title: Understanding the fate of the hungry caterpillar:  Transcriptional and DNA methylation programs during metamorphosis of the butterfly Bicyclus anynana (RNA-Seq).

city: Brighton

first: Andrew

last: Hesketh

state: East Sussex

address: Lewes Road

department: School of Applied Sciences

institute: University of Brighton

summary: An immobile pupal phase in butterfly metamorphosis is central for the production of an airborne adult from the earlier caterpillar feeding stage. Extensive body plan re-organization occurs within the pupal case that is entirely dependent upon nutrients accumulated during caterpillar growth, and sensitive to external environmental conditions. Here, we use DNA and RNA sequencing of a laboratory butterfly population to produce a time course dataset describing changes in DNA methylation and in the transcriptome during progression from the 5th instar caterpillar larval stage through to the latest stage of pupation when the mature butterfly is about to eclose from the pupal case.

overall_design: Gene expression profiling of whole organism samples taken in triplicate at five consecutive time points: L5 (5th instar larva), P0 (the day entering pupation), P2 (2 days into pupation), P4 (4 days into pupation), and P6 (6 days into pupation, where the mature butterfly is about to emerge).

first: Juned

last: Kadiwala

first: Ana

middle: R

last: Garizo

first: Patricia

last: Beldade

first: Rameen

last: Shakur


title: Divergent programming and nonreciprocal plasticity of tissue resident exhaustedand memory CD8+T cell lineages

status: Public on Oct 13 2025

city: Philadelphia

first: E

middle: JOHN

last: WHERRY

state: PA

address: 421 Curie Blvd,354 BRB II/III

department: Systems Pharmacology       and Translational Therapeutics,Institute for Immunology

country: USA

institute: University of Pennsylvania

type: Expression profiling by high throughput sequencing

type: Genome binding/occupancy profiling by high throughput sequencing

summary: persistent antigen stimulation during chronicinfectioninduces apopulationof CD39hiCD69+CD103+/–Hobit+/–tissue-resident TEXcells in non-lymphoid tissuesthataredevelopmentally distinctfrombona fideTRMcells generated afteracutelyresolvedinfection.Tissue-resident TEXcells had reduced function and limited developmentalplasticity compared to TRMcells. Moreover, tissue-resident TEXandbona fideTRMcells weregoverned bydistinct transcriptional and epigenetic programs indicating divergent developmentalpaths.Indeed, whereasestablishedTRMcellscould giverise to secondaryantigen-independentmemory CD8+T cellsafter acute infectionas well as multiple subsets of TEXcells including TCF1+progenitorsduring chronic restimulation,establishedTEXcells were unable to form TRMcells andrequired ongoing antigen stimulation to efficientlyacquire residency features.Moreover,bona fideTRMdevelopedindependently of Tox, whereasTox controlled induction of residency-associatedmolecules in developing CD69+CD103+/–tissue-resident TEXcells and was essential for theiraccumulation in nonlymphoid tissues

overall_design: live CD8β+CD44hiCD45.1+Vα2+ P14 cells from each sample (pooled organs from 20 Arm-infected mice or 20 C13 infected mice) d30 post infection were sorted and stained with TotalSeq-A Oligos and custom pool of antibody derived tags.Also TEA sequencing on these samples for GEX+ATAC

first: Simone

middle: L

last: Park

first: John

middle: E

last: Wherry


title: Understanding the fate of the hungry caterpillar:  Transcriptional and DNA methylation programs during metamorphosis of the butterfly Bicyclus anynana (methylation).

country: United Kingdom

type: Methylation profiling by high throughput sequencing

overall_design: Genomic DNA methylation profiling of whole organism samples taken in triplicate at five consecutive time points: L5 (5th instar larva), P0 (the day entering pupation), P2 (2 days into pupation), P4 (4 days into pupation), and P6 (6 days into pupation, where the mature butterfly is about to emerge).


title: Single-cell RNA sequencing on cord blood-derived HPSCs cultured with or without liproxstatin-1 supplementation in chemically-defined conditions

city: Boston

first: Vijay

middle: G

last: Sankaran

state: MA

address: 1 Blackfan Circle

institute: Boston Children's Hospital / Broad Institute

summary: The aim for this dataset is to demonstrate that blockade of ferroptosis with the small molecule liproxstatin-1 can significantly augment the expansion of human HSCs derived from either cord blood or adult sources using diverse methods, including widely applied serum-free cultures and recently reported chemically-defined conditions. We find that human HSCs treated with liproxstatin-1 display increased ribosome biogenesis and cholesterol biosynthesis, accompanied by elevated 7-dehydrocholesterol levels - a potent endogenous inhibitor of ferroptosis. This study demonstrates the effectiveness of mitigating ferroptosis to enhance human HSC expansion in the setting of therapeutic genome modifications, paving the path to clinical applications.

overall_design: Single-cell transcriptomic profiling by high throughput sequencing

first: Lucrezia

last: della Volpe


title: Profiling of histone modifications in prostate cancer cells in response to  androgen deprivation and the onset of the neuroendocrine phenotype

city: Paris

first: Antonin

last: Morillon

state: Paris

address: 26 rue d'Ulm

country: France

institute: Institut Curie

summary: Androgen deprivation therapy (ADT), also called chemical castration, is one of the prevailing treatments of local and metastatic prostate cancer enabling inhibition of the Androgen Receptor (AR) pathway and tumor regression. However, the response to therapy varies among patients with some showing symptomatic relief and prolonged survival, while others relapsing in less than 5 years or failing to respond (reviewed in Harris et al, 2009). These clinical trajectories are in part due to emergence of mechanisms allowing maintenance of the AR activity, often observed in CRPC tumors, and progressive cell reprograming enabling androgen-independent growth. In some case CRPC tumors progressively evolve in highly agressive AR-negative neuroendocrine prostate cancer (NEPC). In this project we aimed to profile histone modifications associated with actively transcribed and repressed regions in the dynamic in vitro system recapitulating the CRPC and NEPC onset. Hormone-sensitive LNCaP cells were grown in  DHT-supplemented medium. In this condition cells exhibit an epithelial-like morphology and actively proliferate under the control of AR.  Androgen deprivation results in growth arrest and progressive emergence of the neuroendocrine phenotype characterized by AR signalling inactivation, expression of neuroendocrine genes and change in morphology  (Terry et al, 2013).

overall_design: The experiment was performed in duplicates following the protocol from Henikoff lab (Skene et al, 2018) with modifications described in (Jarroux et al, 2021) in prostate cancer adenocarcinoma cells LNCaP growing in the presence of androgen (DHT) or in hormone-depleted media for 1 month (NE1m). Antibodies used : against H3K27ac (Millipore, MABE647, 1:50), H3K27me3 (Cell signaling, C36B11, 1:50), H3K4me3 (Millipore, 04745, 1:50); IgG (Thermo Fisher, 31235). DNA fragments were purified with NEB Monarch PCR & DNA purification kit following the protocol enrichment for short DNA fragments and was quantified by Qubit HS DNA kit. CUT & RUN libraries were prepared using the TruSeq ChIP-Sample Prep Kit-Set A and PCR Box (Illumina) from 5 ng of DNA with 10 PCR cycles for amplification following the manufacture’s procedures. Concentration and quality were assessed by Qubit with dsDNA HS Assay Kit (Thermo Fisher Scientific) and High Sensitivity DNA Analysis Chip Kit (Agilent Technologies). Libraries were sequenced on a NovaSeq – S1 device in a pair-end 100 bp read length mode.

first: Rocco

last: Cipolla

first: Marina

last: Pinskaya

first: Marc

last: Gabriel


title: Interpretable Inflammation Landscape of Circulating Immune cells (ILCIC_RespiratoryDiseases)

city: Barcelona

first: Laura

last: Jiménez-Gracia

address: c/ Baldiri Reixac, 4  Barcelona Science Park - Tower I

country: Spain

institute: Centre Nacional d'Anàlisi Genòmic (CNAG)

summary: Inflammation is a biological phenomenon beneficial for homeostasis, but unfavorable if dysregulated. Although major progress has been made in characterizing inflammation in specific diseases, a global, holistic understanding is still elusive. This is particularly intriguing, considering its function for human health and the potential for modern medicine if fully deciphered. Here, we leveraged advances in single-cell transcriptomics to delineate inflammatory processes of circulating immune cells during infection, immune-mediated inflammatory diseases and cancer. Our single-cell atlas of >6.5 million peripheral blood mononuclear cells from 1047 patients (56% female, 43% male) and 19 diseases allowed us to learn a comprehensive model of inflammation in circulating immune cells. The atlas expanded our current knowledge of the biology of inflammation of immune-mediated diseases, acute and chronic inflammatory diseases, infection and solid tumors, and laid the foundation to develop a disease classification framework using unsupervised as well as explainable machine learning. Beyond a disease-centered analysis, we charted altered activity of inflammatory molecules in peripheral blood cells, depicting discriminative inflammation-related genes to further understand mechanisms of inflammation. We present a rich resource for the community, and  laid the groundwork for learning a classifier for inflammatory diseases, presenting cells in circulation as a potential tool for disease classification.

overall_design: scRNA-seq from 32 human PBMC samples, including 12 Asthma, 12 COPD and 8 HC.

first: Davide

last: Maspero

first: Sergio

last: Aguilar-Fernández

first: Francesco

last: Craighero

first: Juan

middle: C

last: Nieto

first: Holger

last: Heyn


title: Interpretable Inflammation Landscape of Circulating Immune cells (ILCIC_BRCA)

overall_design: scRNA-seq from 6 human PBMC samples of BRCA patients, at the pre-treatment stage.


