title: Transriptional effects of blocking mitochondrial fission-fusion in aging Drosophila clock neurons

city: Waltham

first: Shlesha

last: Richhariya

address: 415 South St

institute: Brandeis University/HHMI

summary: Mitochondria are dynamic organelles and undergo fission-fusion in response to various environemtal cues. But the roles of these two very different mitochondrial forms – predominantly spherical and tubular - are not well-characterized in neurons of animals and especially in aging neurons. This is important because neurons are long-lived and mitochondrial dynamics is associated with neurodegenerative diseases. We used here an efficient cell type-specific CRISPR approach to knockout key fission-fusion genes and disrupt mitochondrial dynamics within the inessential clock neurons of Drosophila. In order to understand the cellular effects of these perturbations, transcriptomic profiling was performed from young and old clock neurons with and without disrupted mitochondrial dynamics.

overall_design:
To perturb mitochondrial dynamics in Drosophila clock neurons we used a cell type-sepcific CRISPR approach. We used CLK856-Gal4 driver to label clock neurons and under UAS-control, expressed Cas9 and 3X-gRNA against gene of interest along with eGFP to label the neurons for sorting. Following genes were targeted: Drp1 (involved in fission), Marf (involved in fusion of the outer mitochondrial membrane) and Opa1 (involved in fusion of inner mitochondrial membrane). Cas9 alone was used as a control.
Bulk RNAseq was performed from FACS-purified clock neurons of the 4 genotypes (Cas9-control, Drp1-mut, Marf-mut and Opa1-mut) at two ages - Young (~15days old) and Old (~35 days old).
Differential expression analysis was performed for each of the mutants from the Cas9 control at both ages independently

first: Michael

last: Rosbash


title: YAP AND TEAD ARE TRANSCRIPTIONAL REGULATORS OF NEUROENDOCRINE DIFFERENTIATION AND GROWTH IN CARCINOID CELLS [RNA-seq]

status: Public on Oct 16 2025

city: Kingston

first: Neil

last: Renwick

state: ON

address: 88 Stuart St

department: Pathology and Molecular Medicine

country: Canada

institute: Queen's University

type: Expression profiling by high throughput sequencing

summary: Molecular regulators of variably aggressive carcinoid tumors are unknown. Since carcinoids have low expression of Yes-associated protein (YAP), we hypothesized that low YAP expression provides a molecular advantage to carcinoids by preventing YAP from binding its partner, TEA domain transcription factor (TEAD). To test this hypothesis, we overexpressed constitutively active YAP and a TEAD-binding defective form of YAP in lung (H727) and pancreatic (BON1) carcinoid cells. We found that active YAP overexpression inhibited neuroendocrine markers, morphology, cell proliferation and anchorage-independent cell growth, while TEAD-binding defective YAP recovered these features. Through integrated ChIP-seq and RNA-seq analyses, we found that YAP-TEAD binding downregulated neuroendocrine transcription factor genes and upregulated transforming growth factor (TGFβ) and Notch genes related to cell growth. We conclude that low YAP expression permits neuroendocrine differentiation and growth in carcinoid cells by preventing YAP-TEAD binding and subsequent dysregulation of neuroendocrine transcription factors, TGFβ and Notch gene targets. These results identify unknown molecular mechanisms in carcinoid development that may apply to the broader family of neuroendocrine cancers.

overall_design: RNA-seq for lung (H727) and pancreatic (BON1) human carcinoid cell lines. Experimental conditions included control and active YAP overexpression.

first: Nanayakkara

last: Jina

first: Yang

last: Xiaojing

first: Damiani

last: Simona

first: Imtiaz

last: Tashifa

first: Wang

last: Xiantao

first: Anastasakis

middle: G

last: Dimitrios

first: Shah

middle: M

last: Girish

first: Tyryskin

last: Kathrin

first: Hafner

last: Markus

last: Xiaolong

first: Renwick

last: Neil


title: Characteristics of Extracellular Vesicle-Derived lncRNAs during the Progression of HBV-Related Hepatocellular Carcinoma

city: 天津

first: Yingtang

last: Gao

address: 83 Jintang Road, Hedong District

country: China

institute: The Third Central Hospital of Tianjin

summary: Using High-Throughput Sequencing to Conduct Integrated Analysis of the Whole Transcriptome in Blood sEVs from HBV-Associated Liver Disease Cohort

overall_design: Patients with HBV-associated liver diseases—chronic hepatitis B (CHB), liver cirrhosis (LC), benign liver disease (HA), and hepatocellular carcinoma (HCC)—were selected as the study cohort. High-throughput sequencing was utilized to perform comprehensive whole transcriptome analysis (mRNA, miRNA, lncRNA, and circRNA) of small extracellular vesicles (sEVs) isolated from serum .

first: Yanan

last: Ma

first: Cheng

last: Lou

first: Jing

last: liang

first: Chunyue

last: Guo

first: Jinjuan

last: Zhang

first: Chengjun

last: Lu

first: Jiandong


title: Head-to-head preclinical treatment design prioritizes promising therapies for Neurofibromatosis 1 optic glioma clinical translation

city: St Louis

first: David

last: Gutmann

state: MO

address: 660 S Euclid Ave

department: Neurology

country: USA

institute: Washington University in St Louis

summary: Authenticated preclinical brain tumor models provide unprecedented opportunities to evaluate next-generation treatments. However, many therapies that exhibit robust anti-tumor activity in mice fail to show efficacy in clinical trials. To prioritize therapeutic candidates for future clinical translation, we implemented a head-to-head preclinical strategy using a well-characterized murine model of NF1-optic pathway glioma (Nf1OPG). Nf1OPG mice were treated with standard of care (carboplatin), clinically evaluated (everolimus, mirdametinib), and investigational (pexidartinib, HBS-101, lamotrigine) drugs during the period of most rapid tumor growth (6-12 weeks of age). Ant-tumoral efficacy was assessed by proliferation (%Ki67+ cells) and optic nerve volume, while vision-related outcomes were measured using retinal nerve fiber layer (RNFL) thickness and retinal ganglion cell (RGC) determinations. Tumor microenvironment (TME) soluble mediator (Ccl2, Ccl3, Ccl4, Ccl5) and tumor cell marker (NeuN, Gpr17) RNA expression was quantitated by qRT-PCR. Outcomes were compared to carboplatin-treated Nf1OPG, untreated Nf1OPG, and Nf1+/- mice. While all agents restored normal tissue architecture, reduced optic nerve proliferation, and decreased TME soluble mediator and tumor cell marker RNA expression, only lamotrigine also reduced optic nerve volume. Everolimus, lamotrigine, and HBS-101 all restored RNFL thickness to wild-type levels, whereas carboplatin showed a trend towards normalization. This referential study design affords direct head-to-head comparisons of investigational therapies relative to standard-of-care-treatment using clinically meaningful outcomes (optic glioma growth and RNFL thickness). Using this strategy, lamotrigine emerged as the most promising therapy for limiting tumor progression and vision loss in Nf1-OPG mice relevant to clinical translation in children with NF1.

overall_design:
Raw sequencing data from Nf1OPG mouse samples were processed using the 10X Genomics Cell Ranger pipeline (version 7.2.0) to generate gene count matrices, which were aligned to the mm10-2020-A mouse reference genome. The aligned data were merged with previously published datasets (GSM7816061 and GSM7816062 from GSE244433), resulting in a total of four samples for analysis. Raw counts were used as input for the Seurat R package (version 5.2.1). For quality control, cells were excluded if they had fewer than 500 or more than 5,000 detected genes, more than 5% mitochondrial gene content, or fewer than 500 or more than 20,000 transcript counts. Normalization and variance stabilization was performed using the SCTransform function and 2,000 highly variable features of each dataset were identified and scaled using the FindVariableFeatures and ScaleData functions. Principal component analysis (PCA) was conducted using RunPCA. The data were integrated using the IntegrateLayers function with CCAIntegration. The integrated data was subjected to dimensional reduction and clustering using RunUMAP, FindNeighbors and FindClusters. Each cell type was identified using cell type-specific markers.

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The table below lists GEO accessions reused/reanalyzed for this study.
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first: Talia

last: Eligator

first: Jit

last: Chatterjee

first: Shintaro

last: Yamada

first: Anthony

last: Kirchner

first: Hareesh B

last: Nair

first: Jason R

last: Fangusaro

first: David H


title: Mitochondrial dysfunction in PRRSV-2 infected macrophages

status: Public on Oct 17 2025

city: Saint-Paul-lez-Durance

first: Thien-Phong

last: Vu Manh

address: CEA Cadarache, Zone Cité des Énergies BIAM

department: BIAM

country: France

institute: CNRS

summary: Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) is one of the most economically devastating viruses for the global swine industry. PRRSV has a known tropism for lung macrophages, where it causes impaired immune responses. This study evaluated the metabolic and immune profiles of primary porcine alveolar macrophages (PAM) and pulmonary intravascular macrophages (PIM) infected with different strains of PRRSV-2 isolated from North Carolina (NC) pig herds (NC134, NC18-9-7 referred to as NC174, NC20-1 referred to as NC144), and VR2232, a PRRSV-2 prototype strain. Primary enriched mononuclear phagocytes were infected ex vivo with NC134 and NC174, sorted, and the total RNA was used for a transcriptomic approach; additionally, gene expression was further validated by RT-qPCR and NanoString technology. Complementary functional assays with additional NC strains were used to further investigate the oxidative stress, mitochondrial and metabolic dysfunction induced by PRRSV-2 infection. PAM infected with both NC PRRSV-2 strains NC174 and NC134 showed similar transcriptomic profiles during the early stage of infection, with downregulation of genes involved in the oxidative phosphorylation and electron transport chain pathways. PIM infected with both NC174 and NC134 strains showed limited alteration in the transcriptomic profiles compared to uninfected cells. The genetic reprogramming matched the PRRSV-2 induced mitochondrial impairment observed in functional assays performed with Seahorse technology. Mitochondrial respiration displayed slightly different profiles between PIM and PAM infected with the different PRRSV-2 strains, with PAM showing a more substantial decrease in mitochondrial fitness compared to control cells. When reactive oxygen species (ROS) and nitric oxide (NO) production were evaluated, no differences were observed between PRRSV-2 infected PAM and PIM and control cells. These results provide valuable insights into the pathogenetic mechanism of different North Carolina PRRSV-2 strains, focusing on the alteration of mitochondrial function in lung macrophages during early infection and highlighting differences in lung macrophages responses to distinct PRRSV-2 strains

overall_design: Lung bronchoalveolar lavage (BAL) and parenchyma (PAR) samples were isolated from two male and two female animals between 8-12 weeks of age were used. For each pig, thirty million enriched mononuclear pahgocytes (MNP) from both BAL and PAR were infected with NC134 and NC174 at MOI=1 or left uninfected in 50 ml falcon tubes for 12h. Infections were synchronized and after 12h cells were washed and stained with a five-color flow cytometry staining to sort AM, PIM, monocyte derived dendritic cells (moDC) and classical DC (cDC),  PAM were sorted from BAL samples and PIM, cDC and moDC were sorted from PAR samples. After sorting, approximately 300,000 PAM and 100,000 PIM were collected for each condition.A range between 63,000 and 100,000 were collected for moDC and cDC. Total RNA was obtained from 63,000-100,000 sorted PAM, PIM, moDC, cDC of four pigs (two females and two males) using the PicoPure RNA Isolation Kit (Thermo Fisher, KIT0204) following manufacturer’s instructions. RNA quantity was determined using a Nanodrop 1000 (Thermo Fisher) and an Agilent Bioanalyzer (Agilent), with RIN values ranging from 7.1-9.6 and concentrations ranging from 0.11-21.61 ng/uL. RNA-seq libraries were generated from 1ng of total RNA per sample, using a NEBNext Single Cell/Low Input RNA Library Prep Kit for Illumina (New England Biolabs) and NEBNext Multiplex Oligos for Illumina (New England Biolabs) following the manufacturer’s instructions. Amplified cDNA quality and quantity were assessed using an Agilent Technologies 2200 TapeStation with high sensitivity D5000 tape. For library preparation, 2ng of amplified cDNA per sample were used. Library quality was assessed using an Agilent Technologies 2200 TapeStation with D1000 tape. Libraries were quantified by RT-qPCR using a NGS Library Quantification kit (Takara Bio) following the manufacturer’s instructions. A total of 47 cDNA libraries were diluted to 10 nM, pooled, and submitted to Novogene for 150-bp paired-end sequencing on a NovaSeq 6000 S4 lane (Illumina).

