title: Exosomal Prognostic Score (EXPS)-based Prognostic Model in Pancreatic Tumours: Construction and Validation

status: Public on Dec 05 2025

city: Wuhan

first: Minghe

state: Hubei

address: Donghu Road

institute: WuHan University

summary: Pancreatic adenocarcinoma (PAAD) is a highly lethal malignancy with limited therapeutic options and poor prognosis. Extracellular vesicles (EVs), essential mediators of intercellular communication, are emerging as non-invasive biomarkers for diagnosis and prognosis. Investigating exosomal gene expression offers a more accurate prognostic tool for PAAD patients.We analyzed four datasets from public databases: PAAD_ExoRbase, TcgaTargetGtex-PAAD, GSE62452_GPL6244, and GSE78229_GPL6244. Differentially expressed exosomal genes were identified, followed by univariate Cox regression to pinpoint prognosis-associated exogenes. Single-cell analysis and single-sample gene set enrichment analysis (ssGSEA) refined the gene selection, assessing their origins and predictive value for immune status. In vitro experiments and RNA-seq validated the regulatory role of the key gene KRT7.LASSO Cox regression identified five prognostic genes: KRT7, KRT19, CXCL5, TNFRSF13C, and GP1BA. The prognostic model accurately predicted overall survival in the TCGA-PAAD, GSE62452, and GSE78229 cohorts. Single-cell analysis revealed the gene signature originated from T-proliferative, malignant, and ductal cells. Immune cell infiltration and immune checkpoint analyses confirmed the model’s predictive strength. In vitro assays and RNA-seq demonstrated that KRT7 promotes PAAD cell proliferation, migration, and invasion.

overall_design: CFPAC1 cells were transfetced with si-Control or si-KRT7, and were  subsequently harvested for RNA sequencing and transcriptome analysis.

first: Tianyin

last: Ma

first: Yufeng

last: Yuan


title: LncRNA and mRNA expression characteristics and bioinformatics analysis of exosomes from sheep ovaries with different reproductive capacities

status: Public on Dec 18 2025

city: nanjing

first: chenbo

last: yan

address: Weigang No.1

country: China

institute: Nanjing Agricultural University

type: Expression profiling by high throughput sequencing

summary: Hu sheep (HS) is known for its year-round estrus and multiple births, and is an ideal model for studying the mechanisms of high reproductive capacity in livestock. We established an RNA sequencing dataset to compare the expression profiles of long non coding RNA (lncRNA) and messenger RNA (mRNA) in the ovarian tissue exosomes of Hu sheep and low reproductive sheep breeds (Mongolian sheep) during estrus period.

overall_design: RNA-seq expression profiles of ovaries during estrus in Hu sheep and Mongolian sheep


title: A 3’UTR-derived small RNA modulates the life-cycle of the cholera toxin-encoding filamentous phage, CTXϕ [RNA-Seq]

status: Public on Dec 03 2025

city: Jena

first: Kai

last: Papenfort

state: Thuringia

address: Winzerlaer Straße 2

department: Faculty of Biological Sciences

country: Germany

institute: Friedrich-Schiller-University Jena

summary: Bacteriophages (phages) are well known to be one of the major driving forces in bacterial evolution. This is also true for virulent microorganisms, such as the major human pathogen Vibrio cholerae, whose pathogenic potential and epidemic proliferation largely depends on the interaction with environmental phages. Specifically, integration of the CTXϕ phage genome into the first chromosome of V. cholerae also involved the ctxAB genes, encoding the principle toxin responsible for the severe acute diarrheal disease, cholera. Whereas the mechanisms underlying CTXϕ-associated horizontal gene transfer and control of the ctxAB genes have been intensively studied over the past years, post-transcriptional regulation affecting the CTXϕ lifecycle has not been documented. Here, we report the discovery and characterization of the CisR small RNA (sRNA) that is produced from the 3’UTR (untranslated region) of the prtV gene and inhibits the expression of the CTXϕ-encoded cep mRNA. CisR-mediated repression of cep involves Hfq-assisted base-pairing of the two transcripts and results in reduced CTXϕ production under stress conditions. We further show that transcription of prtV-cisR requires both, the master quorum sensing transcription factor HapR, as well CRP, which coordinates global carbon metabolism. Taken together, our work provides evidence that V. cholerae employs sRNA-mediated post-transcriptional gene regulation to coordinate CTXϕ activation with both cell density and nutrient availability.

overall_design: RNA-seq expression profiling of Vibrio cholerae strain KPS14 WT grown in LB or AKI medium

first: Anne

last: Lippegaus

first: Malte

last: Siemers

first: Sebastian

last: Krautwurst


title: A 3’UTR-derived small RNA modulates the life-cycle of the cholera toxin-encoding filamentous phage, CTXϕ [RIL-Seq]

overall_design: RILseq RNA-RNA interactome profiling of Vibrio cholerae strains KPS14 and KPS995 grown in AKI medium


title: The spatial transcriptomics of EGFR-mutant non-small cell lung cancer before osimertinib treatment

city: Fukuoka

first: Satoshi

last: Nakamura

state: Fukuoka

address: 3-1-1, Maidashi, higashi-ku

department: Respiratory Medicine

country: Japan

institute: Kyushu University

summary: EGFR-mutant non-small cell lung cancer (NSCLC) is commonly treated with EGFR tyrosine kinase inhibitors (TKIs) such as osimertinib. However, the development of resistance remains a major clinical challenge, with various resistance mechanisms having been identified. Emerging evidence suggests that the tumor microenvironment (TME) may contribute to this resistance. In this study, we analyzed the TME of pre-treatment tumor samples from EGFR-mutant NSCLC patients using the Visium HD spatial transcriptomics platform to explore its potential role in the development of resistance.

overall_design:
Spatial transcriptomic profiling of four pretreatment tumor samples from four patients with EGFR-mutated NSCLC. The samples were analyzed using two Visium HD slides, with two samples placed on each slide, followed by StarDist-based image processing.

UPDATE:
[Jul-27-2026] The GSM9093279 title was corrected from "after treatment" to "before treatment".

first: Ritsu

last: Ibusuki

first: Eiji

last: Iwama

first: Atsushi

last: Shimauchi

first: Hiromu

last: Kawano

first: Yui

last: Miyazaki


title: Gene expression profiling of the whole brain of the normal littermate control for Huntington disease model mouse R6/2 at 5 weeks post-natal age using transcriptome tomography

city: Wako-shi

first: Yuko

last: Okamura-Oho

state: Saitama

address: 2-1, Hirosawa

institute: RIKEN

summary: We developed a novel framework to assess comprehensive endogenous gene expression maps in a broad and isotropic 3D-anatomical context using a relatively small number of original data points: transcriptome tomography. Using this method, we produced a dataset of gene expression maps of the whole brain of the normal control mouse at 5 weeks after birth, computationally reconstructed from fraction data.

overall_design: A total of 43 fraction samples obtained with body axes-based slicing preparation conjugated with anatomical image acquisition were analysed. There are sets of body axes-based preparation series: the S series, composed of10 fractions/ C of 12 fractions/ H of 6 fractions/ L of 8 fractions/ R for 7 fractions.

first: Y

first: H

last: Yokota


title: Spatial transcriptomic based, endocapillary hypercellularity in IgA nephropathy

status: Public on Dec 02 2025

city: Seuol

first: Hwajin

last: Lee

address: 26 Kyungheedae-ro, Dongdaemun-gu

country: South Korea

institute: Kyung Hee University

summary: Immunoglobulin A nephropathy (IgAN) is a leading cause of chronic kidney disease, marked by mesangial IgA1 immune-complex deposition and a multi-hit pathogenesis. The Oxford classification grades histopathological lesions such as endocapillary hypercellularity (E0 and E1), which are associated with disease severity and prognosis. Despite advances in single-cell and spatial transcriptomics, the molecular basis of endocapillary hypercellularity in human IgAN remains unclear. Spatial transcriptomic data obtained using the GeoMx DSP platform were analyzed to compare gene expression profiles across normal, E0, and E1 groups.

overall_design: Human kidney tissues from control subjects and IgA nephropathy patients classified as E0 or E1 were analyzed using spatial transcriptomics to characterize classification-dependent transcriptomic alterations.

first: Jin Sug

last: Kim

first: Hyeon Do

last: Jeon

first: Kyung Hwan

last: Jeong

first: Hyeon Seok

last: Hwang

first: Ji-Youn

last: Sung

first: Kyungsik

last: Ha

first: Woochang

last: Choi


title: Comprehensive gene expression analysis of Huntington disease model mouse brains using Transcriptome Tomography

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

overall_design: Refer to individual Series


title: Bulk RNA sequencing of prostate tissues from BPH model mice and treatment groups

city: Beijing

first: Zheng

last: Li

state: Beijing

address: No. 8 Xishiku Street, Xicheng District

institute: Peking University First hospital

summary: We performed bulk RNA sequencing on fresh prostate tissue serial sections from five randomly selected mice per group.

overall_design:
Differential expression analysis for BPH vs. Control (Figure 6i), BPH + rmCXCL13 vs. BPH (Figure 6k), and BPH + rmCXCL13 + anti-CD4 vs. BPH + rmCXCL13 (Figure 6m) highlighted significant changes in senescence-related genes.
Prostate tissues from BALB/c mice were divided into Control, BPH, BPH + rmCXCL13, and BPH + rmCXCL13 + anti-CD4 groups. Each group contained five mice. RNA was extracted and subjected to bulk RNA-seq. Due to technical issues, raw sequencing files were lost. Processed expression matrices are available and included in this submission.

***************************************************************
Submitter note: Raw sequencing data are not available due to storage limitations
***************************************************************

first: XiaofeI

last: Wang

first: Zhifu

last: Liu

first: Senmao

first: Shuai

last: Hu

first: Wei

last: Yu


title: Gene expression profiling of senescent and non-senescent BPH epithelial cells

summary: RNA-seq analysis of human BPH prostate epithelial cells classified by SA-β-gal staining status.

overall_design: Epithelial cells were isolated from human BPH tissue and divided into senescent (SA-β-gal+) and non-senescent (SA-β-gal−) groups. RNA-seq was performed and gene expression profiles were compared.

first: Frozen tissue sections from human BPH prostate samples were serially sectioned. The first section was subjected to SA-β-gal staining to identify senescent (positive) and non-senescent (negative) regions. The adjacent second section was then used for microdissection to isolate epithelial cells from the corresponding regions based on their senescence status. Total RNA was extracted from the microdissected senescent and non-senescent epithelial cells

last: followed by RNA-seq to profile transcriptomic differences.

first: Xingxing

last: Tang

first: Jie

last: Jin


title: Single-cell RNA-seq of out-of-thaw mesenchymal stromal cells

city: Atlanta

first: Krishnendu

last: Roy

state: Georgia

address: 345 ferst drive NW, marcus nanotechnology building, room no 3102B, 3rd floor

department: IBB

country: USA

institute: Georgia tech

summary:
Purpose: A Multiomics-based Unbiased Computational Modeling Platform Identifies Predictive Attributes of Mesenchymal Stromal Cell Immunomodulatory Potency
Methods: scRNAseq from MSCs with dropseq method on BioRad ddseq platform
Results: framework for identifying putative CQAs and generating MoA hypotheses for therapeutic cells and may help overcome current challenges in advancing large-scale, quality-driven manufacturing of cell therapies for broad clinical use. We used SureCell app to align the reads to human reference genome and used SEURAT for downstream analysis.
Conclusions: Cell therapies are complex “living medicines” with potential to treat chronic, incurable diseases. Despite their success and promise, quality-driven reproducible manufacturing and identification of Mechanisms-of-Action (MoA) remain significant challenges. Specifically, it is difficult to identify which set of cell attributes, among the thousands of proteins, RNA, lipids, and metabolites, are most correlative to their function in a specific disease setting. Here, we report a multiomics-driven unbiased computational platform to identify multivariate features that are predictive of their immunomodulatory functions.