title: Profiling of Androgen Receptor in prostate cancer cells in response to  androgen deprivation and the onset of the neuroendocrine phenotype

summary: Androgen deprivation therapy (ADT), also called chemical castration, is one of the prevailing treatments of local and metastatic prostate cancer enabling inhibition of the Androgen Receptor (AR) pathway and tumor regression. However, the response to therapy varies among patients with some showing symptomatic relief and prolonged survival, while others relapsing in less than 5 years or failing to respond (reviewed in Harris et al, 2009). These clinical trajectories are in part due to emergence of mechanisms allowing maintenance of the AR activity, often observed in CRPC tumors, and progressive cell reprograming enabling androgen-independent growth. In some case CRPC tumors progressively evolve in highly agressive AR-negative neuroendocrine prostate cancer (NEPC). In this project we aimed to profile Andrigen Receptor in the dynamic in vitro system recapitulating the CRPC and NEPC onset. Hormone-sensitive LNCaP cells were grown in  DHT-supplemented medium. In this condition cells exhibit an epithelial-like morphology and actively proliferate under the control of AR.  Androgen deprivation results in growth arrest and progressive emergence of the neuroendocrine phenotype characterized by AR signalling inactivation, expression of neuroendocrine genes and change in morphology  (Terry et al, 2013).

overall_design: The experiment was performed in duplicates following the protocol from Henikoff lab (Skene et al, 2018) with modifications described in (Jarroux et al, 2021) in prostate cancer adenocarcinoma cells LNCaP growing in the presence of androgen (DHT) or in hormone-depleted media for 1 month (NE1m). Antibodies: against AR (Abcam, ab108341) and IgG (Thermo Fisher, 31235). DNA fragments were purified with NEB Monarch PCR & DNA purification kit following the protocol enrichment for short DNA fragments and was quantified by Qubit HS DNA kit. CUT & RUN libraries were prepared using the TruSeq ChIP-Sample Prep Kit-Set A and PCR Box (Illumina) from 5 ng of DNA with 10 PCR cycles for amplification following the manufacture’s procedures. Concentration and quality were assessed by Qubit with dsDNA HS Assay Kit (Thermo Fisher Scientific) and High Sensitivity DNA Analysis Chip Kit (Agilent Technologies). Libraries were sequenced on a NovaSeq – S1 device in a pair-end 100 bp read length mode.


title: RNA-mediated mechanisms of regulation of the Androgen Receptor activity in response to androgen deprivation

summary: Androgen deprivation therapy (ADT), also called chemical castration, is one of the prevailing treatments of local and metastatic prostate cancer enabling inhibition of the Androgen Receptor (AR) pathway and tumor regression. However, the response to therapy varies among patients with some showing symptomatic relief and prolonged survival, while others relapsing in less than 5 years or failing to respond (reviewed in Harris et al, 2009). These clinical trajectories are in part due to emergence of mechanisms allowing maintenance of the AR activity, often observed in CRPC tumors, and progressive cell reprograming enabling androgen-independent growth. Activation and repression of gene exprssion by AR require interactions with numerous proteins, and very recently, with RNAs. Notably, Schmidt et al. identified a specific pyrimidine-rich motif within SRA1 and another SRA-like long noncoding RNA, named SLNCR, both binding directly the AR N-terminal domain in melanoma cells  (Schmidt et al, 2016); (Schmidt et al, 2020). In addition to SLNCR, other RNAs, belonging to the long noncoding (lnc)RNA gene family, contain the aforementioned AR-interacting consensus motif, including a paragon lncRNA - HOTAIR that protects AR from proteolysis in the context of castration-resistant prostate cancer (Zhang et al, 2015) but also tethers AR to the GLI2 promoter to activate its transcription in renal cell carcinoma (Bai et al, 2021). The AR NTD is not the only domain reported to bind RNA. The growth arrest specific-5 gene GAS5, another lncRNA with well-known tumor suppressor functions, interacts with the LBD of AR inhibiting its transactivation activity and proliferation of prostate cancer cells (Lv et al, 2021). In this project we aimed to identify RNAs associated with AR in the androgen-dependent and independent  cell using the technique of RNA immunoprecipitation of the transcription factor (RIP).

overall_design: prostate cancer adenocarcinoma cells LNCaP growing in the presence and absence of androgen were treated with low doses of formaldehyde and 10^7 cells per condition were collected for lysis and immunoprecipitation of AR (G Hendrickson et al, 2016) .Associated RNAs were recovered and analyzed by total stranded RNA-sequencing.  THe experiment was performed in duplicates and AR immunoprecipitation was compared to IgG.


title: Interpretable Inflammation Landscape of Circulating Immune cells (ILCIC_COVID-HC)

overall_design: scRNA-seq from 8 human PBMC samples, 4 patients with COVID and 4 healthy controls.


title: Revealing heterogeneity and damage response in the adult human utricle

city: Toronto

first: Alain

last: Dabdoub

state: Ontario

address: 2075 Bayview Ave., A3 42

country: Canada

institute: Sunnybrook Health Sciences Centre

summary: The human utricle is a vestibular organ composed of sensory and non-sensory cells responsible for maintaining balance. Balance sense gradually deteriorates with age. With the aging population expected to double to 2 billion by 2050, vestibular disorders will pose a significant challenge as no pharmaceutical or biological treatments are available, a current unmet medical need. Here we show, for the first time, the cellular and transcriptional profile of the adult human utricle and its response to damage by performing bulk and single-cell RNA-sequencing from patient-derived utricles. We discovered six transcriptionally distinct cell types, including a unique population, demonstrating the heterogeneity and complexity of the adult human utricle. In addition, using an aminoglycoside damage paradigm, we determined the early transcriptional changes of the utricle after damage. Our findings demonstrate that this organ has the capacity to respond to ototoxic damage within 24 h and potentially initiate a regenerative response via an early-responding supporting cell population. This study represents a major step forward in inner ear regenerative medicine. Our results will serve as a foundation for preclinical studies, paving the way to therapeutic strategies for balance recovery.

overall_design: We cultured six whole organotypic utricles for 24 h, three with vehicle control and three treated with gentamicin to induce hair cell damage. Then, we isolated the sensory epithelium and performed bulk RNA-seq.

first: Luca

last: Emilia

first: Ibeh

last: Neke

first: Yamamoto

last: Ryosuke

first: Bennett

last: Dallas

first: Lin

last: Vincent

first: Chen

last: Joseph

first: Lovett

last: Michael

first: Dabdoub

last: Alain


title: Profiling of transcriptomic changes in androgen-dependent prostate cancer cells  in response to anrogen deprivation.

first: Antonin

last: Morillon

summary: Castration-resistant prostate cancer (CRPC) emerges in response to androgen deprivation therapies and exhibits high cellular plasticity eventually progressing into neuroendocrine prostate cancer (NEPC). In this study, we took advantage of the dynamic prostate cancer cell system recapitulating the CRPC onset to identify lncRNAs induced early in response to androgen deprivation. In this system, first, adenocarcinoma LNCaP cells are grown in the presence of dihydrotestosterone (DHT) mimicking primary epithelial androgen-dependent luminal tumors  (NE_0j). Then, they are subjected to androgen deprivation which induces immediate growth arrest, progressive change in cell morphology and properties towards the neuroendocrine-like phenotype (NE-like cells, NE_15j, 1m, 3m) and finally lead to acquisition of androgen independence (NE_6m).  Total RNA-sequencing followed by differential expression analysis of scallop-assembled transcripts and multiple filtering isolated  gencode annotated protein-coding and long noncoding RNA genes but also  15 novel lncRNAs highly upregulated upon androgen deprivation.

overall_design: Cells were cultured and treated in triplicates for each condition to extract RNA. RNA samples were treated with Dnase, quality controlled (RIN above 9)  and used for the library preparation). To perform differential expression analysis a condition of growth in the presence of androgen NE_0j) was considered as a reference to define up- and down-regulated genes in cells grown in the absence of androgen.

first: Rocco

last: Cipolla

first: Marina

last: Pinskaya

first: Virjinie

last: Firlej


title: Phthalate exposure to adult mice alters non-coding RNAs in cauda epididymosomes

city: Detroit

last: Pilsner

state: MI

address: 275 E Hancock St

department: Department of Obstetrics and Gynecology

institute: Wayne State University

type: Non-coding RNA profiling by high throughput sequencing

summary:
Extracellular vesicles (EVs) are known to contain important cargo of biologically active and regulatory molecules including small non-coding RNA (sncRNA). EVs from cauda epididymis play crucial role in post-testicular maturation of sperm.
We assessed levels of cauda epididymosomes sncRNAs following exposure to low dose anti-androgenic Di-n-butyl phthalate (DBP), Di(2-ethylhexyl) phthalate (DEHP), and their mixtures in mice.

overall_design: Male mice (C57BL/6J) were treated with vehicle (50% DMSO, n = 6), 2.5 mg/kg/day of DBP (n = 6) or DEHP (n = 6), and phthalate mixture (2.5 mg/kg/day each of DBP and DEHP, n = 6) for six weeks. Cauda epididymosomal RNA were extracted and sequenced to analyze their non-coding RNA (ncRNA) content. Mapping of reads to transcriptomes followed the order: microRNA (miRNA) > transfer RNA fragments (tRFs) > piwi-interacting RNA (piRNA) > ribosomal RNA (rRNA) > circular RNA (circRNA) > long non-coding RNA (lncRNA) using STAR alignment tool. Differential expression of normalized read counts between the exposed groups relative to controls was conducted using EdgeR (Fold change, FC ≥ 1.5 and p < 0.01).

