signaling pathway in both human and primary mouse astrocytes. The significant upregulation of MMP14 led to ECM degradation, medium spiny neuron (MSN) damage, and increased mutant huntingtin aggregation in N171-82Q HD transgenic mice. Furthermore, WNT5B gain-of-function exacerbated neuropathology, impaired motor coordination, and shortened the lifespan of N171-82Q mice. We further report that overexpression of estrogen receptor 𝛼 (ER𝛼) suppresses NFATc2 transcriptional activity. Genistein, a phytoestrogen, reduced MMP14 transcription by antagonizing the NFATc2 pathway and prevented ECM degradation in N171-82Q mice. Additionally, genistein administration ameliorated motor behavior and prolonged the lifespan of N171-82Q mice. Together, our findings reveal a molecular pathological mechanism in which astrocytic MMP14 transcription, activated by the non-canonical WNT5B signaling pathway, causes ECM degradation, MSN damage, and accelerates neurodegeneration in HD. Modulation of non-cell-autonomous WNT5B-NFATc2-MMP14 pathway by genistein may serve as a potential therapeutic strategy for ameliorating HD pathogenesis.

overall_design: Whole RNA sequencing to detect gene expression patterns in HD (N171-82Q) mice injected by AAV-GFAP-WNT5B into the striatum.

first: Junhee

last: Lee


title: Alphavirus M1 disrupts super-enhancer-driven oncogenic transcription in osteosarcoma [RNA-seq]

city: Guangzhou

first: Jiajun

last: Zhang

address: #58，Zhongshan 2nd Road

institute: the First Affiliated Hospital of Sun Yat-Sen University

summary: Oncolytic virotherapy has shown promise for various cancers, but its application in osteosarcoma (OS) remains underexplored. This study provides the first evidence of the potent oncolytic activity of M1, a natural Getah-like alphavirus, against OS. We demonstrate that OS cells exhibit heightened sensitivity to M1 infection, with its anti-tumor effects not solely dependent on the canonical ER stress-induced apoptosis. Proteomic and ChIP-seq analyses show the DNA-directed RNA polymerase II subunit RPB1 contributes to oncogenic super-enhancer activity and serves as a direct target of M1-mediated regulation. The oncolytic potency correlated positively with the transcriptional dependency on RPB1 within super-enhancer regions. Mechanistically, the viral non-structural protein NSP2 disrupts super-enhancer activity by recruiting the CUL2-RBX1-ELOC complex, which triggers K63-linked ubiquitination and degradation of RPB1. These findings uncover a previously unrecognized oncolytic mechanism of M1 and its therapeutic potential in OS, with RPB1 as a predictive biomarker for virotherapy response.

overall_design: RNA-seq data of osteosarcoma cells pre- and post-M1 virus infection, as well as pre- and post-Tet-on NSP2 expression plasmid transfection

first: Lifeng

last: Yin

first: Qianqian

first: Yuanyuan

first: Fei

last: Wu

first: Shanyu

last: Huang

first: Jiayu

first: Yiwei

last: Fu

first: Guanyu

first: Yu

first: Hanxiao

first: Jiankai

last: Liang

first: Wenbo

last: Zhu

first: Yuan

last: Lin

first: Guangmei

last: Yan

first: Junqiang

first: Jingnan

last: Shen

first: Jing

first: Weihai


title: Alphavirus M1 disrupts super-enhancer-driven oncogenic transcription in osteosarcoma [ChIP-seq]

first: Jiajun

overall_design: The ChIP-seq data of osteosarcoma cells SJSA-1 pre- and post-M1 virus infection, using anti-H3K27ac and anti-RPB1 antibodies

first: Lifeng

first: Qianqian

last: Cai

last: Liu


title: Design, synthesis and in vitro and in vivo biological evaluation of matrine derivatives as efficient anticancer agents with the characteristics of endoplasmic retic stress induction and apoptosis activation

city: Nanning

first: Xingdong

last: Wang

state: Guangxi

address: Daxuedonglu

institute: Guangxi University

summary: Search for the anticancer pathway of matrine derivatives

overall_design: We then performed gene expression profiling analysis using data obtained from RNA-seq of HeLa cell at two time points.

first: Tingguo

last: Xu


title: Comparative Multi-Omics Evaluation of the Tumor Microenvironment in Canine and Human Hepatocellular Carcinoma

city: Columbia

first: Wesley

last: Warren

state: MO

address: LSC

institute: University of Missouri, Columbia

summary:
Background: Liver cancer remains a leading cause of death in humans. Its primary form, hepatocellular carcinoma (HCC) is frequently resistant to chemotherapy and radiation and often shows insufficient response to immunotherapy. HCC in dogs can arise from various factors but is not typically associated with viral infections, cirrhosis, or alcohol consumption, the more common triggers of spontaneous HCC in humans. This distinction offers a unique comparative perspective on the intrinsic genetic drivers of the disease.
Methods: Using whole exome sequencing (WES) and single nucleus RNA sequencing (snRNA-seq) in tandem, we perform a multi-omic analysis of the dog HCC tumor.
Results: Mutational analysis of impactful polymorphisms revealed a conserved cross-species landscape with genes such as CTNNB1, known for highly recurrent mutations in human HCC, showing similar alterations in dogs. In dog HCC tumors, we identified major cell types commonly observed in human HCC, including T lymphocyte, endothelial, macrophage, fibroblast, hepatocyte, malignant, and non-specific proliferating types. A comparative analysis of intercellular interactions across human and dog HCC cell types revealed intriguing parallels, particularly in macrophage functionality.
Conclusions: These findings underscore the need for expanded genetic studies of dog HCC to further elucidate cross-species commonalities, offering deeper insights into key aspects of HCC biology and identifying novel therapeutic targets.

overall_design: Samples from two dogs with hepatocellular carcinoma were collected and sequenced as described above. Downstream analyses, including clustering, cell type annotation, cell-cell communication, cancer stemness, and cell cycle analysis, were performed. Additionally, we compared the resulting cellular landscape and cell-cell interactions between canine and human HCC samples.