overall_design: BM-MSCs single cell RNAsequences

first: Paramita

last: Chatterjee

first: Carolyn

last: Yeago


title: Gene expression profiling of the whole brain of the Huntington disease model mouse R6/2 at 5 weeks post-natal age using transcriptome tomography

first: Yuko

last: Okamura-Oho

summary: We developed a novel framework to assess comprehensive endogenous gene expression maps in a broad and isotropic 3D-anatomical context using a relatively small number of original data points: transcriptome tomography. Using this method, we produced a dataset of gene expression maps of the whole brain of the Huntington disease model mouse R6/2 at 5 weeks after birth, computationally reconstructed from fraction data.

overall_design: A total of 42 fraction samples obtained with body axes-based slicing preparation conjugated with anatomical image acquisition were analysed. There are sets of body axes-based preparation series: the S series, composed of10 fractions/ C of 12 fractions/ H of 6 fractions/ L of 7 fractions/ R for 7 fractions.

first: Y

first: H

last: Yokota


title: Upper Airway Gene Expression in Hospitalized Children with Rhinovirus-induced Respiratory Illnesses

status: Public on Dec 01 2025

city: Ann Arbor

first: Marc

last: Hershenson

state: Michigan

address: 1150 E. Medical Center Drive

department: Pediatrics

institute: University of Michigan

summary: In this study, we collected nasal swabs from infants and children hospitalized with RV infection and assessed gene expression by next generation sequencing, comparing profiles to swabs obtained from control subjects undergoing otolaryngologic procedures.  We also compared gene expression patterns to those obtained from children with respiratory syncytial virus (RSV) infection, another common respiratory virus well-studied in children.

overall_design:
Flocked nasal swab samples were obtained from children age 0-18 hospitalized with single-virus respiratory infections, as well as uninfected children for comparison.

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

first: Jordan

middle: E

last: Kreger

first: Alex

middle: L

last: Sliwicki

first: Saly

middle: N

last: Essoh

first: Yiran

first: Chaandini

last: Jayachandran

first: Jessica

middle: A

last: Czapla

first: Toby

middle: C

last: Lewis

first: Erin

middle: M

last: Kirkham

first: Rodney

middle: J

last: Vergotine

first: Antonia

middle: P

last: Popova

first: Heidi

middle: R

last: Flori

middle: B


title: Single-cell RNA sequencing data from human CAR-T cell samples

status: Public on Feb 12 2026

city: Tsukiji

first: Yuki

last: Okuhiro

state: Tokyo-to

institute: National cancer center research institute

summary: Raw RNA sequencing data derived from human CAR-T cell samples are deposited in this repository. The datasets include bulk single-cell RNA-seq reads generated for research purposes.

overall_design: CD3+ T cells purified from PBMCs of healthy individuals were activated with anti-CD3 and CD28 monoclonal antibodies and lentivirally transduced with the anti-CD19-BBz CAR gene with DMSO or ponatinib (100 nM) in RPMI-1640 supplemented with 10% Fetal bovine serum (FBS) and 4 mM L-glutamine (Thermo Fisher Scientific; Cat. #25030-081). Recombinant human IL-7 (R&D System, #207-IL) and IL-15 (R&D System, #247-ILB) were added at 10 ng/mL. Beads were removed on day 4 using a magnet, and cells were rested for a further 4 days. CD4+ CAR-T cells and CD8+ CAR-T cells were isolated by Fluorescence-Activated Cell Sorting (FACS). Finally, samples were prepared by mixing CD4+ CAR-T cells and CD8+ CAR-T cells at a 1:9 ratio and analized by scRNA-seq.

first: Yasuhiro

last: Kojima

first: Hiroyoshi

last: Nishikawa


title: T cells in B16 tumor model with ACT and checkpoint blockade - scRNA-seq, CITE-seq and TCRab [i35]

city: Boston

first: Liang

last: Yang

state: MA

address: 77 Avenue Louis Pasteur

department: Pathology

institute: Harvard Medical School

summary: This study is part of the immgenT Open Source Project, specifically from IGT35, which focuses on characterizing T cells in the B16.gp33 melanoma model following adoptive cell therapy (ACT) and immune checkpoint blockade. T cells were isolated from tumors and  draining inguinal lymph nodes of C57BL/6J male mice (7–8 weeks old) subjected to subcutaneous implantation of B16.gp33 melanoma cells, followed by adoptive cell transfer treatment with intravenous transfer of P14 and pmel T cells, and treatment with either isotype control antibodies or a combination of anti-PD-1 and anti-4-1BB antibodies. Samples were collected at day 14 post post-tumor implantation (1 day post-final antibody treatment). The study targeted all CD3+ T cell populations, including transgenic P14 and pmel T cells

overall_design: T cells were isolated from tumors and draining inguinal lymph node samples using mechanical dissociation or collagenase I digestion.  Sorted CD3+ T cell populations, including transgenic P14 and pmel T cells were profiled using single-cell RNA sequencing (10x Genomics), combined with CITE-seq (TotalSeq C) and paired TCR α/β sequencing. Samples from multiple mice were pooled using hashtag oligonucleotides for multiplexing.

first: David

last: Zemmour

first: Christophe

last: Benoist

first: Nicole

last: Scharping

first: Ian

last: Magill


title: TCF3::HLF orchestrates an enhancer-promoter network with activation of MEF2C to promote an immature HSC gene expression program in leukemia

city: Zürich

first: Valdemar

middle: Jacob Sven-Åke

last: Priebe

address: Lengghalde 5

country: Switzerland

institute: Kindersptal Zürich/University of Zurich

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Oncogenic fusion transcription factors (TFs) frequently drive hematopoietic malignancies by altering gene expression in key developmental programs. TCF3::HLF is a fusion TF that characterizes a rare, treatment-resistant subtype of B-cell acute lymphoblastic leukemia (t(17;19) TCF3::HLF-positive B-ALL). Despite its clinical significance, the mechanisms by which TCF3::HLF induces leukemia are unclear. We used HiChIP mapping and genetic interference to analyze TCF3::HLF at the 3D-genome level, revealing enhancer-promoter interactions that control gene activation or repression. Notably, TCF3::HLF directly regulates MEF2C expression through its enhancer, as interference disrupted MEF2C transcription and inhibited leukemia propagation. This disruption also diminished embryonal hematopoietic stem cell (HSC) gene signatures and restored mature HSC and B-lymphoid markers. These findings highlight MEF2C as a critical component of the transcriptional network reprogrammed by TCF3::HLF. Our study provides insight into how TCF3::HLF rewires the 3D genome to drive leukemia and serves as a resource for further exploration of the TCF3::HLF regulome.

overall_design:
To delineate the 3D-genomic interactions orchestrated by the fusion protein TCF3::HLF in t(17;19) ALL cells, we knocked out the  TCF3 wild-type allele, thereby enabling selective immunoprecipitation of the fusion protein when using antibodies against TCF3. We compare the TCF3/TCF3::HLF DNA occupancy profiles of parental HAL-01 and wild-type TCF3 KO HAL-01.
Chromatin prepared from parental HAL-01 cells (TCF3_IP_Parental) and TCF3-KO HAL-01 cells (TCF3_IP_Knockout) was prepared for ChIP assay using E2A (CST #12258) antibody for pull-down.
ChIP-seq outputs were processed to generate bigwig files using bamCoverage from deepTools and call peaks using MACS2 to visualize the enrichment landscapes with the deepTools software.

first: Bartimée

last: Galvan

first: Kaivalya

last: Walavalka


title: Latent MicroRNA Networks in Asthma Endotypes [NS_H_miR_v3a]

city: New Haven

first: Jose

middle: Luis

last: Gomez

state: CT

address: 300 Cedar Street

department: Pulmonary, Critical Care and Sleep Medicine

institute: Yale University

summary:
Transcriptome analysis of whole blood from subjects with asthma and controls
The presence or absence of type 2 inflammation (T2) biomarkers is used to identify T2-high and T2-low endotypes in the clinic. Despite the clinical relevance of these endotypes, the molecular mechanisms of T2-low asthma remain poorly understood. Specific microRNAs may regulate transcriptomic networks associated with asthma endotypes.

overall_design: Cross-sectional study of 88 participants with asthma stratified into T2-high and T2-low asthma by blood eosinophils or Fractional Exhaled Nitric Oxide (FeNO), combined with microRNA and mRNA of whole blood. DIABLO integrated omics of microRNA and mRNA profiles.

first: Maria

last: Ramirez

last: Diaz

first: Ningya

last: Wang

first: Qing

last: Liu

first: Huan

last: Li

first: Shannon

last: Kay

first: Jana

last: Zielonka

first: Gabriella

last: Wilson

first: Zuoheng

first: Xiting

last: Yan

first: Geoffrey

last: Chupp


title: Developmental trajectory of the mouse transcriptome following placental allopregnanolone insufficiency in the somatosensosry cortex, hippocampus and cerebellum

city: New York

first: Jacquelyn

last: Salzbank

state: NY

institute: Columbia University Irving Medical Center

summary: This study investigates the developmental impact of placental allopregnanolone (ALLO) insufficiency on the mouse brain transcriptome in an age-, sex-, and region-specific manner. We generated mice with reduced ALLO levels by specifically deleting the gene encoding the synthetic enzyme for ALLO (Akr1c14) in trophoblasts using an Akr1c14-floxed mouse with a Cyp19a-Cre mouse. The somatosensory cortex, hippocampus, and cerebellum of both WT and plKO mice were collected from males and females at postnatal days 0, 7, 15, and 30. Libraries were prepared using the Illumina TruSeq Stranded mRNA Library prep kit and sequenced on an Illumina NovaSeq sequencer with 2 x 100 bp paired-end cycles. The analysis reveals sex- and region-specific transcriptomic changes following reduced placental ALLO, with differentially expressed genes associated with inflammatory signaling.

overall_design: mRNA profiles for WT and plKO mice at postnatal day 0, 7, 15, and 30, were generated by paired-end sequencing for the somatosensory cortex, hippocampus and cerebellum using and Illumina NovaSeq sequencer.

first: Helene

last: Lacaille

first: Jiaqi

last: O'Reilly


title: RNA-Seq analysis of islets from Akita mice treated with the SGLT2 inhibitor Dapagliflozin and wild-type controls

city: Jerusalem

first: Inbar

last: Plaschkes

address: The Hebrew University of Jerusalem - Ein Kerem

department: The Faculty of Medicine - Ein Kerem

country: Israel

institute: HUJI

summary: In diabetes, hyperglycemia drives the progression of b-cell failure and multi-organ complications. Prolonged exposure to high glucose stimulates mTORC1, resulting in impaired glucose metabolism and exacerbation of ER stress and inflammation. However, the precise mechanism by which glucose regulates mTORC1 activity in diabetes remains unclear. We performed metabolic labeling with 13C6- glucose in diabetic animals treated with or without the SGLT2 inhibitor (SGLT2i) dapagliflozin or insulin, followed by targeted metabolomics and metabolic flux analysis. We found that tissue glucose concentrations strongly correlate with glucosamine, rather than with other glucose or amino acid metabolites. Plasma glucosamine levels are increased in patients with impaired fasting glucose (IFG) and type 2 diabetes (T2D) and are inversely correlated with b-cell function. Glucosamine is synthesized by amine group transfer from glutamine to glucose, which enhances O-GlcNAcylation (O-GlcN) of mTORC1- regulating proteins, including Raptor, via O-GlcNAc transferase (OGT), subsequently activating mTORC1. Genetic inhibition of b-cell mTORC1 by heterozygous Raptor KO and inhibition of the glucosamine-mTORC1 pathway by SGLT2i improved diabetes and b-cell function. We propose that the glucosamine-mTORC1 pathway is a key mediator of glucose toxicity in diabetes.