first: Oladele

middle: A

last: Oluwayiose

first: J. Richard

first: Karolina

last: Nowak


title: The effect of cGAS or STING knockout on gene expression changes in mouse brain after ischemic stroke

city: Shanghai

first: Haiyang

last: Hu

address: 320 Yueyang Road

country: China

institute: PICB

summary: Mounting evidence indicates that the cGAS-STING pathway represents the major DNA sensing pathway to invoke immune and inflammatory responses in neuroinflammatory disorders. Here, we examined the gene expression changes in the brain of cGAS or STING knockout mice after ischemic stroke.

overall_design: Total RNA of brain from cGAS or STING knockout mouse after ischemic stroke was isolated and sequenced by deep sequencing using Illumina HiSeq 2500

first: Chenhui

last: Li

first: Munire

last: Maimaiti

last: Wang


title: Histone H3K4me3 epigenetic modification ChIPseq

city: Gothenburg

first: Maria

middle: I

last: Bokarewa

state: VG

address: Guldhedagatan 10A

department: Rheumatology and Inflammation Research

country: Sweden

institute: Gothenburg University

summary: ChIPseq analysis of histone H3 epigenetic modifications -  K4me3 - chromatin binding in activated CD4+ T cells

overall_design: 3 women, CD4 cells from PBMC isolated by positive selection on Dynabeads (cat.11331D),  ConA+LPS for 48h, pooled from 3 samples. Treated with YM155 for last 24h.   ChIPseq using anti-histone H3 antibodies (0.5 microg/ml, H3K4me3 - C15411003. DNA purified by the EpiTect ChIP OneDay kit (Qiagen).

first: Karin

middle: M

last: Andersson

first: Malin

last: Erlandsson

first: Nina

last: Oparina

first: Chandrasekaran

last: Venkataragavan


title: Anti-uPAR CAR T cells reverse and prevent aging-associated defects in intestinal regeneration and fitness

city: Cold Spring Harbor

first: Vyom

last: Shah

state: New York

address: 1 bungtown road

department: Beyaz Lab

institute: Cold Spring Harbor Laboratory

summary: Intestinal stem cells (ISCs) drive the rapid regeneration of the gut epithelium. However, during aging their regenerative capacity is reduced, possibly through senescence and chronic inflammation, albeit little is known about how aging-associated dysfunction arises in the intestine. We previously identified the urokinase plasminogen activator receptor (uPAR) as a senescence-associated protein in other tissues and developed CAR T cells able to efficiently target it. Harnessing them, here, we identify the accumulation of uPAR-positive cells in the aging gut and uncover their detrimental impact on ISC function in aging. Thus, both therapeutic and prophylactic treatment with anti-uPAR CAR T cells improved barrier function, regenerative capacity, inflammation, and mucosal immune function in aged mice. Overall, these findings reveal the deleterious role of uPAR-positive cells on intestinal aging in vivo and provide proof of concept for the potential of targeted immune-based cell therapies to enhance tissue regeneration in aging organisms.

overall_design: For "control" samples: Young (3 months) and old (20 months) Bl/6J mice had their intestinal crypts isolated and processed for scRNAseq. For "uPAR and UT" experiments: Young (3 months) and old (18 months) mice were treated by tail vein injection with 0.5x10^6 untransduced T cells (UT) or uPAR CAR T cells (m.uPAR-m.28z). The intestinal crypts from these mice were isolated and disociated at 6 weeks after infusion. At this time the young mice were 4.5months old and the old mice were 19.5months old.

first: Corina

last: Amor Vegas


title: Histone H3 epigenetic modifications ChIPseq

summary: ChIPseq analysis of histone H3 epigenetic modification - K27ac - chromatin binding in activated CD4+ T cells

overall_design: 3 women, CD4 cells from PBMC isolated by positive selection on Dynabeads (cat.11331D),  ConA+LPS for 48h, pooled from 3 samples. Treated with YM155 for last 24h.   ChIPseq using anti-histone H3 antibodies (0.5 microg/ml, H3K27ac - C15410196-10, Diagenode). DNA purified by the EpiTect ChIP OneDay kit (Qiagen).


title: Interpretable Inflammation Landscape of Circulating Immune cells (ILCIC_HealthyExercise)

first: Laura

last: Jiménez-Gracia

overall_design: scRNA-seq from 8 human PBMC samples from healthy donors, undergoing different physical activity (4 active and 4 inactive).

first: Davide

last: Maspero

first: Sergio

last: Aguilar-Fernández

first: Francesco

last: Craighero

first: Juan

last: Nieto

first: Holger

last: Heyn


title: Interpretable Inflammation Landscape of Circulating Immune cells (ILCIC_cirrhosis)

overall_design: scRNA-seq from 8 human PBMC samples of patients with cirrhosis.


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

status: Public on Oct 14 2025

city: Palo Alto

first: Lattice

last: Data Coordination

state: CA

address: 3165 Porter Drive

department: Genetics

institute: Stanford University

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

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

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

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

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

first: Rui

last: Chen

first: Jin

first: Jun

first: Ignacio

last: Ibarra

first: Xuesen

last: Cheng

first: Malte

middle: D

last: Luecken

first: Jiaxiong

last: Lu

first: Aboozar

last: Monavarfeshani

first: Wenjun

last: Yan

first: Yiqiao

last: Zheng

first: Zhen

last: Zuo

first: Samantha

last: Colborn

first: Berenice

middle: S

last: Cortez

first: Leah

last: Owen

first: Nicholas

last: Tran

first: Karthik

last: Shekhar

first: Joshua

last: Sanes

first: J

middle: T

last: Stout

first: Shiming

first: Yumei

first: Margaret

last: DeAngelis

first: Fabian

middle: J

last: Theis


title: Effect of TiO2 nanotubes on early gene expression of BMMSCs

city: Xi'an

first: Le

last: Wang

state: shanxi

address: Changle west road

institute: Air Force Medical University

summary: To investigate the effect of naotopography on the gene expression of  BMMSCs in the early stage, we respectively cultured BMMSCs on the surfaces of NT100(100-nanometer nanotubes) and ST (Smooth) for 6 hours.

overall_design:
We then performed gene expression profiling analysis using data obtained from RNA-seq of BMSC on different surface.
Comparative gene expression profiling analysis of RNA-seq data for BMSCs on nanotopograpgy and smooth surface.

first: Xuelian

last: Jia

first: Fuwei

last: Liu


title: The effect of STING antagonist SN-011 on the gene expression changes in the mouse brain after ischemic stroke

first: Haiyang

last: Hu

summary: Mounting evidence indicates that the cGAS-STING pathway represents the major DNA sensing pathway to invoke immune and inflammatory responses in neuroinflammatory disorders. Here, we examined the effect of STING antagonist SN-011 on the gene expression changes in the mouse brain after ischemic stroke

overall_design: Total RNA of mouse brain were sequenced by deep sequencing using Illumina HiSeq 2500

first: Munire

last: Maimaiti

first: Chen


title: Histone H3 epigenetic modifications ChIPseq K27me3

first: Maria

last: Bokarewa

summary: ChIPseq analysis of histone H3 epigenetic modification - K27me3 - chromatin binding in activated CD4+ T cells

overall_design: 3 women, CD4 cells from PBMC isolated by positive selection on Dynabeads (cat.11331D),  ConA+LPS for 48h, pooled from 3 samples. Treated with YM155 for last 24h.   ChIPseq using anti-histone H3 antibodies (0.5 microg/ml,  H3K27me3 - C15410195-10, Diagenode). DNA purified by the EpiTect ChIP OneDay kit (Qiagen).

first: Karin

last: Andersson

first: Malin

last: Erlandsson

first: Nina

last: Oparina

first: Chandrasekaran

last: Venkataragavan


title: Revealing heterogeneity and damage response in the adult human utricle [scRNA-Seq]

first: Alain

last: Dabdoub

overall_design: We cultured a total of six organotypic utricles, two with 24h vehicle control, two treated with gentamicin for 24h to induce hair cell damage, and two with no treatment (time 0). Then, we isolated the sensory epithelium and performed scRNA-seq.

first: Luca

last: Emilia

first: Ibeh

last: Neke

first: Yamamoto

last: Ryosuke

first: Bennett

last: Dallas

first: Lin

last: Vincent

last: Joseph

first: Lovett

last: Michael

first: Dabdoub

last: Alain


title: RNA sequencing to identify daf-10-regulated genes and che-3-regulated genes in C. elegans defense against pathogen P. aeruginosa infection

city: Tianjin

first: Ming

last: Lei

address: Weijin Road, Heping District, Tianjin

institute: Tianjin University

summary: Purpose: To gain molecular insights on how daf-10 and che-3 regulates C. elegans innate immunity, we used RNA sequencing to profile gene expression in daf-10 and che-3 animals relative to wild-type animals with or without P. aeruginosa (PA14) infection.

overall_design: Gene expression was compared between groups to identify daf-10 and che-3-regulated genes under uninfection or infection conditions.Three replicates of three groups of RNA samples (daf-10(e1387) and che-3(e1124) and wild-type L4-stage animals with or without exposure to P. aeruginosa for 24 hrs) were sequenced. Gene expression was compared between groups to identify daf-10 and che-3-regulated genes under uninfection or infection conditions.