first: Yulia

last: Nussbaum

first: Edward

last: Ricemeyer


title: Reprogramming-driven drug discovery uncovers sildenafil as a candidate drug for mitochondrial disease

city: Berlin

first: Pawel

last: Lisowski

address: Hannoversche Str. 28

institute: Max-Delbrück-Center for Molecular Medicine (MDC) in the Helmholtz Association

summary: Mitochondrial disease is a group of rare inherited conditions affecting mitochondrial function. A severe untreatable form of mitochondrial disease is Leigh syndrome (LS) characterized by psychomotor regression and acute metabolic crises. To accelerate drug discovery for mitochondrial disease, we focused on drug repurposing and made use of induced pluripotent stem cell (iPSC)-derived neuronal precursor cells (NPCs) from LS patients to screen a library of 5,632 repurposable compounds. We identified phosphodiesterase 5 inhibitors (PDE5i) as leads capable of normalizing mitochondrial polarization in LS NPCs. Among PDE5i, we prioritized Sildenafil due to its established safety profile in children. Sildenafil restored key pathways regulating nervous system development, enhanced neurite outgrowth in LS neurons, and mitigated abnormal calcium responses in LS brain organoids under metabolic stress. In a mouse model of LS, Sildenafil led to lifespan extension and amelioration of metabolic and encephalopathy phenotypes. Lastly, chronic off-label treatment with Sildenafil in six LS patients demonstrated good tolerability and clinical improvements. Our findings highlight the potential of iPSC-driven drug discovery for rare diseases and position Sildenafil as a promising candidate drug for patients with mitochondrial disease.

overall_design: Single-nucleus RNA sequencing (snRNAseq) of AggreWell™ cortical brain organoids (ACOs). For snRNAseq, we used (day invitro) DIV 72 Aggrewell Cortical Organoids (ACOs)generated with the second appraoch83. ACOs  were treated with either DMSO (XM001_DMSO/CTRL_DMSO and 267B_DMSO/ATP6_DMSO) or 10 µM Sildenafil resuspended in DMSO (XM001_Sil/CTRL_Sil  and 267B_Sil/ATP6_Sil ) from DIV 18  to DIV 72. We used 15 pelleted organoids per sample (n=8 samples) with n=2 replicates per condition (n=120 ACOs in total).

first: Tancredi

last: Pentimalli

first: Alessandro

last: Prigione


title: IL-6-induced C/EBPα drives follicular regulatory T cell differentiation to regulate humoral immunity in mice

city: Pohang

first: Haena

last: Lee

state: Kyungbuk

address: POSTECH Biotech Center, 77 Cheongam-ro

department: Department of Life Sciences

institute: Pohang University of Science and Technology

summary: To investigate the C/EBPα-dependent mechanism of follicular regulatory T (Tfr) cell differentiation and function under pathological settings, we analyzed the transcriptomic profile of wild-type (WT) and Cebpa knock-out (KO) Tfr cells in autoimmune condition.

overall_design: Tfr cells (live CD4+Foxp3+CXCR5+PD-1+ICOS+) were sorted from the spleens of Foxp3-GFP reporter mice and Foxp3-Cre Cebpa-flox/flox mice 21 days after imiquimod treatment using FACS (CytoFLEX SRT sorter). To obtain sufficient cells for RNA isolation, sorted cells from more than two mice were pooled in TRIzol reagent to generate a single biological sample. RNA was extracted via a RNeasy Micro Kit (Qiagen) according to manufacturer's instructions, and subjected to RNA-seq.

first: Sin-hyeog

last: Im


title: BASELINE: single cell lineage tracing with Cas12a-ABE

city: Lebanon

first: Evan

last: Winter

state: NH

address: 1 Medical Center Dr.

department: Molecular and Systems Biology

institute: Dartmouth

summary: A cell’s fate is shaped by its inherited state, or lineage, and the ever-shifting context of its environment. CRISPR-based recording technologies are a promising solution to map the importance of lineage, yet challenges remain regarding single-cell recovery, engineering complexity, and scale. Here, we introduce BASELINE, which uses base editing to generate high-resolution lineage trees in conjunction with single-cell profiling. BASELINE uses the Cas12a adenine base editor to irreversibly edit nucleotides within 50 synthetic target sites, which are integrated multiple times into a cell’s genome. We show that BASELINE accumulates lineage-specific marks over a wide range of biologically relevant intervals, recording more than 4300 bits of information in a model of pancreatic cancer. Single-cell sequencing reveals high-fidelity capture of these lineage recorders, recovering lineage reconstructions up to 46 cell-divisions deep, within the estimated range of mammalian development. We expect BASELINE to be applicable to various lineage-tracing projects in development and disease, especially in which cellular engineering makes small, more distributed systems challenging.

overall_design: BASELINE-KPCY clones were transfected with Cas12a-ABE before being single cell sorted into 96-well plates. Colonies were expanded and passages at confluency until a single confluent well of a 6-well plate was obtained. At which point, cells from 2 distinct clones were combines (1:1) and subjected to scRNAseq (10X Chromium).

first: Aaron

last: McKenna


title: Fgf18 marks reserve skeletal stem or progenitor cells in the outer periosteum responsible for bone fracture repair

city: 杭州

first: XING

last: JI

state: State

address: 余杭塘路866号

institute: zhejiang university

summary: Purpose: The periosteum plays a crucial role in regulating bone growth and repair; however, the histological and transcriptomic characteristics of the long bone periosteum remain largely unknown. In our study, we aimed to investigate the cellular composition and gene expression profiles of the periosteum in long bones.

overall_design: scRNAseq of periosteum from WT  at 8wks

first: Xing

last: Ji

first: Fanxin

last: Long


title: 3D enhancer dynamics dictate treatment response in T-cell acute lymphoblastic leukemia

city: Boston

first: Valeriya

last: Dimitrova

state: MA

address: 450 Brookline Av

department: Pediatric Oncology

institute: Dana Farber Cancer Institute

summary: Background Cellular plasticity frequently contributes to treatment resistance in cancer, yet the 3D chromatin dynamics driving this plasticity are unknown. To investigate how enhancer remodeling maintains transcriptional heterogeneity and modulates treatment response, we use T-cell acute lymphoblastic leukemia (T-ALL) patient-derived xenograft (PDX) models carrying activating NOTCH1 mutations treated with Notch-inhibitor as a model of therapeutic resistance. Methods Here, we assessed alterations in 3D chromatin structures differentiating responder and non-responder models by evaluating enhancer rewiring and mapping of the associated loops using H3K27ac HiChIP. After performing full-length single-cell RNA sequencing of 3,129 leukemic cells from both models, before and after treatment with a NOTCH inhibitor, we characterized transcriptional states by assessing developmental potential using CytoTRACE and identified state-specific gene-regulatory networks (GRN) driving state transitions using SCENIC. Apoptotic priming and functional validation of anti-apoptotic dependencies were determined by BH3 profiling. Results Analyzing 3D chromatin architecture and single-cell transcriptomics from responder and non-responder models, we show that gain of short enhancer-promoter interactions underlies increased developmental potential in non-responders. Moreover, this extensive enhancer rewiring is associated with the loss of active transcriptional regulators and a state transition towards more immature states co-expressing multi-lineage markers allowing for the emergence of novel dependencies such as the transcription factor ATF4 and its downstream anti-apoptotic target MCL1 Conclusions: Resistance to NOTCH inhibition remains a therapeutic challenge in T-ALL. We revealed that 3D enhancer mapping and detailed characterization of developmental states present a novel approach to develop biomarkers that predict treatment response and may allow to identify subsets of T-ALL patients resistant to therapy upfront.