first: Alba

last: Frias-De-Diego

first: Abigail

last: Williams

first: John

last: J. Byrne

first: Chaitawat

last: Sirisereewan

first: Julie

last: Hicks

first: Liu

last: Hsiao-Ching

first: Elisa

last: Crisci


title: YAP AND TEAD ARE TRANSCRIPTIONAL REGULATORS OF NEUROENDOCRINE DIFFERENTIATION AND GROWTH IN CARCINOID CELLS [ChIP-seq]

first: Neil

last: Renwick

type: Genome binding/occupancy profiling by high throughput sequencing

overall_design: ChIP-seq for YAP and TEAD immunoprecipitation in lung (H727) and pancreatic (BON1) human carcinoid cell lines. Experimental conditions included control and active YAP overexpression.

first: Nanayakkara

last: Jina

first: Yang

last: Xiaojing

first: Damiani

last: Simona

first: Imtiaz

last: Tashifa

first: Wang

last: Xiantao

first: Anastasakis

last: Dimitrios

first: Shah

last: Girish

first: Tyryskin

last: Kathrin

first: Hafner

last: Markus

last: Xiaolong

first: Renwick

last: Neil


title: Multi-layer stratified oncology platform utilizing transcriptomics, prostate cancer organoids, and modeling of drug response

city: Bern

first: Panagiotis

last: Chouvardas

address: Murtenstrasse 24

country: Switzerland

institute: University of Bern

summary: The high intra-patient heterogeneity in multifocal primary prostate cancer (PCa) has curtailed the efficacy of current treatment options. By employing twin biopsies from multiple lesions with matched Patient-derived organoids (PDO) models, the PCa molecular heterogeneity was investigated. We utilized genomics, transcriptomics and machine learning (ML) approaches to elucidate and predict the underlying mechanisms of pharmacological heterogeneity. Our data indicate a vulnerability of primary PCa organoids for small molecule inhibitors targeting receptor tyrosine kinases (MET, ALK, SRC). By exploring gene expression data from matched parental tissue in an unsupervised manner, we identified two distinct clusters of samples. Interestingly, the PDO drug responses were significantly different between the two clusters for 4/11 compounds tested. We developed a transcriptomics-based, cluster prediction model, which can accurately stratify samples into the two clusters. Notably, our prediction model is based on tissue profiles; therefore, it can be utilized to rapidly evaluate new cases and suggest promising drug candidates, even when PDO derivation is not feasible. Taken together, we propose a novel flexible stratified oncology approach that can swiftly and accurately highlight promising drug vulnerabilities of PCa patients.

overall_design: Prostate cancer tissue samples (FFPE) RNA sequencing

first: Juening

last: Kang

first: Andrew

last: Maalouf

first: Daniel

last: Hanhart

first: Laura

last: Fernárdez Cerro

first: Eva

last: Comperat

first: Katja

last: Ovchinnikova

first: Ulrich

last: Schneeberger

first: Beat

last: Roth

first: George

last: N. Thalmann

first: Sofia

last: Karkampouna

first: Marianna

last: Kruithof-de Julio


title: Transcriptome profiling of Actr3 KO mIMCD3 cells

city: Freiburg

first: Manuel

last: Rogg

state: Baden Wuerttemberg

address: Breisacher Straße 115a

department: Institute of Surgical Pathology

country: Germany

institute: University Medical Center Freiburg

summary: Actr3 WT (control) and Actr3 KO mIMCD3 cells were generated using CRISPR/Cas9 and independent gRNAs for control and KO cell lines. Single cells clones (Ctrl.-1, Crtl.-2, KO-1, KO-2) were selected and validated by western blotting confirming loss of Actr3 in KO cell lines on protein level. Transcriptome profiling (RNA-Sequencing) and differential gene expression analysis of independent replicates per cell line was performed.

overall_design: mRNA sequencing analysis of control and Actr3 KO mIMCD3 cell lines

first: Christoph

last: Schell


title: Enhancement of melanoma aggressiveness via p38-MAPK, HIF-1α pathways, and metabolic reprogramming induced by Candida albicans

city: Derio

first: Ana

middle: Maria

last: Aransay

state: BIZKAIA

address: Parque tecnologico de Bizkaia, Building 801-A

department: Genome Analysis Platform

country: Spain

institute: CIC bioGUNE

summary: Recent studies have increasingly focused on the role of fungi, including Candida albicans, in carcinogenesis. Since C. albicans is a component of the human microbiota, particularly on the skin, we investigated its effect on the phenotype and signalling pathways of melanoma cells. Assays for migration, adhesion, angiogenesis, and hepatic metastasis showed that C. albicans promotes a more malignant phenotype in melanoma cells. At the transcriptomic level, C. albicans increased the expression of VEGF (Vegfa), and genes associated with MAPK and HIF-1 signalling pathways, and with aerobic glycolysis. Further in vitro analysis revealed that TLRs and EphA2 receptors are involved in the recognition of live C. albicans, stimulating VEGF secretion and expression of the AP-1 transcription factor component c-Fos through p38-MAPK and HIF-1α. These pathways also regulate the expression of other AP-1 constituents such as Atf3, Jun, and Jund. Moreover, p38-MAPK regulates glycolytic genes like Hk2, Slc2a1, and Eno2. In conclusion, C. albicans activates the p38-MAPK/c-Fos/AP-1 and HIF-1/HIF-1α/c-Fos/AP-1 pathways in melanoma cells, promoting a pro-angiogenic environment and metabolic reprogramming. Therefore, this study clarifies the impact of C. albicans on melanoma cells, which can lead to the use of antifungal therapies as complementary to traditional treatments for melanoma.

overall_design: Three independent biological replicates of B16-F10 murine melanoma cell line were co-incubated with Candida albicansor cell growth media (RPMI) and, after six hours, RNA was isolated and RNA sequencing was performed.

first: Leire

last: Aparicio-Fernandez

first: Aitziber

last: Antoran

first: Nuria

last: Macias-Cámara

first: Monika

last: Gonzalez

first: Jose Ezequiel

last: Martin Rodriguez

first: Ana M.

first: Juan

last: Anguita

first: Andoni

last: Ramirez-Garcia


title: The 3’-5’ exoribonuclease ISG20L2 contributes to 3’ terminus maturation of 18S and 28S ribosomal RNAs (revision)

city: Strasbourg

first: Dominique

last: Gagliardi

address: 12, rue du General Zimmer

department: IBMP

summary: Ribosome biogenesis is a nodal process in cell growth and proliferation, and its dysfunction is associated to human congenital diseases and tumorigenesis. Despite extensive mechanistic characterization, several processing steps of human pre-ribosomal RNAs remain elusive. The 47S primary transcript contains 3 out of 4 ribosomal RNAs flanked by external (5’ETS, 3’ETS) and internal (ITS1, ITS2) transcribed spacers. The molecular processes leading to the removal of the 3’ETS, one of the earliest maturation steps, is not fully understood. Combining loss-of-function experiments and 3’-RACE high-throughput sequencing, we showed that the vertebrate-specific 3’-5’ exoribonuclease ISG20L2, a DEDDh RNase T superfamily member, is critical for efficient removal of the 3’ETS and formation of large ribosomal subunits. ISG20L2 inactivation led to accumulation of various forms of 3’-extented pre-rRNAs and disorganized PDFC, a sub-nucleolar compartment recently linked to 3’ETS processing. The function of ISG20L2 also extends to the trimming of ITS1 after endonucleolytic cleavage at site 2 and its knockdown reveals the precise location of site 2. Altogether, the present work uncovers the landscape of two pre-rRNA processing steps at nucleotide resolution, and restricts the function of ISG20L2 to the nucleoli where it contributes to the maturation of 18S and 28S 3’ ends.

overall_design: HeLa cells were treated with a control siRNA duplex (siRNA scramble) or siRNA duplexes targeting ISG20L2, DDX51, URB1, RPL3 or RPL26 mRNA.

first: Maxime

last: Aubert

first: Hélène

last: Zuber

first: Marine

last: Mommert-Tripon

first: Sarah

last: Le Page

first: Nathalie

last: Montel-Lehry

first: Vanessa

last: Soldan

first: Stéphanie

last: Bosch

first: Pierre-Emmanuel

last: Gleizes

first: Marie-Françoise

last: O'Donohue


title: Targeting calcium signaling with synthetic EB3 inhibitor promotes lung repair through FOXM1 pathway

city: Chicago

first: Mark

last: Maienschein-Cline

state: IL

address: 900 S Ashland Ave, Rm 1058, M/C 937

department: Research Resources Center

institute: University of Illinois at Chicago

summary: Acute respiratory distress syndrome (ARDS) is a severe pulmonary disease characterized by acute, noncardiogenic pulmonary edema and hypoxemia leading to respiratory failure with a diverse array of etiologies, including the recent SARS-CoV-2 infection. The current standard of care for ARDS remains predominantly supportive, underscoring the urgent need for targeted pharmacological interventions. To address this critical gap, we have developed an inhibitor to the microtubule accessory factor end binding protein 3 (EB3), a key mediator in the pathogenesis of ARDS. During injury, EB3 in endothelial cells facilitates the cluster of inositol 1,4,5-trisphosphate receptor 3 (IP3R3) clustering on the endoplasmic reticulum surface activating pathological calcium signaling. Building on our prior research, we have designed and optimized an EB3 inhibitor, termed Vascular Therapeutics (VT)-109, with enhanced physicochemical properties using NMR approaches. Recognizing the diverse etiologies of ARDS, we evaluated the therapeutic potential of VT-109 using a range of preclinical models, including PAR-1 agonist-, endotoxin-, polymicrobial sepsis-, mechanical ventilation-, SARS-CoV-2-induced models of ARDS in mice. Treatment of VT-109 protects the lungs of mice from vascular leakage caused by ARDS by upregulating VE-cadherin at the endothelial junctions. Molecularly, VT-109 reduces the inflammatory NFAT and NFκB pathways while simultaneously activating the endothelial regenerative FOXM1 pathway. Additionally, VT-109 mitigated ARDS-induced lung injury, reduced inflammatory cytokine production, decreased morbidity and mortality, and improved lung functions. Collectively, these data demonstrate that targeting EB3-mediated pathological calcium signaling within pulmonary endothelial cells with VT-109 could provide a promising therapeutic strategy for the treatment of ARDS.

overall_design: CD1 mice were first challenged with LPS and treated with VT-109 . At endpoint, the lung tissues from all mice were obtained and pulmonary endothelial cells were isolated. Bulk RNA-sequencing was performed on the isolated endothelial cells to investigate VT-109's molecular mechanisms.