overall_design: To investigate the molecular mechanisms underlying glucotoxicity in beta cells, we performed RNA-seq analysis on whole islets from wild-type (WT) and Akita mice, a model of endoplasmic reticulum (ER) stress-mediated diabetes. Akita mice were treated with or without a glucose-lowering sodium-glucose cotransporter 2 inhibitor (SGLT2i). SGLT2i-treated Akita mice received the drug in their drinking water for two weeks immediately after weaning. Islets were subsequently collected from all groups and processed for RNA-seq analysis. Each experimental group included three biological replicates, with each replicate consisting of pooled islets (50 islets pooled) from 2–3 mice.

first: Yael

last: Riahi

first: Elisheva

last: Zemelman


title: TCF3::HLF orchestrates an enhancer-promoter network with activation of MEF2C to promote an immature HSC gene expression program in leukemia.

first: Valdemar

last: Priebe

overall_design:
To delineate the 3D-genomic interactions orchestrated by the fusion protein TCF3::HLF in t(17;19) ALL cells, we knocked out the  TCF3 wild-type allele, thereby enabling selective immunoprecipitation of the fusion protein when using antibodies against TCF3.  We compare the RNAseq expression profile for wild-type TCF3 knockout  HAL-01 with parental HAL-01 control samples to verify that no major changes occure. We included 697 with shSCR as an additional control representing the TCF3::PBX1 fusion protein.
Expression datasets for parental HAL-01 cells, TCF3-KO HAL-01 cells (TCF3_KO) and 697 cells with shSCR (X697) were used to generate PCA plots visualizing the variability among the cell lines.

first: Bartimée

last: Galvan


title: Latent MicroRNA Networks in Asthma Endotypes [HuGene-1_0]

first: Jose

last: Gomez

first: Maria

last: Ramirez

last: Diaz

first: Ningya


title: TCF3::HLF Orchestrates an Enhancer-Promoter Network with Activation of MEF2C to Promote Immature HSC Gene Expression in Leukemia [RNA-seq]

overall_design:
To directly assess the regulatory impact of the TCF3::HLF-bound MEF2C enhancer, we employed CRISPR editing to eliminate the HLF binding site within the enhancer in Cas9GPF expressing HAL-01 cells.
Comperative gene expression profiling was done on Day13 samples  for MEF2C enhancer KO (sgRNA_96, sgRNA_97) and scrambled controls (sgRNA_SCR1)


title: TCF3::HLF Orchestrates an Enhancer-Promoter Network with Activation of MEF2C to Promote Immature HSC Gene Expression in Leukemia [HiChIP]

overall_design:
To delineate the 3D-genomic interactions orchestrated by the fusion protein TCF3::HLF in t(17;19) ALL cells, we performed MNase-HiChIP with two independent replicates using the TCF3::HLF positive cell line HAL-01, with the TCF3 wild-type allele knocked out, thereby enabling selective immunoprecipitation of the fusion protein when using antibodies against TCF3.
We performed the HiChIP following the Dovetail®-HiChIP-MNase-Kit-User-Guide-Version-1.3. with modefications using E2A (CST #12258) antibody for pull-down.
Interaction events were analyzed using FitHiChIP.


title: Advantages of Magnetic Compression in Rat Colonic Anastomosis: A Comparative Study with a Transcriptomic Perspective

status: Public on Nov 30 2025

city: Xi'an

first: Shuqin

last: Xu

address: Zhuque street

institute: xianjiaotong univeisity

summary: Background: Colorectal anastomosis is a common procedure in colorectal cancer surgery, but traditional suturing is technically demanding and prone to complications. Magnetic compression anastomosis (MCA) offers a simpler, minimally invasive alternative with favorable outcomes. This study compares the healing effects of MCA and conventional suturing in rat colonic anastomosis and investigates the molecular mechanisms involved.  Methods: Twenty male Sprague-Dawley rats (200-230 g) were randomly divided into an MCA group and a suture (control) group. The survival rates, and histological and transcriptomic profiles of the anastomotic sites were compared. Results: The survival rate of the MCA group (100%) was significantly higher than that of the control group (70%). Histological examination showed improved tissue alignment and more continuous mucosal surfaces in the MCA group. Transcriptomic analysis revealed that differentially expressed genes between the MCA and control groups were highly enriched in immune-inflammatory pathways. PPI network analysis identified IL-1β as a key molecule, with significantly elevated expression in the MCA group. Results: The survival rate of the MCA group (100%) was significantly higher than that of the control group (70%). Histological examination showed improved tissue alignment and more continuous mucosal surfaces in the MCA group. Transcriptomic analysis revealed that differentially expressed genes between the MCA and control groups were highly enriched in immune-inflammatory pathways. PPI network analysis identified IL-1β as a key molecule, with significantly elevated expression in the MCA group. Conclusion: MCA is a simple, low-complication method for colonic anastomosis in rats. Transcriptomic analysis suggests that IL-1β may play a pivotal role in enhancing the efficacy of MCA in promoting anastomotic healing.

overall_design: Six colonic anastomotic tissue samples were collected from rats, including three from the magnetic compression anastomosis (MCA) group and three from the suture (control) group. After two weeks of healing, tissues at the anastomotic sites were excised, immediately frozen in liquid nitrogen, and stored at −80 °C. Total RNA was extracted using TRIzol reagent, and sequencing libraries were prepared with the NEBNext Ultra RNA Library Prep Kit. High-throughput RNA sequencing was performed on the DNBSEQ-T7 platform. The aim was to compare gene expression profiles between the MCA and suture groups to explore molecular mechanisms associated with enhanced anastomotic healing.


title: Rapamycin limits peritendinous fibrosis but does not affect intratendinous healing in a rodent Achilles tendon injury model

status: Public on Dec 09 2025

city: London

first: Chavaunne

last: Thorpe

address: Royal College Street

country: United Kingdom

institute: Royal Veterinary College

type: Non-coding RNA profiling by high throughput sequencing

summary: Tendon  injuries are common, affecting both athletes and the general population. Healing is often poor, with deposition of fibrotic, disorganised scar-like tissue leading to continued pain, dysfunction and reinjury. While a variety of therapeutics are available clinically to treat tendon injuries, outcomes remain variable and no treatments are able to fully restore tendon structure and function, hence novel regenerative therapies are required. The pathogenesis of many fibrotic diseases is influenced by the mammalian target of rapamycin (mTOR) signalling pathway, which modulates processes required for cell growth and proliferation. Rapamycin, an mTOR inhibitor, is a promising therapeutic for several fibrotic diseases, and can facilitate musculoskeletal tissue repair. Therefore, we used a needle injury model in the rat Achilles tendon to test the hypothesis that rapamycin treatment during the early stages of tendon injury enhances tendon healing via modulation of resident tendon cell populations and autophagy. The results demonstrate that, while rapamycin treatment decreased peritendinous fibrosis and appeared to modulate cell recruitment, it did not enhance healing of lesions within the tendon core, up to three weeks post-injury. Therefore, rapamycin is not an effective therapeutic for tendon injury in young adults. Future studies should establish if rapamycin is able to improve tendon healing in aged animals or with longer-term administration.

overall_design: RNAseq profiling of Evs isolated from serum of rats subjected to tendon injury and treated either with rapamycin or vehicle control, 7 or 21 days post injury

first: Neil

last: Marr

first: Danae

last: Zamboulis

first: Ross

last: Beaumont

first: Zofia

last: Tatarczyk

first: Yu-Mei

last: Chang

first: Richard

last: Piercy

last: Meeson

first: Mandy

last: Peffers

first: John

last: Hildyard

first: Marianne

last: Pultar


title: Polyethylene Microplastics Breach Chorion Protection, Triggering Cardiotoxicity Across Aquatic Models

city: Yangsan-si

first: Hyerin

last: Lee

address: 49, Busandaehak-ro

institute: Pusan National University

summary: Polyethylene microplastics are pervasive environmental pollutants that pose potential risks to aquatic organisms. This study investigates the effects of polyethylene microplastics on zebrafish (Danio rerio) embryo development, with a focus on whether the chorion, a protective barrier surrounding the embryo, is effective in blocking polyethylene penetration. Contrary to previous findings that suggested the chorion could prevent larger microplastics (>0.7 µm) from entering, our study demonstrates that polyethylene particles sized 1-4 µm can still negatively impact embryo development without dechorionation. Embryos were exposed to polyethylene at concentrations of 0.01, 0.1, and 1 mg/L, followed by RNA sequencing to assess gene expression changes. Despite no significant differences in survival, hatching, or body length between control and treated groups, a significant reduction in heart rate was observed at higher concentrations, indicating potential sub-lethal cardiotoxicity. Further, qRT-PCR validation confirmed significant downregulation of key heart development-related genes, particularly fbln1 and fn1b, in polyethylene-exposed embryos. Additionally, polyethylene exposure also impacted Daphnia magna, reducing heart rate and delaying growth. These findings highlight the ability of polyethylene microplastics to penetrate natural barriers such as the chorion and induce physiological and developmental changes. Our results emphasize the need for further research into the long-term effects of microplastic exposure on aquatic ecosystems.

overall_design: To confirm whether PE particles larger than the pore size of the zebrafish chorion truly have no effect on zebrafish embryos, PE was administered without dechorionating the embryos, followed by bulk RNA sequencing analysis.

first: Yejin

last: Kim

first: Yun Hak

first: Chang-kyu

last: Oh


title: A blueprint for local and distal glioblastoma invasion programs

city: Rehovot

first: Rony

last: Chanoch

state: Israel

address: Weizmann Institute of Science, 234 Herzl Street

institute: Weizmann Instititue

summary: Glioblastoma (GBM) invasion into brain parenchyma presents significant challenges for treatment but remains poorly understood. In this study, we combined single-cell RNA sequencing (scRNA-seq), spatial transcriptomics, and multiplexed imaging of orthotopic xenograft models to investigate GBM invasion. We first screened 20 patient-derived gliomasphere models for their distal (i.e., extending to the contralateral hemisphere) and local invasive potential in mice. We found that models with distal invasion potential are enriched with oligodendrocyte progenitor-like (OPC-like) cells, while models with only local invasion potential are enriched with mesenchymal-like (MES-like) cells. These patterns reflect predominantly peri-axonal vs peri-vascular invasion routes, respectively. Next, we analyzed the transcriptomes of invading cells within models (compared to tumor core) and identified novel programs associated with distal and local invasion. Thus, we decouple transcriptional features associated with invasion potential from those associated with the process of invasion. We validated our findings by spatial transcriptomics and multiplexed imaging, further describing the spatial niche of invasive cells. Taken together, our results provide a blueprint for the invasive potential of GBM cell states and of the programs associated with invasion across different scales.