overall_design:
Single cell expression profiles of 5 PDX models harbouring NOTCH1 activating mutations treated with the Notch1 inhibitor DBZ (Dipenzazepine)

***************************************************************
Due to ethical consideration in keeping patients privacy we are not sharing raw fastq files submit only the processed data.
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first: Julia

last: Frede

first: Anna

last: Montanaro

first: Noori

last: Sotudeh

first: Hannah

last: Stuart

first: Huiyoung

last: Yun

first: Sayalee

last: Potdar

first: Alexandria

last: Van Scoyk

first: Shruti

last: Bhatt

first: Praveen

last: Anand

first: Jake

last: Kloeber

first: Antonis

last: Kokkalis

first: Amy

last: Guillaumet-Adkins

first: Johannes

last: Waldschmidt

first: Jun

last: Qi

first: Anthony

middle: G

last: Letai

first: David

last: Weinstock

first: Jon

last: Aster

first: Jens

last: Lohr

first: Birgit

last: Knoechel


title: A novel combination of CDK4/6 and PI3K inhibitors exhibits highly synergistic activity and translational potential in Ewing sarcoma.

first: Brian

last: Crompton

state: Massachusetts

address: 450 Brookline Ave

institute: Dana-Farber Cancer Institute

summary: Ewing sarcoma is a highly aggressive solid tumor malignancy and the second most common bone cancer in children. Ewing sarcoma is driven primarily by EWS-FLI, a fusion oncoprotein that has been notoriously difficult to target with traditional pharmacological agents. Compared to adult cancers, pediatric malignancies are rarely driven by readily druggable oncogenic targets and there are few incentives for developing drugs for challenging targets restricted to relatively uncommon cancer types. In addition, the effectiveness of single-agent therapies for cancer treatment is often limited. Furthermore, there are numerous examples of promising combinations of preclinical small molecules that are never tested in pediatric clinical trials because agents fail to reach the market due to limited efficacy for common adult cancers. Therefore, the identification of novel effective candidate treatment combinations comprised of anti-cancer drugs already commercially available would likely expedite the development of clinical trials for patients with pediatric cancers. To identify candidate treatment combinations for Ewing sarcoma, we performed a high-throughput drug screening with 180 combinations of tyrosine kinase inhibitors, cell cycle inhibitors, and chemotherapies, that were largely FDA approved or in late stages of clinical development. The results of the screen revealed that a CDK4/6 inhibitor ribociclib combined with a PI3K inhibitor copanlisib exhibited strong synergistic anti-Ewing sarcoma activity. We showed that this combination induced apoptosis and cell cycle arrest more effectively than either agent alone in vitro and impaired tumor proliferation and prolonged survival in vivo compared to mice treated with vehicle or single-agent therapy. Our findings identified a new candidate therapeutic option for Ewing sarcoma patients using FDA-approved drugs and provide a resource of additional potential synergistic combinations for future validation.

overall_design: To understand the impact of PI3K and CDK4/6 inhibition on protein expression and kinase signaling cells were treated with single agent control, Ribociclib as a single agent, Copanlisib as a single agent, or the combination of both and submitted for RNA-sequencing to determine these changes.

first: Maria Ana Isabel

last: De Los Santos

first: Helen

middle: F

last: Gloege

first: Alejandra

last: Aguilar Quintero

first: Caleb

last: O'Donnell Heaslip

first: Mohammad

last: Tanhaemami

first: Stephanie

last: Meyer

first: Kelly

last: Klega

first: Brigit

last: McDannel

first: Ya-Qin

last: Zhang

first: Min

last: Shen

first: Matthew

last: Hall

first: Anne-Florence

last: Blandin


title: Axin1 and Axin2 regulate the WNT-signaling landscape to promote distinct mesoderm programs [E6.5]

city: San Francisco

first: Rocio

last: Hernandez-Martinez

state: California

address: 513 Parnassus Ave

department: Orofacial Sciences

institute: UCSF

summary: How distinct mesodermal lineages – extraembryonic, lateral, intermediate, paraxial and axial – are specified from pluripotent epiblast during gastrulation is a longstanding open question. By investigating AXIN, a negative regulator of the WNT/b-catenin pathway, we have uncovered new roles for WNT signaling in the determination of mesodermal fates. We undertook complementary approaches to dissect the role of WNT signaling that augmented a detailed analysis of Axin1;Axin2 mutant mouse embryos, including single-cell and single-embryo transcriptomics, with in vitro pluripotent Epiblast-Like Cell differentiation assays. This strategy allowed us to reveal two layers of regulation. First, WNT initiates differentiation of primitive streak cells into mesoderm progenitors, and thereafter, WNT amplifies and cooperates with BMP/pSMAD1/5/9 or NODAL/pSMAD2/3 to propel differentiating mesoderm progenitors into either posterior streak derivatives or anterior streak derivatives, respectively. We propose that Axin1 and Axin2 prevent aberrant differentiation of pluripotent epiblast cells into mesoderm by spatially and temporally regulating WNT signaling levels

overall_design: To analyze differential gene expression we performed bulk RNA-seq analysis in E6.5 control and Axin1/Axin2 mutant embryos

first: Rocío

last: Hernández-Martínez

first: Sonja

last: Nowotschin

first: Luke T

last: Harland

first: Ying-Yi

last: Kuo

first: Bart

last: Theeuwes

first: Berthold

last: Göttgens

first: Elizabeth

last: Lacy

first: Anna-Katerina

last: Hadjantonakis

first: Kathryn

middle: V

last: Anderson


title: Axin1 and Axin2 regulate the WNT-signaling landscape to promote distinct mesoderm programs [E7.5]

overall_design: To analyze differential gene expression we performed bulk RNA-seq analysis in E7.5 control and Axin1/Axin2 mutant embryos


title: Fructose feeding on Asxl1-mutant clonal hematopoiesis [single-cell RNA-seq]

city: Houston

first: Jong

middle: H

last: Kim

state: TX

address: One Baylor Plaza

institute: Baylor College of Medicine

summary: Single-cell profiling of wild-type (WT) or mutant hematopoietic stem and progenitor cell (HSPC)-enriched hematopoietic cells from the bone marrow of mice harboring Asxl1Y588X clonal hematopoiesis of intermediate potential (CHIP) after 40 weeks of high-fructose corn syrup (HFCS) feeding to determine genes involved in the inflammatory response to HFCS between WT and Asxl1Y588X hematopoietic cells. These data provide new information on the difference in the inflammatory, pro-survival, and proliferative responses between WT and Asxl1Y588X hematopoietic cells after fructose feeding.