first: Wan Ching

last: Chan

first: Man Long

last: Kwok

first: Xinyan

last: Qu

first: Hazem

last: Abdelkarim

first: Jonathan

last: Le

first: Deying

last: Yang

first: Benjamin

last: Hitchinson

first: Avik

last: Banerjee

first: Shuangping

last: Zhao

first: Chongxu

last: Zhang

first: Jake

last: Class

first: Marlen

first: Harry

last: Hailemeskel

first: Raman Ghotra

last: Singh

last: Maieschein-Cline

first: Patrick

last: Belvitch

first: Vadim

last: Gaponenko

first: Justin

last: Richner

first: Yulia A

last: Komarova


title: Long Noncoding RNA LncBAR Enhances BRG1 Protein to Promote Cardiomyocyte Cell Cycle Progression and Cardiac Repair

city: wuhan

first: li

last: jun

state: hubei

address: donghu street

department: wuhan

institute: wuhan university

summary: The mammalian heart retains regenerative capacity during the early postnatal period, but this ability declines as it matures. Enhancing cardiomyocyte proliferation represents a key therapeutic approach to promote heart regeneration and repair, yet the molecular mechanisms remain elusive. Here, we identified LncBAR (BAF complex-associated lncRNA) as a critical regulator of cardiac regeneration. LncBAR expression declines during heart development but is upregulated following cardiac injury. Loss of LncBAR impairs cardiomyocyte growth, suppresses cell cycle gene expression, and diminishes heart regeneration, as evidenced by reduced cytokinesis and cardiac function. Conversely, cardiac specific overexpression of LncBAR restores cardiomyocyte proliferation and enhances cardiac regeneration, especially in adult myocardial infarction model. Mechanistically, LncBAR interacts with Brg1, stabilizing BRG1 protein level and activating cell cycle progression to drive cardiomyocytes proliferation. Collectively, our study identified LncBAR as a crucial regulator for heart regeneration, highlighting the LncBAR-BRG1 axis as a promising therapeutic strategy for cardiac repair.

overall_design:
To investigate the function of LncBAR in regulating the proliferation of mouse cardiomyocytes, we isolated primary neonatal mouse cardiomyocytes to perform loss-of-function or gain-of-function experiments
To explore the effect of LncBAR on cardiac regeneration, we constructed an AR model of LncBAR knockout mice and LncBAR transgenic mice
To explore the effect of LncBAR on adult cardiac regeneration, we constructed an MI model of  LncBAR transgenic mice
To explore the mechanism of LncBAR regulates cardiomyocyte proliferation, we performed RNA seq of LncBAR knockdown in cardiomyocytes

first: Jun

last: Li

first: Huanhuan

last: Cai

first: Yufan

last: Chen

first: Ruiqi

last: Pi


title: Lung adenocarcinoma cells respond differently to mechanical stress in 3D versus 2D environments

city: Toyama

first: Naoya

last: Kitamura

state: Toyama

address: 2630, Sugitani

department: Thoracic Surgery

country: Japan

institute: University of Toyama

summary: Two-dimensional (2D) culture models are commonly used in cancer research, but fail to recapitulate complex mechanical cues of native tissues. In this study, we developed an ex vivo three-dimensional (3D) lung cancer model by seeding human lung adenocarcinoma cells into decellularised rat lungs and culturing them in a pressure chamber and perfusion system mimicking respiratory motion (RM) and blood flow. In 3D culture, RM promoted cell adhesion and proliferation, enhanced the nuclear translocation of β-catenin and YAP, and increased the expression of integrin β1 and E-cadherin. In addition, upregulation of extracellular matrix- and cell adhesion-related genes was particularly notable. In contrast, in 2D culture, RM suppressed cell proliferation and induced apoptosis, with prominent upregulation of tumour suppressor genes. Our findings demonstrate that dimensionality and mechanical stress synergistically influence lung cancer cell dynamics and underscore the need for 3D models in cancer research that closely replicate the native lung tissue microenvironment.

overall_design: A549 human lung adenocarcinoma cells were divided into two groups: one subjected to respiratory motion and the other not. After four days of culture, samples were collected and subjected to RNA sequencing.

first: Mayumi

last: Iwatake

first: Satoshi

last: Mizoguchi

first: Shadil

last: Wani

first: Komei

last: Kobayashi

first: Muhammad

last: Hasnain

first: Dung

middle: V

last: Nguyen

first: Ryo

last: Yokoyama

first: Naru

last: Kitade

first: Toshihiro

last: Ojima

first: Koichiro

last: Shimoyama

last: Koba

first: Hideki

last: Hatta

first: Micha Sam

middle: B

last: Raredon

first: Kenichi

last: Hirabayashi

first: Yoshitomo

last: Morinaga

first: Tomoshi

last: Tsuchiya


title: Capicua regulates the survival of Cajal-Retzius cells in the postnatal hippocampus

city: Edmotnotn

first: Qiumin

last: Tan

state: Alberta

address: 114 St and 87 Ave

department: Cell Biology

institute: University of Alberta

summary: Programmed cell death is crucial for organ morphogenesis and tissue homeostasis. Understanding programmed cell death in the developing brain is essential for comprehending both normal brain development and neurological disorders. In this study, we utilize Cajal-Retzius (CR) cells, transient neurons that populate the embryonic cortex and are predominantly eliminated in early postnatal stages, as a model to investigate the regulation of programmed cell death. While many CR cells typically undergo postnatal cell death, some persist into adulthood in the hippocampus, influencing local circuits and behaviors. Here, we show that the loss of capicua (CIC), a transcriptional repressor implicated in a rare neurodevelopmental syndrome and multiple cancers, results in aberrant survival of CR cells in the adult hippocampus. Altered cell survival is mediated by the cell-autonomous function of CIC in hippocampal CR cells. Surprisingly, the atypical persistence of CR cells following CIC loss does not impact hippocampal-dependent behaviors or susceptibility to kainic acid-induced seizures. Single-cell transcriptomic analysis unveils previously unrecognized heterogeneity among hippocampal CR cells and suggests a role of CIC in repressing Fgf1 expression. Additionally, we reveal that FGF1 and BCL2 serve as pivotal regulators enhancing CR cell survival in the postnatal hippocampus. Our findings shed light on a previously unacknowledged role of CIC upstream of FGF signaling and elucidate the apoptosis mechanism governing developmental programmed CR cell death.

overall_design: Four ΔNp73-Cre; Cicflox/+; tdT and four ΔNp73-Cre; Cicflox/flox; tdT mice (littermates) at P14 were perfused with artificial cerebrospinal fluid (aCSF; 87 mM NaCl; 2.5 mM KCl; 1.25 mM NaH2PO4; 26 mM NaHCO3; 75 mM sucrose; 20 mM glucose; 2 mM CaCl2; 2 mM MgSO4) equilibrated in carbogen (95% O2, 5% CO2) via a gas stone. The brain was promptly removed and kept in aCSF as the hippocampus was dissected. Dissected tissue was kept submerged in aCSF saturated with carbogen on ice.


title: SF3B1 K700E Mutation Induces Genome-Wide Enhancement of Transcriptional Pause Release in ES Cells [RNA-seq]

city: Boston

first: Claudia

middle: A

last: Mimoso

state: MA

address: 45 Shattuck St. LHRRB

institute: Harvard Medical School

summary: SF3B1, a critical component of the U2 snRNP splicing factor, is frequently mutated in cancer and plays a crucial role in pre-mRNA splicing. We investigated the effects of the most common SF3B1 mutation, heterozygous substitution of Lysine 700 to Glutamate (K700E), in human embryonic stem (hESC) cells using CRISPR-Cas9 to generate heterozygous SF3B1K700E clones. We observed the upregulation of several key transcription regulators associated with hematopoiesis and a broad range of immune genes in SF3B1K700E hESCs. Despite transcriptional differences between hESC and myelodysplastic syndrome (MDS) cells harboring the SF3B1K700E mutation, several common gene programs were identified in both cell types, independent of splicing alterations. To further elucidate the molecular mechanisms underlying dysregulated gene expression in SF3B1K700E hESCs, we performed Precision Run-On sequencing (PRO-seq) in SF3B1K700E hESCs. These analyses revealed alterations in RNA polymerase II (Pol II) elongation properties induced by the SF3B1K700E mutation. Specifically, a general increase in pause release was noted in SF3B1K700E hESCs. This study identifies several downstream candidate genes that could contribute to the SF3B1 mutated phenotype, shedding light on the impact of the U2 snRNP on transcription by Pol II.

overall_design: Examination of 6 biological conditions by RNA-seq; 3 biological replicate sets of SF3B1 K700E Mutant and SF3B1 WT libraries. 3 technical replicates per biological replicate.

first: Mahtab

last: Dastpak

first: Moein

last: Farshchian

first: Christina

middle: L

last: Paraggio

middle: E

last: Leonard

first: Shanye

last: Yin

first: Binkai

last: Chi

first: Kelsey

middle: W

last: Nassar

first: RGrant

last: Rowe

first: Jiuchun

last: Zhang

first: George

middle: Q

last: Daley

first: Karen

last: Adelman

first: Robin

last: Reed


title: Transcriptome profiling of starved Actr3 KO mIMCD3 cells

first: Manuel

last: Rogg

summary: Actr3 WT (control), Actr3 KO and Actr3-Ift88 double KO mIMCD3 cells were generated using CRISPR/Cas9. Single cells clones (Actr3 Ctrl.-1, Actr3 KO-1, Actr3-Ift88 dKO) were selected and validated by western blotting confirming loss of Actr3 or Ift88 in KO cell lines on protein level. Transcriptome profiling (RNA-Sequencing) and differential gene expression analysis of three independent replicates of starved (ciliated) Actr3 Ctrl.-1, Actr3 KO-1, Actr3-KO Ift88-KO (dKO) and 0.5 µM Ciliobrevin D treated Actr3 KO-1 cells was performed.

overall_design: mRNA sequencing analysis of control, Actr3 KO, Actr3-KO Ift88-KO (dKO) and 0.5 µM Ciliobrevin D treated Actr3 KO-1 mIMCD3 cells

first: Christoph

last: Schell


title: Transcriptome profiling of kidney medulla of Actr3 KO mice

summary: Renal tubule-specific Actr3 knockout mice (Actr3-fl/fl*Cdh16-Cre) were generated. Transcriptome profiling (RNA-Seq) and differential gene expression analysis of isolated renal medulla from KO and WT mice at p14 was performed. Actr3 KO mice showed transcriptional changes associated with Actr3 loss and kidney disease.

overall_design: mRNA sequencing analysis of  kidney medulla of WT control and Actr3-fl/fl*Cdh16-Cre mice


title: RNASeq-based identification of extracellular matrix components impacted by FasL deficiency in osteoblasts

city: Brno

first: Martina

last: Zapletalová

address: Kamenice 5

department: Department of Biochemistry

country: Czech Republic

institute: Masaryk University

summary: Osteoblasts and osteoclasts are two critical cell populations in bone remodelling. FasL is known from osteoblast-induced osteoclast apoptosis. Notably, FasL deficient (gld) mice display increased bone mass pointing to non-apoptotic functions of FasL. Some key extracellular matrix associated molecules, such as osteoprotegerin, osteocalcin, osteopontin and alkaline phosphatase were reported to be affected by FasL deficiency in osteoblasts but a complex insight has been missing. To fill this gap and provide a robust dataset, gld calva-derived cells were differentiated along with controls and subjected to RNASequencing. The analysis revealed statistically significant changes in expression of 1,710 genes. 15 % (263) out of them were associated with the extracellular matrix. This applied for the collagen components,  but also non-collagenous proteoglycans including versican and aggrecan. This report provides enrichment analysis of statistically significant expression changes in calva-derived osteoblastic cells with focus on extracellular matrix components. The dataset further provides a solid background for further functional analyses revealing the exact mechanisms behind and consequences of such dysregulations in pathophysiology.