first: Haijun

last: Tu

first: Jingyi

last: Ke

first: Guangshuo

last: Ou


title: Interpretable Inflammation Landscape of Circulating Immune cells

first: Laura

last: Jiménez-Gracia

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

Inflammation is a biological phenomenon beneficial for homeostasis, but unfavorable if dysregulated. Although major progress has been made in characterizing inflammation in specific diseases, a global, holistic understanding is still elusive. This is particularly intriguing, considering its function for human health and the potential for modern medicine if fully deciphered. Here, we leveraged advances in single-cell transcriptomics to delineate inflammatory processes of circulating immune cells during infection, immune-mediated inflammatory diseases and cancer. Our single-cell atlas of >6.5 million peripheral blood mononuclear cells from 1047 patients (56% female, 43% male) and 19 diseases allowed us to learn a comprehensive model of inflammation in circulating immune cells. The atlas expanded our current knowledge of the biology of inflammation of immune-mediated diseases, acute and chronic inflammatory diseases, infection and solid tumors, and laid the foundation to develop a disease classification framework using unsupervised as well as explainable machine learning. Beyond a disease-centered analysis, we charted altered activity of inflammatory molecules in peripheral blood cells, depicting discriminative inflammation-related genes to further understand mechanisms of inflammation. We present a rich resource for the community, and  laid the groundwork for learning a classifier for inflammatory diseases, presenting cells in circulation as a potential tool for disease classification.

overall_design: Refer to individual Series


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


title: RNA-Seq shows the changes on transcriptomes after Nsd2 overexpression in mice.

city: shanghai

first: wenxin

last: feng

address: 1954 Huashan Road, Shanghai

institute: shanghai jiaotong university

summary: To explore the possible role of Nsd2 in pancreatic carcinogenesis in vivo, the gene expression profile of pancreas tissue from PKNO(Pdx-Cre;LSL-KrasG12D;Nsd2oe/+) and littermate PK(Pdx-Cre;LSL-KrasG12D) mice (8 weeks old) was examined by RNA sequencing(RNA-Seq).

first: Feng

last: Wenxin

first: Li

last: Li


title: The gene expression profiling in the brain of cGAS or STING deficiency mice

first: Haiyang

last: Hu

summary: Mounting evidence indicates that the cGAS-STING pathway represents the major DNA sensing pathway to invoke immune and inflammatory responses in neuroinflammatory disorders. Here, we examinedgene expression profiling in the brain of cGAS and STING deficiency mice

first: Munire

last: Maimaiti

first: Chen

last: Wang


title: Histone H3 epigenetic modifications

first: Maria

last: Bokarewa


title: Targeted CRISPR-Cas9 screening identifies core transcription factors controlling murine haemato-endothelial fate commitment [RNA-seq]

status: Public on Oct 12 2025

city: Zürich

first: Nina

last: Schmolka

address: Winterthurerstrasse 190

country: Switzerland

institute: University of Zurich

summary: During development, blood generation begins in the yolk sac with the differentiation of haemato-endothelial mesoderm generating haematopoietic progenitors. This study aimed to identify the crucial molecular regulators of haemato-endothelial mesoderm formation and to extend our knowledge of the process in an unbiased way. We employed a murine embryonic stem cell model that recapitulates embryonic blood development, and performed targeted CRISPR-Cas9 knock out screens focusing on transcription factors and chromatin regulators, which highlighted the transcription factors Smad1, Ldb1, Six4 and Zbtb7b. Embryonic stem cells lacking these regulators gave rise to mesodermal subsets with a defined lineage differentiation bias, while transcriptome analysis of these cells uncovered the precise impact of each factor on gene expression in the developing mesoderm. Our study reveals novel molecular pathways governing mesodermal development crucial to allow endothelial and haematopoietic lineage specification and paves the way for future advances in haematopoietic stem cell applications.

overall_design: Viable single cells were FACS sorted into 384-well cell capture plates (Single Cell Discoveries, Netherlands), in which each well contained 50 nl of barcoded primers and 10 µl of mineral oil (Sigma M8410). After sorting, plates containing cells were centrifuged at 1500x g for 1 minute then placed on dry ice before storage at -80° C. Single-cell RNA sequencing was performed by Single Cell Discoveries according to an adapted version of the SORT-seq protocol57

first: Michael

last: Teske


title: Alteration of the N6-methyladenosine methylation landscape in a mouse model of polycystic ovary syndrome

city: Changsha

first: Waixing

address: Tongzipo

institute: The Third Xiangya Hospital of Central South University

type:
Non-coding RNA profiling by array
Other

summary: To explore the N6-methyladenosine (m6A) methylation abnormality of mRNAs and its potential roles in the mouse model of polycystic ovary syndrome (PCOS)

overall_design: Ovary tissues from the mouse model of PCOS were distributed into two experimental groups: control group and PCOS group, then perform lncRNAs chips by the Arraystar Mouse m6A-mRNA&lncRNA Epitranscriptomic microarray.

first: Bin

last: Jiang


title: Targeting FABP4 Improves Healthy Aging by Rejuvenating Liver Metabolism

city: Shenzhen

first: Zhihua

address: No. 12, Langshan Road, Xili Street, Nanshan District, Shenzhen

department: Shenzhen Key Laboratory of Cardiovascular Disease

institute: Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen

summary: Aging is characterized by progressive metabolic dyshomeostasis that increases morbidity and mortality. It remains underexplored whether metabolic aging is a targetable process to improve healthy aging. Here, we performed a proteomic analysis in a cohort of young and elderly adults. Among 9 aging-sensitive proteins shared by both female and male, fatty acid binding protein 4 (FABP4) was identified as a reliable biomarker that was consistently upregulated in aged mice. Silencing FABP4 in the elderly mice by adeno-associated virus significantly rejuvenated metabolic activity, and improved glucose intolerance and steatosis. Transcriptome analysis revealed a restoration of the pro-aging gene reprogramming towards inflammation and metabolic disorders in the liver after FABP4 knockdown. Specifically, FABP4 knockdown promoted degradation of cholesterol and fatty acids, while repressing gluconeogenesis. Furthermore, administration of an FABP4 inhibitor BMS309403 delivered similar metabolic benefits in the elderly mice. Thus, FABP4 is a practicable target to improve metabolic aging in the elderly.

overall_design: All animals were housed in a constant environment (room temperature, 24 ± 3 °C; room humidity,55 ± 5%) with a standard 12-h light/12-h dark cycle. Mice were fed with normal chow and with free access to water. A total of thirty 14-month-old male WT mice were randomly divided into two groups as the following: (1) mice injected with AAV9-shRNA-Fabp4 by tail vein and sWAT in situ injection with a dose of 4×10^11 viral genomes, n=15; (2) mice injected with AAV9-shRNA-Neg with the same way and same amount, n=15. The above animals were kept until 20-month-old after AAV injection for sundry experiments. A group of 8-week-old WT mice were regarded as young control group (n=15). The mice were anaesthetized with inhalational anaesthetic and euthanized by cervical dislocation. Liver were immediately dissected and stored at -80°C. Three independent biological replicate samples from Young or Old group were used for RNA extraction. RNA-seq was completed by Novogene.

first: Jian

last: Lv

first: Yimeng

first: Lili

first: Jingjing

first: Yuan

last: He

first: Ningning

last: Guo

first: Yu

last: Fang

last: Tong

first: Lixu

last: Tang


title: Targeted CRISPR-Cas9 screening identifies core transcription factors controlling murine haemato-endothelial fate commitment [SORT-seq]

overall_design: Viable single cells were FACS sorted into 384-well cell capture plates (Single Cell Discoveries, Netherlands), in which each well contained 50 nl of barcoded primers and 10 µl of mineral oil (Sigma M8410). After sorting, plates containing cells were centrifuged at 1500x g for 1 minute then placed on dry ice before storage at -80° C. Single-cell RNA sequencing was performed by Single Cell Discoveries according to an adapted version of the SORT-seq protocol.


title: Profiling the host defense responses against the emerging fungal pathogen Candida auris in a reliable Drospophila melanogaster infection model

city: Shang hai

first: li

last: jie

address: No. 320 Yueyang Road

institute: Shanghai lnstitute of lmmunity and Infection

summary: The ‘superbug’ Candida auris has been ranked as a priority fungal pathogen and is becoming a serious threat to public health. However, the underlying mechanisms of real-world pathogen-host interactions remain elusive, in part due to the lack of powerful immunocompetent animal models. In this study, we report that selected wild-type strains of Drosophila melanogaster can be developed as a promising infection model to recapitulate C. auris bloodstream infection. The systemic and organ-specific responses to C. auris infection in vivo were evaluated, as well as the corresponding transcriptional profiling. Our findings confirm that Toll and JAK-STAT signaling pathways mediate antifungal responses in the Drosophila model following C. auris infection. Moreover, we identified certain conserved novel factors required for host-C. auris interactions, highlighting the fly model's potential to reveal subtle immune mechanisms not readily observed in mammalian systems. Taken together, our work demonstrates that wild-type Drosophila offers a robust immunocompetent animal model for the further in-depth investigation of dynamic C. auris-host interactions in vivo.

overall_design: To investigate the effects of Candida auris infection on the host transcriptome in Drosophila melanogaster, we performed a series of experiments involving infection and control groups. Adult flies were injected with either C. auris or PBS as a control. We collected samples at two time points post-infection: 6 hours and 24 hours. At each time point, we either harvested whole flies or dissected the fat body tissue for analysis.


title: Irinotecan activates anti-tumor immunity in CT26 tumor cells

city: Nanjing

first: Xinghua

last: Gao

state: Jiangsu

address: #639 Longmian Dadao

institute: China Pharmaceutical University

summary: Topoisomerase I (Top1) is a classical drug target for anticancer therapy, but its role in immune signaling in cancer cells remain unclear. Here, we aimed to explore the possible role and mechanism of Irinotecan (CPT-11) in anti-tumor immunity.

overall_design: mRNA expression profiles of CPT-11-treated CT26 tumor cells were generated by deep sequencing, in duplicate.