overall_design: Single-cell mRNA sequencing of mouse lineage-Sca1+c-Kit+ - enriched bone marrow freshly isolated from chimeric mice harboring Asxl1Y588X mutant hematopoietic cells fed HFCS for 40 weeks, purified by flow cytometry. WT and Asxl1Y588X samples are paired from the same mouse. Each condition has three replicates each.

first: Jonathan

last: Tiessen

first: Daisuke

last: Nakada

first: Jong Hwan

first: James

last: Martin


title: Gene expression profile at single cell level of immune cells and gastric cancer cells from multipoint biopsy samples of 2 gastric cancer patients treated by PD-1 antibody-based therapy

city: Shanghai

first: Chenfei

last: Zhou

address: Ruijin No.2 Road

institute: Ruijin Hospital

summary: To analyze the correlation between the neutrophil-to-lymphocyte ratio (NLR) and prognosis of advanced gastric cancer (AGC) patients treated by PD-1 antibody-based therapy and to delineate molecular characteristics of circulating neutrophils by single-cell RNA sequencing (scRNA-seq).

overall_design: The clinicopathological information of 45 AGC patients receiving PD-1 antibody-based regimens at the Department of Oncology, Ruijin Hospital, was  reviewed. Treatment outcomes including objective response rate (ORR), progression-free survival (PFS), and overall survival (OS) were recorded. The correlation between NLR and efficacy of PD-1 antibody-based treatment was analyzed. Single-cell RNA sequencing (scRNA-seq) analysis was performed based on multisite biopsy samples from two AGC patients to explore the molecular characteristics of circulating neutrophils and their pro-tumor mechanisms. Tissue samples from 88 gastric cancer patients who underwent radial gastrectomy were collected for immunochemistry staining.

first: Liting

last: Guo

first: Qu

last: Cai

first: Wenqi

last: Xi

first: Fei

last: Yuan

first: Huan

last: Zhang

first: Chao

last: Yan

first: Lei

last: Huang

first: Zhenggang

last: Zhu

first: Jun


title: Chinmo maintains adult stem cell sex identity by directly regulating Doublesex and Insulin signaling [bulk RNA-seq]

city: Shenzhen

first: Qing

last: Ma

address: 1068 Xueyuan Avenue, Shenzhen University Town, Shenzhen, P.R.China

institute: Shenzhen Institutes of Advanced Technology

summary: After sex specification during development, inappropriate sex maintenance in adults can lead to numerous defects and pathologies across many species. The molecular and cellular signals involved remain unknown. In the adult Drosophila testis, removing the JAK-STAT downstream effector Chinmo from adult somatic cyst stem cells (CySCs) causes their feminization, such that the sex-concordant interactions between male germ cells and the adjacent somatic cells are disrupted, causing gradual formation of testis germ cell tumors (GCT). Here we use single cell RNA-Seq to characterize cell-type specific transcriptional profiles for chinmo mutant testes undergoing sex transformation. This revealed both expected and novel mutant-specific cell populations and the full repertoire of transcriptomic changes accompanying sex transformation. Cell-cell communication networks were computed among all major cell types, revealing that feminized CySCs have reduced outgoing signaling to themselves and hub cells but elevated outgoing signaling including insulin signaling to germline stem cells (GSCs) /spermatogonia. Using Chinmo CUT & Tag, we identified Chinmo’s direct targets including the sex determination factor dsx and members of the insulin signaling pathway. We also found that Chinmo mainly functions as an activator in CySCs. By functional assays, we found ectopic expression of insulin pathway members in GSCs/spermatogonia phenocopies feminized chinmo mutant testes. In addition, knocking down insulin signaling in germ cells partially rescues the chinmo mutant phenotype. Altogether, we uncovered that Chinmo directly regulates canonical sex determination signals, as well as insulin signaling, to drive sex conversion of CySCs and germline tumorigenesis.

overall_design: Bulk RNA-seq of testes and ovaries from adult wild-type flies and testes from chinmoST at 1-, 3-, 5-, 7-, 9- and 11-days of adulthood using DNBSEQ Platform to generate 100 bp paired-end Reads.

first: Rui

first: Peiyu

last: Shi

first: Shuyang

last: Xu


title: Single-cell CNV dataset by Cell Ranger from severe aplastic anaemia patients

city: Bethesda

first: Shouguo

last: Gao

state: MD

address: 9000 Rockville Pike

department: NHLBI

institute: National Institutes of Health

type: Genome variation profiling by high throughput sequencing

summary: Single Cell CNV experiment was performed in severe aplastic anaemia patients with known chromosome 7 abnormality. The goal of this project is to use single cell CNV to assess whether these abnormalities existed prior to immunosuppressive treatment (baseline) and were just too small to detect it with standard cytogenetics.

overall_design: Bone marrow cells were sorted into myeloid and lymphoid. For each subject, samples were selected from time of clonal evolution to chromosome 7 and at baseline when the standard cytogenetics were normal. The goal was to get 2 paired samples for myeloid and 2 paired samples for lymphoid for all subjects but some subjects only had 2-3 samples due to low cell counts. Using 10X Genomics, single cell DNA sequencing for CNV was performed. 2 healthy samples were also included.

first: Bhavisha

last: Patel


title: RNA-seq of paraventricular thalamus (PVT) and posterior insular cortex (pIC) in a mouse model of STZ-induced painful diabetic neuropathy with anxiety-like behavior

status: Public on May 30 2026

city: Beijing

first: Min

last: Wei

address: Xueyan RD

institute: Peking University

summary: We generated poly(A)-selected, stranded mRNA-seq profiles from the paraventricular thalamus (PVT) and posterior insular cortex (pIC) of mice with streptozotocin (STZ; 200 mg/kg, i.p.)–induced painful diabetic neuropathy (PDN) and anxiety-like behavior, alongside vehicle controls. Twenty brain tissue samples (PVT and pIC from PDN and control groups) were sequenced. The dataset enables region-wise differential expression analysis and comparison of convergent versus region-specific remodeling between PVT and pIC.