overall_design: We developed a pooled in vivo system to simultaneously analyze the contralateral invasion capacity of multiple patient-derived GBM models. In this assay, we grew 20 GBM patient-derived gliomasphere models separately and pooled them for stereotaxic injection into the mouse brains (10 models per pool – [Pool #1, Pool #2] with 2 mice replicates). At symptom onset, the mice were euthanized, and brains were dissected under a stereomicroscope and separated into the primary injection site and the contralateral hemispheric invasion fractions. Malignant cells from each site were isolated by flow cytometry based on GFP expression and profiled by scRNA-seq using the 10X Genomics 3’ gene expression platform.To characterize the program expressed by locally-invading glioma, we employed fluorescent-guided microdissection and isolated around 200 malignant cells associated with vasculature within the ipsilateral hemisphere of two non-distally invasive models (MGG65 and MGG123). These cells were profiled by scRNA-seq using SS2, along with around 200 cells of the tumor core of each model.

last: Chanoch-Myers

first: Toshiro

last: Hara

first: Alissa C.

last: Greenwald

first: Itay

last: Tirosh

first: Mario L.

last: Suva


title: Spatial transcriptomics of bladder cancer with squamous differentiation

status: Public on Nov 29 2025

city: Suita

first: Daisuke

last: Motooka

state: Osaka

address: 3-1, Yamadaoka

institute: NGS core facility, Research Institute for Microbial Diseases, Osaka University

summary: We analyze the gene expression of bladder cancer with squamous differenciarion using spatial gene expression analysis techniques (Visium HD, 10x genomics).

overall_design: Formalin-fixed, paraffin-embedded (FFPE) sample of bladder cancer is analyzed with using the CytAssist Visium HD (10x genomics) spatial transcriptomics platform.

first: Ryuta

last: Watanabe

first: Shunsuke

last: Haga

first: Noriyoshi

last: Miura

first: Tadahiko

last: Kikugawa

first: Takashi

last: Saika


title: The Phosphate-Specific Transport System Gene pstA1 Contributes to Rifampin Tolerance in Mycobacterium tuberculosis

status: Public on Nov 27 2025

city: Baltimore

first: Venkata Anoushka Chinmayi

last: Gudipudi

state: MD

address: 1550 Orleans Street

department: Medicine

institute: Johns Hopkins University School of Medicine

summary: This study investigates the role of the phosphate-specific transport system gene pstA1 in rifampin tolerance in Mycobacterium tuberculosis. We constructed a pstA1 deletion mutant (ΔpstA1) and demonstrated that it exhibits enhanced rifampin susceptibility compared to wild-type H37Rv. To explore the molecular mechanisms underlying this phenotype, we performed RNA-seq transcriptomic analysis comparing wild-type and ΔpstA1 strains grown in standard Middlebrook 7H9 broth under exposure to sub-inhibitory rifampin (7.5 ng/ml, 1/4 MIC) for 30 or 60 minutes. The analysis revealed substantial transcriptional reprogramming in ΔpstA1, providing insights into how loss of PstA1 function leads to increased rifampin susceptibility.

overall_design: RNA-seq profiling of wild-type Mycobacterium tuberculosis H37Rv and ΔpstA1 strains with and without rifampin treatment. Strains were cultured in Middlebrook 7H9 broth and sampled at three timepoints: untreated control (0 min), 30 minutes after sub-inhibitory rifampin exposure (7.5 ng/ml), or 60 minutes after rifampin exposure. Three biological replicates per strain per condition.

first: Carina

last: Danchik

first: GV Anoushka

last: Chinmayi

first: Gi Yong

first: Joel

middle: S

last: Bader

first: Hyungjin

last: Eoh

first: Petros

last: Karakousis


title: RIPK1 regulates beta-cell fate and autoimmunity in type 1 diabetes

status: Public on Nov 24 2025

city: Indianapolis

first: Madeline

last: Peyton

state: IN

address: 410 W 10th St

institute: Indiana University

summary: Type 1 diabetes (T1D) results from autoimmune destruction of pancreatic beta-cells. RIPK1, a key regulator of cell death and inflammation, has been implicated in beta-cell responses to cytokines and immune attack. To investigate RIPK1's role in beta-cell fate during autoimmune stress, we generated CRISPR/Cas9-mediated Ripk1-deleted NIT-1 beta-cells and exposed them to TNFα+IFNγ or self-reactive diabetic NOD splenocytes. Using RNA-seq, kinome profiling, flow cytometry, and small molecule inhibitors, we demonstrate that RIPK1 deletion or pharmacological inhibition protects beta-cells from cytokine-induced and autoimmune cell death. This study provides insights into RIPK1-dependent pathways in beta-cell vulnerability and suggests potential therapeutic strategies for T1D.

overall_design: 2x2 factorial design: Genotype (Control NIT-1 vs Ripk1-deleted NIT-1) x Treatment (Vehicle vs TNFα+IFNγ). NIT-1 beta-cells from NOD mice; CRISPR-engineered Ripk1Δ vs control cells. Cells treated with TNFα (40 ng/mL) + IFNγ (100 ng/mL) or vehicle. Six biological replicates per condition (24 samples total). Multi-modal analyses: RNA-seq, kinome profiling, flow cytometry, small molecule inhibitor testing.

first: Christopher

last: Contreras

first: Andrew

middle: T

last: Templin


title: m6A RNA modification cooperates with alternative polyadenylation to control T cell homeostasis via mTOR signaling

city: shanghai

first: Xingli

last: Zhang

address: 280 Chongqing South Rd

institute: Shanghai Jiao Tong University School of Medicine

summary: To identify all of the APA targets of NUDT21 or METTL3 and obtain  gene expression profile, RNA from WT, Nudt21-deficient and Mettl3-deficient naïve CD4+ T cells stimulated with anti-CD3/CD28 for 0hr or 48hr were subject to RNA-Seq. By using a custom-designed algorithm and Gene ontology (GO) analysis, we found mRNA 3'UTR shortening phenomenon after TCR stimulation and both METTL3 and NUDT21 regulate 3'UTR length. In addition, we found most of up-regulated genes after Nudt21 deficiency are associated with immune activation pathway.

overall_design: mRNA profiles of WT, Mettl3-deficient and Nudt21-deficient naïve CD4+ T cells stimulated with anti-CD3/CD28 for 0hr or 48hr were generated by RNA-sequencing analysis.

first: Gaoyang

last: Wang

first: Haixin

last: Li

first: Youqiong

last: Ye

first: Hua-Bing


title: Structural and molecular insights into specialized translation mediated by the ribosome mRNA-binding channel [Ribo-Seq]

first: Ariel

last: Ogran

address: 234 Herzl Street

department: Bimolecular Sciences

institute: Weizmann Institute of Science

summary: The ribosome mRNA channel is central for translation, but its involvement in specific regulatory mechanisms remains unexplored. Employing Cryo-EM on ribosomal complexes bound to Kozak and TISU mRNAs from wild-type and RPS26 mutant cells (RPS26dC), we demonstrate that RPS26/eS26 adopts distinct conformations, providing a structural basis for its opposing effect on their activity. Translatome studies of wild-type and RPS26dC revealed AUG-context-dependent rearrangements in key intermediates of the 48S and full 80S initiation complexes and slower scanning. Downregulated mRNAs are enriched with AUG upstream nucleotides and a C at position -1 that contacts 18S rRNA nucleotide G1207, a contact lost in the mutant structure. The top downregulated mRNAs are replication-dependent histones, which, despite having short 5’UTRs and suboptimal Kozak, exhibit robust translation activity that is RPS26/eS26-dependent. We identified a translational enhancer in H2B 5’UTR, spanning nucleotide -16 to -9, overlapping the predicted RPS26/eS26-binding sites. Intriguingly, the H2B mRNA-ribosome complex structure adopts a conformation distinct from the Kozak and TISU. Exploiting these features, we designed a high-efficiency translational cassette with minimal leaky scanning, improving efficacy and safety for mRNA-based therapy. These findings underscore the central importance of the ribosome’s mRNA-binding channel in selective translation regulation and its potential for therapeutic applications.

overall_design: Ribo-seq profling of WT human embryonic kidney cells (HEK293T) and RPS26dC HEK293T cells

first: Davide

last: Fraticelli

first: Disha-Gajanan

last: Hiregange

first: Benjamin

last: Weiss

first: Tal

last: Havkin-Solomon

first: Irene

last: Martinez-Roman

first: Anat

last: Bashan

first: Ada

last: Yonath

first: Rivka

last: Dikstein


title: Structural and molecular insights into specialized translation mediated by the ribosome mRNA-binding channel [RNA-Seq]


title: Meningeal-derived retinoic acid regulates neurogenesis via suppression of Notch and Sox2 [ATAC-seq]

city: Aurora

first: Christina

last: Como

state: CO

institute: University of Colorado

summary: The meninges act as a regulator of brain development by secreting ligands that act on neural cells to regulate neurogenesis and neuronal migration. Meningeal-derived retinoic acid (RA) promotes neocortical neural progenitor cell cycle exit; however, the underlying molecular mechanism is unknown. Here, we used spatial transcriptomics and profiling of retinoic-acid receptor-a (RARa) DNA binding in Foxc1-mutant embryos that lack meninges-derived ligands to identify the neurogenic transcriptional mechanisms of RA signaling in telencephalic neural progenitors. We determined that meningeal-derived RA promotes neurogenesis by suppressing progenitor self-renewal pathways Notch signaling and the transcription factor Sox2. We show that RARα binds in the Sox2ot promoter, a long non-coding RNA that regulates Sox2 expression, and RA promotes Sox2ot expression in neocortical progenitors. Our findings elucidate a previously unknown mechanism of how meningeal RA coordinates neocortical development and insight into how defects in meningeal development may cause neurodevelopmental disorders.

overall_design: Bulk ATAC-seq data from Prom1+ magnetically separated E14 forebrain neural progenitors

first: Julie

last: Siegenthaler


title: The contribution of formyl peptide receptor 2 to intestinal epithelium homeostasis

status: Public on Nov 23 2025

city: Shanghai

first: shuting

last: Yu

address: 320 Yueyang Road, Xuhui District

institute: Shanghai Institute of Nutrition and Health

summary: To elucidate the mechanisms involved in maintaining intestinal epithelial homeostasis through formyl peptide receptor 1 (FPR2), small intestinal organoids derived from Fpr2f/f mice were used as an ex vivo model. Transcriptomics were examined via RNA-seq following FPR2 activation with MMK-1.

overall_design: RNA-seq profiling of small intestinal organoids derived from Fpr2f/f mice treated with 1 M MMK-1 or a vehicle control (0.1% DMSO) for 5 days.

first: Shuting

first: Yingying

last: Le


title: Metabolic Adaptations Rewire CD4 T Cells in a Subset-Specific Manner in Human Critical Illness with and without Sepsis

status: Public on Nov 21 2025

city: Nashville

first: Matthew

middle: Tyler

last: Stier

state: TN

address: 1161 21st Avenue South

department: Internal Medicine

institute: Vanderbilt University Medical Center

summary: Bioenergetic dysfunction is an archetypal finding in critical illness, particularly among patients with severe sepsis. A central feature of sepsis is the shift towards pathologic immunosuppression, especially among CD4 T cells, predisposing to secondary infections and ineffectual organ recovery. However, it remains unknown whether metabolic abnormalities contribute to CD4 T cell dysregulation in critically ill sepsis patients. We collected PBMC from medical and surgical ICU patients at Vanderbilt University Medical Center or community-matched healthy controls. We performed single cell RNA-sequencing with 10x Genomics droplet-based technology on a subset of 9 healthy controls, 19 ICU patients without sepsis, and 19 ICU patients with sepsis to generate a 644,147 cell map of critical illness.

overall_design:
Peripheral blood mononuclear cells (PBMCs) were collected from critically ill patients in the medical and surgical intensive care units (ICUs) at Vanderbilt University Medical Center 48-72 hours after admission to the ICU. This includes crtiically ill patients with sepsis (CI-Sep) and non-septic critically ill patients (CI-NS). Non-acutely ill healthy control participants (NHC) were recruited from the community including bedside surrogates of enrolled ICU patients. Cryothawed PBMC were analyzed by scRNA-seq.