first: Yong

last: Yang

first: Yanting

last: Lin


title: Gene expression profile at single cell level of human melanoma cell lines, normal human melanocytes and human nevus cells.

city: Salt Lake City

first: Robert

last: Judson-Torres

state: Utah

address: 2000 Circle of Hope

department: Dermatology

institute: Huntsman Cancer Institute at the University of Utah

summary: Melanomas are considered highly heterogenous in transcriptional state. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of melanoma cells as compared to primary melanocytes and nevus melanocytes. Sample 1 contain KIT postitive melanocytes sequenced directly ex vivo from human nevi. Sample 2 contains different human melanoma cell lines and primary human melanocytes grown in vitro.

overall_design: Melanoma cell lines were grown in RPMI media supplemented with 10% FBS. NHMs were grown in 254 media supplemented with HGMS. Nevus cells were obtained by excising nevi and sorting for KIT positive cells using the protocol in PMID: 34475532


title: Dynamic transcriptional and epigenetic changes define postnatal tendon growth

city: Boston

first: Jenna

last: Galloway

address: 185 Cambridge St.

department: Orthopaedics

institute: Massachusetts General Hospital

summary: Tendons are dynamic structures that efficiently transmit forces and enable movement. From birth, tendons undergo dramatic changes from a principally cellular tissue to a hypocellular one characterized by a dense and highly ordered extracellular matrix. During this time, tendon cells change morphology from rounded to stellate in appearance and their proliferative rates decline. There is also significant expansion and maturation of the extracellular matrix (ECM) as tendons grow in length and diameter and alter their biomechanical properties to sustain increased physical activities. Surprisingly, for such an important stage of tendon maturation, we understand very little about the transcriptional and epigenetic regulators that direct these processes. Here, we present a roadmap of genes that are differentially regulated during the early neonatal and postnatal time period. We find differentially expressed genes fall into specific transcriptional modules, representing expression increases, decreases, or gene sets undergoing dynamic changes over postnatal time. By pairing our transcriptomic data with epigenetic data, we were able to perform an integrative analysis of the datasets and further define modules with highly correlated changes in gene expression and chromatin accessibility.  From this analysis, several new pathways emerge. Among them, we focus on Yap1, a transcriptional co-activator of the Hippo signaling pathway. We observe accessible regions near to differentially expressed genes, containing motifs for TEAD, the transcription factor that binds Yap to regulate transcription. Conditional loss of Yap1 at postnatal stages results in altered expression of Col1a1 and disrupted matrix organization and density, suggesting that Yap is important for refining tendon ECM maturation. Together, our analyses identify a regulator of matrix maturation and provides a rich dataset with which to interrogate transcriptional networks and pathways during this poorly understood time in tendon growth.

overall_design: Tendon samples from weekly timepoints during postnatal development were subjected to both RNAseq and ATACseq to profile transcriptional and chromatin level changes during postnatal tendon growth and development.

first: Heather

last: Dingwall

first: Terence

last: Capellini


title: Whole-exome sequencing of normal lung tissues, precursor lesions and invasive lung adenocarcinomas

status: Public on Oct 11 2025

city: Houston

first: Humam

last: Kadara

state: TX

address: 2130 W. Holcombe Blvd

institute: University of Texas MD Anderson Cancer Center

type: Genome variation profiling by high throughput sequencing

summary: Understanding cellular processes underlying early lung adenocarcinoma (LUAD) development is needed to devise intervention strategies. Here, we performed whole exome sequencing (WES) of human treatment-naive lungs comprising various stages in the sequence of pathogenesis of LUAD including normal lung tissues, atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA) and LUAD.

overall_design:
WES of tissues was performed on DNA isolated from formalin-fixed paraffin embedded tissues using the TWIST-WES protocol. Sequencing was done on the NovaSeq 6000 platform from Illumina.

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

first: Fuduan

last: Peng

first: Ansam

last: Sinjab


title: Single-nucleus RNA-sequencing (snRNA-seq) analysis of normal lung tissues, precursor lung lesions and invasive lung adenocarcinomas

summary: Understanding cellular processes underlying early lung adenocarcinoma (LUAD) development is needed to devise intervention strategies. Here, we performed snRNA-seq analysis of human treatment-naive lungs comprising various stages in the sequence of pathogenesis of LUAD including normal lung tissues, atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA) and LUAD.

overall_design:
snRNA-seq was performed on isolated nuclei from tissue scrolls of formalin-fixed parafin embedded tissues using the 10x Genomics Chromium Fixed RNA protocol.

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

first: Sujuan


title: Targeted CRISPR-Cas9 screening identifies core transcription factors controlling murine haemato-endothelial fate commitment

first: Nina

last: Schmolka

overall_design: Viable FLK1+ single cells from different genotypes ( Ctrl,  Etv2 KO, Ldb1 KO, Six4 KO, Smad1 KO, Zbtb7b KO) were FACS sorted and fixed using the 10x Chromium Next GEM Single Cell Fixed RNA Sample Preparation Kit (PN-1000414) and stored at -80°C. The quantity of fixed cell suspension was assessed using an automated cell counter (LUNA-FX7, Logos). Library preparation was conducted using the 10x Chromium Fixed RNA Profiling Reagent Kits for Multiplexed Samples. Briefly, four fixed samples underwent probe hybridization, pooling, and loading onto the chip. Approximately 66,000 cells from the sample pools were loaded into the 10x Chromium X. Library preparation followed the manufacturer's guidelines (Guide CG000527, Rev E).

first: Michael

last: Teske


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

first: Chenfang

last: Si

address: Haike Road 100

institute: Chinese Academy of Sciences

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

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

first: Bing

last: Shan

first: Yaoyang

last: Zhang


title: Spatial transcriptomics analysis of normal lung tissues, precursor lung lesions and invasive lung adenocarcinomas

summary: Understanding cellular processes underlying early lung adenocarcinoma (LUAD) development is needed to devise intervention strategies. Here, we performed spatial trancriptomics analysis of human treatment-naive lungs comprising various stages in the sequence of pathogenesis of LUAD including normal lung tissues, atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA) and LUAD.

overall_design:
Spatial transcriptomics analysis of samples was done using the Visium CytAssist platform from 10x Genomics. All tissues were surgically resected and formalin-fixed paraffin embedded.

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


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

city: wuhan

first: yu

middle: zhang

last: yi

state: hubei

address: donghu street

department: wuhan

institute: wuhan university

summary: Direct reprogramming of scar-forming fibroblasts into induced cardiomyocytes (iCMs) offers a regenerative strategy to repair injured myocardium. However, reprogramming efficiency remains low in fibroblasts from adult and aged hearts, and the molecular barriers underlying this resistance remain poorly understood. Here, we used transcriptomic and epigenetic profiling to uncover cellular senescence as a key obstacle limiting fibroblast plasticity and cardiogenic conversion. Fibroblasts from post-neonatal stages exhibited impaired activation of cardiac gene programs and persistent expression of fibrotic and inflammatory signatures. A loss of function screen identified Nr4a3 as a key repressor of cardiac reprogramming, particularly in senescent and aged cardiac fibroblasts (CFs). Nr4a3 overexpression promoted senescence and suppressed iCM reprogramming, whereas Nr4a3 knockdown significantly enhanced iCM induction from both murine and human senescent CFs. Mechanistically, Nr4a3 depletion remodeled the chromatin landscape by shifting it from a fibrotic and inflammatory state to a regenerative cardiac program. We further identified Cxcl14, a senescence-associated secretory phenotype (SASP) factor upregulated by Nr4a3, as a key downstream effector. Blocking Cxcl14 restored reprogramming in otherwise refractory fibroblasts. In vivo, Nr4a3 knockdown enhanced reprogramming-based improvement of heart function following myocardial infarction. These findings demonstrated that cellular senescence is a major barrier to direct cardiac reprogramming and identified Nr4a3 as a central regulator of this block. Targeting Nr4a3 and its downstream effectors may represent a promising therapeutic avenue to enhance cardiac regeneration in aged individuals following injury.

overall_design: To determine the molecular basis by which knockdown Nr4a3 enhances iCM reprogramming, we conducted RNA-seq using shNr4a3-CFs and shNT-CFs collected at  day 7 of treatment.

first: Li

last: Wang

first: Mengxin

last: Liu

first: Zhangyi

last: Yu


title: Single-cell and spatial transcriptomics analysis of tobacco-associated lung adenocarcinoma development, and in response to targeting inflammation alone or in combination with immune checkpoint blockade in precancerous phase [Spatial transcriptomics]

summary: Understanding cellular processes underlying early lung adenocarcinoma (LUAD) development is needed to devise intervention strategies. Here, we performed single-cell RNA sequencing (scRNA-seq) of mouse lungs from Gprc5a−/− mice during lung tumor development and also following therapeutic targeting of inflammation (IL-1𝛽) alone and in combination with immune checkpoint blockade in precancerous stages. We coupled scRNA-seq analysis with spatial transcriptomics of mouse lungs under different conditions.

overall_design: Gene expression profiling by high throughput single-cell sequencing and spatial transcriptomics


title: Myeloid Cell Adhesion Molecule 1 (CADM1) promotes pro-inflammatory signaling in human Inflammatory Bowel Diseases

city: Chapel Hill

first: Shehzad

middle: Z.

last: Sheikh

address: 111 Mason Farm Road

department: Department of Medicine

institute: University of North Carolina School of Medicine

summary: Cytotoxic T cells have been postulated to facilitate the destruction of intestinal epithelium in inflammatory bowel diseases (IBDs). CADM1, which encodes a membrane adhesion protein that can bind the T cell receptor CRTAM, was markedly up regulated in colon of IBD patients compared to non-IBD (NIBD) patients. We then identified CADM1 enrichment in multiple immune cell clusters including macrophages and dendritic cells in the colons of IBD patients. Increased numbers of CADM1+ myeloid cells were measured adjacent to CD8+ T cells within colons of ulcerative colitis patients compared to NIBD patients. Conditional deletion of Cadm1 in myeloid cells resulted in reduced numbers of activated T cell populations and protected mice from chemical-induced colitis. Similarly, administration of a Cadm1 ‘neutralizing’ antibody which binds its extracellular domain reduced tissue inflammation and breakdown of the intestinal epithelium and crypts after induction of colitis in mice. Lastly, serum levels of sCADM1 were elevated in IBD patients compared to NIBD controls and treatment of LPMCs with recombinant sCADM1 enhanced inflammatory STAT3 phosphorylation. Therefore, we concluded that CADM1 is a mediator of pro-inflammatory signaling cascades in the colon and a potential therapeutic target for the IBDs.

overall_design: We performed comprehensive small RNA and RNA profiling on colon tissue from IBD and NIBD control patients in addition to characterizing the cleaved extracellular domain of CADM1 (sCADM1) function in lamina propria mononuclear cells (LPMCs) isolated from these patients. Lastly, a conditional loss-of-function mouse was developed to assess Cadm1 function in the myeloid compartment during chemical-induced colitis.

first: Kimberly

last: Darlington

first: Alexandria

last: Shumway

first: Chandon

last: Sona

first: Matthew

last: Poy


title: Single-cell and spatial transcriptomics analysis of tobacco-associated lung adenocarcinoma development, and in response to targeting inflammation alone or in combination with immune checkpoint blockade in precancerous phase [scRNA-seq]

first: Humam

last: Kadara

first: Fuduan


title: Distinct Layer 6b transcriptomic subtypes parcellate the cortical mantle

city: Vancouver

first: Mark

middle: Steven

last: Cembrowski

state: BC

address: 2350 Health Sciences Mall

department: Cellular and Physiological Sciences

institute: University of British Columbia

summary: Here, we examined the transcriptomic heterogeneity of mouse Layer 6b (L6b) neurons using single-cell spatial transcriptomics.

overall_design: Examination of layer 6b neuron transcriptomes.

first: Margarita

last: Kapustina

first: Brianna

middle: N

last: Bristow


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

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


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

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


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

city: Wuhan

address: 115 Donghu Road

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


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


title: tRNA m1A modification is essential for gut homeostasis and function of group 3 innate lymphoid cells

city: Shanghai

middle: jing

last: yu

address: south Chongqing road 280

institute: Shanghai Jiaotong university school of medcine

summary: Group 3 innate lymphoid cells (ILC3s) play crucial roles in maintaining intestinal homeostasis and defending against bacterial infections. However, the epigenetic mechanisms that regulate ILC3 responses are not well understood. In this study, we show that Trmt61a, the methyltransferase responsible for the m1A58 tRNA modification, is predominantly expressed in ILC3s. We found that specific depletion of TRMT61A in ILC3s leads to dysregulated cell cycle and a reduction in cell numbers. Notably, mice with an ILC3-specific TRMT61A deficiency exhibit dysbiosis, but antibiotic treatment can restore colonic ILC3 levels. Furthermore, these mice exhibit increased susceptibility to experimental intestinal inflammation and enteric bacterial infection. Our findings uncover a previously unrecognized role for TRMT61A mediated m1A modification in the regulation of intestinal ILC3s, essential for protecting intestinal tissue during inflammation and enhancing innate immunity against enteric pathogens.

overall_design: To study the function of Trmt61a and tRNA m1A modification in ILC3 biology, we crossed Trmt61afl/fl mice with Rorccre mice to specifically delete Trmt61a expression in ILC3s. To explore the underlying molecular mechanism by which TRMT61A regulates ILC3 homeostasis, we isolated ILC3s from the intestines of Trmt61a△Rorc and Trmt61afl/fl mice and performed transcriptome sequencing.

first: Jingyu

last: Li

first: Zirun

last: Tang

first: Yunzhu

last: Chen


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

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


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

first: yujing

last: lin

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

institute: Southern University of Science and Technology

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

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

first: Jiahui

first: Yujing

last: Lin

first: Chengguo

last: Duan


title: Impaired CD103+ T cell accumulation facilitates oxidative damage induced lung adenocarcinoma

first: Yu

last: Xu

address: 320 Yueyang Road

institute: Shanghai Institue of Biochemistry and Cell Biology

summary: Immune microenvironment plays essential roles in tumor progression. The molecular mechanism underlying the regulation of immune surveillance in tumor initiation remains to be elucidated. Here we show that mice with T cell-specific deletion of the mediator subunit Med23 develops the alveolar epithelial type II cells (AT2 cells) originated lung adenocarcinoma, and such lung tumors displays an increased mutation frequency of oncogenes. Notably, the tumorigenesis of lung adenocarcinoma in Med23-deficient mice is promoted by the accumulation of AT2 cells under oxidative stress and oxidative DNA damage. Antioxidant treatment partially rescues spontaneous lung adenocarcinoma in Med23-deficient mice. Moreover, we find that loss of MED23 impairs the accumulation of lung CD103+ T cells, usually recognized as tissue resident T cells. CD103+ T cells have the ability to scavenge AT2 cells bearing oxidative DNA damage and prevent the tumorigenesis of lung adenocarcinoma. Mechanistically, CD103+ T cells predispose cells with high-level of oxidative stress to apoptosis. Collectively, our study finds MED23 is the key regulator of CD103+ T cell in lungs and reveals the immunosurveillance of CD103+ T cells in tumorigenesis.

overall_design:
To investigate the tumor type and charateristics of the spontaneous lung tumors in mice with Med23 deletion in T cells, lung tumors and adjacent normal tissues were analyzed using RNA-seq.
To investigate the phenotype of AT2 cells before tumorigenesis in mice with Med23 deletion in T cells, AT2 cells were isolated by Fluorescence-activated cell sorting (FACS) and analyzed using RNA-seq.

first: Haorui

last: Luo

first: Jiahao

last: Wang

first: Haifeng

last: Liu

first: Junwei

last: Ma

first: Hetian

last: Yuan

first: Jiao

last: Wu

first: Luonan

first: Zimu

last: Deng

first: Xiaolong


title: Screening and identification of transcriptomic expression profiles of mice with bone cancer pain

city: Beijing

first: Guangda

last: Zheng

address: No. 5, North Line Pavilion, Xicheng District

institute: Guang anmen Hospital

summary: To map the transcriptomic expression profiles of mice with bone cancer pain (BCP).

overall_design: C57BL/6 mice were processed by the LL/2-cell implantation in left femur to establish bone cancer pain. left spinal cord was collected for transcriptomic analysis. RNA-sequencing was processed using a high-throughput sequencing platform (illumine).

first: Yiting

first: Yupeng

first: Yaoyuan

first: Mingzhu

last: Yang

first: Qiuhu

first: Yanju

last: Bao


first: yu

last: yi

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

first: Li

first: Mengxin

first: Zhangyi

last: Yu


title: Molecular remodeling of myocardium in mice with melanocortin-4 receptor deletion before cardiac function impairment

city: Jining

first: Xiaomei

address: No. 133 Hehua Road，Taibai Lake New District

institute: Jining Medical University

summary: The melanocortin-4 receptor (MC4R) is highly expressed in the hypothalamus and mutations in this gene are closely associated with the development of hereditary obesity and early onset severe obesity in humans. It has been demonstrated that Mc4r is involved in the development of dilated cardiomyopathy. However, the current system of early diagnosis and treatment of heart disease is not well established. In this study, we analyzed the effects of Mc4r knockout on cardiac function and cardiomyocyte morphology, fibrosis, and apoptosis in mice. Meanwhile, we explored the possible early molecular mechanisms of Mc4r affecting cardiac dysfunction by transcriptome sequencing of cardiac cells combined with bioinformatics analysis. The results showed that although the overall heart does not show organic changes, our study suggests that cardiomyocytes already show abnormal changes at the early molecular level. The sequencing results showed that the differentially expressed genes between the two groups of mice were mainly enriched in the p53 signaling pathway and HIF-1 signaling pathway. We screened 10 key target genes using PPI network and Module analysis. Subsequently, drugs targeting key genes were screened and seven genes were identified as potential drug targets. This study will provide important reference and guidance for early prevention, treatment and drug targeting of heart-related diseases caused by Mc4r gene deletion.

overall_design: To investigate the role of Mc4r in the development of early cardiac disease, We constructed Mc4r knockout mice. Comparative gene expression profiling analysis of RNA seq data for heart tissues of 12 week old Mc4r knockout mice (MC4R_KO, n=3) and wild-type mice (WT, n=3)


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


title: Identification of Whole Blood Gene Expression Signature to Predict the Therapeutic Effect of Nintedanib in Idiopathic Pulmonary Fibrosis

city: TSUKUBA

first: Masashi

last: Matsuyama

state: IBARAKI

address: 1-1-1 AMAKUBO

department: respiratory medicine

country: Japan

institute: Tsukuba university

summary:
We aimed to determine gene expression signature associated with the therapeutic effect of nintedanib in patients with IPF using whole blood cells.
A total of 87 IPF patients treated with nintedanib were prospectively analysed in this study. RNA from whole blood cells was collected from all patients at enrollment (0M), 3 months (3M) after treatment with nintedanib, and/or at the onset of an acute exacerbation (AE).  We then performed gene expression profiling analysis using data obtained from RNA-seq.