overall_design: Organism: Mus musculus. Condition: STZ-induced PDN (single 200 mg/kg i.p.) vs vehicle control; tissue collected at the model endpoint (week 7). Tissues: paraventricular thalamic nucleus (PVT) and posterior insular cortex (pIC). Library strategy: poly(A)-selected, stranded mRNA-seq. Platform / layout / read length: Illumina NovaSeq X Plus, paired-end 2×150 bp. Notes: Sample naming and RNA QC follow the sequencing provider’s report (20 samples total). FASTQ filenames map 1:1 to sample_name in the SRA table.


title: Multicellular senescence impairs skeletal muscle recovery following disuse in aging

city: Salt Lake City

first: Micah

last: Drummond

address: 15 North 2030 East

institute: University of Utah

summary: Aged skeletal muscle has a diminished capacity to recover after disuse. Although muscle regrowth requires coordinated interactions between immune and progenitor cells, the mechanisms of impaired remodeling in aged skeletal muscle remain poorly understood, yet possibly involving the accumulation of senescent cells. We used a novel flow cytometry approach coupled with scRNAseq to determine the muscle senescent cell identity and transcriptional landscape during skeletal muscle recovery following disuse atrophy. Young and aged mice underwent 14d of hindlimb unloading followed by reloading (7 or 14d). At recovery, old mice showed smaller myofibers and abnormal muscle macrophage dynamics corresponding to greater collagen content. These outcomes coincided with elevated markers of muscle senescence (p21, γH2AX) and increased SPiDER-β-Gal⁺ cells, which inversely correlated with muscle mass. Single-cell resolution of SPiDER+ cells unmasked several senescent interstitial muscle vascular and stromal populations. Senescent interstitial cell populations were enriched in aged muscle and displayed a senescence-associated secretory phenotype (SASP) across multiple stromal, vascular, and immune cell types. Senolytic treatment reduced overall senescent cell burden, attenuated macrophage accumulation, and restored muscle mass and function in aged mice following disuse. These findings identify a multicellular senescence environment within the muscle interstitial niche as a hallmark of impaired muscle recovery following disuse.

overall_design: Single-cell RNA sequencing was performed on senescent (SPiDER-βGal⁺) and non-senescent (SPiDER-βGal⁻) cells isolated by FACS (Cytek Aurora). Cells were obtained from pooled gastrocnemius muscles ofold mice (~26mo)  at RL14 after 14 days of hindlimb unloading (n=10 mice per group)

first: Paul-Emile

last: Bourrant


title: Virus-inclusive single-nucleus RNA sequencing reveals two distinct endothelial response patterns in infectious salmon anaemia.

city: Ås

first: Adriana Magalhaes

middle: Santos

last: Andresen

state: Other

address: Elizabeth Stephansens v. 1

country: Norway

institute: Veterinærinstituttet

summary: This study investigates the Atlantic salmon response to infectious salmon anemia virus (ISAV) infection using single-nucleus RNA sequencing of the head kidney, a key immune and hematopoietic organ. Providing a detailed characterization of the endothelial response to ISAV infection in its natural host.

overall_design: Snap-frozen head kidney were used for nuclei isolation, following a TST base method. Targeting 6000 nuclei, libraries were generated using the 10X Genomics Plataform, and sequencing was performed using Illumina NextSeq 2000 with NextSeq 1000/2000 P3 reagents (200 cycles) v3 Kit, 1.2B paired-end reads.

first: Adriana

last: Magalhaes Santos Andresen

first: Richard

middle: S

last: Taylor

first: James

last: Furniss

first: Maryam

last: Saghafian

first: Raoul

last: Kuiper

first: Daniel

last: Macqueen

first: Johanna

last: Fosse


title: Coexistent alterations of BAFF and B cell phenotypes in complicated CVID course

status: Public on May 29 2026

first: Feng

last: Feng

state: United States

address: 650 Albany Street X248

institute: Boston University

summary:
Background: Common variable immunodeficiency (CVID) is a primary immunodeficiency marked by impaired antibody production and infection susceptibility, with about half developing non-infectious complications. BAFF elevation and genetic variants in a BAFF receptor, transmembrane activator and CAML interactor (TACI), frequently occur in CVID. While these findings associate with autoimmune and lymphoproliferative complications, pathogenic mechanisms remain incompletely defined.
Objective: This work explored how coexistent changes in BAFF, its receptors, and B cell subsets may shape CVID.
Methods: Plasma protein measurement, spectral flow cytometry, and single-cell RNA sequencing was applied.
Results: CVID with autoimmune cytopenias and lymphoid hyperplasia had elevated plasma BAFF:TACI ratio and increased transitional and activated naïve B cells. Activated naïve B cells from CVID patients had increased mRNA of genes downstream of BAFF receptor (BAFF-R) that promote B cell survival. Also on these expanded subsets, BAFF-R surface protein decreased, consistent with negative feedback, while autoreactive B cell receptor (BCR) VH4-34 clonality increased.
Conclusions: Novel application of spectral flow cytometry, paired BCR sequencing RNA-seq, and measurement of BAFF and related proteins in plasma found CVID with autoimmune and lymphoproliferative complications to be marked by coexistent BAFF and B cell subset dysregulation. This included increased plasma BAFF, BAFF:TACI ratio, and transitional and activated naïve B cells with reduced BAFF-R expression and BCR repertoire diversity. The expanded activated naïve B cell subset in CVID had increased expression of BAFF-R-driven genes that subvert B cell tolerance as well as increased autoreactive VH4-34 clonality. Convergence of BAFF, its receptors, and B cell subset dysregulation, should be further explored in CVID.

overall_design: Single cell RNA-seq profiling of peripheral blood B cells from common variable immunodeficiency patients and healthy donors. Prior to RNA collection, cells were sorted into transitional, naïve, and activated naïve B cells using flow cytometry. Joint gene expression and B cell receptor (BCR) libraries were prepared using 10X genomics platform.