overall_design: Mice homozygous for the FasL gld mutation (B6Smn.C3-Faslgld/J) were purchased from The Jackson Laboratory (Bar Harbor, ME). C57BL/6 were used as a wild-type control. Mice were kept at the Department of Biomedical Research of the Medical University of Vienna. Calvaria-derived cells (gld and wt) were isolated and expanded as described in Kratochvilova et al. (2022). Differentiation was performed in osteogenic media consisting of MEM alpha (Gibco, Waltham, MA, USA), 10% fetal bovine serum (Sigma-Aldrich, Burlington, MA, USA), 1% penicillin/streptomycin (Sigma-Aldrich), 50 mg/ml ascorbate and 4 mM β-glycerophosphate in 37˚C and 5% CO2. For the stimulatory experiment of gld cells, the osteogenic medium was supplemented with 150 ng/ml recombinant human sFas ligand (Peprotech, 310-03H) at day 14 of differentiation. The cells were then cultured for 72 h, the medium/medium+FasL was changed once during this time, wt cells (wt), gld cells (gld) and gld cells treated by FasL (gld+FasL) were cultured in parallel. Samples for RNA isolation were lysed in 350 μl of RLT lysis buffer (Qiagen) with β-ME (Sigma-Aldrich), total RNA was extracted using RNeasy Mini Kit (Qiagen, Germany) and cDNA was synthesized using the gb Elite Reverse Transcription Kit (Generi Biotech, Czech Republic). Total RNA samples were sent for QuantSeq analysis to Lexogen GmbH, Campus Vienna Biocenter 5, Vienna, where the samples were processed and sequenced according to the company's standard operating procedure. In brief, the library for sequencing was prepared using the QuantSeq 3′mRNA-Seq Library Prep Kit FWD for Illumina (Lexogen) and the Lexogen i5 6 nt Unique Dual Indexing Add-on Kit (Lexogen). Single-read RNA-Seq (1 × 75) was performed using an Illumina NextSeq 500 System (Illumina). Comprehensive analysis of the RNA-Seq data, including demultiplexing, read quality assessment, trimming and filtering, read mapping, and differential expression analysis, was carefully performed by Lexogen GmbH. This analysis was performed according to their standardized pipeline for QuantSeq FWD data. In brief, read quality was assessed using the FastQC , RSeQC  and MultiQC  packages. Samples were trimmed using the Cutadapt  tool and aligned to the reference genome using the STAR  aligner.


title: Genome-scale transcriptome augmentation during Arabidopsis thaliana photomorphogenesis

city: Paris

first: Clara

last: Bourbousse

address: 9 quai Saint Bernard

department: UMR 8263 Dev2A

institute: Sorbonne Université

summary: Plant photomorphogenesis is a light-induced developmental switch combining rapid enrichment in RNA Polymerase II activity and massive gene expression reprogramming. Yet, all former transcriptome analyses of this transition detected no average tendency toward gene upregulation. By applying a spike-in RNA-seq approach, we solved this conundrum and reconciled transcriptome dynamics with epigenomic and cytogenetic data. This further unveiled that Arabidopsis cotyledon photomorphogenesis involves a ~2-fold expansion of the transcriptome, a trend that we reproducibly observed in datasets from independent laboratories upon normalization using a set of stable genes defined ad hoc. This new standpoint enabled us to reinterpret light-mediated gene regulatory paths and unveil a quasi-exclusive positive effect of light-induced transcription factors on target genes. Collectively, this study reveals how environmentally controlled variations of the transcriptional regime can functionally impact plant genome expression. It further establishes a framework for investigating the mechanisms of global genome regulation in these organisms.

overall_design: RNA-seq with drosophila spike-in on dissected cotyledons

first: Geoffrey

last: Schivre

first: Léa

last: Wolff

first: Fredy

last: Barneche


overall_design: ChIP-seq of RNA pol II and H2Bub of dissected cotyledons from 5-day-old Arabidopsis thaliana light and dark-grown seedlings. 3 Replicates are available for RNA Pol II, 2 for H2Bub. A spike-in was included (Drosophila S2 cells chromatin).

first: Elodie

last: Armanet

first: Delphine

last: Cuménal


title: PCBP1 binding to single-stranded poly-cytosine motifs enhances cGAS sensing and impairs breast cancer development [snRNA-Seq]

status: Public on Oct 15 2025

city: Charleston

first: Cécile

last: Fréreux

state: SC

address: 173 Ashley Avenue

institute: Medical University of South Carolina

summary: The cGAS-STING pathway plays a central role in controlling tumor progression through nucleic acid sensing and type I Interferon production. Here, we identify Poly(rC) Binding Protein 1 (PCBP1) as a tumor suppressor that amplifies cGAS-STING signaling in breast cancer. Using patient datasets and a transgenic mouse model with conditional PCBP1 knockout in mammary epithelial cells, we show that PCBP1 expression correlates with improved survival, reduced tumor burden, increased type I IFN and ISG expression, and elevated cytotoxic T cell infiltration. Mechanistically, PCBP1 binds cytosine-rich single-stranded motifs via its KH domains and increases cGAS affinity to these nucleic acids. Disruption of the conserved GXXG motif impairs PCBP1's nucleic acid binding and cGAS activation. Although cGAS is a double-stranded DNA sensor with no intrinsic sequence specificity, we uncover that the single-stranded nucleic-acid binding protein PCBP1 enhances cGAS sensing by engaging sequence-specific motifs, acting as an important nucleic acid co-sensor that impairs tumorigenesis.

overall_design:
We used sized-matched mammary tumors (~100mg) from a C57BL/6 transgenic mouse model expressing the MMTV-PyMT (polyomavirus middle T antigen) oncogene, which drives mammary tumorigenesis, in addition to a MMTV-Cre PCBP1(fl/fl) system that selectively knocks out PCBP1 in mammary epithelial cells. These mice, abbreviated as PyMT PCBP1–/–, were compared to control animals expressing the MMTV-PyMT and MMTV-Cre constructs along with the non-floxed PCBP1(wt/wt) alleles, referred to as PyMT PCBP1+/+. The mammary tumors were dissociated, the nuclei sorted by flow cytometry and analyzed by single-nuclei RNA-sequencing.
Please note that the same mouse model associated with GSE307616 RNA-seq dataset was used for the current study

first: Joseph

last: Karam

first: Breege

last: Howley

first: Bryan

last: Granger

first: Paramita

last: Chakraborty

first: Annamarie

middle: C

last: Dalton

first: Bidyut

middle: K

last: Mohanty

first: Silvia

last: Vaena

first: Romeo

last: Martin

first: Shikhar

last: Mehrotra

first: Philip

middle: H

last: Howe


title: Transcriptome analysis of human monocyte-derived myeloid cells

city: Nantes

first: Aurelie

last: Moreau

address: 30 bd Jean Monnet

institute: INSERM U1064

summary: Transcriptome analysis of different populations of human monocyte-derived myeloid cells: Autologous Tolerogenic Dendritic Cells (ATDCs), Monocyte-derived Dendritic Cells (MoDCs) and IL-10 induced dendritic cells (DC-10). GSM 2800573 to GSM 2800584 that were re-analyzed from GSE104438.

overall_design:
CD14+ sorted monocytes from 6 different donors were used to differentiate ATDCs, MoDCs and DC-10 from the same samples. We analyzed transcriptomic profiles from these monocytes-derived cells using Agilent whole genome oligo Microarrays (8x60K).

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The table below lists GEO accessions reused/reanalyzed for this study.
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first: A

first: S

last: Gregori

first: G

last: Amodio


title: Tissue-resident macrophages co-develop with myocardial tissue in human induced pluripotent stem cell-derived organoids

city: Würzburg

first: Anna

middle: Frederike

last: Rockel

address: Koelliker Straße 6

department: Institute of Anatomy and Cell Biology

institute: University of Würzburg

summary: The heart is the first functional organ to develop during embryogenesis, forming in parallel with the vasculature and hematopoietic cell lineages. To advance our understanding of human cardiac development and disease, human induced pluripotent stem cell-derived cardiomyocytes offer a promising in vitro model. However, conventional 2D culture systems lack the complexity required to recapitulate the intricate interactions of different cell types leading to fully functional and mature cardiac tissue. Here, we present a cardiac organoid model that mimics several aspects of cardiogenesis. The organoids develop a functional myocardium consisting of cardiomyocytes and fibroblasts capable of spontaneous rhythmic contractions. The myocard is interspersed with a branched endothelial network. Additionally, macrophages develop within the organoids and integrate into the myocardium. In summary, we describe a complex 3D cell culture platform to study human heart tissue development with all the involved cell types (cardiomyocytes, fibroblasts, endothelial cells, macrophages), paving the way for new insights into the role of macrophages in cardiac development and disease.

overall_design: RNA-seq profiling of human wildtype cardiac organoid at day 35

middle: F

first: Tobias

last: Brunnenbauer

first: Nicole

last: Wagner

first: Brenda

last: Gerull

first: Süleyman

last: Ergün

first: Philipp

last: Wörsdörfer


title: PCBP1 binding to single-stranded poly-cytosine motifs enhances cGAS sensing and impairs breast cancer development

first: Cécile

last: Fréreux

overall_design: We used mammary tumors from a C57BL/6 transgenic mouse model expressing the MMTV-PyMT (polyomavirus middle T antigen) oncogene, which drives mammary tumorigenesis, in addition to a MMTV-Cre PCBP1(fl/fl) system that selectively knocks out PCBP1 in mammary epithelial cells. These mice, abbreviated as PyMT PCBP1–/–, were compared to control animals expressing the MMTV-PyMT and MMTV-Cre constructs along with the non-floxed PCBP1(wt/wt) alleles, referred to as PyMT PCBP1+/+. RNA was prepared from the mammary tumors and RNA-sequencing performed.

first: Joseph

last: Karam

first: Breege

last: Howley

first: Bryan

last: Granger

first: Paramita


title: The 3’-5’ exoribonuclease ISG20L2 contributes to 3’ terminus maturation of 18S and 28S ribosomal RNAs

first: Dominique

last: Gagliardi

overall_design: HeLa cells were treated with a control siRNA duplex (siRNA scramble) ou siRNA duplexes targeting ISG20L2 mRNA.

first: Maxime

last: Aubert

first: Hélène

last: Zuber

first: Marine

last: Mommert-Tripon

first: Sarah

last: Le Page

first: Nathalie

last: Montel-Lehry

first: Vanessa

last: Soldan

first: Stéphanie

last: Bosch

first: Pierre-Emmanuel

last: Gleizes

first: Marie-Françoise

last: O'Donohue


title: SF3B1 K700E Mutation Induces Genome-Wide Enhancement of Transcriptional Pause Release in ES Cells [PRO-seq]

first: Claudia

last: Mimoso

overall_design: Examination of 6 samples by PRO-seq; 3 biological replicate sets of SF3B1 K700E Mutant and SF3B1 WT libraries.

first: Mahtab

last: Dastpak

first: Moein

last: Farshchian

first: Christina

last: Paraggio

last: Leonard

first: Shanye

last: Yin

first: Binkai

last: Chi

first: Kelsey

last: Nassar

first: RGrant

last: Rowe

first: Jiuchun

last: Zhang

first: George

last: Daley

first: Karen

last: Adelman

first: Robin

last: Reed


title: Gene expression profiling of skin and blood in human acute cutaneous Lyme disease

city: Vienna

first: Georg

last: Stary

address: Waehringer Guertel 18-20, 1090 Wien

department: Department of Dermatology

country: Austria

institute: Medical University Of Vienna

summary: We investigated T cell polarization and Langerhans cell gene expression in acute Lyme disease compared to autoloagous healthy control skin.

overall_design:
Single cell suspensions were obtained from skin and blood of LD patients, FACS-sorted and sequenced using the 10XGenomics platform as previously described (Saluzzo et al. STAR Protoc. 2022 Jun 17;3(3):101470. doi: 10.1016/j.xpro.2022.101470. PMID: 35769924; PMCID: PMC9234085.