***************************************************************
Raw files for human/patient samples are available in dbGaP (accessions phs004377.v1.p1 and phs004258.v1.p1) for controlled access to the personally identifiable sequence data. All subjects with age >89 have been assigned an age of 90 consistent with current HHS policy regarding de-identification of protected health information.
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first: Paul

last: Lindau

first: Jeffrey

last: Rathmell


title: A non-toxic, abscisic acid-based anchor-away system for efficient nuclear depletion of budding yeast proteins

status: Public on Nov 22 2025

city: Edinburgh

first: Sander

last: Granneman

address: Mayfield Road, Kings Buildings, Waddington building, room 3.06

department: Centre for Synthetic and Systems Biology

institute: University of Edinburgh

summary: With the aim of overcoming some of the problems associated with yeast genetic depletion systems, we developed a modified anchor-away (AA) system that relies on a chemically induced dimerization system involving the plant phytohormone abscisic acid (ABA). An advantage of employing this CID in an anchor-away system is that ABA is inexpensive, non-toxic to humans and it is easy to reverse the effect of ABA by simply washing out the hormone. Here we demonstrate that the ABA CID can be effectively employed as an AA system in Saccharomyces cerevisiae. We tested the ABA-AA with three proteins that accumulate at very different levels in the cell. We found that even for a highly abundant and essential proteasome component we were still able to get a ~50% decrease in cell growth upon ABA treatment. Compared to the rapamycin AA system, higher concentrations of the chemical is needed to observe a phenotypical effect. Nevertheless, we show that even at these high concentrations, ABA does not noticeably impair cellular growth nor does it cause major changes in gene expression in exponentially growing yeast. We propose that the ABA anchor-away system is highly complementary to existing tools but has no toxicity issues. Because of its simplicity, we anticipate it will be broadly useful.

overall_design: Developing a new anchor-away system for removing yeast proteins from the nucleus.

first: Hanne

last: Grosemans


title: Single-cell heterogeneity in interferon induction potential is heritable and governed by variation in cell state III

status: Public on Dec 13 2025

city: Urbana

first: Elizabeth

middle: Anne

last: Thayer

state: IL

address: 407 S Goodwin Ave

department: Microbiology

institute: University of Illinois at Urbana-Champaign

summary: Type I and III interferons (IFNs) are among the first lines of defense against viral infections, yet they are generally only produced by a tiny fraction of infected cells. Here, we show that variability in tonic cell signaling significantly influences cells’ ability to produce IFN upon stimulation with the synthetic double-stranded RNA, polyinosinic:polycytidylic acid (pIC). Using single-cell approaches, we found that members of the activator protein (AP)-1 transcription factor were implicated in IFNL1 expression predisposition. This guided us to investigate the role of the mitogen-activated protein kinase (MAPK) pathway, specifically the c-Jun N-terminal kinase (JNK), in IFNL1 production. We found that inhibition of JNK signaling severely altered the nature of the innate antiviral response upon pIC stimulation, independently of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. Together, our study emphasizes the influence of intrinsic stochasticity in cell state on heterogeneity in IFN expression.

overall_design: scRNAseq data of A549 cells either untreated or treated with 5 ng/mL pIC for 4, 8, 12, or 16 hours before being collected and processed for fixed scRNA sequencing.

first: Gabriela

last: Shipman

first: Joel

last: Rivera-Cardona

first: Tarun

last: Mahajan

first: QiWen

last: Teo

first: Sebastian

last: Paez

first: Joseph

last: Lederer

first: Jie

last: Chen

first: Nicholas

last: Wu

first: Sergei

last: Maslov

first: Christopher

last: Brooke


title: Deciphering Precursor Cell Dynamics in Esophageal Preneoplasia via Genetic Barcoding and Single-Cell Transcriptomics

status: Public on Nov 20 2025

city: Houston

first: Kyung Pil

last: Ko

state: Tx

address: 1515 Holcombe Blvd

institute: The University of Texas M.D. Anderson Cancer Center

summary: Esophageal preneoplastic cells, despite appearing histologically normal, exhibit early genetic alterations and lineage plasticity, yet their origins and trajectories remain unclear. This study employs genetic barcoding combined with single-cell RNA sequencing to trace the lineage of esophageal preneoplastic cells and identify a distinct progenitor-like population with high plasticity. Through a newly developed scoring system, high-plasticity cells are mapped, revealing their contributions to proliferative and basal cell populations. The study identifies key molecular markers, including Nfib and Qk, that define these precursor cells. These findings provide critical insights into early tumorigenesis, highlighting the potential of precursor cells as biomarkers for early cancer detection and therapeutic targeting. By elucidating the cellular dynamics underlying esophageal cancer initiation, this research lays the foundation for strategies to prevent malignant progression, offering broader implications for improving cancer diagnostics and treatment approaches.

overall_design: For Xenium In Situ experiment, a single FFPE block was prepared from normal esophagus and Trp53, Cdkn2a dKO cell-derived subcutaneous tumor samples and placed onto a Xenium slide.  Mouse 5K gene panel was used.


title: A receptor kinase complex refines cambium activity in Arabidopsis

status: Public on Nov 19 2025

city: Durham

first: Wenbin

last: Wei

address: Stockton Road

department: Biosciences

institute: Durham University

summary: The largest reservoir of terrestrial biomass is the wood within plant stems. Consisting of xylem cells, wood is derived from the cambium, a stem cell population that is maintained by non-cell autonomous signalling. The central component of this system is PXY, a receptor protein present on the plasma membrane of cambium cells. Here, we show that PXY protein interacts with a second membrane-localised receptor kinase, ER, to promote cambium fate. Combinatorial mutations between ER, ERL1 and ERL2 and receptor kinases of a second family, PXY, PXL1, and PXL2, show severe cambial defects, but the mechanism underpinning these phenotypes is not known. Here we discovered that PXY and PXL proteins form protein complexes with ER family members. In genetic analyses, plant lines in which PXY signalling was constitutively active had dramatic phenotypic changes that required the presence of ER or ERL2. Our results demonstrate that PXY signalling mediated cambium regulation depends on ER signalling and explains ER function in the cambium. Because the cambium produces xylem, which constitutes the wood in vascular plants, our findings position PXY-ER complexes at the centre of the accumulation of this versatile biomaterial and essential carbon sink.

overall_design: RNA-Seq profiling of 7-day-old wild type, er mutant and XVE:ER transformed er mutant at 0h, 3h and 8h Estradiol induction.

first: Qing

last: He

first: Peter

last: Etchells


title: Bi-directional regulation between NAD/NAMPT and IFN-γ/PD-L1 axes via BRD4/IRF1 and mitochondrial respiration in metastatic cutaneous melanoma

status: Public on Nov 18 2025

city: Alessandria

first: Valentina

last: Audrito

address: Viale Teresa Michel 11

department: DIST

country: Italy

institute: University of Eastern Piedmont

summary: Nicotinamide phosphoribosyltransferase (NAMPT) is a key enzyme in NAD biosynthesis and is frequently upregulated in tumors, including melanoma, where it drives disease progression and resistance to targeted therapies. Beyond its metabolic role, NAMPT also exerts immune-modulatory functions, acting as a cytokine-like mediator that shapes tumor–host interactions and influences the efficacy of immunotherapy. Building on recent evidence indicating a connection between the pro-inflammatory cytokine interferon-gamma (IFN-γ) signaling and NAD metabolism, we sought to explore this poorly understood relationship in melanoma context. Analysis of the TCGA melanoma cohort revealed a significant correlation between NAMPT expression and IFN-γ signaling, including specific genes belonging to this pathway, such as IRF1, STAT1, and CD274/PD-L1. The correlation between NAMPT and PD-L1 was also confirmed at the protein level in more than 100 cases included in a melanoma tissue microarray (TMA). Functionally, IFN-γ treatment (100ng/ml for 24h) of three MM cell lines led to increased NAMPT transcription and intracellular expression, as well as increased release. Molecularly, as previously demonstrated for IFN-γ-inducible PD-L1, also NAMPT expression upon IFN-γ signaling activation is regulated at epigenetic/transcriptional level via bromodomain protein BRD4/IRF1 complex, as revealed using BRD4 inhibitors and chromatin immunoprecipitation (ChIP)-RT-PCR experiments. In the second part of our results, we showed a bidirectional regulation between NAD/NAMPT axis and IFN-γ signaling. NAMPT inhibition, as well as genetic silencing, reduced IFN-γ signaling activation, as highlighted by RNAseq data and confirmed by biochemical validation. This reciprocal regulation involved the modulation of mitochondrial respiration, specifically mitochondrial Complex I. Analysis of the melanoma TCGA cohort revealed a significant correlation between NAMPT expression, IFN signaling and several mitochondrial Complex I subunit genes. Consistently, activation of IFN-γ signaling in melanoma cell lines induced an increase in oxygen consumption rate, which was completely abrogated by NAD/NAMPT-dependent inhibition of complex I activity, indicating a direct metabolic crosstalk.

overall_design: Overall, these findings highlight a novel reciprocal regulatory loop between NAMPT/NAD axis and IFN γ signaling, linking NAMPT-dependent metabolic reprogramming and immune regulation.

first: Irene

last: Fiorilla

first: Lidia

last: Avalle


title: Spatial and single cell transcriptomics in the human Entorhinal Cortex across diverse risk of Alzheimer’s disease

status: Public on Nov 14 2025

first: Keri

last: Martinowich

state: Maryland

address: 855 N Wolfe St Suite 300

institute: Lieber Institute for Brain Development

summary: We present the first spatially-resolved transcriptomics and single-nucleus RNA-sequencing integrated dataset from the entorhinal cortex (ERC) of postmortem human brain donors. ERC is implicated in early progression of Alzheimer’s Disease (AD) and we chose this brain region to study gene expression changes associated with AD risk by comparing APOE E2 and E4 allele carriers. Donors with no AD diagnosis or widespread neurodegeneration were exclusively selected. As AD risk is increased in African Ancestry in contrast to European Ancestry backgrounds, and AD risk is also increased in women compared to men, our dataset included donors from these different backgrounds. We identified a pre-myleinating oligodendrocyte sub-cluster with transcriptomic changes strongly associated with APOE E4 carriers. These changes were present in both ancestry backgrounds, although they were more pronounced in African Ancestry donors. To facilitate future studies based on this dataset, we provided the raw and processed data, and created interactive web applications.

overall_design:
We obtained tissue blocks of postmortem human brain entorhinal cortex (ERC) from 31 neurotypical adult brain donors carrying either E2 or E4 APOE alleles from both African and European ancestry. For each donor, a sample was generated for both spatially resolved transcriptomics with 10x Visium, and single nucleus RNA-seq with 10x Chromium. Visium data showed 9 transcriptional distinct spatial domains. snRNA-seq data was clustered into 38 fine subtypes across 8 broad cell types. Differential expression between APOE carrier status (E2+ vs. E4+) was performed at the cluster level in both data types.