first: Erik

last: Matson

first: Matthew

last: Ware

first: Lingge

last: Yu

first: Jennifer

last: Beane

first: Anna

last: Belkina

first: Paul

last: Maglione


title: Hopx is a dual-gatekeeper of astrocyte fate enabling in vivo reprogramming and neural repair

city: beijing

first: yani

last: zhang

state: beijing

address: tsinghua

institute: tsinghua university

summary: Astrocyte-to-neuron conversion provides a potential strategy for neural repair, but the endogenous mechanisms that maintain astrocytic identity and restrict neuronal fate acquisition remain incompletely understood. In this study, we investigated the role of Hopx, an astrocyte-enriched transcriptional regulator, in maintaining astrocyte fate and limiting astrocyte-to-neuron conversion. We developed an AAV-compatible TIGR interference (TIGRi) system to repress Hopx expression in vivo and applied this strategy in Aldh1l1CreERT2;Rosa26-LSL-tdTomato lineage-tracing mice. To define the transcriptional changes associated with Hopx knockdown-induced astrocyte-to-neuron conversion, we performed single-cell RNA sequencing on hippocampal cells collected after AAV-TIGRi-Hopx delivery and tamoxifen induction. scRNA-seq dataset was generated to characterize the transcriptomic states of virus-transduced astrocyte-lineage cells, identify intermediate cell populations during conversion, and reconstruct the trajectory from astrocyte-like cells toward progenitor-like and neuron-like states. The analysis revealed Hopx knockdown-associated induction of neurogenic and neuronal transcriptional programs in AAV-transduced astrocyte-lineage cells, including increased expression of progenitor- and neuron-associated markers and gene modules related to generation of neurons and neuron fate commitment. These data support the conclusion that Hopx repression promotes a progressive transcriptional transition from a glial state toward a neuron-like state and provide a transcriptomic resource for studying endogenous regulation of astrocyte plasticity during in vivo neural reprogramming. In parallel, we performed HOPX ChIP-seq to define the genome-wide binding landscape of HOPX and identify HOPX peak-associated candidate genes. Together, the scRNA-seq and ChIP-seq datasets provide complementary resources for investigating the transcriptional and genomic regulatory mechanisms underlying astrocyte-to-neuron conversion in vivo.

overall_design: Single-cell RNA-seq experiment was designed to characterize the transcriptional trajectory of astrocyte-lineage cells undergoing Hopx knockdown-induced astrocyte-to-neuron conversion in vivo. Five Aldh1l1CreERT2;Rosa26-LSL-tdTomato mice received hippocampal injection of Cre-dependent AAV-TIGRi-Hopx carrying an EGFP reporter, followed by tamoxifen induction to activate lineage tracing and virus-dependent expression in astrocyte-lineage cells. Hippocampal tissues were collected at 3 weeks after tamoxifen induction, a time point selected to capture intermediate cell states during astrocyte-to-neuron conversion. The dissected hippocampal tissues from the five mice were dissociated into single-cell suspensions, and tdTomato-positive/EGFP-positive cells were enriched by fluorescence-activated cell sorting. The sorted cells were subjected to single-cell RNA sequencing. The main experimental variable was Hopx repression in AAV-transduced astrocyte-lineage cells. scRNA-seq dataset was used to compare AAV-transduced astrocyte-lineage cells with non-transduced astrocytes present in the same samples and to identify astrocyte-like, progenitor-like astrocyte-derived, and neuron-like astrocyte-derived cell states during the conversion process. For ChIP, chromatin was prepared from mouse primary astrocyte and immunoprecipitated using anti-Flag antibody or control IgG.


title: Effect of HNF1A-MODY in glucagon expressing cells in the duodenal intestine [Bulk RNA-seq]

city: Bergen

first: Ulrik

last: Larsen

address: Haukelandsbakken 15

department: Clinical Science

institute: University of Bergen

summary: This project investigates the impact of the Hnf1a hotspot mutation similar to HNF1A-MODY (Maturity-Onset Diabetes of the Young) on glucagon expressing cells in the intestine. RNA sequencing (RNA-seq) data was preformed on intestinal crypts isolated from duodenum from mutant and control Hnf1a mice to study the mutation's effect on gene expression. By comparing the transcriptomcis profiles of these crypts, the study aims to uncover molecular mehcnaisms underlying the phenotype caused by HNF1A-MODY during adulhood.

overall_design: Study included mice with Hnf1a mutation mimicking HNF1A-MODY in glucagon producing cells and wild-type controls. RNA-sequencing was done on isolated duodenal crypts to compare gene expression profiles and assess the impact of the mutation on intestinal morphology and function.

first: Lucas

last: Unger

first: Simona

last: Chera


title: 3D Chromatin Dynamics during Immune Memory Acquisition

status: Public on May 28 2026

city: New York

first: Hyunu

last: Kim

state: NY

address: 417 E 68th St

department: Immunology

institute: Memorial Sloan Kettering Cancer Center

summary: Immune cells responding to pathogens undergo molecular changes that are intimately linked to genome organization. Recent work has demonstrated that natural killer (NK) and CD8+ T cells experience substantial transcriptomic and epigenetic rewiring during their differentiation from naive to effector to memory cells. Whether these molecular adaptations are accompanied by changes in three-dimensional (3D) chromatin architecture is unknown. In this study, we combine histone profiling, ATAC-seq, RNA-seq and high-throughput chromatin capture (HiC) assay to investigate the dynamics of one-dimensional (1D) and 3D chromatin during the differentiation of innate and adaptive lymphocytes. To this end, we discovered a coordinated 1D and 3D epigenetic remodeling during innate immune memory differentiation, and demonstrate that effector CD8+ T cells adopt an NK-like architectural program that is maintained in memory cells. Altogether, our study reveals the dynamic nature of the 1D and 3D genome during the formation of innate and adaptive immunological memory. Histone CUT&RUN data of differentiating NK cells (H3K4me1) during MCMV infection.

overall_design: Ly49H+ NK cells were sorted from C57BL/6 mice infected with mouse cytomegalovirus (MCMV) at different time points post infection.