overall_design: Participants were classified into 56 responders and 22 non-responders and 9 AE patients. Comparative gene expression profiling analysis between 0M and 3M was performed in 56 responders and 22 non-responders, respectively. Comparative gene expression profiling analysis between 0M and the onset of AE was performed in 9 AE patients. In addition, comparative gene expression profiling analysis between the onset of AE and 3M in 56 responders was also performed.

first: Naoki

last: Arai

first: Masayuki

last: Nakajima

first: Masafumi

last: Muratani

first: Nobuyuki

last: Hizawa


title: TDO2 promotes hepatocellular carcinoma by regulating tryptophan-kynurenine pathway

status: Public on Oct 10 2025

first: Y

last: Su

address: No. 1200, Huatuo Road, Shanghai University of Traditional Chinese Medicine

summary: Objective: This study aims to investigate the impact of differentially expressed tryptophan 2,3-dioxygenase (TDO2) on hepatocellular carcinoma (HCC) growth and its role in regulating ADCY5 and PRKAR2B expression in cells and tissues. Methods: Serum amino acid profiles in patients with HCC were analyzed via metabolomics. Lentiviral transfection was used to knock down and overexpress TDO2 in cells, with corresponding subcutaneous tumor models established in nude mice. A rat model of primary hepatocellular carcinoma was generated through intraperitoneal injection of N-nitrosodiethylamine (DEN). Cellular responses were assessed using CCK8, Annexin V-PE/7ADD double staining, and scratch assays. Transcriptome sequencing was performed to analyze genetic alterations in subcutaneous tumor tissues, while RT-qPCR and Western blotting were employed to quantify mRNA and protein levels. Results: TDO2 knockdown inhibited hepatocellular carcinoma cell proliferation and migration, while promoting apoptosis. Conversely, TDO2 overexpression enhanced cell proliferation and migration. Moreover, ADCY5 overexpression reverses the tumor-suppressive effects elicited by TDO2 knockdown. Transcriptome sequencing revealed an association between TDO2 and the downstream genes ADCY5 and PRKAR2B. In both cellular and animal models, mRNA levels of ADCY5 and PRKAR2B were positively correlated with TDO2 expression. Conclusion: TDO2 may facilitate HCC growth and metastasis by activating ADCY5 expression and its downstream target PRKAR2B.

overall_design: To investigate the impact of differentially expressed tryptophan 2,3-dioxygenase (TDO2) on hepatocellular carcinoma (HCC) growth and its role in regulating ADCY5 and PRKAR2B expression in cells and tissues，we made a rat model of primary hepatocellular carcinoma which was generated through intraperitoneal injection of N-nitrosodiethylamine (DEN).

first: Tao

first: Hongjiao

last: Xiang

first: Yanqun

last: Luo

first: Junmin

first: Caiyun

last: Zhang


title: Transcriptomic profiling of THP-1 and RPMI-8226 cells stimulated with innate immune agonists

first: Yuanhanyu

state: Beijing

address: No.7, Science Park Road, Zhongguancun Life Science Park, Beijing

institute: National Institute of Biological Sciences

summary: This study aimed to investigate the transcriptional responses of human THP-1 monocytes and RPMI-8226 multiple myeloma cells to various innate immune agonists. Cells were treated with ALPK1 agonist (ADP-Hep or UDSP-Hep), TLR7/8 agonist (R848), or STING agonist (ADU-S100) at different concentrations for 4 hours, and RNA-seq was performed to characterise the downstream gene expression programmes triggered by these stimuli.

overall_design: THP-1 and RPMI-8226 cells were cultured under standard conditions and exposed to different concentrations of the innate immune agonists ADP-Hep, UDSP-Hep, R848, or ADU-S100 for 4 hours. Total RNA was extracted from treated and untreated control samples, and RNA sequencing was performed using an Illumina platform. This design enables comparison of the gene expression profiles induced by different innate immune pathways across two human cell lines.

first: Xiaoying

last: Tian

first: Jiaqi

last: Liu

first: Feng

last: Shao


first: yu

overall_design: To determine the molecular basis by which knockdown Nr4a3 enhances iCM reprogramming, we conducted RNA-seq using shNr4a3-iCMs and shNT-iCMs collected at reprogramming day 7.

first: Li

last: Wang

first: Mengxin

first: Zhangyi


title: SPOCK1 activates Wnt/β-Catenin signaling to drive colorectal cancer stemness and progression

city: Fuzhou

first: Nathaniel

last: Weygant

state: Fujian

address: Qiuyang street

department: Academy of Integrative Medicine

institute: FJTCM

summary: Colorectal cancer (CRC) ranks second in cancer-related mortality worldwide, with clinical intractability and chemoresistance representing significant challenges driven by cancer stem cells (CSCs). Wnt/β-catenin signaling is a lynchpin of CSC self-renewal, but targetable upstream drivers remain elusive. Using bioinformatics we identified the proteoglycan SPOCK1 as a Wnt-associated CSC target. Critically, high SPOCK1 expression predicted poor patient prognosis and reduced progression-free survival following first-line chemotherapy. In vitro assays demonstrated that SPOCK1 levels modulated Wnt/β-catenin activity. SPOCK1 silencing inhibited β-catenin nuclear translocation and TCF/LEF-mediated transcription, which concurrently suppressed CRC proliferation and stemness. Conversely, SPOCK1 overexpression promoted β-catenin nuclear translocation and TCF/LEF-mediated transcription, which enhanced CRC proliferation and stemness. This SPOCK1-driven pro-tumorigenic effect was significantly reversed by the β-catenin/TCF/LEF inhibitor iCRT3, demonstrating SPOCK1’s dependence on Wnt transcriptional activation. The functional role was validated in vivo using a SPOCK1-overexpressing xenograft model and ex vivo using patient-derived organoids (PDOs), both confirming increased growth and β-catenin nuclear localization. Furthermore, data-independent acquisition (DIA) mass spectrometry of SPOCK1-overexpressing tumors revealed pro-tumorigenic signaling including c-Myc activity, oxidative phosphorylation, epithelial-mesenchymal transition. Notably, SPOCK1 drove remodeling of the tumor microenvironment, characterized by desmoplasia and fibrosis. Overall, our findings establish a SPOCK1/Wnt/β-catenin axis as a novel mechanism driving CRC tumorigenesis and stemness, positioning it as a promising therapeutic target to overcome Wnt-mediated progression and resistance.

overall_design: SW480 cells stably overexpressing SPOCK1-flag or vector control were submitted for RNA-Seq

first: Zhiyun

last: Cao

last: Yi


title: Challenge agent strain selection and characterization for a first-in-human Salmonella Typhimurium controlled human infection model

city: Liverpool

first: Lijuan

address: University of Liverpool

institute: University of Liverpool

summary: Nontyphoidal Salmonella (NTS) infections cause significant illness worldwide, particularly in sub-Saharan Africa, where invasive NTS (iNTS) disease leads to life-threatening bloodstream infections. Developing vaccines to prevent iNTS is a public health priority, but progress has been slow due to gaps in understanding how these bacteria cause disease and how the immune system responds. Controlled human infection models (CHIMs) can accelerate vaccine development by allowing detailed investigation of infection biology in a controlled setting.  This study describes the selection, production, and detailed characterisation of two Salmonella Typhimurium strains for the first-in-human iNTS CHIM. The strains – one associated with diarrhoeal disease and the other with bloodstream infections – were chosen based on their global relevance and comprehensive prior testing. We confirmed their stability, antibiotic susceptibility, and behaviour in conditions mimicking the human gut. Importantly, we found that sodium bicarbonate, used to neutralise stomach acid before infection, does not alter bacterial virulence.  These findings ensure that the selected strains accurately represent real-world infections while maintaining safety for use in human trials. This CHIM will be a valuable platform for testing new iNTS vaccines and improving our understanding of NTS infections.

sample_organism: Salmonella enterica subsp. enterica serovar Typhimurium

overall_design: RNA-seq profiling of Salmonella Typhimurium strain 4/74 and D23580 before and after 30 minute bicarbonate treatment.

first: Xiaojun

last: Zhu

first: Christopher

last: Smith


title: Transcriptomic analysis of ALPK1-dependent responses in BMDMs from WT and ALPK1 knockout C57BL/6 mice upon ADP-Hep stimulation

summary: The ALPK1 pathway is a cytosolic sensor for the bacterial metabolite ADP-heptose (ADP-Hep), triggering innate immune signalling. To investigate ALPK1-dependent transcriptional responses, bone marrow-derived macrophages (BMDMs) were generated from wild-type (WT) and Alpk1 knockout C57BL/6 mice using L929 cell-conditioned medium. On day 7 of differentiation, BMDMs were treated with either PBS (control) or ADP-Hep. RNA sequencing was performed to characterise gene expression changes, allowing assessment of ALPK1 pathway activation.

overall_design: Bone marrow cells were isolated from WT and Alpk1 knockout C57BL/6 mice and differentiated into BMDMs over 7 days in the presence of L929 cell-conditioned medium. Differentiated BMDMs were then treated with PBS (control) or ADP-heptose for 4 hours. Total RNA was extracted from each sample and sequenced to evaluate transcriptional changes. The design allows comparison between PBS and ADP-Hep-treated cells within each genotype, as well as assessment of ALPK1-specific transcriptional responses by comparing WT and Alpk1-/- BMDMs.

first: Ping

last: Zhou


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

last: yi

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

overall_design: Refer to individual Series


title: SALL1 is an orchestrator of uterine receptivity in part via titration of estrogen signaling [ChIP-seq]

city: St. Louis

first: Liang

last: Ma

state: MO

address: 660 S. Euclid Ave

department: Medicine, Obstetrics and Gynecology

institute: Washington University

summary: SALL1 is a critical regulator of embryonic development across a wide swath of tissues, including vital organs, but little is known about its function in adult tissues. Recent work from our group demonstrates that SALL1 is involved in urogenital development. This study delineates the role of SALL1 transcription factor in the adult reproductive system by demonstrating its requirement at multiple levels of uterine function during the implantation phase of early pregnancy. By generating a conditional knockout mouse model of Sall1 exclusively in female reproductive organs, it is demonstrated herein that SALL1 is independently required both in the uterine luminal epithelium for the attachment of competent blastocysts to the uterine wall, as well as in the uterine stroma for the process of decidualization, another prerequisite for pregnancy success. This robust, multi-tissue-layer requirement for SALL1 across multiple stages in the process of implantation makes it a newly identified regulator of early pregnancy. Herein it is shown that loss of SALL1 causes misexpression of estrogen receptor alpha (ESR1) during the window of implantation, and subsequent pathological deregulation of multiple estrogen response genes whose tight titrations are prerequisites of pregnancy. RNA sequencing of independent knockout uterine compartments at multiple timepoints, and ChIP sequencing to identify direct transcriptional targets, elucidated multiple powerful regulatory pathways downstream of SALL1. Importantly, the use of a selective estrogen receptor antagonist, fulvestrant, at a precise timepoint and dose, offers a partial rescue of embryo attachment to the uterine luminal epithelium, further demonstrating that SALL1 is upstream of ESR1 during implantation phase signaling.

overall_design:
Binding of SALL1 to chromatin was measured using ChIP in 3.5dpc CD1 mouse uterine luminal epithelia and stroma.
Please note that merged processed data files (generated from both rep1 and rep2 samples) are linked to the corresponding rep1 sample records.

first: Jeannine

last: Basta

first: Lynn

last: Robbins

first: Meade

last: Haller

first: Yan

last: Yin

first: Michael

last: Rauchman


title: Cilia Spin the Reissner fiber, an extracellular thread required for morphogenesis

city: Eugene

first: Samuel

last: Bertrand

state: OR

address: 1318 Franklin Blvd

department: IMB

institute: University of Oregon

summary: The Reissner fiber (RF) is an extracellular thread composed of the glycoprotein SCO-spondin (Sspo) that forms within cerebrospinal fluid (CSF) in the brain ventricles and central canal (CC) of vertebrates. Its assembly depends on motile cilia, yet how cilia and CSF flow transform secreted Sspo into a fiber that spans the length of the body axis has remained unknown. Using live imaging in zebrafish, we show that globular Sspo is remodeled into fibrils that anchor to the floor plate, elongate, and spin together into a tensioned, posteriorly translocating RF. Fiber assembly draws on a shared CSF pool of Sspo but requires local ciliary activity for globule-to-fibril remodeling. Once assembled, the RF is anchored by dynamic fibrils that stabilize the fiber and preserve its tension. Perturbations that locally disrupt ciliary motility and RF integrity along the CC result in region-specific defects in axial morphogenesis. These findings identify the RF as a flow-responsive extracellular system that converts ciliary beating into mechanical structure, linking fluid dynamics to the large-scale shaping of the vertebrate body.

overall_design: RNA-seq profiling of whole embryo cebra mutants and heterozygous siblings at 28 hpf.

first: Elizabeth

last: Bearce

first: Zoe

last: Irons

first: Adamend

last: Freda

first: Calvin

last: Chmelir

first: Sophie

last: Fisher

first: Samara

last: Williams

first: Daniel

last: Grimes


title: SALL1 is an orchestrator of uterine receptivity in part via titration of estrogen signaling [RNA-seq]

summary: SALL1 is a critical regulator of embryonic development across a wide swath of tissues, including vital organs, but little is known about its function in adult tissues. Recent work from our group demonstrates that SALL1 is involved in urogenital development. This study delineates the role of SALL1 transcription factor in the adult reproductive system by demonstrating its requirement at multiple levels of uterine function during the implantation phase of early pregnancy. By generating a conditional knockout mouse model of Sall1 exclusively in female reproductive organs, it is demonstrated herein that SALL1 is independently required both in the uterine luminal epithelium for the attachment of competent blastocysts to the uterine wall, as well as in the uterine stroma for the process of decidualization, another prerequisite for pregnancy success. This robust, multi-tissue-layer requirement for SALL1 across multiple stages in the process of implantation makes it a newly identified regulator of early pregnancy. Herein it isshown that loss of SALL1 causes misexpression of estrogen receptor alpha (ESR1) during the window of implantation, and subsequent pathological deregulation of multiple estrogen response genes whose tight titrations are prerequisites of pregnancy. RNA sequencing of independent knockout uterine compartments at multiple timepoints, and ChIP sequencing to identify direct transcriptional targets, elucidated multiple powerful regulatory pathways downstream of SALL1. Importantly, the use of a selective estrogen receptor antagonist, fulvestrant, at a precise timepoint and dose, offers a partial rescue of embryo attachment to the uterine luminal epithelium, further demonstrating that SALL1 is upstream of ESR1 during implantation phase signaling.

overall_design: RNA sequencing was performed on control and Sall1 cKO uteri for both isolated luminal epithelia and isolated stroma at both 3.5dpc and 4.5dpc.


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

city: Paris

first: Michèle

last: SABBAH

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

institute: INSERM U938

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

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

first: Lara

last: Closset

first: Jean-Philippe

last: Foy

first: Lila

last: Louadj

first: Elodie

last: Pramil

first: Elisabetta

last: Marangoni

first: Ivan

last: Bieche

last: Sabbah


title: Diabetes-associated MYT1 and ST18 regulate human b-cell insulin secretion and survival via other diabetes-risk genes

city: Nashville

first: guoqiang

last: Gu

state: Tennessee

address: 9415D Medical Research Building IV

department: Department of Cell and Developmental Biology

institute: Vanderbilt University Medical Center

summary: Genetic and environmental factors together cause islet beta-cell failure, leading to Type 2 diabetes (T2D). Here, we study how two members of the Myelin transcription factor family (MYT1, MYT1L, and ST18) prevent human beta-cell failure under obesity-related stress. We have reported that these factors are induced by high levels of obesity-related nutrients. They prevent beta-cell failure in mouse islets and human beta-cell lines. Their variants are all associated with human T2D, and their downregulation accompanies beta-cell dysfunction during T2D development. By knocking down MYT1 or ST18 separately in primary human donor islets, we show here that they have overlapping but distinct functions. Under normal culture conditions, MYT1-knockdown (KD) causes beta-cell death, while ST18-KD compromises glucose-stimulated insulin secretion. Under obesity-induced metabolic stress in vivo, ST18-KD also causes beta-cell death. These findings led us to explore the molecular mechanisms by which MUYT1/ST18 regulate beta cells. The data presented here are the RNAseq of human islet beta cells with knockdown of these factors.

overall_design: MYT1 or ST18 were knocked down in primary human beta cells using shRNA, made as pseudo-islets. Gene expression in resulting cells were examined with scRNA-seq uisng the In-Drop platform.

first: Ruiying

last: Hu

first: Nala

last: Hamilton

first: Yu

last: Wang

first: Qi

last: Liu

first: Lau

last: Ken

first: Xanwen

last: Xu

first: Alan J.

last: Simmons

first: Guoqiang


title: 3D Biomechanics and Epigenomics Reveal Atypical Fibroblast Responses in Cardiometabolic Disease

city: Little Rock

first: Se-Ran

last: Jun

address: 4301 W Markham St

institute: University of Arkansas for Medical Sciences

summary: Cell behavior is influenced by substrate stiffness and cell-cell and cell-environment interactions. The limitations of two-dimensional (2D) culture, such as its inability to fully capture the complexity of cell interactions and tissue structure, highlights the necessity of three-dimensional (3D) cell culture. This explicitly applies to ‘disease modeling in a dish’ platforms for translational studies. 3D bioprinting demonstrates significant potential in recapitulating the intricate physiological environments of human tissues in both healthy and pathological states. With the alarming rise in obesity, addressing systemic pathophysiological dysfunction beyond adipose tissue itself, such as the heart, is inevitable. To capture cellular and tissue-level responses to overnutrition, we employed state-of-the-art 3D bioprinting technology to understand the acute response of 3D matrix-embedded human cardiac fibroblasts (HCFs) to a ‘high-fat diet’ mimic. Chromatin accessibility profiling revealed that excess fatty acid (FA) exposure in 2D induces a non-canonical extracellular matrix (ECM) gene program that is minimally expressed in healthy adult myocardium. In contrast, 3D cultures exhibited reduced fibroblast proliferation and blunted transcriptional responses to the impact of biomechanical cues under metabolic stress, reflecting a more quiescent and physiologically relevant phenotype. Furthermore, we incorporated human induced pluripotent stem cell-derived cardiac fibroblasts (iPSC-CFs), which mirrored key transcriptional changes, including sex-dependent gene regulation. Notably, male iPSC-CFs showed stronger fibrotic gene induction than females, reinforcing the need to account for biological sex in disease modeling. Together, our results highlight the limitations of 2D systems and demonstrate that 3D-bioprinted platforms provide a scalable, physiologically relevant tool for investigating cardiometabolic diseases and therapeutic targets.

overall_design: ATAC-seq on nuclei isolated from 2D cultured human cardiac fibroblasts (HCFs) treated with fatty acid enriched or vehicle medium

first: Somaya

middle: Y

last: Ibrahim

first: Ryan

last: Holdiness

first: Ashira

last: Thadisena

first: Kristen

last: Boyle

first: Rushita

last: Bagchi