***************************************************************
Raw files for human/patient samples are being made available in dbGaP (https://www.ncbi.nlm.nih.gov/gap/) for controlled access to the personally identifiable sequence data.
***************************************************************

first: Louise

last: Huuki-Myers

first: Heena

last: Divecha

first: Svitlana

middle: V

last: Bach

first: Madeline

last: Valentine

last: Eagles

first: Bernard

last: Mulvey

first: Rahul

last: Bharadwaj

first: Ruth

last: Zhang

first: James

last: Evans

first: Melissa

last: Grant-Peters

first: Ryan

last: Miller

last: Kleinman

first: Shizhong

last: Han

first: Thomas

last: Hyde

first: Stephanie

last: Page

first: Danie

last: Weinberger

first: Mina

last: Ryten

first: Kristen

last: Maynard

first: Leonardo

last: Collado-Torres


title: Nox4 inhibitor treatment ameliorates cardiac function in mouse models of Duchenne Muscular Dystrophy

city: Tampa

first: Da-Zhi

last: Wang

state: FL

address: 560 Channelside Dr.

institute: University of South Florida

summary: Duchenne Muscular Dystrophy (DMD) is caused by mutations in dystrophin, leading to degeneration and weakness of the skeletal and cardiac muscles. Despite numerous efforts in developing therapies for this devastating disease, DMD remains a fatal disease. Our recent study showed that loss of the cardiac Isl1-interacting protein (CIP), which interacts with dystrophin in sarcolemma of cardiomyocytes, accelerates the progression of dystrophic cardiomyopathy. We identified Nox4 as one of the downstream mediators of this process. Here, we report that Setanaxib, a Nox1/4 inhibitor, protected the heart of CIP/Mdx double knockout (dKO) mice from heart failure and reduced cardiac fibrosis. Similarly, Setanaxib treatment exhibited lower cardiac fibrosis and protection against heart failure in Mdx/Utrn dKO mouse, another murine model for dystrophic cardiomyopathy. Additionally, treatment with Nox4 inhibitor reduced the expression of cardiomyopathy genes in dystrophic mice. Interestingly, transcriptomic analysis of the hearts from Mdx/Utrn dKO mice treated with Nox4 inhibitor reveals an enrichment of genes associated with fatty acid metabolism, oxidative phosphorylation, and protein binding, while genes related to inflammation and epithelial-mesenchymal transition were downregulated. Consistent with these results, we found increased expression of Pgc1a and Tcap in the hearts of Mdx/Utrn dKO mice treated with Nox 4 inhibitor, and reduced expression of Mcp1. Collectively, these findings suggest that Nox4 plays a key role in development of myocardial fibrosis and heart failure caused by dystrophin deficiency, and suggest that Nox4 inhibition could be a potential novel therapy to alleviate cardiomyopathy in DMD patients.

overall_design: In order to characterize the role of Nox4 in dystrophic cardiomyopathy, Mdx/Utrn dKO male mice (2 to 3-month-old) were daily treated with Setanaxib (60 mg/kg/day) or vehicle (corn oil) via oral gavage for 12 weeks. After the treatment, mice were euthanized and the hearts were collected for transcriptomic analysis.

first: Rui

last: Deng

first: Tabatha

last: De Oliveira Silva

first: Xiang

last: Liu

first: Cheng

last: Fan

first: Hee

last: Young Seok

first: Jingjing

last: Wu

first: Haipeng

last: Guo

first: Tian

last: Lin

first: Shiju

first: Nihan

last: Gunay

first: Yao Wei

last: Lu

first: Zhan-Peng

last: Huang

first: John

middle: D

last: Mably

first: Mingxiang

last: Teng

first: Hong

last: Chen

first: Gabriela

last: Diniz


title: Spatial and single cell transcriptomics in the human Entorhinal Cortex across diverse risk of Alzheimer’s disease [Visium]

first: Keri

last: Martinowich

first: Louise

last: Huuki-Myers

first: Heena

last: Divecha

first: Svitlana

last: Bach

first: Madeline

last: Valentine

first: Nicholas

last: Eagles

first: Bernard

last: Mulvey

first: Rahul

last: Bharadwaj

first: Ruth

last: Zhang

first: James

last: Evans

first: Melissa

last: Grant-Peters

first: Ryan

last: Miller

first: Joel

middle: E

last: Kleinman

first: Shizhong

last: Han

first: Thomas

last: Hyde

first: Stephanie

last: Page

first: Daniel

last: Weinberger

first: Mina

last: Ryten

first: Kristen

last: Maynard

first: Leonardo

last: Collado-Torres


title: Single-cell sequencing unveils CD34+ membranous cells (CMCs) in subcutaneous fascia of the abdominal midline

city: Nanjing

first: Haixiang

last: Huang

state: 江苏

address: No.1, Weigang, Xuanwu district

department: College of veterinary

institute: Nanjing Agricultural University

summary: ScRNA data of the abdominal skin and subcutaneous fascia

overall_design: we performed scRNA-seq to compare the cellular constitution of the skin(n=2) and subcutaneous fascia (n=2)

first: Zhenwei

first: Jianming

last: Yue

first: Lu

last: Mei

first: Qiusheng

last: Chen


title: A comprehensive study on the co-culture interaction between endophytic Fusarium and host Sanghuangporus

status: Public on Nov 15 2025

city: Lanzhou City

first: Lan

middle: Lan

last: Yu

state: Anning District

address: Northwest Normal University, Shi Street, Anning District, Lanzhou City, Gansu Province, China

department: College of Life Sciences

institute: Northwest Normal University

summary: Fungal-fungal interactions frequently result in alterations to the metabolomic profiles of the interacting fungi, with potential ramifications in both industrial and agricultural contexts. In this present study, an endophytic strain of Fusarium sp. MF20 was isolated from the fruiting bodies of Sanghuangporus vaninii. An optimized co-culture system was then established to explore the changes in metabolite profiles resulting from the fungal-fungal interaction, employing a comprehensive analysis integrating transcriptomics and metabolomics. This foundational work paves the way for the enhanced industrial exploitation of Sanghuangporus, a medicinally valuable and rare fungi

sample_organism:
Fusarium sp.
Sanghuangporus vaninii

platform_organism:
Fusarium sp.
Sanghuangporus vaninii

overall_design: Comparative gene expression profiling analysis using data obtained from RNA-seq of twelve samples in two different treatment groups

first: Yanjun

last: Ma

first: Lanlan

first: Jingming

first: Rong

last: Li


title: LHPP expression in triple-negative breast cancer promotes tumor growth and metastasis by modulating the tumor microenvironment

status: Public on Nov 07 2025

city: La Jolla

first: Jeffrey

last: Reina

state: CA

address: 10010 N Torrey Pines Rd

institute: Salk Institute for Biological Studies

summary: Triple-negative breast cancer (TNBC) is a highly aggressive and metastatic form of breast cancer that lacks an effective targeted therapy. To identify potential therapeutic targets, we investigated the phosphohistidine phosphatase, LHPP, which has been implicated in the development of several types of cancer. However, the full significance of LHPP in cancer progression remains unclear due to our limited understanding of its molecular mechanism. We found that levels of the LHPP phosphohistidine phosphatase were significantly increased in human breast cancer patients compared to normal adjacent tissues, with the highest levels in the TNBC subtype. When LHPP was knocked out in the MDA-MB-231 human TNBC cell line, cell proliferation, wound healing capacity, and invasion were significantly reduced. However, LHPP knockout in TNBC cells did not significantly affect overall phosphohistidine protein levels. Interestingly, LHPP knockout in MDA-MB-231 cells delayed tumor growth and reduced metastasis when orthotopically transplanted into mouse mammary glands. To investigate LHPP’s role in breast cancer progression, we used next-generation sequencing and proximity-labeling proteomics, and found that LHPP regulates gene expression in chemokine-mediated signaling and actin cytoskeleton organization. Depletion of LHPP reduced the presence of tumor-infiltrating macrophages in mouse xenografts. Our results support a tumor promoter role for LHPP phosphohistidine phosphatase in MDA-MB-231TNBC cells and suggest that targeting LHPP phosphatase could be a potential therapeutic strategy for TNBC.

overall_design: To understand the molecular pathways regulated by LHPP, RNAseq was performed on human breast cancer cells with and without LHPP expression. LHPP was genetically depleted in the MDA-MB-231 and MCF7 cell lines via CRISPR-Cas9, generating LHPP knockout (KO) and wild-type (WT) control cells. RNA was extracted from both cell types, followed by library preparation and RNA sequencing to capture differences in gene expression profiles when LHPP is depleted. Three replicates for each cell type were used

first: Queralt

last: Vallmajo-Martin

first: Jia

last: Ning

first: Aubrey

last: Michi

first: Kay

last: Yeung

first: Geoffrey

last: Wahl

first: Tony

last: Hunter


title: Receptor kinase heterodimers refine cambium activity in Arabidopsis

first: Wenbin

last: Wei

summary: In plant development, a receptor kinase may be active in disparate cell types, with each requir-ing different signalling outputs. The ERECTA (ER) receptor kinase and its homologs ERL1 and ERL2 exemplify this pleiotropy. In Arabidopsis, they influence stomatal patterning, shoot meristem function, ovule morphogenesis, xylem fiber differentiation, and cell division in the vascular cambium1–6. Such diverse expression and functionality raise the question of how ER signalling can specify such distinct cell behaviours. One explanation is that cell-type specific interactions with co-receptors, ligands, or other proteins modulate signalling. However, little is known about ER interactors in the vascular cambium, a bifacial stem cell niche that generates phloem and xylem. Combinatorial mutations between ER, ERL1 and ERL2 and receptor kinases of a sec-ond family, PXY, PXL1, and PXL2, show severe cambial defects5,7. Here we discovered that PXY and PXL proteins form heterodimers with ER and ERL2. PXY signalling can be manipulated by altering levels of its cognate ligand, TDIF. In genetic analysis, plant lines in which TDIF levels were altered had dramatic phenotypes that required the presence of ER or ERL2. Our results demonstrate that PXY signalling mediated cambium regulation depends on ER signalling and explains ER function in the cambium. Because the cambium produces xylem, which constitutes the wood in vascular plants, our findings position PXY-ER heterodimers at the centre of the ac-cumulation of this versatile biomaterial and carbon sink.

overall_design: There were triplicates in each of the four groups (wild type, er, IRX3:CLE41, er IRX3:CLE41)

first: Qing

last: He

first: Ehmke

last: Pohl

first: Changyin

last: Wu

first: Raymond

last: Wightman

first: Peter

last: Etchells


title: Whole blood transcriptomic profiling identifies expression signatures for sepsis mortality

status: Public on Nov 03 2025

city: Philadelphia

first: Blanca

last: Himes

state: PA

address: 423 Guardian Dr

department: Department of Biostatistics, Epidemiology and Informatics

institute: University of Pennsylvania

summary:
Sepsis is the leading cause of death in U.S. hospitals and affects nearly 50 million people globally per year. Sepsis is defined as the ‘dysregulated host response to infection’, however, identifying specific and targetable immune abnormalities for therapeutic intervention has been challenging. An effective immune response clears pathogen but also protects host tissues from collateral damage. In sepsis, however, broad immune dysregulation causes organ failure and increased risk of mortality. Therapeutic trials targeting known inflammatory markers in sepsis have failed to improve outcomes. Efforts to identify sepsis therapies may have been thwarted by a focus on the wrong targets, undetected or unaccounted-for heterogeneity among study participants, or issues of timing in a highly dynamic immune response and clinical syndrome.
Analysis of the leukocyte transcriptome can reveal elements of the dysregulated host response to infection that characterizes sepsis. We hypothesized that sepsis nonsurvivors have a distinct transcriptional signature, and we thus sought to identify, validate, and contextualize the whole blood transcriptomic changes associated with sepsis mortality in patients with and without septic shock.