first: Endi

last: Santosa

first: Joseph

last: Sun


title: Interleukin-12 drives a rapid STAT4/DDX5-dependent change in the RNA polymerase II landscape for IFN-γ production by NK cells [Pol II CUT&RUN]

summary: Natural killer (NK) cells are innate lymphocytes that respond to inflammatory cytokines produced during infection by mounting a rapid response. However, the mechanisms that allow NK cells to launch such a swift response upon inflammation remains incompletely understood. Here, we investigate whether RNA Polymerase II (Pol II) may regulate this rapid responsiveness of NK cells. Exposure of NK cells to the proinflammatory cytokine interleukin-12 (IL-12) results in a highly dynamic Pol II genomic landscape mediated by the transcription factor STAT4, especially at the interferon-gamma (Ifng) locus. We identify a STAT4 interacting partner, the RNA helicase DDX5, that was required for optimal IFN-γ production by modulating Pol II occupancy following IL-12 stimulation. Thus, our findings highlight STAT4/DDX5-mediated regulation of Pol II binding as a critical mechanism driving the rapid responsiveness of NK cells to proinflammatory cytokines.

overall_design: To determine the global Pol II landscape in NK cells at baseline and during cytokine stimulation, we performed Pol II CUT&RUN in NK cells of various mouse strains at rest or stimulated with specified cytokine(s).


title: Interleukin-12 drives a rapid STAT4/DDX5-dependent change in the RNA polymerase II landscape for IFN-γ production by NK cells [CUT&RUN]

overall_design: To determine the global Pol II landscape in NK cells at baseline and during cytokine stimulation, we performed CUT&RUN in NK cells of various mouse strains at rest or stimulated with specified cytokine(s).


title: Functional characterization of androgen receptor dimerization interfaces [RNA-seq]

status: Public on May 27 2026

city: Istanbul

first: Emirhan

last: Tekoglu

address: Rumelifeneri Yolu

country: Turkey

institute: Koc University

summary: The activity of the androgen receptor (AR) is thought to rely on interactions between its functional domains, including dimerization of the DNA-binding domain (DBD), the ligand-binding domain (LBD), and the N-terminal domain (NTD) with the LBD (N/C interaction). However, their contributions to genome-wide AR signaling remain unclear. Using U2OS cell lines expressing AR mutants that selectively disrupt each dimerization interface, we dissected their roles in transactivation, chromatin binding, cofactor recruitment, and transcriptional regulation. The disruption of LBD dimerization or N/C interactions had limited effects. Both AR mutants largely preserved enhancer activity, chromatin occupancy, AR-associated interactomes and androgen-responsive transcriptional programs. In contrast, disruption of DBD dimerization profoundly rewired AR function. Although this mutant lost binding to many AR chromatin sites and attenuated the classical androgen-responsive transcriptome, it also retained activity at a subset of loci. In addition, it gained binding at new chromatin regions enriched for half-site androgen response elements and other transcription factor motifs. RUNX factors, whose binding motifs were among the enriched motifs, directly contributed to part of the altered AR program. These data identify DBD dimerization as the principal determinant of canonical AR signaling, while revealing that monomeric DNA-binding of AR adopts alternative, cofactor-assisted chromatin-binding strategies.

overall_design:
RNA-seq profiling of U2OS cells and U2OS cells stably expressing AR WT, AR Dmon, AR Lmon, or AR NoC upon stimulation with androgens
AR Mutant definitions:
AR Lmon: W752R
AR Dmon: A597T and S598T
AR NoC: 23-27 from FQNLF to AQNAA
RNA-seq of U2OS cells stably expressing AR WT or AR Dmon, in which RUNX factors are perturbed by knockout (RUNX1, RUNX2), knockdown (RUNX3) or addition of an anti-CBFB compound (AI-14-91).

first: Kaat

last: Peperstraete

first: Frank

last: Claessens


title: Multiomic profiling of vascular endothelial cell differentiation from human embryonic stem cells

city: Daejeon

first: Inkyung

last: Jung

address: KAIST, 291 Daehak-ro, Yuseong-gu

department: Biological Sciences

institute: KAIST

summary: To investigate gene regulatory dynamics of normal endothelial cell (EC) differentiation at high resolution, an in vitro differentiation system was employed to derive functional vascular ECs from human embryonic stem cells. Human embryonic stem cells, mesodermal cells, and differentiating cells following VEGF-A stimulation at eight time points (1–48 hours), along with internal controls without VEGF-A treatment (referred to as non-ECs), were collected to profile global RNA expression and H3K27ac signals. In addition, in situ Hi-C data were generated for ECs and non-ECs at 24 hours after VEGF-A treatment to characterize global chromatin contact profiles associated with the EC progenitor state.

overall_design: Refer to individual Series


title: Multi‑omics analysis of anxiolytic gut–brain pathways induced by heat‑killed Lactobacillus brevis in zebrafish [intestinal 16S rRNA-seq]

city: Kanazawa

first: Azusa

last: Kubota

state: Ishikawa

address: 13-1 Takara-machi

department: Graduate School of Advanced Preventive Medical Sciences

institute: Kanazawa University

summary: This study aimed to elucidate the molecular gut-brain pathways underlying the anxiolytic effects of heat-inactivated L. brevis SBC8803 using zebrafish as a translational model. Adult fish received oral SBC8803 and were assessed in the novel tank test. To interrogate mechanisms, we combined brain RNA sequencing with 16S rRNA gene profiling of the gut microbiota and performed integrative multi‑omics analyses to identify host gene expression changes and microbial functional alterations associated with anxiolysis.

overall_design: To investigate the anxiolytic effects of L. brevis SBC8803 in zebrafish, we compared the brain transcriptome and gut microbiota of Control (n=6) and SBC8803-treated (n=6) groups. Brain RNA-seq (MGI DNBSEQ-T7) and intestinal 16S rRNA-seq (Illumina MiSeq) were performed on the same individuals to identify host-microbe interactions associated with behavioral changes.

first: Liqing

last: Zang

first: Takuro

last: Shinkai

first: Misa

last: Nakai

first: Atsushi

last: Tajima

first: Yasuhito

last: Shimada


title: Multi‑omics analysis of anxiolytic gut–brain pathways induced by heat‑killed Lactobacillus brevis in zebrafish [Brain RNA-seq]


title: H4K16ac contributes to chromatin compartment reorganization during mitotic and meiotic transitions [CUTnTAG]

city: Freiburg

first: Asifa

last: Akhtar

address: Stuebeweg 51

department: Chromatin Regulation

institute: Max Planck Institute of Immunobiology and Epigenetics

summary: Chromatin compartments reorganize dramatically during cell cycle transitions, shifting from a compartmentalized interphase to a condensed mitotic configuration in which large-scale compartment signals are attenuated. While histone modifications are linked to compartment identity, their contribution to compartment organization remains unclear. Using meiotic (mouse spermatogenesis) and mitotic (mouse neuronal progenitor cell, mNPC) models, we mapped histone landscapes alongside compartment dynamics. We found that histone H4 lysine 16 acetylation (H4K16ac) strongly tracked compartment reorganization, remaining enriched in A compartments during compartmentalization but redistributing upon chromatin compaction. In spermatogenesis, H4K16ac loss on the X chromosome coincided with condensation and H3K9me3 spreading. Machine learning highlighted H4K16ac as a stronger predictor of compartment transitions than H3K27ac. Acute degradation of MOF, the principal H4K16ac acetyltransferase, disrupted both the spatial distribution and global abundance of H4K16ac and progressively impaired compartmentalization in mNPCs. These results position H4K16ac as a histone modification selectively coupled to chromatin compartment transitions.

overall_design: CUT&Tag of major histone marks and related transcription/chromatin structure regulators to explore the correlations among epigenetic landscape dynamics, chromatin compartment remodeling and transcription status in different models across cell cycle and development.

first: Yuling

last: Zhao

first: Laura

last: Arrigoni


title: GM-CSF-derived DCs from BM and BM progenitors and Spleen(SP) in vitro

city: Seoul

first: Wanho

last: Choi

address: Yonsei-ro 50-1

institute: Yonsei University

summary: To investigate the heterogeneity of BM GM-DCs using progenitor-derived GM-DCs

overall_design: Bulk RNA sequencing of DC subsets derived from BM or DC progenitors cultured with GM-CSF

first: Chae Gyu

last: Park

first: Seul Hye

last: Ryu


title: Baseline interferon signaling in monocytes and antibody-mediated innate activation at injection site shape mRNA vaccine reactogenicity

status: Public on May 26 2026

city: Lausanne

first: Gustavo

middle: Agustín

last: Ruiz Buendía

state: Vaud

address: Amphipôle, Quartier UNIL-Sorge

country: Switzerland

institute: Swiss Institute of Bioinformatics

summary: The local and systemic symptoms that follow vaccination -collectively referred to as reactogenicity- are common, yet the mechanisms underlying individual variability remain poorly understood. Through longitudinal immune profiling of vaccinated individuals and mechanistic studies in mice, we identified key immunological determinants of reactogenicity induced by mRNA vaccines. Systemic adverse events were associated with stronger interferon and pro-inflammatory responses following the second dose of COVID-19 vaccine, which were also correlated with the magnitude of the antigen-specific adaptive responses. This heightened inflammation occurred within 24 hours of vaccination and originated primarily from the injection site and was characterized by enhanced recruitment and activation of myeloid cells, particularly monocytes. Two mechanisms contributed to this response: (1) early interferon production by muscle T cells generated after the first dose and (2) FcγR-dependent chemokine induction by antigen-specific antibodies. Consistently, serum antibody levels prior to vaccination correlated positively with reactogenicity. In addition to this local amplification mechanism, variability in reactogenicity was influenced by the baseline immune state, as individuals with a pre-existing interferon-stimulated gene signature in monocytes, detectable at both transcriptomic and epigenetic levels, were more prone to systemic symptoms. Our findings reveal molecular and cellular mechanisms driving vaccine reactogenicity, providing a framework for the design of less reactogenic vaccines.

overall_design: RNA-seq profiling of gene expression of monocytes isolated from the blood and dLN of mice vaccinated with a prime or booster dose of Spike mRNA COVID19 vaccine (6 hours post-vaccination).

first: Natacha

last: Madelon

first: Arnaud

last: Didierlaurent


title: Inflammatory immune modulators of AML lung infiltration and respiratory failure

status: Public on May 22 2026

first: Ziyan

last: Lin

department: Applied Bioinformatics Laboratories

institute: NYU Grossman School of Medicine

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


title: Polyphosphates attenuate interleukin-12 production in macrophages infected with Legionella pneumophila

status: Public on May 21 2026

city: Boston

first: Markus

last: Bosmann

address: 72 E Concord Street

department: Pulmonary Centre, Department of Medicine

summary: Polyphosphates are evolutionarily conserved linear chains of phosphate residues present in all living cells. Bacteria accumulate polyphosphates under stress and starvation for energy and phosphate storage, protein folding, and stress adaptation. During infection, bacteria release polyphosphates that may impair host responses, although the exact mechanisms remain elusive. In this study, polyphosphates were found to be elevated in bronchoalveolar lavage fluids from patients with Legionnaires’ disease, in Legionella pneumophila cultured alone, or during infection of bone marrow-derived macrophages (BMDMs) from C57BL/6J mice. We performed RNA-sequencing of infected BMDMs co-incubated with or without long-chain, bacterial-type polyphosphates. Among nearly 500 differentially expressed genes, Il12b (p40) showed the strongest suppression among highly expressed genes. IL-12p40 protein release was dose-dependently reduced by long-chain polyphosphates (~Pi 700), but not by short-chain, mammalian-type polyphosphates (Pi 70), indicating a specific bacterial mechanism targeting innate immune signaling. In contrast, IL-18, processed by inflammasome activation and synergizing functionally with IL-12, was not consistently suppressed. Polyphosphates predominantly inhibited LPS/TLR4 signaling, with Legionella-induced IL-12 relying on the MyD88 pathway, but not TRIF. RAGE and P2Y1, previously implicated in polyphosphate biology, were not required for IL-12 suppression. However, PI3K/AKT signaling appeared to mediate polyphosphate effects, which were reversed by the PI3K inhibitors, LY294002, copanlisib and eganelisib. Finally, long-chain polyphosphates suppressed IL-12 release also from human monocyte-derived macrophages exposed to L. pneumophila or LPS. In summary, our findings identify a selective inhibition of IL-12 by long-chain bacterial polyphosphates, suggesting that these molecules act as bacterial effectors capable of suppressing protective innate immune responses.

overall_design: Bone marrow was isolated from naïve C57BL/6J mice (n=4, 6 week-old, females, Jackson Laboratories, Bar Harbor, ME) and incubated for seven days with 49% RPMI 1640, 30% L-929 cell supernatant, 20% FBS and 1% Penicillin/Streptomycin medium to generate bone-derived macrophages (BMDM). The BMDM were challenged in vitro with exogenous long-chain polyphosphates (50 μM), Legionella pneumophila (strain JR32, MOI = 1 [500,000 CFUs/500,000 cells]), a combination of both long-chain polyphosphates and L. pneumophila, or left unstimulated. BMDM were harvested 10 h post-challenge and subject to RNA-sequencing.

first: Kara

last: Vasilew

first: Archana

last: Jayaraman