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

last: Strobl

first: Florian

last: Winkler

first: Ruth

last: Dingelmaier-Hovorka


title: Impact of somatic XIST deletions on ongoing XIST expression and inactive X silencing and heterochromatin

city: Vancouver

first: Carolyn

last: Brown

address: 2350 Health Sciences Mall

institute: University of British Columbia

summary: The long non-coding RNA XIST is critical during early female development for establishing X-chromosome inactivation. XIST continues to be expressed from the inactive X throughout life, and can establish silenced heterochromatin when ectopically expressed; yet silencing of most genes on the inactive X has been shown to continue in the absence of XIST in somatic cells. As changes in XIST expression are observed in cancers and aging we sought to re-examine the impact of complete or partial XIST loss on gene expression and chromatin structure in the hTERT RPE-1 cell line. Loss of the A repeat region resulted in complete loss of XIST expression. While loss of an adjacent enhancer region spanning the small F repeat region impacted expression and loss of the repeat E region impacted localization, both deletions maintained partial silencing. Upon XIST loss there was reactivation of a subset of X-linked genes, with escape genes showing an average 20% increase in expression; consistent with other studies. Comparison with other studies of XIST loss in human somatic cells revealed some common XIST-dependent escapees, while autosomal genes demonstrated no consistent XIST-dependencies. Loss of XIST in hTERT RPE-1 resulted in loss of H3K27me3 and H2AK119ub; however, inhibition of each of these pathways failed to upregulate candidate escapees on the inactive X. In contrast, reduction of H3K9me3 caused partial reactivation of USP9X but not MED14. XIST regulatory elements lie within the gene, with ongoing expression dependent on the A repeat region, as well as enhancer function from the adjacent F-containing region. Unlike the E region, the F region is not involved in XIST localization. Our work, in agreement with previous studies, reveals that in somatic cells XIST expression and localization suppresses the expression of escape genes, likely through loss of XIST-dependent chromatin modifications. No single chromatin modification was responsible for the XIST-dependency, varying across both genes and studied cell lines, thus implicating combinatorial action of silencing pathways on the inactive X. While disruption of autosomal gene expression is observed, there are no consistent autosomal XIST-dependencies to implicate a direct action of XIST on autosomes across cell types.

overall_design: RNA-seq profiling of wild-type RPE1 cells and RPE1 cells with CRISPR-mediated interal deletion of XIST gene

first: Karanveer

middle: S

last: Bhangu

first: Christine

last: Yang

first: Hannah

middle: J

last: Illing


title: The regulatory code of injury responsive enhancers enables precision cell state targeting in the CNS [enhancer_aav]

city: Stockholm

first: Margherita

last: Zamboni

address: Solnavägen 9

department: Cell and Molecular Biology

country: Sweden

institute: Karolinska Institutet

summary: Enhancer elements in the genome direct cell type-specific gene expression programs. In response to injury, cells undergo dynamic changes in gene expression that drive adaptation and initiate tissue repair. Here, we investigate how injury-induced gene expression programs are encoded within enhancer elements in the mammalian CNS. Leveraging single-nucleus transcriptomics and chromatin accessibility profiling, we identify thousands of injury-induced, cell type-specific enhancers in the mouse spinal cord. These enhancers are more abundant in glial cells and retain cell type specificity, even when regulating shared wound response genes. By modeling glial injury-responsive enhancers using deep learning, we reveal that their architecture encodes cell type specificity by integrating generic stimulus response elements with cell identity programs. Finally, through in vivo enhancer screening, we demonstrate that injury-responsive enhancers can selectively target reactive astrocytes bordering lesion sites across the CNS using therapeutically relevant gene delivery vectors. Our decoding of the principles of injury-responsive enhancers enables the design of sequences that can be programmed to therapeutically target disease related cell states.

overall_design: Animals from a Cx30-Tom transgenic line were injected with an enhancer AAV library to test the activity of injury-responsive enhancers identified in our analysis. Mice were then injured with a spinal cord contusion model (14dpi) and samples were collected after 3 days (or from uninjured controls). Single cells were obtained through tissue digestion and sorting and were processed using a transcriptomics experiment that included enrichment for barcodes associated with the enhancer viruses. Each condition encompassed 1-2 animals per sex.

first: Enric

last: Llorens Bobadilla


title: Mechanisms of assembly and function of the Hsp70-Hsp40 chaperone machinery

city: Heidelberg

first: Santiago

last: Maya

address: Im Neuenheimer Feld 329

institute: Zentrum für Molekulare Biologie der Universität Heidelberg (ZMBH)

summary: Hsp70 and Hsp40 molecular chaperones form a central machinery that remodels client proteins involved in numerous biological processes. Here, we integrated cryo-electron microscopy and nuclear magnetic resonance spectroscopy to determine the architecture of the full-length Hsp70-Hsp40 machinery. The structure of the complex in a physiologically inhibited state reveals distinct regulatory mechanisms. In the active state, the Hsp40 glycine-phenylalanine (G/F)-rich region acts as a pseudo-substrate for Hsp70, directly modulating refolding. This region also maintains Hsp40 in an autoinhibited state; upon binding to Hsp70, the inhibition is disrupted, exposing a cryptic client-binding site that enables client engagement and refolding. Transitions between these states are central to controlling refolding efficiency. Disrupting either the autoinhibited state or the G/F-Hsp70 interaction impairs function and elicits a compensatory heat shock response in cells. Our findings uncover the regulatory dynamics of a fundamental chaperone system, with broad implications for understanding protein homeostasis and the cellular response to stress.

sample_organism: Escherichia coli str. K-12 substr. MG1655

overall_design: Ribosome profiling analalysis of wt E. coli MG1655 and mutant (DnaJF98A - F102A, CbpAF98A - F102A) cells, at optical density (OD600) of 0.5 and 2.0.

first: Yajun

last: Jiang

first: Ziad

last: Ibrahim

first: Mary

last: Clay

first: Youlin

last: Xia

first: Alexandre

last: Myasnikov

first: Kaylan

last: Immadisetty

first: Zhilian

first: Liang

last: Tang

first: Paolo

last: Rossi;

first: Pritha

last: Ganguly

first: Jiangshu

last: Liu

first: Darcie

last: Miller

first: Meixia

last: Che

last: palacios

first: Gunther

last: Kramer

first: Bernd

last: Bukau

first: Charalampos

last: Kalodimos


title: SF3B1 K700E Mutation Induces Genome-Wide Enhancement of Transcriptional Pause Release in ES Cells

first: Claudia

last: Mimoso

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

overall_design: Refer to individual Series


title: The regulatory code of injury responsive enhancers enables precision cell state targeting in the CNS [CUT&Tag]

first: Margherita

last: Zamboni

overall_design: CUT&Tag for Sox9 was performed on spinal cord samples from animals subjected to contusion injury (1dpi) or uninjured controls.

first: Enric

last: Llorens Bobadilla


title: The regulatory code of injury responsive enhancers enables precision cell state targeting in the CNS [multiome]

overall_design: Single nuclei from the mouse spinal cord were processed with a multiomic approach, sampling transcriptomics and chromatin accessibility information. We collected tissue from uninjured mice, as well as mice subjected to a spinal cord injury (ie., contusion, at 1, 3, 7, and 28 dpi). Nuclei were either sampled unbiased or subjected to FAC sorting to enrich for specific populations (e.g., astrocytes, ependymal cells, immune cells and perivascular cells). Each experimental condition encompassed 1-2 animals per sex.


title: An early-stage 3D fibroblast-featured tumor model mimics the gene expression of the naïve tumor microenvironment, including cancer progression and drug resistance phenotype.

city: Philadelphia

first: Francesca

last: Costabile

address: 3400 Civic Center BLVD

institute: University of Pennsylvania

summary: The tumor microenvironment (TME) plays a crucial role in cancer progression, yet the interactions between tumor cells and stromal components, such as fibroblasts, remain poorly understood. Traditional two-dimensional (2D) culture models fail to accurately replicate the complexities of the TME, hindering progress in cancer research and drug development. This study presents a novel 3D spheroid model, generated using the hanging drop system, that incorporates both tumor cells (B16F10 mouse melanoma) and fibroblasts (NIH/3T3), and aimed at simulating the early-stage TME. We demonstrate that fibroblasts are essential for ECM deposition, a key feature absent in tumor cells-only spheroids. Co-cultured spheroids exhibited a more organized structure, enhanced ECM deposition (type-VI collagen), and more closely resembled the morphology of native tumors compared to monocultures. RNA sequencing analysis revealed that the gene expression profile of B16F10–NIH/3T3 spheroids closely matched that of in vivo tumors, with 693 genes involved in critical pathways such as “pathways in cancer” and those linked to drug resistance. These findings highlight the importance of fibroblast inclusion in 3D models to replicate the genetic and structural features of the TME. Our spheroid system provides a more accurate representation of early tumor stages and offers a promising platform for drug screening, reducing the need for in vivo models by allowing the selection of the most effective compounds for further testing. This work underscores the potential of 3D culture systems in advancing our understanding of tumor biology and improving the precision of cancer therapeutics.

overall_design: RNA-seq profiling of B16F10 cells cultured in the different condition: sorted from B16F10–NIH/3T3 spheroids, sorted from B16F10 generated - in vivo tumor, sorted from standard two dimentional B16F10–NIH/3T3 coculture, B16F10 standard two dimentinally cultured.

first: Subin

last: George

first: Andrea

last: Facciabene

first: Gilberto

last: Filaci

first: Maddalena

last: Mastrogiacomo


title: Single Nucleus Profiling Highlights the All-Brain Echinoderm Nervous System

city: Napoli

first: Maria Ina

last: Arnone

address: Villa Comunale 1

department: Biology and Evolution of Marine Organisms

country: Italy

institute: Stazione Zoologica Anton Dohrn

summary: By combining single nucleus transcriptomics with spatial gene expression analysis and high-resolution electron microscopy, we reconstructed the cell type atlas of post-metamorphic Paracentrotus lividus juveniles.

overall_design: Generation and analysis of Paracentrotus lividus juvenile snRNA-seq data to use along with imaging techniques to generate P. lividus juvenile cell atlas.

first: Paganos

last: Periklis

first: Ullrich-Lüter

last: Jack

first: Almazán

last: Alba

first: Voronov

last: Danila

first: Carl

last: Jil

first: Zakrzewski

last: Anne-C.

first: Zemann

last: Berit

first: Rusciano

last: Maria Lorenza

first: Sancerni

last: Tiphaine

first: Schauer

last: Maria

first: Akar

last: Oğuz

first: Caccavale

last: Filomena

first: Cocurullo

first: Benvenuto

last: Giovanna

first: Croce

last: Jenifer Carol

first: Lüter

last: Carsten

first: Arnone

last: Maria Ina


title: Single cell multi-omic sequencing of human peripheral mononuclear cells (PBMCs) post heart transplantation

city: La Jolla

first: Yuko

last: Tada

state: CA

address: 9500 Gilman Dr

institute: UC San Diego

summary: PBMCs collected from patients with or without graft dysfunction post heart transplantation  were analyzed using the BD Rhapsody CITE-seq and VDJ-seq. The study groups include patients with cardiac allograft dysfunction (CAV), non-specific graft dysfunction (NGD), and normal graft function (Normal HTx).

overall_design:
Cryopreserved PBMCs were thawed and labeled with antibody derived tags followed by single cell CITE-seq and VDJ-seq.

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Submitter states that missing raw files are due to file loss.
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first: Paul

last: Kim

first: Klaus

last: Ley


title: The role of Endothelial cell-derived Extracellular Vesicles in modulating Fibroblast Function in Skin Wound Healing

city: Chicago

first: Heidi

last: Yuan

address: 801 S Paulina St

institute: University of Illinois Chicago

summary: An adequate wound healing response requires the coordination of intercellular signals between multiple cell types. Following skin injury, endothelial cellsand fibroblasts provisionally replace the site of injury with newlyvascularized granulation tissue. Given the spatial and temporal overlap ofthese two cell types in the healing response, we hypothesize that endothelial cell-derived extracellular vesicles (ECEVs) could provide a communication pathway by which ECs influence fibroblast behavior. In this study we investigated the effects of ECEVs on fibroblast function both in vitro and in vivo through a murine skin wound healing model. Transcriptomic analysis showed that the uptake of ECEVs by fibroblasts altered functions and pathways relating to cel ldivision, ECM organization, and fibrosis. This transcriptomic analysis was functionally corroborated through in vitro assays in which fibroblasts demonstrated enhanced proliferation, migration, cell cycle progression,collagen contraction, and altered ECM deposition following ECEV treatment. Administration of ECEVs to healing mouse wounds led to greater collagen density and an upregulated fibroblast quantity in the wound bed of scar tissue. Our study highlights a novel role for ECEVs in affecting fibroblast function in the context of wound repair. Future studies can extrapolate this to other contexts where vascularization may affect tissue fibrosis.

overall_design: RNA-sequencing (RNA-seq) profiling of primary human dermal fibroblasts treated with control media or control media containing endothelial cell-derived extracellular vesicles (ECEVs) for 72h.

first: Anna

last: Salapatas

first: Trevor

middle: R

last: Leonardo

first: Chen

last: Han

first: Bhavya

last: Vegesna

first: Koushik

last: Debnath

first: Lin

last: Chen

first: Sriram

last: Ravindran

first: Luisa

last: DiPietro


title: Genome-wide DNA methylation profiling of human CD4+ T helper cells define epigenetic signatures for Th1, Th17 and non-classic Th1 cells

city: Braunschweig

first: Stefan

last: Floess

address: Inhoffenstr. 7

department: Experimental Immunology

institute: Helmholtz-Centre for Infection Research

type: Methylation profiling by high throughput sequencing

summary: Naive CD4+ T cells are highly plastic cells that - upon activation - can differentiate into various T helper (Th) cell fates characterized by the expression of specific transcription factors and effector cytokines. Their expression can be stabilized by epigenetic mechanisms including DNA methylation. So far, our knowledge about the link between DNA methylation and T helper cell differentiation processes is fragmentary. In this study, we generated methylomes of CD4+ T helper cells by performing a whole-genome bisulfite sequencing analysis of ex vivo isolated human naïve T cells and selected clones of Th1, non-classic Th1 and Th17 cells. The pairwise comparison of the methylomes identified differentially methylated regions (DMRs) mainly located within introns, followed by promoter regions and exons. In accordance with literature, several DMRs were identified within lineage-specific loci like IFNG, TBX21, IL-17A and RORC. Thus, the identified DMRs are suitable to further characterize the T helper lineages and might be helpful to define lineage-specific regulatory modules involved in human T helper cell differentiation.

overall_design: Whole-genome bisulfite sequencing (WGBS) of human ex vivo isolated naive T cells and Th1, Th17 and non-classic Th1 cell clones.

first: Michael

last: Beckstette

last: Ntalli

first: Jochen

last: Huehn


title: WAGO-4 Germ Granule Localization Ensures Fidelity in Small RNA Loading

city: Wien

first: Stela

last: Jelenic

address: Dr. Bohr-Gasse 3

institute: Institute of Molecular Biotechnology

type: Non-coding RNA profiling by high throughput sequencing

summary: Germ granules are liquid-like condensates that regulate small RNA pathways and gene expression, ensuring genome stability and fertility in animals. In C. elegans, several Argonaute proteins, central players of small RNA pathways, localize to germ granules, yet the functional significance of this spatial enrichment remains unclear. Here, we disrupted the localization of WAGO-4 to germ granules by introducing targeted mutations in the FG repeats of Vasa-like GLH proteins. These mutations did not disrupt overall germ granule architecture but significantly reduced WAGO-4 partitioning, leading to its predominant localization in the cytoplasm. Functional analyses revealed that this mislocalization partially compromised WAGO-4 activity, resulting in reduced WAGO-4 binding of small RNAs targeting specific genes, particularly those not co-regulated by CSR-1. This selective effect highlights the importance of WAGO-4’s spatial localization for efficient small RNA loading and gene regulation. Our findings demonstrate that germ granules serve as specialized compartments that fine-tune Argonaute function, emphasizing the role of phase-separated condensates in modulating RNA pathways and gene regulatory networks.

overall_design: Comparative rRNA depleted RNA-seq of C. elegans mutants 3xFG, WAGO-4 KO (200a) and WAGO-4(Y611E)(272a) compared to the WT

first: Mathias

last: Renaud

first: Samantha

last: Del Borrello

first: Joseph

last: Gokcezade

first: Janos

last: Bindics

first: Lisa

last: Frasz

first: Philipp

last: Czermak

first: Peter

last: Duchek

first: Julie

middle: M

last: Claycomb


title: Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging

city: Baltimore

first: Supriyo

last: De

state: Maryland

address: 251 Bayview Blvd

department: Laboratory of Genetics and Genomics

institute: NIA-IRP, NIH


title: Effects of Bach2 on pancreatic gene expression in mice

city: Rostock

first: Robert

last: Jaster

address: Ernst-Heydemann-Str. 6

department: Dept. of Medicine, Div. of Gastroenterology

institute: Rostock University Medical Center

summary: The role of Bach2, a transcriptional repressor and key regulator of adaptive immunity, in the pathogenesis of autoimmune pancreatitis (AIP) is incompletely understood. Here, we used C57BL/6N mice with a targeted deletion of the Bach2 gene (Bach2 knockout mice) to study their susceptibility to AIP. The mice were kept for 18 weeks, before the pancreas and further organs were assessed histopathologically and by molecular methods. Results: Consistent with previous studies, Bach2 knockout mice showed reduced growth and developed a fatal lung disease necessitating humane euthanasia at the age of 18 weeks. Pancreatic infiltrates with lymphocytes frequently occurred in Bach2 knockout mice but not in wild-type animals. In more severe cases, this was associated with the focal destruction of exocrine pancreatic tissue and mild fibrosis. In the principal component analysis of pancreatic RNA-seq data, Bach2 knockout mice clustered separately from wild-type comtrols. Further data analysis revealed the activation of processes linked to adaptive immunity in pancreatic tissue of Bach2 knockout mice. We conclude that Bach2-deficient C57BL/6N mice are prone to the spontaneous development of AIP. This could be due to a disturbed immune homeostasis with dysregulated B and T cell activation. We thank Helmholtz Zentrum Muenchen - German Research Center for Environmental Health  (GmbH) for providing the mutant mouse line (Allele:  Bach2tm1b(EUCOMM)Wtsi), INFRAFRONTIER/EMMA (www.infrafrontier.eu, PMID: 25414328), and EMMA node at Helmholtz Zentrum Muenchen - German Research Center for Environmental Health (GmbH) from which the mouse line was distributed (RRID:IMSR_EM:09104). Associated primary phenotypic information may be found at www.mousephenotype.org.

overall_design: Mice with a constitutive whole-body knockout of the Bach2 gene and wild-type controls were kept until they reached 18 weeks of age. RNA was isolated from pancreatic tissue of 2 males and 2 females per group and subjected to RNA seq analysis.


title: An intracellular magnetic torque-regulator drives mechano-sequential antitumor immunity

city: Shanghai

first: Rui

last: Gao

address: Zhennan rode

department: School of Medicine

institute: Tongji University

summary: Nature creates specific structures to control mechanical plasticity for cell fate regulation. Although immune cells can sense and adapt to extracellular mechanical cues, how to activate immune responses via intracellular mechanical stimulation remains a mystery. Here, we present an intelligent intracellular magnetic torque (IIMT) paradigm that is coupled with programmed rotating magnetic fields to generate the selective mechano-stimulations in lysosomes and induce sequential antitumor immune responses. A magnetic rod-shaped micromotor (MagRM) with the a unique geometric aspect ratio is designed to exert tunable torques in antigen-presenting cells (APCs) and tumor cells. Low-intensity torque induces the mild lysosomal membrane damage to trigger antigen cross-presentation and canonical NLRP3 inflammasome activation in APCs, whereas high-intensity torque causes lysosomal membrane rupture for immunogenic cell death. In vivo studies unveil that the optimal antitumor activity is achieved by generating sequential torques from high to low intensities, which is illuminating to explore mechano-immunotherapy with selective and spatiotemporal control.

overall_design: The underlying mechanism of mechano-regulation for tumor cell death post high-frequency megneic field (HMF) were explored for the analysis. The RNA sequencing was performed on OVA-expression B16F10 (B16-OVA) melanoma cells collected at 6 h after Control, magnetic rod-shaped micromotors (MagRMs) with HMF treatments.

first: Chang

last: Xu

first: Zhenyan

last: Zhu

first: Chen

last: Liu

first: Min

last: Wang

first: Xueyan

last: Wei

first: Peng

last: Ning

first: Wei

last: Zhang

first: Yingze

last: Li

first: Junwu

last: Shen

first: Yajuan

first: Yifan

last: Tong

first: Feng

last: Tao

first: Xiaolei

last: Chen

first: Xiaoyi

last: Jiang

first: Huan

last: Ren

first: Cheng

last: Lv

first: Gustavo

last: Plaza

first: Jason

last: Miska

first: Haiming

last: Fan

first: Yichao

last: Tang

first: Yalei

last: Dai

first: Weiwei

last: Yang

first: Bin

last: He

first: Yu

last: Cheng


first: Rui

last: Gao

overall_design: To fully explore the effects of IIMT-activated immune response in tumor microenvironment, we performed single-cell RNA sequencing (scRNA-seq) on all cells in tumors isolated at 24 h after IIMT (HL-2), MagRMs (M-1), and PBS (P-2) treatments for 10 days from the B16-OVA (BO) mice on day 11.

first: Chang

last: Xu

first: Zhenyan

last: Zhu

first: Chen

last: Liu

first: Min

last: Wang

first: Xueyan

last: Wei

first: Peng

last: Ning

first: Wei

last: Zhang

first: Yingze


title: Mesenchymal Colorectal Cancers Secrete Vesicles With Unique Cargo That Can Be Used For Liquid Biopsy Based Diagnostics

city: Amsterdam

first: Sander

middle: Roeland

last: van Hooff

address: Meibergdreef 9

department: Center for Experimental and Molecular Medicine (CEMM),

country: Netherlands

institute: AUMC


title: Mesenchymal Colorectal Cancers Secrete Vesicles With Unique Cargo That Can Be Used For Liquid Biopsy Based Diagnostics [miRNA-seq plasma]

summary: Tumor-derived extracellular vesicles (TEVs) play a crucial role in cancer progression, metastasis and therapy resistance but their distinct profiles across different cancer stages and molecular subtypes remain underexplored. This study analyzed TEVs from epithelial (CMS2) and mesenchymal (CMS4) subtypes of colorectal cancer (CRC) using six cell lines and clinical samples. Investigation of the cargo of vesicles secreted by the two subtypes revealed significant differences in mRNA, miRNA, and protein profiles between the two subtypes. Notably, CMS2 predominantly secreted smaller, Tetraspanin-8 (TSPAN8) enriched EVs, while CMS4 produced both larger and smaller EVs, enriched in TSPAN4. This underscores the complexity of vesicle heterogeneity between these subtypes. Additionally, we assessed miRNA profiles from plasma-derived bulk TEVs in CRC patients. Our integrative analysis identified a distinct miRNA signature specific to each subtype, indicating that TEVs from CMS2 and CMS4 cells can be detected in circulation and may serve as potential diagnostic tool for CRC.

overall_design:
To investigate the miRNA profiles from plasma-derived TEVs in CMS2 and CMS4 subtyped CRC patients.