overall_design: We conducted a prospective observational cohort study of 161 critically ill sepsis patients with whole blood RNA samples collected within 24 hours of admission to the ICU. Differential gene expression analysis was conducted to identify transcriptomic changes in 1) nonsurvivors versus survivors at 30 days and 2) patients with versus without septic shock, adjusted for age, sex, and absolute neutrophil count. We performed gene set enrichment analysis (GSEA) to describe overrepresented ontological pathways.

first: Nuala

last: Meyer

first: Mengyuan

last: Kan


title: Direct ERG-to-glucocorticoid receptor interactions enhance tumorigenicity and might explain the enigmatic responses of prostate cancers to corticosteroids (RNA-Seq)

status: Public on Nov 01 2025

city: Rehovot

first: Arunachalam

last: Sekar

address: Herzl street

department: IRB

summary: Patients with prostate cancer (PCa) frequently express fusions between an androgen-regulated gene and anETSfamily gene, especiallyERG. Our protein complementation assays revealed that the glucocorticoid receptor, GR, physically interacts with ERG. This alleviates allosteric autoinhibition, stabilizes ERG and protects it from chemotherapy-induced degradation. Promoter-reporter assays indicated that GR transactivates ERG’s target genes, includingMYC. In PCa models, antagonizing GR or lowering cortisol increased apoptosis and decreased tumorigenic growth of ERG-positive, not ERG-negative PCa cells. Likewise, ERG+patient-derivedxenografts displayedintensifiedsensitivity tothe combination of aGRantagonist and an inhibitor of the androgen receptor (AR). In summary, we uncovered an oncogenic partner of ERG, identified a potential molecular basis for the association of corticosteroid use with poor responses to AR signaling inhibitors, as well as offer new strategies to treat a sizable group of patients with PCa.

overall_design: To investigate the ERG target gene transcativation by GR, we stimulated the human prostate cancer cells (VCaP, Du145-EV and DU145-tERG) with dexamethasone (DEX) for 24 hours.

first: Eviatar

last: Weizmann

first: Ronnie

last: Blecher-Gonen


title: Direct ERG-to-glucocorticoid receptor interactions enhance tumorigenicity and might explain the enigmatic responses of prostate cancers to corticosteroids

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

overall_design: Refer to individual Series


title: Direct ERG-to-glucocorticoid receptor interactions enhance tumorigenicity and might explain the enigmatic responses of prostate cancers to corticosteroids (ChIP-Seq)

overall_design: Chromatin immunoprecipitation and DNA sequencing (ChIP-seq) for ERG and GR in dexamethasone (DEX) stimulated VCaP and DU145-tERG cells


title: tRF-394 has the potential to be a RNA-based therapy for H. pylori-infected gastric cancer

status: Public on Oct 31 2025

first: Han

last: Chen

state: Jiangsu

address: #300 Guzhou Road, Gulou District

institute: Nanjing Medical University

summary: HGC-27 GC cells were stimulated with Helicobacter pylori. PANDORA-seq sequencing was employed to elucidate the potential roles of these relatively uncharacterized novel small non-coding RNAs (sncRNAs) in Hp-infected gastric cancers. RNA-seq was performed to identify diffferentially-expressed gene in Hp-infected gastric cancers.

overall_design: PANDORA-Seq profiling of the GC cells after stimulated by H. pylori compared with H. pylori-negative controls.


title: Therapy-persistent leukemia is selectively vulnerable to SLC23A1 restoration via targeting KHSRP (KHSRP knockdown in CAL-1 cells)

status: Public on Oct 28 2025

city: Boston

first: Qingyu

last: Luo

state: MA

address: 450 Brookline Ave

institute: Dana-Farber Cancer Institute

summary: KHSRP was knocked down in CAL-1 cells by CRISPR interference, then RNA-seq was performed in control and KHSRP knockdown cells to assess differentially expressed genes.

first: Andrew

last: Lane


title: Deep Learning Models for Cell Cycle Phase Prediction from Single-Cell RNA Sequencing Data

status: Public on Oct 22 2025

city: Morgantown

first: Halima Akhter

last: Akhter

state: West Virginia

address: 1 Medical Center Dr, Morgantown, WV 26506

department: Immunology, and Cell Biology

institute: West Virginia University

summary: Accurate prediction of cell cycle phases is essential for mitigating confounding effects in single-cell RNA sequencing (scRNA-seq) analysis and for understanding how certain diseases (e.g. cancer) develop and respond to treatment. We evaluated traditional machine learning (AdaBoost, Random Forest, LightGBM) and deep learning approaches (DNN3, DNN5, CNN, hybrid models, ensembles) for cell cycle phase prediction from scRNA-seq data. Models were trained using consensus phase labels derived from four established tools (CellCycleScore, ccAFv2, Revelio, and Tricycle) applied to single-cell gene expression datasets representing diverse biological contexts, including a human leukemia cell line (REH), peripheral blood mononuclear cells (10× PBMC), human pluripotent stem cells and their differentiated derivatives (GSE75748), 10 k embryonic mouse brain cells, and mouse hematopoietic stem and progenitor cells (GSE81682). Performance was evaluated on three independent datasets: human embryonic stem cells (GSE64016; 247 cells), human osteosarcoma cells (GSE146773; 1152 cells), and mouse embryonic stem cells (E-MTAB-2805; 288 cells), all with experimentally verified labels. REH-trained models achieved strong cross-dataset performance, reaching 74.35% accuracy on GSE146773 (Top 3 decision fusion (DF), and score fusion (SF)) and 72.9% on GSE64016, while attaining 56.9% on the cross-species Buettner mESC benchmark. SHapley Additive exPlanations (SHAP) analysis confirmed enrichment in cell-cycle-related gene sets for features. Notably, models trained on samples with lower recovery rates of cell cycle markers exhibited lower performance. These results highlight the strength of deep learning for robust, scalable cell cycle phase prediction from scRNA-seq data.

overall_design:
We ran an experiment using two types of human leukemia cell lines. These include REH (ATCC #CRL-8286) and SUP-B15 (ATCC #CRL-1929). We prepared scMultiome libraries for each cell line for both gene expression (scRNA-seq) and chromatin accessibility (single-cell Assay for Transposase-Accessible Chromatin; scATAC-seq) at the same time at single-cell levels. In this study we focused only on scRNA-seq data.

Funding: This work was partially supported by the National Institute of General Medical Sciences of the National Institutes of Health under award numbers P20 GM103434, U54 GM104942, and 2P20 GM121322 (G.H.), and by the National Science Foundation under award numbers 2125872 (G.H. and D.A.A.) and 2318708 (D.A.A.).

first: Gangqing

last: Hu

first: Donald

last: Adjeroh

first: Debra

last: Piktel

first: Laura

middle: F

last: Gibson

first: Halima


title: Gestational Feed Restriction Induces Differential Expression of Novel Long Non-Coding RNAs in Offspring Skeletal Muscle

city: Viçosa

first: Maria Malane

last: Muniz

state: MG

address: Av Peter Henry Rolfs S

department: Animal Science

country: Brazil

institute: University Federal of Vicosa

summary: Fetal programming via maternal nutrition during gestation plays a key role in shaping skeletal muscle development, directly affecting meat quality and production efficiency. This study examines how maternal feed restriction at different gestational stages alters the expression of novel long non-coding RNAs (lncRNAs) in the skeletal muscle of goat offspring. LncRNAs are emerging as important regulators of biological processes, including myogenesis, yet their role in fetal programming remains largely unexplored. Using RNA sequencing (RNA-Seq), we analyzed lncRNA expression in the Longissimus thoracis muscle of kids born to goats exposed to two feeding regimens: early gestation restriction (50% of maintenance from day 8–84 of gestation, then 100% until parturition; RM, n=6) and late gestation restriction (100% from day 8–84, then 50% until parturition; MR, n=8). RNA-Seq data underwent quality control, alignment, transcript assembly, and differential expression analysis using Cufflinks and FEELnc pipelines. Three differentially expressed (DE; FDR ≤ 0.05) lncRNAs were identified and classified based on genomic context and potential regulatory function. The upregulated lncRNA_10996.1 in the RM group was linked to ENSCHIG00000020055 and ENSCHIG00000024132. Downregulated lncRNA_1180.1 and lncRNA_7992.1 were associated with ZNF546, PSMC4, SNORA65, ZNF79, LRSAM1, and ENSCHIG00000023017. These results suggest that maternal nutrition-induced shifts in lncRNA expression may influence muscle development through regulatory interactions with protein-coding genes. Our findings identify candidate lncRNAs as potential biomarkers and contribute novel insights into the molecular mechanisms underlying fetal programming in livestock.

overall_design: RNA-Seq profilling of Longissimus thoracis muscle  from newborn male goat kids.60 nulliparous Saanen dairy goats underwent estrous synchronization using prostaglandin administered at a 7-day interval, followed by artificial insemination with semen from a single male.The day of the insemination was considered the day 0 of the pregnancy and the beginning of the experiment. All the animals were kept under the same diet and management conditions for an adaptation period of 7 days. After that, the animals were randomly assigned to one of two feeding regimens: Restriction-Maintenance (RM) group (n = 6): fed 50% of maintenance requirements from days 8–84 of gestation, followed by 100% from day 85 to parturition. Maintenance-Restriction (MR) group (n = 8): fed 100% of maintenance requirements from days 8–84, followed by 50% from day 85 to parturition. Both groups received the same diet composition; only the timing of the restriction varied according to gestational stage.

first: Maria

first: Thais

last: Costa

first: Nicola

last: Serão

first: Mateus

last: Gionbelli

first: Marcio

last: Duarte


title: Increased LEF1 protein levels and isoform switching drive cell proliferation in chronic lymphocytic leukemia [CUT&Tag]

status: Public on Oct 08 2025

city: Barcelona

first: Jose Ignacio

last: Martin-Subero

state: Barcelona

address: c/Rosselló, 149-153

country: Spain

institute: IDIBAPS

summary: The main goal of this study was to assess the role of LEF1 in patient-derived CLL cells.

overall_design: Comprehensive functional analyses to define the role of LEF1 (LEF1 CRISPR in primary CLL cells and LEF1 isoforms overexpression in CLL cell lines).