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

first: Paris

last: Asif

first: Lauri

last: Borghuis

first: Anita

last: Grootemaat

first: Monique

last: van Eijndhoven

first: Johan

last: de Rooij

first: Nils

last: Groenewegen

first: Nicole

middle: N

last: van der Wel

first: Arezo

last: Torang

first: Tineke

last: Buffart

first: D

last: Pegtel

first: Jan Paul

last: Medema


title: Mesenchymal Colorectal Cancers Secrete Vesicles With Unique Cargo That Can Be Used For Liquid Biopsy Based Diagnostics [RNA-seq]

overall_design: To investigate the mRNA profiles of TEVs derived from CMS2 and CMS4 subtyped cell lines, we used two CMS2 and two CMS4 cell lines.

first: Michiel

middle: D


title: Mesenchymal Colorectal Cancers Secrete Vesicles With Unique Cargo That Can Be Used For Liquid Biopsy Based Diagnostics [RNA-seq plasma]

overall_design:
To investigate the mRNA profiles from plasma-derived TEVs in CMS2 and CMS4 subtyped CRC patients.

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

middle: A

first: Inne

last: Borel Rinkes

first: Cristina

last: Gómez-Martín

first: Hans

last: Pruijt

first: Jennifer

last: Perez Boza

first: Onno

last: Kranenburg


title: ChIP-Seq analysis of DMTF1 in mouse neural stem cells; ChIP-Seq analysis of H2AZ in mouse neural stem cells with or wihtout Dmtf1 knockdown.

city: Singapore

first: Oleg

last: Grinchuk

address: 61 Biopolis Dr, Proteos

country: Singapore

institute: IMCB

summary: Neural stem cells (NSCs) contribute to embryonic brain development and adult brain homeostasis via their unique properties of self-renewal and differentiation. The Cyclin D binding Myb‑like transcription factor 1 (DMTF1) is reported to be a tumor supressor gene in cancer cells. However,the role of DMTF1 in NSCs is poorly understood. The aim of this study is to determine the role of Dmtf1 in NSCs and elucidate the underlying mechanism.

overall_design: DMTF1 ChIP-Seq in mNSCs; H2AZ ChIP-Seq in mNSCs without and with treatment shRNAs against mouse Dmtf1.

first: Yajing

last: Liang

middle: V

first: Derrick

last: Ong


title: Mesenchymal Colorectal Cancers Secrete Vesicles With Unique Cargo That Can Be Used For Liquid Biopsy Based Diagnostics [miRNA-seq]

first: Sander

last: van Hooff

overall_design: To investigate the miRNA profiles of TEVs derived from CMS2 and CMS4 subtyped cell lines. We used three CMS2 and three CMS4 cell lines.

first: Paris

last: Asif

first: Lauri

last: Borghuis

first: Anita

middle: E

last: Grootemaat

first: Monique


title: Chaperone-mediated autophagy sustains muscle stem cell regenerative functions but declines with age

city: Barcelona

first: Ignacio

last: Ramirez Pardo

state: Barcelona

address: Carrer del Doctor Aiguader, 88, Ciutat Vella

department: Department of Medicine and Life Sciences

institute: Universitat Pompeu Fabra

summary: Proteostasis supports stemness and its loss correlates with the functional decline of diverse stem cell types. Here we identify that chaperone-mediated autophagy (CMA), a selective autophagy pathway, is necessary for the regenerative capacity of muscle stem cells (MuSCs) throughout life. We show that CMA is active in MuSCs, while genetic loss of CMA in MuSCs or failure of CMA in normally aged cells causes a proliferative impairment, resulting in defective skeletal muscle regeneration. Reactivation of CMA in old MuSCs boosts their proliferative capacity and improves their regenerative ability. Using comparative proteomics to identify CMA substrates, we uncovered actin cytoskeleton and glycolytic metabolism as key processes altered in aged mice and human MuSCs. Our findings reveal CMA to be a decisive stem-cell-fate regulator, with implications for fostering muscle regeneration in old age.

overall_design: bulk RNA-seq of isolated muscle stem cells (MuSCs) at 0 (uninjured), 1 and 4 dpi (days post injury) from Lamp2a-WT and Lamp2A-Pax7CreER mice.

last: Ramírez-Pardo

first: Silvia

last: Campanario-Sanz

first: Eusebio

last: Perdiguero

first: Joan

last: Isern

first: Pura

last: Muñoz-Cánoves

first: Ana Maria

last: Cuervo


title: An intracellular magnetic torque-regulator drives mechano-sequential antitumor immunity [RNA-seq]

first: Rui

last: Gao

overall_design: The underlying mechanism of mechano-stimulation for dendritic cell (DC) activation post low-frequency megneic field (LMF) were explored for the analysis. The RNA sequencing was performed on bone marrow-drived dendritic cells (BMDCs) collected at 6 h after Control, magnetic rod-shaped micromotors (MagRMs), and LMF treatments.

first: Chang

last: Xu

first: Zhenyan

last: Zhu

first: Chen

last: Liu

first: Min

last: Wang

first: Xueyan

last: Wei

first: Peng

last: Ning

first: Wei

last: Zhang

first: Yingze

last: Li

first: Junwu

last: Shen

first: Yajuan

first: Yifan

last: Tong

first: Feng

last: Tao

first: Xiaolei

last: Chen

first: Xiaoyi

last: Jiang

first: Huan

last: Ren

first: Cheng

last: Lv

first: Gustavo

last: Plaza

first: Jason

last: Miska

first: Haiming

last: Fan

first: Yichao

last: Tang

first: Yalei

last: Dai

first: Weiwei

last: Yang

first: Bin

last: He

first: Yu

last: Cheng


title: RNA-Seq analysis of mouse neural stem cells with or wihtout DMTF1 knockdown.

first: Oleg

last: Grinchuk

overall_design: RNA-seq analysis of neural stem cells that are derived from wild type control mice without and with treatment  shRNAs against mouse Dmtf1.

first: Yajing

last: Liang

first: Derrick

last: Ong


title: Gestational Low-Protein Diet Impairs Mitochondrial Function and Skeletal Muscle Development by Inducing Immune Responses in Male Offspring

status: Public on Oct 14 2025

city: Liverpool

first: Atilla

last: ALTINPINAR

address: 6 West Derby street

country: United Kingdom

institute: University of Liverpool

summary: To elucidate the potential underlying mechanisms of protein restriction during gestation, we compared the transcriptomic profiles of GAS muscles from 21-day-old offspring of mothers on a low-protein diet during gestation with those of a control group using RNA-seq analysis.

overall_design: Two weeks prior to mating, nulliparous 8-weeks old female mice were fed either a normal-protein diet (N, 20% crude protein; code 824226, Special Diet Services, UK) or a low-protein diet (L, 8% crude protein; code 824248, Special Diet Services, UK) ad-libitum. Male mice of the same age, which had been fed on a normal-protein diet, were used for mating. The male pups born from both groups were used for this study. New-born offspring were cross-fostered to dams fed normal-protein diet within 24 hours of birth, creating Normal-Normal (NN) and Low-Normal (LN) groups. NN and LN mice were kept on a normal-protein diet after weaning (day 21), generating Normal-Normal-Normal (NNN) and Low-Normal-Normal (LNN) groups of mice respectively.

last: Altinpinar

first: Moussira

last: Alameddine

first: Ufuk

last: Ersoy

first: Ioannis

last: Kanakis

first: Vanja

last: Pekovic-Vaughan

first: Susan

last: Ozanne

first: Katarzyna

last: Goljanek-Whysall

first: Aphrodite

last: Vasilaki


title: UBA2A is a regulator of seed dormancy and DOG1 mRNA chromatin retention in Arabidopsis

city: Warsaw

first: Michal

last: Krzyszton

address: Pawinskiego 5a

country: Poland

institute: Institute of Biochemistry and Biophysics, Polish Academy of Sciences

summary: Multiple factors control primary seed dormancy established during seed maturation and secondary seed dormancy established when a non-dormant seed is exposed to adverse conditions during imbibition. A key player in the control of both primary and secondary dormancy in Arabidopsis thaliana is the DOG1 gene, whose expression is extensively regulated at the transcriptional level. Despite its importance, the influence of posttranscriptional RNA processing and mRNA storage of DOG1 on the determination of dormancy depth remains elusive. We show that the UBA2A protein, a member of the hnRNP family, suppresses primary and secondary seed dormancy through the regulation of the DOG1 gene expres-sion at the posttranscriptional level. Surprisingly, single-molecule FISH, chromatin-attached RNA analysis and Pol II ChIP demonstrated that UBA2A do not control DOG1 gene transcription but rather DOG1 mRNA chromatin retention. Our study highlights chromatin retention as an important step in DOG1 gene expression regulation during dormancy establishment and shows that UBA2A like its human homolog hnRNPAB is implicated in RNA transport in the cell.

overall_design: Comparison of Col-0 and uba2a mutants (uba2a-1 and uba2a-3) dry seed transcriptomes (four biological replicas).

first: Ce

last: Wang

first: Szymon

last: Swiezewski


title: Analysis of microRNA-transcript regulatory networks in the hippocampus of the BTBR mouse model of autism

city: Rome

first: Valerio

last: Licursi

address: via degli Apuli, 4

department: c/o Dept. Biology and Biotechnologies "C. Darwin", Sapienza University of Rome

institute: Institute of Molecular Biology and Pathology (IBPM), National Research Council (CNR)

summary: Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition with unknown etiology. Currently, the role of post-transcriptional mechanisms in ASD remains unclear. microRNAs (miRNAs) are small non-coding regulatory RNAs that mediate mRNA destabilization and/or translational repression. To explore the potential role of miRNAs in ASD, we performed miRNA expression profiling in the hippocampus of the BTBR ASD mouse model and age-matched C57BL/6J mice. Alongside, we analyzed the BTBR hippocampal transcriptomic profile to identify differentially expressed transcripts (DETs). By integrating differentially expressed miRNA (DEmiRNA) and DET lists, we discovered mRNA transcripts putative targets of BTBR DEmiRNAs and with an anti-correlated differential expression in the BTBR hippocampus. They represent potential regulatory networks related to gene transcription regulation, and synaptic structure and function relevant for ASD. Thes include miR-200 family members, miR-200a-3p, miR-200b-3p, miR-200c-3p, and miR-429, and the experimentally validated target Zeb2. Moreover, we identified a set of non-canonical interactions characterized by extensive pairing between BTBR DEmiRNAs and DETs, potentially triggering Target-directed miRNA degradation (TDMD). Our findings support a role for miRNA dysregulation in the pathophysiology of ASD.

first: Silvia

last: Gasparini

first: Carlo

last: Presutti

first: Cecilia

last: Mannironi


title: Transcriptional Profile in Allergic Contact Dermatitis to Methylisothiazolinone

city: São Paulo

first: Maria

middle: Notomi

last: Sato

state: São Paulo

address: Av. Dr. Eneas de Carvalho Aguia, 470

department: Dermatology

country: Brazil

institute: University of São Paulo

summary: This study aimed to investigate the signaling pathways induced by MI in the skin test of individuals with MI-sensitized ACD, comparing them to healthy controls. Individuals initially testing positive only for MI were recruited at the Contact Dermatitis Clinic at Hospital das Clínicas of São Paulo, re-exposed to MI or saline, and biopsied 48 hours after exposure. Negative controls for the patch test were also exposed to MI and saline for comparison. Histopathological and transcriptomic (RNAseq) analyses identified two groups among the ACD patients: Group A (GA), with more pronounced histopathological features such as spongiosis and microvesicles, and Group B (GB), which showed milder reactions and absence of spongiosis. In GA, a total of 1588 genes were upregulated and 2090 downregulated in response to MI, compared to GB. These differentially expressed genes (DEGs) were associated with inflammation and neurological signaling, such as IL-24, IL-9, IL-13, and NTRK1, while IL-37 and IL-18 were downregulated. Similarly, GA compared to the MI-negative ACD group showed 1169 upregulated and 321 downregulated genes. DEG validation in GA through qPCR confirmed increased expression of NTRK1, IL-9, IL-6, IL-13, and CXCL8, with a reduction in IL-18. Protein analysis of IL-24 and IL-9 revealed higher expression in the dermal layer of GA. These results indicate distinct transcriptional profiles in MI-sensitized individuals, despite positive patch tests in all cases. The observed heterogeneity, not previously described in ACD, points to new potential therapeutic targets, such as IL-9, IL-37, and NTRK1. Furthermore, the study suggests that inflammatory and neurological cytokines, such as IL-9 and NTRK1, play key roles in the pathogenesis of ACD.

overall_design: ACD patients as well as skin from health individuals undergoing the same the same conditions and exposion to MI and saline, for histopathological analysis, RNA sequencing, PCR, immunohistochemistry.

first: Taynah

last: Melo

first: Iara

middle: G

last: Fernandes

first: Frederico

last: Ferreira

first: Emanuella

last: Souza

first: Gabriel

middle: B

last: Simões

first: Mirian

last: Sotto

first: Yasmim

last: Ramos

first: Vitor

last: Reis


title: Integrated landscape of renal metabolism in domestic cats with spontaneous chronic kidney disease: a multi-omics study

city: Lausanne

first: James

middle: Holzwarth

last: A

address: EPFL Innovation Park

institute: Nestlé

summary: Chronic kidney disease (CKD) is the leading cause of mortality in aged cats. After injury, feline kidneys undergo extensive metabolic reprogramming, but a comprehensive evaluation is lacking. We integrate serum metabolome from 15 early stages, 6 late stages CKD and 14 healthy control cats, with renal cortex and medulla transcriptome and proteome. Our analysis reveals spatiotemporal patterns of gene and protein expression changes. In the early stages, there are ~2000 differentially expressed genes in the medulla, but 6 in the cortex. The number in the cortex increases to >4000 in the late stages. We provide evidence of deranged bioenergetics in CKD: circulating fatty acids and acylcarnitines accumulate, while genes and proteins involved in fatty acid transport and oxidation are downregulated. Glucose and pyruvate metabolism is altered in CKD. Impaired glutamine metabolism contributes to both energy deficiency and acid-base imbalance. Additionally, there is a downregulation of redox enzymes, and overexpression of proinflammatory and profibrotic markers in CKD. Finally, hypoxia signaling pathway is upregulated, and negatively correlated with SGLT2 expression. These data unveil profound metabolic abnormalities in feline CKD.

overall_design: 40 samples total, 22 kidney cortex and 18 kidney medulla from 23 separate cats, with 6 non-CKD control, 10 CKD stage 1/2 and 7 CKD stage 3/4 cats.

first: Qinghong

last: Li

first: Ornella

last: Cominetti

first: James A

last: Holzwarth

first: Stacie

last: Summers

first: Loïc

last: Dayon


title: WAGO-4 Localization to Germ Granules Is Important for Its Accurate Small RNA Loading

city: Toronto

first: Julie

last: Claycomb

address: 661 University Ave

country: Canada

institute: University of Toronto

overall_design: small RNA sequencing of immunoprecipitated WAGO-4 complexes and whole worms

first: Stela

last: Jelenic

first: Mathias

last: Renaud

first: Samantha

last: Del Borrello

first: Joseph

last: Gokcezade

first: Janos

last: Bindics

first: Lisa

last: Frasz

first: Philipp

last: Czermak

first: Peter

last: Duchek


title: DEK function in silencing of Polycomb-target genes

city: Uppsala

first: Miyuki

last: Nakamura

address: Ulls Grand1

institute: Swedish University of Agricultural Sciences

summary: Chromatin-bound protein DEK is potentially related to a DNA topology change. In Arabidopsis, mutations in the DEK genes enhance the aberrant morphology in the background of lhp1 (Like Heterochromatin Protein) mutant.  LHP1 is responsible for the silencing of Polycomb target genes. We investigated whether defects in DEK genes affect transcriptional profiles in the presence and absence of the lhp1 mutation. Topoisomerase 1α is also known that affects DNA topology and interact with the DEK3 protein (Waidmann et al., 2014). ATRX is known as one of the LHP1 interacting proteins (Wang et al., 2018). By comparing these mutant transcriptomes, we addressed how these mutants are related to each other. We found that there is a synergistic effect on the misregulation of Polycomb target genes in the multiple mutant lhp1;dek2;3;4.

overall_design: Seedling sample of 5 different genetic background including wild-type (Wild-type x3, lhp1 x 3, dek1;2;3;4 quadruple x3, atrx x 3, lhp1;dek2;3;4 x2 biological replications)


title: CHD7 Regulates Cardiac Neural Crest Cell Differentiation Through SOX5-Mediated Self-Activation

city: Augusta

first: Kai

last: Jiao

state: GA

address: 1120 15th Street, Rm. CA4098

department: Center for Biotechnology and Genomic Medicine

institute: Augusta University

summary: CHARGE syndrome, primarily caused by CHD7 haploinsufficiency, is a complex developmental disorder frequently associated with congenital heart defects. Our comprehensive single-cell RNA sequencing analysis of cardiac neural crest cells (cNCCs) with Chd7 inactivation reveals impaired myocyte differentiation by cNCCs as a major cellular defect; loss of Chd7 disrupts myogenic transcriptional programs, alters cell fate trajectories, and activates cellular stress responses. These results significantly advance our understanding of the NCC-autonomous role of CHD7 and the mechanisms underlying CHARGE-associated heart defects driven by cNCC dysfunction. We further discovered that CHD7 enhances its own expression through interaction with SOX5 at an upstream, evolutionarily conserved enhancer. Notably, SOX5 overexpression in cultured Chd7-haploinsufficient cNCCs restores Chd7 expression from the intact allele, and rescues myocyte differentiation. These findings uncover a SOX5-mediated Chd7 autoregulatory mechanism and suggest that enhancing the SOX5-CHD7 axis may represent a promising strategy to mitigate cardiovascular defects caused by CHD7 insufficiency.

overall_design: GFP+ cells were isolated by fluorescence-activated cell sorting from the PA3–6 trunk and outflow tract (OFT) regions of control (Wnt1-Cre2; R26 +/mtmg; Chd7 +/+) and mutant (Wnt1-Cre2; R26 +/mtmg; Chd7 loxp/loxp) embryos at E10.5. Cells were pooled from three embryos of the same genotype. Single-cell transcriptome libraries were prepared using the 10x Genomics Chromium Single Cell 3ʹ v3 Reagent Kits, following the manufacturer’s standard protocol.

first: Shun

last: Yan

first: Andrey

last: Bombin

first: Jiao

last: Kai


title: Analgesia through FKBP51 inhibition at disease onset confers lasting relief from sensory and emotional chronic pain symptoms

city: London

first: Sandrine

last: Géranton

address: Medawar Building, Malet Place

department: Cell and Developmental Biology

institute: University College London

summary: Chronic pain affects 20-30% of the population and imposes a significant socio-economic burden as it is often accompanied by substantial emotional comorbidities such as anxiety and depression. Yet, the mechanisms underlying the interactions between the sensory and emotional aspects of chronic pain remain poorly understood. Here, we investigated the role of FKBP51, a regulator of the stress response, in mediating both sensory and emotional symptoms of chronic pain. Inhibition of FKBP51, via genetic deletion or pharmacological blockade, in persistent joint pain reduced fast-onset sensory, functional and activity-related symptoms, as well as late anxio-depressive comorbidities. FKBP51 inhibition after the establishment of the hypersensitive state provided only temporary symptoms relief, while acute inhibition at disease onset protected from the full development of sensory and anxio-depressive symptoms for up to 6 months. Our results also indicated that early pain symptoms could predict the late sensory and emotional outcomes of chronic pain. RNA sequencing of spinal cord tissue revealed that late FKBP51 inhibition transiently altered nociceptive genes associated with mechanical hypersensitivity. In contrast, early inhibition persistently downregulated the Naaa gene, a key regulator of the transition to chronic pain, and reorganized spinal cilia. Our results indicate that early FKBP51 inhibition after injury can persistently reduce chronic pain and prevent the onset of associated emotional comorbidities by modulating critical spinal neurobiological pathways that play pivotal roles in the transition to chronic pain.

overall_design: RNA Sequencing (NextSeq 500, Illumina) of mouse lumbar (L4-l6) spinal cord on day 30 after injection of sodium iodoacetate (MIA; 1 mg) into the knee joint. The aim of the study was to establish the mechanisms conferring anti-allodynia by the FKBP5 inhibitor SAFit2 in the MIA model of osteoarthritis and the influence of time of SAFit2 administration. Early samples were injected with vesicular phospholipid gel (VPG)-SAFit2 on days -3 before MIA and day 4 after MIA whilst late samples were injected on days 20 and 27 after MIA. Matched vehicle injections (VPG) occured at the same time points.

first: Sara

last: Hestehave

first: Roxana

last: Florea

first: Samuel

last: Singleton

first: Alexander

last: Fedorec

last: Caxaria

first: Oakley

last: Morgan

first: Katharina

last: Tatjana Kopp

first: Laurence

last: Brown

first: Tim

last: Heymann

first: Shafaq

last: Sikandar

first: Felix

last: Hausch

first: Stuart

last: Peirson


title: A direct role for a mitochondrial targeting sequence in triggering a stress response

city: Vancouver

first: Stephane

last: Flibotte

state: BC

address: 2370-6270 University Blvd.

department: Faculty of Science

institute: University of British Columbia

summary: Mitochondrial protein import is required for maintaining organellar function. Perturbations in this process are associated with various physiological and disease conditions. Several stress responses, including the mitoCPR, combat damage caused by mitochondrial protein import stress. However, it remains unknown how this defect is sensed. Here, we reveal that the conserved mitochondrial Hsp70 co-chaperone, Mge1, acts as a stress messenger in budding yeast. During mitochondrial stress, unimported Mge1 entered the nucleus and triggered the transcription of mitoCPR target genes. This was mediated by Mge1’s interaction with the transcription factor Pdr3 on DNA regulatory elements. Mge1’s mitochondrial targeting sequence was both sufficient and essential for mitoCPR induction, demonstrating that in addition to their roles in mitochondrial protein import, targeting sequences can also function as signaling molecules.

overall_design: Experiments was performed using three biological replicates for each of the following six conditions: (1) PSD1 overexpressors, (2) PSD1 overexpressors harboring a PDR3 deletion, (3) overexpressors of the N-terminal 44 amino acids of MGE1, (4) overexpressors of the N-terminal 44 amino acids of MGE1 with a PDR3 deletion, (5) overexpressors of the N-terminal 53 amino acids of MSS116.

first: Hilla

last: Weidberg

first: Zixuan

last: Yuan


title: Plate-based 10X Genomics-compatible single-cell RNA-sequencing based on Smart-seq3xpress

city: Gent

first: Koen

last: Deserranno

address: Ottergemsesteenweg 460

department: Department of Pharmaceutics

country: Belgium

institute: Ghent University

summary: In this study, we developed a novel plate-based 10X-compatible (PB10X) scRNA-seq strategy. By leveraging the Smart-seq3xpress (SS3X) principle, PB10X supports single-cell indexed sorting and cDNA generation that is downstream compatible with any commercially available 10X Single Cell 5' library construction kits such as the 10X Single Cell 5' Gene Expression and 5' V(D)J library construction kits. We demonstrated PB10X's performance on Jurkat T lymphoblasts by generating gene expression and V(D)J sequencing libraries, benchmarking it against 10X and SS3X.

overall_design: scRNA-seq;Smart-seq3xpress profiling of Jurkat cells

first: Elise

last: Callens

first: Dieter

last: Deforce

first: Filip

last: Van Nieuwerburgh