first: Mateos-Jaimez

last: Judith

first: Charalampopoulou

last: Stella


title: Increased LEF1 protein levels and isoform switching drive cell proliferation in chronic lymphocytic leukemia [RNA-Seq]


title: Notch interaction with RUNX factors regulates initiation of the T-lineage program [ChIP-seq]

status: Public on Oct 14 2025

city: Isehara

first: Hiroyuki

last: Hosokawa

address: 143 Shimokasuya

department: Immunology

institute: Tokai Univ

summary: RUNX factors play an essential role in the development of T cell. Dynamic interacting partner switching of RUNX1 induces the redeployment of RUNX1 at the T-lineage commitment checkpoint. Here, we attempted to reveal functional differences in RUNX factors between lymphoid progenitor (LP) and Noth-stimulated the earliest T progenitor stage, phase1. We identified CTCF as a LP-specific RUNX1-interacting partner. Indeed, LP-specific RUNX1 binding genomic sites had significantly enriched CTCF consensus motif and co-occupied with CTCF. After Notch stimulation, Notch1-IC directly interacted with RUNX1 and recruited it to the Notch-regulated T-signature gene loci with the Mediator/p300 transcriptional activation complex. CRISPR/Cas9-mediated stage-specific deletion of RUNX factors and its binding partners revealed that the RUNX1/CTCF complex in LP and the RUNX1/Mediator/p300 complex in phase1 negatively and positively regulate T-signature genes expression, respectively. Our results indicate that the Notch-mediated functional conversion of RUNX factors; re-organization of protein complexes and redeployment of genomic binding sites, has a crucial role in the initiation of T-lineage program.

overall_design: Ten million of Cas9-LPs with or without Notch stimulation were fixed with 1 mg/ml disuccinimidyl glutarate (Thermo Scientific) in PBS for 30 min at room temperature followed by an additional 10 min with addition of formaldehyde up to 1 %. The reaction was quenched by addition of 1/10 volume of 0.125 M glycine and the cells were washed with cold PBS. Pelleted nuclei were dissolved in lysis buffer (0.5 % SDS, 10 mM EDTA, 0.5 mM EGTA, 50 mM Tris-HCl [pH 8.0], and PIC) and sonicated on a Bioruptor (Diagenode) for 18 cycles of 30 sec sonication followed by 30 sec rest, with high power. Five micrograms of anti-RUNX1 (abcam; ab23980), anti-CTCF (CST; 3418), anti-Med12 (Bethyl; A300-774A), or anti-p300 Abs (CST; 57625) were prebound to Dynabeads anti-rabbit Ig and then added to the diluted chromatin complexes. The samples were incubated overnight at 4 ℃, then washed and eluted overnight at 65 ℃ in ChIP elution buffer (20 mM Tris-HCl, pH 7.5, 5 mM EDTA, 50 mM NaCl, 1 % SDS, and 50 mg/ml proteinase K). Eluted chromatin fragments were cleaned up using ChIP DNA Clean & Concentrator (Zymo). ChIP-seq libraries were constructed using NEBNext Ultra Ⅱ DNA Library Prep with Sample Purification Beads (E7103S, NEB) and NEBNext Multiplex Oligos for Illumina (E7500S, NEB) and sequenced on Illumina NextSeq500 in single read mode with the read length of 75 nt.

first: Yuichi

last: Kama

first: Ken-ichi

last: Hirano

first: Kaori

last: Masuhara

first: Yusuke

last: Endo


title: Increased LEF1 protein levels and isoform switching drive cell proliferation in chronic lymphocytic leukemia [CUT&Run]


title: Proteolytic disruption of renal endothelial glycocalyx in sepsis: Dexamethasone inhibition via TLR4/NF-κB/MMP axis

status: Public on Oct 01 2025

city: HANGZHOU

first: MINGJIE

last: FU

state: ZHEJIANG

address: 79#QINGCHUN ROAD

institute: THE FIRST AFFILIATED HOSPITAL OF ZHEJIANG UNIVERSITY

summary: Investigate the differences in gene expression in the kidneys of mice with sepsis, and by comparing with the sham operation group, analyze the differentially expressed genes and signaling pathways.

overall_design: Compare the differences in gene expression between the kidneys of CLP sepsis mice and those of the sham-operation mice

first: Mingjie

last: Fu


title: MLL2 facilitates long-range gene regulation through LINE1 elements [RNA-Seq]

city: Santander

first: Lucio

last: Di Filippo

address: PCTCAN - Cl. Albert Einstein, 22

institute: IBBTEC

summary: Transcriptional regulation is tightly linked to chromatin organization, with H3K4me3 commonly marking both active and bivalent promoters. In embryonic stem cells (ESC), MLL2 is essential for H3K4me3 deposition at bivalent promoters, which has been proposed to facilitate the induction of major developmental genes during pluripotent cell differentiation. However, prior studies point to a functional discrepancy between the loss of H3K4me3 at bivalent promoters and the largely unaltered transcription of major developmental genes in Mll2-/- cells. In this study, we investigated MLL2-dependent gene regulation in mouse ESC and during their differentiation. Contrary to the prevailing view, we show that MLL2’s primary role is not to oppose Polycomb-mediated repression at the bivalent promoters of developmental genes. Instead, we identify a previously unrecognized regulatory function for MLL2 at the CG-rich 5' untranslated regions (5'UTR) of evolutionarily young LINE-1 (L1) transposable elements (TE). We found that MLL2 binds to the 5’UTR of L1 elements and is critical for maintaining their active state (H3K4me3 and H3K27ac), while preventing the accumulation of repressive H3K9me3. Using both global genomic approaches (i.e. RNA-seq, ChIP-seq and Micro-C) as well as targeted L1 deletions, we demonstrate that these MLL2-bound L1 elements act as enhancers, modulating the expression of neighboring genes in ESC and, more prominently, during differentiation. Together, our findings illuminate novel aspects of MLL2 regulatory function during early developmental transitions and highlight the emerging role of TE as key components of long-range gene expression control.

overall_design: Transcriptional profiles on WT, Mll1-KO, Mll2-KO and double-KO at day 0 (mESC) and day 4 of a multilineage differentiation protocol.

first: Lara

middle: Z

last: Shahidian

last: di Filippo

first: Sarah

last: Robert

first: Álvaro

last: Rada-Iglesias


title: Antibiotic resistance in Aeromonas hydrophila associated with exposure to low levels of oxytetracycline

city: Hong Kong

first: Sophie

middle: Natasha

last: ST-HILAIRE

address: Kowloon Tong, Hong Kong SAR, PR China

institute: City University of Hong Kong

summary: Antibiotic resistance (AMR) in aquatic bacteria affecting aquaculture has been a growing concern given the potential for mixing of bacterial populations in the aquatic environment and exposure to different pharmaceuticals from drugs used in aquaculture, as well as wastewater effluent and agricultural run-off.  To better understand the mechanism for AMR in a common aquatic fish pathogen exposed to low dose antibiotics we monitored the genetic changes, as well as gene expression, in Aeromonas hydrophila as the bacteria was exposed to incremental doses of oxytetracycline (OTC), a commonly used drug in aquaculture.  We were able to render all three isolates of our original A. hydrophila resistant to therapeutic levels of OTC (i.e.  ≥100ppm). The relatively quick phenotypic adaptation (often less than 3 days) to different OTC concentrations was very similar across our replicates.  Our whole genome sequencing data and transcriptome results suggested several genes underwent point mutations across all replicates.  Further differential gene expression was observed and likely impacted several pathways which may explain the progressive resistance to OTC associated with incremental exposure to the drug.  The specific mutations consistently identified in isolates exposed to OTC were on AHA_ 2785 (associated with an outer membrane protein), AHA_2910 (involved in the efflux pump mechanism), and AHA_0308 (associated with the small ribosomal subunit protein S10). The pathways involved in the differential gene expression included efflux- pump mechanisms, outer membrane proteins, and ribosomal protein OTC target.  Our findings support the notion that AMR can occur via genetic regulation of several intrinsic mechanisms within a bacterial population. This finding could have implications in aquaculture where bacteria such as A. hydrophila can be exposed to varying levels of antibiotics during in-feed treatments.

overall_design: We trained  original Aeromonas hydrophila ATCC9766 to get resistance to different levels of oxytetracycline (i.e., 5ppm, 20ppm, 50ppm, 100ppm, and 200ppm). The data contains all RNAseq samples from original Aeromonas hydrophila ATCC9766 (R0), and all the resistant Aeromonas hydrophila (i.e., R5, R20, R50, R100, and R200).

first: Ju

last: Zhang

first: Liqing

last: Huang

first: Liang

first: Zhaogyang

last: Wang

first: Celia

last: Schunter

last: St-Hilaire


title: Human pancreatic ductal cells from non-T1D donors respond to T1D cytokines and function as non-professional antigen presenting cells

status: Public on Sep 30 2025

city: Duarte

first: WenYong

last: Chen

address: 1500 E. Duarte Road

department: Cancer Biology and Molecular Medicine

institute: City of Hope

summary: Aims/Hypothesis: Type 1 diabetes (T1D) is an autoimmune disease marked by the destruction of beta cells in the pancreatic islets, with an incomplete picture of disease pathogenesis/progression and a lack of definitive cure. A recent finding linked pancreatic ductal cells of T1D donors with elevated levels of human leukocyte antigen (HLA) Class II molecules; however, the causal relationship and functional significance of this finding remain unknown. Because HLA Class II molecules are typically expressed by professional antigen presenting cells (APCs), this raises the possibility of ductal cells functioning as non-professional APCs. In this study, we test the hypothesis that non-T1D ductal cells are responsive to T1D-associated proinflammatory cytokines, TNF-α, IL-1β, and IFN-γ, and can act as non-professional APCs. Methods: Pancreatic exocrine cells, after the removal of islets, were obtained from cadaveric donors without apparent diseases and with appropriate consent. Cells were cryopreserved, thawed into a defined culture medium tailored to support ductal cell survival in a 3D suspension culture system. Ductal cells were exposed to various doses of cytokines for 48 hours and analyzed for gene and protein expression, using qRT-PCR, bulk-RNAseq, flow cytometry and Western blot analyses. Functional ability of cytokine-treated ductal cells to present an exogenous autoantigen (glutamate decarboxylase 65kD isoform [GAD65]) to T cells was tested using a GAD65-specific autoreactive CD4+ T cell clone (named BRI4.13) isolated from a T1D donor. Results: We found that within 48 hours a combination of TNF-α, IL-1β, and IFN-γ stimulated the expression of HLA Class II, co-stimulatory, and antigen-processing molecules at mRNA and protein levels in non-T1D ductal cells. Bulk RNAseq analysis showed that cytokines most significantly upregulated biological pathways in “antigen processing and presentation” and “T1D”. When cytokine-treated ductal cells were pulsed with an exogenous GAD65 peptide and cocultured with the BRI4.13 T cells, these T cells became activated and proliferated. Unexpectedly, we also found ~1% of KRT19+ ductal cells express GAD protein endogenously. Conclusions/interpretation: These results demonstrate that non-diseased primary ductal cells are sensitive to TNF-α, IL-1β, and IFN-γ stimulation, and can upregulate APC molecules and function in antigen presentation to autoreactive CD4+ T cells. To the best of our knowledge, our results provide the first evidence demonstrating antigen presentation by non-T1D human ductal cells to T cells, which implicate ductal cells in contributing to T1D progression.

overall_design: Bulk mRNA-sequencing of human ductal cells derived from non-T1D subjects treated with "250x" (250 IU/ml TNF-α, 25 IU/ml IL-1β, and 250 IU/ml IFN-γ) and "500x" (500 IU/ml TNF-α, 50 IU/ml IL-1β, and 500 IU/ml IFN-γ) doses as well as vehicle control for 48 hrs (N=4 donors)

first: Neslihan

last: Erdem

first: Min-Hsuan

first: Hsun Teresa

last: Ku


title: CK2-mediated DEK Phosphorylation Drives PBX3 Overexpression: A Core Event in Hematopoietic Stem Cell-to-Leukemia Stem Cell Transformation

city: Chongqing

first: Zhe

address: 1 Yixueyuan Road, Yuzhong District

institute: Chongqing Medical University

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus