title: An ancient enhancer rapidly evolving in the human lineage promotes neural development and cognitive flexibility

city: La Jolla

first: Kun

last: Tan

state: CA

address: 9500 Gilman Drive # 0695

department: Dept. of Obstetrics, Gynecology & Reproductive Science

institute: UCSD

summary: An unsolved mystery in biology is how human-specific traits were acquired during evolution.  Here, we report that an evolutionary ancient non-coding element—human accelerated region 123 (HAR123)—has undergone rapid evolution specifically in the human lineage and confers human-specific functions.  HAR123 is a neural enhancer that promotes the generation of human neuroectoderm and neural progenitor cells by upregulating the transcriptional repressor HIC1.  The human and chimpanzee versions of HAR123 exhibit different properties, consistent with HAR123 being selected for new functions since the human-chimpanzee split.  To address the in vivo functions of HAR123, we generated HAR123-knockout mice, which exhibit a specific defect in “re-learning.”  Together, our study supports a model in which HAR123 has rapidly evolved in the human lineage to influence neural generation and, ultimately, cognitive flexibility.

overall_design: To examine the role of HAR123 in NPC generation, we performed single-cell RNA-sequencing (scRNAseq) analysis.  For these experiments, we also compared the function of hHAR123 with chimpanzee (c) HAR123 and mouse (m) HAR123 by replacing hHAR123 with cHAR123 or mHAR123, respectively, in human embryonic stem cells (ESCs).  We then differentiated these 3 genotypes of hESCs, along with HAR123-knock out (KO) hESCs, in parallel, using a standard NPC generation protocol.

first: Miles

last: Wilkinson


status: Public on Jul 15 2025

country: USA

overall_design: Given that HAR123 is a transcriptional enhancer, to identify HAR123-target genes, we performed Hi-C analysis on hESCs and neuroectodermal cells.

middle: F


type: Expression profiling by high throughput sequencing

overall_design: To define potential underlying mechanism by which HAR123 functions in cognitive flexibility, we identified HAR123-regulated genes in the frontal cortex, as this region has previously been shown to be involved in cognitive flexibility.


title: Insights into Intestinal Barrier Disruption During Long-Term Gut Chlamydia Colonization in Mice: A Single-Cell Transcriptomic Approach

status: Public on Jul 14 2025

city: Changsha

first: Qi

last: Tian

state: Hunan

address: No. 59, Xiangchun Road, Changsha City, Hunan Province

department: Department of Obstetrics & Gynecology

country: China

institute: Hunan Provincial Maternal and Child Health Care Hospital

summary: Chlamydia trachomatis, an intracellular pathogen, stands as the most prevalent sexually transmitted bacterial infection among women globally. Traditionally recognized as a genital pathogen, recent research indicates that the gastrointestinal tract may also act as a reservoir for its long-term colonization. However, the mechanisms underlying Chlamydia's ability to persist in the gut remain poorly understood. This gap in knowledge limits our ability to develop effective treatments for persistent Chlamydia infections. In this study we utilized single-cell RNA sequencing to analyze the gene expression profiles and cellular heterogeneity of mouse colonic tissues during Chlamydia long- term infection. This approach provided detailed insights into the transcriptional changes and cellular interactions involved in the persistence of Chlamydia in the gut. Our results revealed significant alterations in the gene expression profiles of various intestinal cell populations, with distinct molecular pathways contributing to Chlamydia persistence. Notably, we observed a reduction in the expression of markers associated with epithelial tight junctions, indicating a potential breakdown of the intestinal epithelial barrier. This impairment may facilitate the penetration of Chlamydia into deeper tissues and contribute to the initiation of infection. We also found dysregulation of the transcriptional networks in goblet cells and an imbalance in communication between immune and epithelial cells. These disruptions were linked to the pathogen's ability to establish persistent colonization and infection.

overall_design: 59197 cells from 3 Control samples, 3 De_Chlamydia-treated samples and 3 Chlamydia-treated mouse large intestine tissue samples were analyzed using scRNA-seq.

first: Tianyuan

last: Zhang

first: Ziqing

last: Wan


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

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Refer to individual Series


title: L-Arabinose alters the E. coli transcriptome to favor biofilm growth and enhances survival with fluoroquinolone stress

city: Oberlin

first: Lisa

last: Ryno

state: Ohio

address: 119 Woodland St

department: Chemistry and Biochemistry

institute: Oberlin College

summary: Environmental conditions, including nutrient composition and temperature, influence biofilm formation and antibiotic resistance in Escherichia coli. Understanding how specific metabolites modulate these processes is critical for improving antimicrobial strategies. Here, we investigated the growth and composition of Escherichia coli in both planktonic and biofilm states under the influence of L-arabinose, with and without exposure to the fluoroquinolone antibiotic levofloxacin, at two temperatures: 28 °C, optimal for biofilm development, and 37 °C, representative of human physiological conditions. L-arabinose increased the growth rate of planktonic E. coli but resulted in less total planktonic growth overall; L-arabinose addition also enhanced biofilm growth at 37 °C. L-arabinose reduced the efficacy of the fluoroquinolone levofloxacin and promoted growth in sub-minimum inhibitory concentrations of the antibiotic.  We conducted transcriptomic analyses at both temperatures to gain insight into the molecular basis of arabinose-mediated reduced susceptibility of E. coli to levofloxacin. We found that L-arabinose had a temperature- and state-dependent impact on the transcriptome. Using gene ontology overrepresentation analyses, we found that L-arabinose modulated the expression of many critical antibiotic resistance genes, including efflux pumps, transporters, and biofilm-related genes for external structures like pili and curli. This study demonstrates a previously uncharacterized role for L-arabinose in modulating antibiotic resistance and biofilm-associated gene expression in E. coli and provides a foundation for additional exploration of sugar-mediated antibiotic sensitivity in bacterial biofilms.

overall_design: PHL628 E. coli cells were grown in rich (LB) media supplemented with either L-arabinose at 0.5% (w/w) or no sugar (0%, LB samples).  Cells were grown at either 28 °C or 37 °C and three biological replicates of planktonic and biofilm samples of each experimental condition type were harvested (8 conditions, 24 samples total).

first: Ryno

last: Lisa M.

first: Austin

last: Katherine M.

first: Frizzell

last: Jenna K.

first: Neighmond

last: Audrey A.

first: Moppel

last: Isabella J.


title: CYP1B1-AS1 regulates CYP1B1 to promote Coxiella burnetii pathogenesis by inhibiting ROS and host cell death

city: COLLEGE STATION

first: Doyoung

last: Kwak

state: Texas

address: 302 Ball Street

institute: Texas A&M

summary: Coxiella burnetii (Cb), the causative agent of Q fever, replicates within host macrophages by modulating immune responses through poorly understood mechanisms. Long non-coding RNAs (lncRNAs) are crucial yet underexplored regulators of inflammation, particularly in Cb pathogenesis. Employing a comparative transcriptomic analysis of THP-1 macrophages infected with 16 different microbes, we dissected a core set of immune-responsive lncRNAs such as MAILR, LINC01215, PACER, and MROCKI-common to human anti-pathogen responses, and distinguished them from lncRNAs specifically altered at early (1 h) time points in individual infections. In particular, our approach unveiled lncRNA CYP1B1-AS1 as specifically upregulated in a spatiotemporal manner along with CYP1B1 in cis during Cb infection. Promoter assays confirmed their co-regulation via a shared bidirectional promoter, while aryl hydrocarbon receptor (AHR)-lucia luciferase and nuclear translocation assays demonstrated that Cb infection activates AHR, driving their transcription. Knockdown of CYP1B1-AS1 or CYP1B1 alone disrupted mitochondrial homeostasis, increased ROS and mitochondrial dysfunction, and exacerbated apoptosis during infection. These findings position the CYP1B1-AS1/CYP1B1 axis as a key regulator of mitochondrial homeostasis under AHR signaling, supporting an intracellular environment that benefits Cb replication. Our results highlight the critical roles of lncRNAs in immune regulation and provide a valuable resource for future lncRNA research.

overall_design: THP-1 monocytes were differentiated into macrophages using Phorbol 12-myristate 13-acetate (PMA, 100 ng/mL, 48 h) before infection with various bacterial strains. Infections were carried for 1 hour, after which cells were collected for RNA extraction. Bacterial Strains used,Pathogenic strains: Coxiella burnetii Nine Mile Phase II (NMII), Coxiella burnetii NMII dotA::Tn (T4SS mutant), Coxiella burnetii NMII dotB::Tn (T4SS mutant), Enterohemorrhagic Escherichia coli (O157, O157 Δstx), Francisella novicida U112, Pseudomonas aeruginosa PAO1, Staphylococcus aureus JE2, Salmonella enterica subsp. Typhimurium SL1344, Rhizobium radiobacter, Micrococcus luteus, Enterococcus faecalis, Brucella melitensis ΔvjbR. Non-pathogenic controls: Escherichia coli DH5α, Listeria innocua, Bacillus subtilis P31K6. Total RNA was extracted using TRIzol™ reagent (Invitrogen) following manufacturer protocols. RNA-seq libraries were generated using the TruSeq Stranded Total RNA-Seq Library Kit (Illumina), incorporating rRNA depletion. cDNA synthesis was performed using random primers, and paired-end libraries were constructed following the manufacturer’s instructions. Differentially expressed long non-coding RNAs (lncRNAs) and associated mRNAs were identified using DESeq2, comparing C.burnetii-infected samples to control and other microbial infections.

first: Aryashree

last: Arunima

first: James

middle: E

last: Samuel

first: Erin

last: vanSchaik

first: Paul

last: deFigueiredo

first: Xiaoning

last: Qian

first: Seyednami

last: Niyakan


title: Epigenetic liquid biopsies reveal elevated vascular endothelial cell turnover and erythropoiesis in asymptomatic COVID-19 patients

city: Jerusalem

first: Tommy

last: Kaplan

address: Givat Ram Campus

department: School of Computer Science and Engineering

country: Israel

institute: Hebrew University

type: Methylation profiling by high throughput sequencing

summary: Understanding the full spectrum of tissues affected by SARS-CoV-2 infection is crucial for deciphering the heterogenous clinical course of COVID-19. Here, we analyzed DNA methylation and histone modification patterns in circulating chromatin to assess cell type-specific turnover in severe and asymptomatic COVID-19 patients, in relation to clinical outcome. Patients with severe COVID-19 had a massive elevation of circulating cell-free DNA (cfDNA) levels, which originated in lung epithelial cells, cardiomyocytes, vascular endothelial cells and erythroblasts, suggesting increased cell death or turnover in these tissues. The immune response to infection was reflected by elevated B cell and monocyte/macrophage cfDNA levels, and by evidence of an interferon response in cells prior to cfDNA release. Strikingly, monocyte/macrophage cfDNA levels (but not monocyte counts), as well as lung epithelium cfDNA and vascular endothelial cfDNA, predicted clinical deterioration and duration of hospitalization. Asymptomatic patients had elevated levels of immune-derived cfDNA but did not show evidence of pulmonary or cardiac damage. Surprisingly, these patients showed elevated levels of vascular endothelial cell and erythroblast cfDNA, suggesting that sub-clinical endothelial and erythrocyte turnover are universal features of COVID-19, independent of disease severity. Epigenetic liquid biopsies provide non-invasive means of monitoring COVID-19 patients and reveal sub-clinical vascular damage and red blood cell turnover.

overall_design:
Plasma cell-free DNA samples were collected from COVID-19 patients (n=6) and healthy controls (n=6) and were whole-genome bisulfite sequenced (WGBS)

***************************************************************
Raw sequencing files were not uploaded due to privacy concerns
***************************************************************

first: Roni

last: Ben-Ami

first: Netanel

last: Loyfer

first: Eden

last: Cohen

first: Sheina

last: Piyanzin

first: Gavriel

last: Fialkoff

first: Israa

last: Sharkia

first: Naama

last: Bogot

first: Danit

last: Kochan

first: George

last: Kalak

first: Amir

last: Jarjoui

first: Chen

last: Chen-Shuali

first: Hava

last: Azulai

first: Hezi

last: Barhoum

first: Nissim

last: Arish

first: Moshe

middle: M

last: Greenberger

first: David

last: Vellema

first: Ramzi

last: Kurd

first: Eli

middle: B

last: Chetrit

first: Davina

last: Bohm

first: Talya

last: Wolak

first: Ahmad

last: Quteineh

first: Gordon

last: Cann

first: Benjamin

last: Glaser

first: Nir

last: Friedman

first: Ruth

last: Shemer

first: Ariel

last: Rokach

first: Yuval

last: Dor


title: Single-cell DNA methylome and 3D genome atlas of human subcutaneous adipose tissue [snRNA-Seq]

city: Los Angeles

first: Asha

last: Kar

address: 695 Charles E. Young Drive South

department: Human Genetics

institute: University of California Los Angeles

summary: We performed single-nucleus RNA-seq and single-nucleus methyl-3C seq on subcutaneous adipose tissue (SAT) biopsies from Finnish women who underwent abdominal SAT liposuction at Tilkka Hospital, Helsinki, Finland. The purpose of this study was to understand the epigenomic, 3D topology, and transcriptomic dynamics across the SAT cell-types.

overall_design:
We performed snRNA-seq on subcutaneous adipose tissue (SAT) biopsies from eight participants, and snm3C-seq3 on five of the eight SAT biopsies.
snm3C-seq3: An Arima Genomics Arima-HiC Kit was used for the in situ chromatin conformation capture (3C), the fluorescence-activated nuclei sorting (FANS) and library preparation were performed using the snm3C-seq3 workflow, and libraries were sequenced using the Illumina NovaSeq 6000 instrument with S4 flow cells generating 150 bp paired-end reads.
snRNA-seq: The single-nucleus sequencing libraries were either constructed using the Chromium Single Cell 3’ v3.1 chemistry and sequenced on an Illumina NovaSeq S4 with a target sequencing depth of 600 million read pairs (n=6), or constructed using the Single Cell Multiome ATAC + Gene Expression Reagent Kit and sequenced on an Illumina NovaSeq SP with a target sequencing depth of 400 million reads (n=5).

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

first: Zeyuan Johnson

last: Chen

first: Seung Hyuk

middle: T

last: Lee

first: Kevin

middle: D

last: Abuhanna

first: Marcus

last: Alvarez

first: Yi

last: Zhang

first: Sini

last: Heinonen

first: Hilkka

last: Peltoniemi

first: Kirsi

middle: H

last: Pietiläinen

first: Chongyuan

last: Luo

first: Paivi

last: Pajukanta


first: Kun

last: Tan

overall_design: To identify HAR123-regulated genes potentially important for NPC generation, we performed bulk RNA sequencing (RNAseq) analysis on HAR123-KO, hHAR123, cHAR123, and mHAR123 cells.  Since HAR123 is critical for promoting NPC generation derived from ESCs, we performed RNAseq analysis at both the ESC and neuroectoderm stages of these 4 genotypes.

first: Miles

last: Wilkinson


title: Spatial multi-omics defines a shared glioblastoma infiltrative signature at the resection margin [RNA-seq]

city: NEW YORK

first: Nadejda

last: Tsankova

state: NY

address: 1425 MADISON AVE ICAHN BUILDING FLOOR 9, 9-20B

department: Pathology

institute: Icahn School of Medicine at Mount Sinai

summary: Glioblastoma (GBM) remains an untreatable disease. Understanding of GBM’s infiltrative biology at the resection margin is limited, despite causing disease recurrence and progression. To address this, we generated a high-throughput single-nucleus (sn)RNA-seq and snATAC-seq multi-omic dataset from six tumors with distinct genomic drivers and combined it with spatial transcriptomics to characterize the unique molecular phenotype of GBM near the margin. By contrasting GBM-specific biology in matching “Core” vs. “Margin” dissections, we define unique, shared “GBM infiltration” and chromatin accessibility signatures near the margin. We prioritize EGFR as a top differentially expressed and accessible “Margin” marker across GBM subtypes, show its dynamic expression along a core-to-margin infiltration trajectory, and validate its role in migration through CRISPR/Cas9 deletion in two patient-derived models. ChIP-seq studies furthermore corroborate preferential TEAD1 binding at EGFR’s accessible regulatory elements. This validated multi-omic dataset enables further studies into tumor and microenvironment biology in the context of residual GBM disease.

overall_design: Surgical glioma tissue was collected from 6 patients with confirmed diagnosis of glioblastoma, WHO grade 4 (2016 and 2021 diagnostic criteria), representing diverse genetic backgrounds and all major mutational drivers. Tissue procurement was coordinated with neurosurgery to include contrast-enhancing tumor “Core” (C) and FLAIR-hyperintense infiltrative “Margin”  (M) representing the distal extent of gross supratotal resection and having a “normal brain” appearance on fresh tissue inspection. Experienced neuropathologist confirmed the presence of necrosis in “Core” and the presence of infiltrative brain parenchyma without necrosis in “Margin” tissues, during frozen section dissection. Sections were snap-frozen, stored at -80°C for snRNA-seq (n=6).

first: Pai

last: Balagopal

first: Ramos

last: Susana

first: Cheng

last: Wan Sze

first: Joshi

last: Tanvi

first: Price

last: Gabrielle

first: Tome-Garcia

last: Jessica

first: Nudelman

last: German

first: Shroff

last: Sanjana

first: Beaumont

last: Kristin

first: Yong

last: Raymund

first: Sebra

last: Robert

first: Zaslavsky

last: Elena

first: Tsankova

last: Nadejda Mincheva


title: Spatial multi-omics defines a shared glioblastoma infiltrative signature at the resection margin [10x Spatial]

overall_design: Surgical glioma tissue was collected from 2 patients with confirmed diagnosis of glioblastoma, WHO grade 4 (2021 diagnostic criteria), representing diverse genetic backgrounds and of each sex. Tissue procurement was coordinated with neurosurgery to include contrast-enhancing tumor “Core” (C) and FLAIR-hyperintense infiltrative “Margin”  (M) representing the distal extent of gross supratotal resection and having a “normal brain” appearance on fresh tissue inspection. Tissues were fixed in 10% formalin for spatial transcriptomics (n=2). Serial formalin-fixed and paraffin embedded (FFPE) sections from samples were kept for histological analysis.


title: Spatial multi-omics defines a shared glioblastoma infiltrative signature at the resection margin [snATAC-seq]

type: Genome binding/occupancy profiling by high throughput sequencing


title: Chromatin retained MUSHER lncRNA integrates ABA and DOG1 signalling pathways to enhance Arabidopsis seeds dormancy.

city: Warsaw

first: Michal

last: Krzyszton

address: Pawinskiego 5a

country: Poland

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

summary: Many plant lncRNAs regulate gene expression by binding to chromatin, but how they are retained at the target loci is unclear. We identify a new, chromatin-localized lncRNA - MUSHER, which activates two parallel regulatory pathways to increase Arabidopsis seed dormancy. MUSHER is upregulated in response to high temperatures, contributing to the induction of secondary dormancy. It promotes DOG1 expression by recruitment of the CPSF complex to enhance the proximal cleavage and polyadenylation at the DOG1 transcript. It also increases ABA sensitivity in seeds by activating PIR1 gene transcription. These genes, located on different chromosomes, are both bound by MUSHER, despite lacking sequence homology. The chromatin association of MUSHER enables the integration of the DOG1- and ABA pathways to adjust seed germination timing. Additionally, MUSHER and other lncRNAs interact with U1 snRNP, which is required for their chromatin localisation, revealing a novel function of U1 snRNP in plants.

overall_design:
3'RNA-seq: Comparison of Col-0 and msh-1 mutant siliques transcriptomes (13-20 days after pollination - four biological replicas).
ChIRP-seq: Chromatin Isolation by RNA Purification using MUSHER probes for Col-0 and msh-1 mutant siliques (13-20 days after pollination - two biological replicas). For Col-0 samples, lacZ probes were used as a negative control. Each sample used for purification with probes has a sequenced input sample.
ChIDP-seq: Chromatin Isolation by DNA Purification was employed to identify genomic regions physically interacting with the PIR1 locus using PIR1 probes and Col-0 siliques (13-20 days after pollination - two biological replicas). Samples used for purification with the PIR1 probe have a sequenced input samples.

first: Sebastian

middle: P

last: Sacharowski

first: Lien

last: Brzezniak

first: Szymon

last: Swiezewski


title: O-GlcNAc transferase senses influenza viral RNA and restricts viral infection by integrating innate immunity and lipid metabolism

city: Columbus

first: Weidong

last: Wu

address: 2255 Kenny Rd

institute: Ohio State University

summary: Viral infection induces robust reprogramming of metabolic pathways in host cells. However, whether host metabolic enzymes detect viral components remains unknown. Our group and others previously identified O-GlcNAc transferase (OGT), an important glucose metabolic enzyme, as a crucial mediator of the antiviral immune responses. Here, we discover an enzyme-independent function of OGT in restraining influenza A virus (IAV) infection in addition to its enzyme-dependent effect on MAVS-mediated antiviral immunity by studying a mouse model with an enzyme-inactive OGT. Biochemical studies reveal a critical antiviral effect based on OGT N-terminal tetracopeptide repeat-4-domain binding to IAV genomic RNA. This binding causes the translocation of nuclear OGT to cytosolic lipid droplets (LDs) to destabilize LDs-coating perilipin 2, thereby limiting LDs accumulation and in turn virus replication. In sum, our findings reveal OGT as a multifaceted metabolic sensor that integrates MAVS signaling and lipid metabolism to combat viral infection.

overall_design:
In this project we study the binding of OGT protein and influenza A virus (IAV) genomic RNA, the experiment design is below:
We transfected 293T cells with pFlag-OGT plasmid (Flag empty plasmid as control) and infected the cells with influenza virus (no infection as control, we labeled them with “Mock” groups), then harvested the cells for the immunoprecipitation (IP) assay (including input samples and IP samples), total are 8 samples as below:
1,FM_IP:Flag empty vector Mock IP sample; 2, GM_IP: Flag-OGT Mock IP sample; 3,F8_IP: Flag empty vector IAV (PR8 strain) IP sample; 4, G8_IP: Flag-OGT IAV (PR8 strain) IP sample; 5,FM_N: Flag empty vector Mock Input sample; 6, GM_N: Flag-OGT Mock Input sample; 7, F8_N: Flag empty vector IAV (PR8 strain) Input sample; 8,G8_N: Flag-OGT IAV (PR8 strain) Input sample. After IP assay, we extracted the total RNA using TRIzol from all samples for RNA-Seq.

first: Hong

last: Dong

first: Haitao

last: Wen

first: Anjun

last: Ma


title: Mapping the axolotl chromatin accessibility landscape by UUATAC-seq

city: Hangzhou

first: Guoji

last: Guo

state: Zhejiang

address: Yuhangtang street 866

department: Zhejiang University School of Medicine

institute: Center for Stem Cell and Regenerative Medicine

summary: The current understanding of regulatory sequences in the vertebrate genome is still incomplete. By introducing an adapter switching strategy, we developed an ultra-throughput ultra-sensitivity single-nucleus ATAC-seq (UUATAC-seq) protocol that enables construction of high-quality chromatin accessibility landscape from one species in a one-day experiment. By using UUATAC-seq, we mapped open chromatin regions for five representative vertebrate species at the landscape scale.

overall_design:
UUATAC-seq was performed across 15 tissues from one axolotl to profile over 130,000 nuclei. Axolotl tissues were obtained from the d/d Ambystoma mexicanum strain (1-year old).
Please note that the processed data file generated from all replicates is linked to the corresponding *_A sample records.

first: Xiaoping

last: Han

first: Hanyu

first: Xueyi

last: Wang

first: Daiyuan

last: Liu


title: Mapping the male mouse chromatin accessibility landscape by UUATAC-seq

overall_design: UUATAC-seq was performed across 23 tissues from one male mouse to profile over 290,000 nuclei. Mouse tissues were obtained from the C57BL/6J strain (8 weeks).


title: Novel environment exposure drives temporally defined and region-specific chromatin accessibility and gene expression programs in the hippocampus

status: Public on Jul 16 2025

city: Boston

first: Erin

middle: Elizabeth

last: Duffy

state: MA

address: 200 Longwood Ave, Goldenson 405

department: Neurobiology

institute: Harvard Medical School

summary: Curiosity-driven interactions with novel cues in our environment represent a common behavioral trait across the animal kingdom. Exposure to a novel environment (NE) reshapes the brain via structural and functional changes in multiple brain areas, including the hippocampus. This experience-dependent circuit reorganization is thought to be driven in part by changes in gene expression. While substantial progress has been made in generating atlases of cell-type-specific gene expression and chromatin state, these datasets largely reflect conditions in naïve animals, thereby missing transient gene expression programs induced by salient environmental stimuli. NE exposure, for example, has been shown to rapidly induce the expression of Fos and other immediate-early gene transcription factors (IEG TFs). However, the downstream IEG-driven genes (e.g. late response genes, LRGs) that serve to mediate NE-dependent circuit remodeling, as well as the genomic elements that drive the expression of these genes, remain largely unexplored. We employed a combination of single-nucleus multiomics and bulk RNA sequencing of the hippocampal DG, CA3, and CA1 regions to characterize the temporal evolution of cell-type-specific NE-driven gene expression and chromatin accessibility patterns downstream of IEG induction. We observe strong hippocampal regional specificity in excitatory neuron LRG programs, as well as diversity in the inhibitory neuron and non-neuronal transcriptional responses. LRGs were particularly enriched for secreted factors, where we observed cell type-specific expression of their receptors in our snRNA-seq data. These ligands and their cognate receptors represent promising candidates for future study to examine their region- and cell-type-specific effects on learning and memory. In addition, compared to a short exposure, prolonged exposure to NE caused more robust induction of late-response genes, suggesting that sustained environmental stimulation is more effective at triggering the long-lasting molecular changes that support memory formation. In addition, chromatin-level analyses revealed thousands of cell-type-specific changes in chromatin accessibility in response to NE exposure. Coordinated analysis of both chromatin accessibility and gene expression within individual cells revealed the Fos/AP-1 motif as a major predictor of neuronal cell-type-specific LRG expression, suggesting that AP-1 TFs play a regulatory role in NE-driven neuronal gene expression patterns. Together, these data provide a rich resource of hippocampal chromatin accessibility and gene expression profiles in response to novel experience, a physiological stimulus that affects learning and memory.

overall_design: Bulk RNA-seq and snRNA-seq+ATAC-seq (10X Multiome) from adult mouse hippocampus following novel environment exposure

first: Lisa

last: Traunmüller

first: Hanqing

first: Michael

last: Greenberg


title: Themis differentially regulates T follicular helper cell differentiation during early and late stages of chronic viral Infection

city: Xiamen City

first: GUO

last: FU

address: No. 4221, Xiang'an South Road, Xiang'an District, Xiamen, Fujian Province

institute: Xiamen University

summary: TFH cells play an important role in chronic viral infection by helping B cells produce antibodies. Recent studies have identified a novel CD4+ T cell progenitor population in chronic LCMV infection that sustains the differentiation of TFH and other effector CD4+ T cells. However, the details of this differentiation process remain unclear. Here, we report an unprecedented dual role for Themis in regulating the differentiation of CD4+ T cell progenitors into TFH cells during chronic LCMV infection. Themis expression is strongly upregulated in TFH cells at early stages of infection, and as expected, Themis promotes TFH cell differentiation at this stage. However, unexpectedly, at the late stages of chronic LCMV infection, Themis-deficient CD4+ T cells favored TFH cell differentiation and helped control the virus by enhancing GC responses and antibody production, suggesting that Themis inhibits TFH cell differentiation at this stage. In the late stage we found that Themis inhibits the differentiation of CD4+ T cell progenitors into TFH cells through transcriptional regulation.

overall_design: Primary murine tissues were collected from co-transfer p14 mice, with tissues isolated at different time points following infection with LCMV-clone 13. A total of 2 single-cell samples were prepared, consisting of CD4+ T cells from spleen tissues, with both wild-type (WT) and knockout (KO) groups, at 21 days post-infection (dpi). The isolated single-cell suspensions were processed using the DNBSEQ platform, which was run on the DNBelab C4 portable single-cell system (BGI). This system facilitates high-throughput cell capture and gene expression profiling.

first: yuzhen

last: Zhu

first: yuzhou

last: Bao


title: Mapping the zebrafish chromatin accessibility landscape by UUATAC-seq

overall_design: UUATAC-seq was performed across 11 tissues from 4 male and 4 female zebrafish to profile over 90,000 nuclei. Zebrafish tissues were obtained from wild-type D. rerio AB strain.


title: Expanded Neuronal Migration Supports Region-specific Distribution of Inhibitory Neurons in the Gyrencephalic Brain

city: San Francisco

first: Aunoy

last: Poddar

institute: UCSF

summary: Neurodevelopmental mechanisms have evolved to support the formation of more complex brain structures, such as the neocortex. While there are increasing examples of persistent migration of GABAergic inhibitory neurons (interneurons) in the neonatal brain, the breadth and impact of postnatal neuronal migration in the cortex remain unknown. Here, we demonstrate that neonatal gyrencephalic brains harbor an expanded subventricular zone, termed the Arc, defined by a tiered arrangement of neuroblasts and vascular enrichment at the ventricular wall. The Arc is a neonatal reservoir of diverse immature inhibitory subpopulations that supply higher cognitive cortical regions. Migration from the Arc is primarily related to the caudal ganglionic eminence and results in higher VIP+ neuron densities in the cingulate and temporal cortex of the piglet and human brains. Our findings indicate the Arc is a developmental structure present in phylogenetically divergent species and supports the expansion of postnatal neuronal migration, contributing to regional patterning of cortical interneurons in gyrencephalic brains. The recruitment of Arc-derived neuroblasts provides a mechanism to postnatally influence plasticity and has neuroprotective implications for late-migratory neurons given the presence of perinatal injuries, such as hypoxia-ischemia.

overall_design: To explore the molecular and cellular diversity of the Arc, we performed single-nucleus RNA sequencing (snRNA-seq) on the human Arc using sub-dissected ventricular tissue from 3 postmortem human brains between gestational week (GW) 30 to 39 (Fig.2a). We obtained the transcriptional profiles of 28,550 single nuclei (Extended Data Fig.4a-c)

first: JaeYeon

last: Kim

first: Kadellyn

last: Sandoval

first: Julia

last: Chu

first: Emma

last: Horton

first: Di

last: Cui

first: Keira

last: Nakamura

first: I-Ling

last: Lu

last: Mui

first: Theresa

last: Bartels

first: Christian

last: Wood

first: David

last: Rowitch

first: Hosung

first: Chet

middle: C

last: Sherwood

first: Boris

middle: W

last: Kramer

first: Angela

last: Roberts

first: Pablo

middle: J

last: Ross

first: Duan

last: Xu

first: Nicola

last: Robertson

first: Peng

last: Ji

first: Elizabeth

middle: A

last: Maga

first: Mercedes

last: Paredes


title: Diversity of molecular interactions between NK cells and acute leukemic cells: KIR2DL5 drastically limits NK cell responses against leukemic cells

city: NANTES

first: Enora

last: Ferron

address: 34 boulevard Jean Monnet

department: Research

country: France

institute: Etalissement Français du Sang

summary: NK cells naturally recognize and eliminate leukemic cells. However, the molecular interactions that govern these responses are diverse due to the large number of activating and inhibitory NK receptors that modulate NK functions and the diversity of corresponding ligands that are differentially expressed in acute lymphoblastic and myeloid leukemias. We identified resting NKG2A+ NK cells and NKG2A+KIR+ NK cell subsets that are most effective in eliminating lymphoid and myeloid leukemic cells respectively. The NKG2A+KIR+/-CD57- subsets show high expression of activating receptors and a functional transcriptomic profile, but differ in KIR2DL5 expression. The frequency of KIR2DL5+ NK cells increases with the number of expressed KIR. Furthermore, KIR2DL5 is preferentially co-expressed with KIR2DL1 and is negatively regulated by NKG2A. Of note, CD57 expression, regardless of the subset considered, is associated with reduced receptor expression, consistent with its reduced cytotoxic potential. Furthermore, we have shown that molecular interactions between NK cells and leukemic cells influence NK cell responses, particularly the inhibitory KIR2DL5-PVR axis. The integration of these data is of importance for the optimization of NK cell-based immunotherapies, as the selection of NK cell donors represents a key parameter for the improvement of these therapies.

overall_design: In this study, we aim to identify NK subsets with the highest efficacy against acute leukemia by considering the NK cell phenotype in the context of KIR and HLA genotypes, age, sex, and CMV status. To complement the phenotypic study, we analyzed the transcriptional profiles of the three cell subsets NKneg, NKALL and NKAML. RNA-seq was then applied to the different samples in order to establish the transcriptomic signature associated with these different NK cell subsets.

first: Martin

last: Braud

first: Cynthia

last: Fourgeux

first: Jeremie

last: Poschmann

first: Christelle

last: Retière


title: Mapping the gecko chromatin accessibility landscape by UUATAC-seq

first: Guoji

last: Guo

overall_design: UUATAC-seq was performed across 19 tissues from one female leopard gecko (Eublepharis macularius) to profile over 150,000 nuclei.

first: Xiaoping

last: Han

first: Hanyu

last: Wu

first: Xueyi

last: Wang

first: Daiyuan

last: Liu


title: Conserved and Unique Features of Terminal Telomeric Sequences in ALT-Positive Cancer Cells

status: Public on Jul 13 2025

city: BETHESDA

first: Benura

last: Azeroglu

state: Maryland

address: National Cancer Institute, NIH, Building 37, Room 1108 37 Convent Drive

institute: NIH

summary: A significant portion of human cancers utilize a recombination-based pathway, Alternative Lengthening of Telomeres (ALT), to maintain telomere length. Targeting the ALT is of growing interest as a cancer therapy, yet a substantial knowledge gap remains regarding the basic features of telomeres in ALT-positive cells. To address this, we adopted END-seq, an unbiased sequencing-based approach, to define the identity and regulation of the terminal sequences of chromosomes in ALT cells. Our data reveal that the terminal portions of chromosomes in ALT cells contain canonical telomeric sequences with the same 5’ terminus bias (-ATC) observed in non-ALT cells. Furthermore, as reported for non-ALT cells, POT1 is required to preserve the precise regulation of the 5’ end in cells that maintain telomere length using the ALT pathway. Thus, the regulation of the terminal 5’ of chromosomes occurs independently of the mechanism of telomere elongation. Additionally, we employed an S1 endonuclease-based sequencing method to determine the presence and origin of single-stranded regions within ALT telomeres. These data shed light on conserved and unique features of ALT telomeres.

sample_organism:
Homo sapiens
Canis lupus familiaris
Mus musculus

overall_design: We used END-seq and S1-END-seq to investigate features of telomeres in human, mouse and dog cell lines

first: Wei

first: Raphael

last: Pavani

first: Ranjodh

last: Sandhu

first: Tadahiko

last: Matsumoto

first: Andre

last: Nussenzweig

first: Eros

last: Lazzerini Denchi


title: Mapping the chromatin accessibility landscape by UUATAC-seq

sample_organism:
Danio rerio
Ambystoma mexicanum
Gallus gallus
Mus musculus
Eublepharis macularius

overall_design: Refer to individual Series


title: Mapping the chicken chromatin accessibility landscape by UUATAC-seq

overall_design: UUATAC-seq was performed across 18 tissues from one female chicken to profile over 200,000 nuclei.


title: Mapping the female mouse chromatin accessibility landscape by UUATAC-seq

overall_design: UUATAC-seq was performed across 23 tissues from one female mouse to profile over 180,000 nuclei. Mouse tissues were obtained from the C57BL/6J strain (8 weeks).


title: Transcriptome-proteome profiling in Burkholderia thailandensis  during the transition from exponential to stationary phase

city: Baton Rouge

first: Anne

last: Grove

state: LA

address: 103 Life Sciences Building

department: Biological Sciences

institute: Louisiana State University

summary: Burkholderia thailandensis is closely related to highly pathogenic Burkholderia species, and it is an excellent surrogate as it rarely causes disease in humans. Understanding the complex molecular mechanisms that characterize the transition of B. thailandensis from exponential to stationary phases is critical to understanding bacterial responses to stress or nutrient limitation. We present here an integrated transcriptomic and proteomic analysis to profile gene and protein expression changes during entry into stationary phase. We identified 928 differentially expressed genes (DEGs) and 832 differentially expressed proteins (DEPs), highlighting significant transcriptional and translational reprogramming. Genes encoding proteins involved in benzoate degradation and O-antigen nucleotide sugar biosynthesis were among the most highly upregulated in stationary phase, whereas processes such as nitrogen metabolism, translation, and flagellar biosynthesis were downregulated. At the proteome level, proteins related to fatty acid degradation and butanoate metabolism accumulated along with proteins involved in synthesis of secondary metabolites. Markedly downregulated proteins included ribosomal proteins and translation factors as well as the house-keeping iron-sulfur biogenesis proteins. A protein-protein interaction (PPI) network analysis identified clusters involved in processes such as fatty acid metabolism and amino acid degradation. Surprisingly, the RpoS sigma factor, which has been shown to accumulate in stationary phase in several bacterial species, was not significantly increased in B. thailandensis during stationary phase. These findings offer comprehensive insights into B. thailandensis adaptive strategies and provide a foundation for developing interventions against pathogenic Burkholderia species.

overall_design: Three biological replicates were analyzed for each of 2 conditions (three exponential  phase; three stationary phase)

first: Ahmed

last: Al-Tohamy


title: Transcriptome analyses of bEV treated HEK293T cells

status: Public on Jul 12 2025

city: Pyeongchag

first: seoah

last: Park

address: 1447-1, Pyeongchang-daero, Daehwa-myeon, Pyeongchang-gun, Gangwon-do, Republic of Korea

country: South Korea

institute: Seoul National University

summary:
To get insight of molecular effects of bEV on HEK293T cells, we investigated transcriptomic response in bEV treated HEK293T cells
We identified differentially expressed genes (DEGs) fold change cutoff = 1.5 in the bEV treated HEK293T cells
These findings suggest that bEV would be putative ingredients by modulating signaling pathways in human cells

overall_design: HEK293T cell line was treated with bEV

first: Joonghoon

first: Seoah


title: Ethanolamine phosphate phospholyase knockout mice have reduced weight gain and altered lipid metabolism when fed a high-fat diet

status: Public on Jul 11 2025

city: Edmonton

first: René

last: Jacobs

state: Alberta

address: Room 4002E, Li Ka Shing Building, 11300 87 Ave NW

department: Department of Agricultural, Food and Nutritional Science

country: Canada

institute: University of Alberta

summary: Ethanolamine phosphate phospholyase (ETNPPL) is an enzyme that irreversibly degrades phospho-ethanolamine (p-ETN), an intermediate in the Kennedy pathway of phosphatidylethanolamine (PE) synthesis. Whole-body knockout Etnppl mice were fed a high-fat diet (HFD) containing 45% kcal fat for 10 weeks. Etnppl-/- female mice were resistant to HFD-induced obesity and adiposity and had decreased liver weight compared with Etnppl+/+ mice. Furthermore, Etnppl-/- female mice had improved glucose sensitivity and increased energy expenditure compared to Etnppl+/+ mice. Plasma triglycerides (TG) levels were elevated in Etnppl-/- female mice, although the rate of very low-density lipoprotein (VLDL) secretion was not increased. The hepatic expression of PCSK9 was elevated, indicating a possible decrease in VLDL uptake. Interestingly, both plasma and hepatic cholesterol levels were reduced in Etnppl-/- female mice relative to Etnppl+/+ mice. No difference in hepatic phosphatidylcholine, PE or TG was detected between groups. Histopathological examination of hepatic tissues revealed decreased lipid deposition in Etnppl-/- mice that may be explained by the lower hepatic cholesterol level. Additionally, RNA sequencing analysis showed upregulation in genes related to cholesterol metabolism in Etnppl-/- female mice. In male mice, a slight decrease in weight gain was observed in Etnppl-/- mice compared to Etnppl+/+ mice. No change in plasma and hepatic lipid levels was detected in Etnppl-/- male mice. To conclude, ETNPPL impacts whole-body energy expenditure, weight gain, cholesterol metabolism, and hepatic lipoprotein metabolism without altering hepatic phospholipid levels.

overall_design: Full body Etnppl knockout (KO) and wild type (WT) female mice were fed a standard chow diet for 8 weeks, then fed a HFD containing 45% kcal fat for 10 weeks.Livers were harvested, total RNA extracted, and poly-A selected mRNA was processed for paired-end sequencing.

first: Kholoud

last: Elmihi

first: Kelly-Ann

last: Leonard

first: Randy

last: Nelson

first: Aducio

last: Thiesen

first: Robin

last: Clugston

middle: L


title: Temporal multiomics gene expression data across human embryonic stem cell derived cardiomyocyte differentiation [Ribo-seq]

city: New York

first: Marko

last: Jovanovic

address: 1212 Amsterdam Avenue

institute: Columbia University

summary: Embryonic development has not been fully understood, despite significant advances in molecular and systems-level approaches. Human embryonic stem cells (hESCs) serve as a valuable in vitro model for studying early human developmental processes due to their ability to differentiate into all three germ layers. Here, we present a comprehensive multi-omics dataset generated by differentiating hESCs into cardiomyocytes via the mesodermal lineage, collecting samples at 10 distinct time points. We measured mRNA levels by mRNA sequencing (mRNA-seq), translation levels by ribosome profiling (Ribo-seq), and protein levels by quantitative mass spectrometry. Technical validation confirmed high quality and reproducibility across all datasets, with strong correlations between replicates. This extensive dataset provides critical insights into the complex regulatory mechanisms of cardiomyocyte differentiation and serves as a valuable resource for the research community, aiding in the exploration of mammalian development and gene regulation.

overall_design: To gain a deeper understanding of the gene regulatory mechanisms that drive embryonic development, we conducted simultaneous genome-wide measurements of mRNA, translation, and protein levels during hESC differentiation. This involved differentiating hESCs into the three distinct germ layers—endoderm, mesoderm, and ectoderm—and subsequently further differentiating them into polyhormonal cells, cardiomyocytes, and motor neurons, respectively. In this study, we specifically focus on the differentiation process from hESCs to cardiomyocytes via the mesodermal lineage. We collected samples at 10 distinct time points during cardiomyocyte differentiation, which allows us to track the differentiation of cells over time, providing valuable insights into the temporal regulation of gene expression. We measured mRNA levels by mRNA sequencing (mRNA-seq), translation levels by ribosome profiling (Ribo-seq), and protein levels by quantitative mass spectrometry on the matched samples. The differentiation and subsequent measurements were conducted in duplicates.

first: Abdurrahman

last: Keskin

first: Hani

last: Shayya

first: Dario

last: Sirabella

first: Achchhe

last: Patel

first: Barbara

last: Corneo


title: Temporal multiomics gene expression data across human embryonic stem cell derived cardiomyocyte differentiation [RNA-seq]


title: Thor: a platform for cell-level investigation of spatial transcriptomics and histology [Heart Failure]

city: Houston

first: Tu N

last: Tran

address: 6670 Bertner Ave,

department: Cardiovascular

institute: Houston Methodist Research Institute

summary: Spatial transcriptomics links gene expression with tissue morphology, however, current tools often prioritize genomic analysis, lacking integrated image interpretation. To address this, we present Thor, a comprehensive platform for cell-level analysis of spatial transcriptomics and histological images. Thor employs an anti-shrinking Markov diffusion method to infer single-cell spatial transcriptome from spot-level data, effectively combining gene expression and cell morphology. The platform includes 10 modular tools for genomic and image-based analysis, and is paired with Mjolnir, a web-based interface for interactive exploration of gigapixel images. Thor is validated on simulated data and multiple spatial platforms (ISH, MERFISH, Xenium, Stereo-seq). Thor identifies regenerative signatures in heart failure, unbiasedly screens breast cancer hallmarks, resolves fine layers in mouse olfactory bulb, and annotates fibrotic heart tissue. In high-resolution Visium HD data, it enhances spatial gene patterns aligned with histology. By bridging transcriptomic and histological analysis, Thor enables holistic tissue interpretation in spatial biology.

overall_design:
Sample collection and preparation Tissues were collected from patients wearing LVAD before a heart transplant. All samples were obtained under an approved IRB protocol (Pro00006097:1 Congestive Heart Failure) at Houston Methodist Hospital. FFPE heart failure tissue samples were collected using standard-of-care procedures. Tissue sections (10 μm) obtained from the FFPE tissues were mounted on Visium spatial gene expression slides (10x Genomics, 1000520). The samples were processed as described in the manufacturer’s protocols.  ST by 10x Genomics Visium The tissue slides were permeabilized at 37 °C for 6 min, and polyadenylated mRNA was captured by oligonucleotides bound to the slides. Reverse transcription, second-strand synthesis, complementary DNA (cDNA) amplification and library preparation proceeded using the Visium Spatial Gene Expression Slide & Reagent Kit (10x Genomics, 1000520) according to the manufacturer’s protocol. After evaluation by real-time PCR, cDNA amplification included 13-14 cycles. Indexed libraries were pooled equimolarly and sequenced on a NovaSeq X Plus instrument in a PE28/150 run (Illumina). An average of 26, 011 paired reads were generated per spot and the median genes per spot were 2,277. Tissues were stained with H&E, and slides were scanned on a Pannoramic MIDI scanner (3DHISTECH) using a ×20, 0.8-NA objective.

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patient privacy, this data does not have fastq file
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first: Pengzhi

last: Zhang

first: Weiqing

last: Chen

first: Guangyu

last: Wang

first: Lai

last: Li


title: Eradicating Drug Tolerant Persister Cells in EGFR-Mutated Non-Small Cell Lung Cancer by Targeting TROP2 with CAR-T cellular therapy

status: Public on Jul 10 2025

first: Zhaorong

address: 60 Fenwood Road

institute: Dana Farber Cancer Institute

summary: EGFR tyrosine kinase inhibitors (TKIs) have dramatically improved outcomes for EGFR-mutated non-small cell lung cancer (NSCLC) patients, but relapse frequently occurs due to drug tolerant persister (DTP) cells that can evolve and develop diverse mechanisms of drug resistance. In samples from patients with EGFR-mutated NSCLC treated with an EGFR-TKIs in the neoadjuvant setting, we observed uniformly elevated expression of the cell surface protein TROP2, a target of clinically active antibody drug conjugates (ADCs). We further confirmed that TROP2 expression is enriched in DTPs following osimertinib treatment of EGFR-mutated NSCLC cell lines and xenograft models. At the time of osimertinib-induced minimal residual disease, treatment with TROP2 ADC sacituzumab govitecan had only a modest impact on delaying tumor recurrence in vivo. In contrast, a single treatment of TROP2 directed CAR-T treatment significantly prolonged relapse-free survival with evidence of cure, highlighting the ability of CAR-T therapy to eliminate DTPs in vivo.

overall_design: scRNA-Seq samples of residual tumor tissues and lymph nodes from patients after treatment

first: Simon

last: Baldacci

first: Elliott

last: Brea

first: Francesco

last: Facchinetti

first: Soumya

last: Malhotra

first: Matthew

last: Booker

first: David

last: Barbie

first: Pasi

last: Jänne


title: Immune Composition of the Mononuclear Cell Fraction of Human Umbilical Cord Blood

city: Stanford

first: Esmond

last: Lee

address: 450 Jane Stanford Way

institute: Stanford University

summary: Despite its therapeutic potential and unique immunological properties, the immune composition of umbilical cord blood lacks consistent and comprehensive characterizations. Human umbilical cord blood (UCB) is often discarded after delivery and is difficult to obtain for research purposes. Furthermore, most research on UCB is focused on properties of CD34+ hematopoietic stem cells for transplantation. The Binns Program for Cord Blood Research at Stanford University has the unique advantage of regular collection and isolation of mononuclear cells (MNC) from UCB donors. This study provides a robust characterization of the immune subset compositions of the CD34-negative MNC fraction of UCB (n=50). The study also compares the UCB data to adult peripheral blood (PB) mononuclear cells to identify differences in immune maturity. Using flow cytometry and single-cell RNA sequencing (scRNA-seq), we analyzed UCB and adult PB MNC samples to characterize the cell surface protein and transcriptomic profiles of different immune subsets. Our study findings bring a higher-definition understanding of the unique immunological properties of umbilical cord blood. Study findings reveal a distinct immune profile in UCB, such as a higher average percentage of CD19 B Lymphocytes, CD4 T Cells, CD4 Naive T Cells, CD4 Recent Thymic Emigrants, CD8 Naive T Cells, CD8 Recent Thymic Emigrants, and CD19 Naive B Cells compared to adult PB. Additionally, there were fewer CD19 Memory B Cells in UCB compared to PB. The scRNA-Seq showed concordance in the proportion of immune cell types but captured more differentiated subtypes of cells. Additionally, scRNA-Seq showed unique clustering patterns in UCB, which reflect cell types that converge in adulthood as the immune system matures. These analyses yield the intriguing possibility that the immune heterogeneity of individuals at birth gives way to more stereotyped immune subsets as the immune system is exposed to the external environment and undergoes maturation. Overall, our findings provide a robust characterization of MNC UCB immune subsets and insights into how immune function develops from birth to adulthood.

overall_design: Mononuclear cells (MNCs) in 2 umbilical cord blood (UCB) and 3 adult peripheral blood (PB) samples were analyzed by single-cell RNA sequencing (scRNA-seq).

first: Karen

last: Kikuta

first: Talia

last: Menezes

first: Hannah

last: Fung

first: Alvaro

last: Amorin

first: Aditi

last: Agrawal

first: Theodore

last: Roth

last: Porteus


title: RNA sequencing data from Atlantic silverside (Menidia menidia) exposed to combined hypoxia and acidification

city: Woods Hole

first: Christopher

last: Murray

state: Massachusetts

address: 266 Woods Hole Rd

department: Biology

institute: Woods Hole Oceanographic Institution

summary: Silverside adults and their offspring (embryos and early larvae) were exposed to control conditions or a combined hypoxia and acidification treatment (~35% dissolved oxygen, ~2500 µatm pCO2; hereafter HypOA). They were collected at 10 days post-hatch and sampled for RNA sequencing.

overall_design: Spawning adults were acclimated to contorl or HypOA conditions during final stages of gonad maturation. Their offspring were reared under both treatments in a fully factorial design to form four experimental groups. The offspring were reared from fertilization to 19 days post-fertilization (~10 days post hatch). Each group had 6 biological replicates; 24 larvae total larvae were sequenced.

first: Neelakanteswar

last: Aluru


title: Single nuclei multiomics analysis of cardiogenic transcription factors in a new murine model of cardiac development.

city: Iowa City

first: Brad

last: Amendt

state: IA

address: 51 Newton Road

department: Anatomy and Cell Biology

institute: University of Iowa

summary: Transcription factors such as Tbx5, Gata4, Mef2c and Pitx2 are required during cardiac development, and in adult cardiac homeostasis. We demonstrate that the gene dosage and modulation of these factors are mediated in vivo by the miR-200 family. These microRNAs (miRs) are expressed during early stages of heart development, and they regulate a highly complex gene regulatory network (GRN). To study the in vivo and in vitro function of specific miR-200 family members we inhibited individual members of the miR-200 family during embryonic development. Inhibition of a single miR-200 family member within the cluster caused defects in the left ventricle and cardiomyocyte maturation during development. Inhibition of the entire miR-200 family resulted in a ventral septal defect and embryonic lethality by embryonic day (E)16.5. In cardiomyocytes, the miR-200 family targets the transcripts of Tbx5, Gata4, Mef2c and Pitx2. Inhibition of this family increased expression of Tbx5, Gata4, Mef2c and Pitx2 in both the left ventricle and atria across multiple stages of cardiac development. Embryos with reduced levels of a single miR-200 family member were non-lethal and pups survived into adulthood. At postnatal day (P) 1 these pups had a reduced heart rate and increased ventricular wall thickness. Each miR-200 family has distinct heart phenotypes in cell specific differentiation and maturation. snRNA-sequencing revealed a new cardiomyocyte cell state, suggesting these cells were less differentiated due to inhibition of the miR-200 family. We have identified several new transcription factors regulated by miR-200 during heart development. The miR-200 family are critical regulators of early cardiac development through maintaining gene dosage of Tbx5, Gata4, Mef2c and Pitx2, which affects cardiomyocyte differentiation and maturation. The multiomics analyses of early heart development after miR-200 inhibition reveals a new cardiomyocyte less differentiated cell state and chromatin modifications due to the function of the miR-200 family.

overall_design: To evalute the effect of inhibitng the miR-200 family on cardiac development.

first: Riley

last: Leonard

first: Mason

last: Sweat

first: Xiao

last: Li

first: Yi

last: Xiao


title: B3GALT6 mutations trigger sequential molecular events leading to compromised connective tissue biomechanics in Ehlers-Danlos syndrome

city: Vandoeuvre-lès-Nancy

first: Sebastien

last: Hergalant

address: Faculté de Médecine. 9 avenue de la forêt de Haye

department: Bioinformatics

institute: INSERM

summary: Ehlers-Danlos syndromes (EDS) comprise a genetically and clinically heterogenous group of rare diseases that cause severe, often fatal, damage to connective tissue. The molecular basis of EDS implicates defects in extracellular matrix components, including various fibrillar collagens and glycosaminoglycans (GAGs). However, the precise pathogenic mechanisms behind EDS remain elusive. Here, we have implemented a multi-tiered approach to demonstrate the functional impact of B3GALT6 mutations on biochemical and developmental processes, ultimately leading to the spondylodysplastic subtype of EDS (spEDS), characterized by severe musculoskeletal symptoms. We show that the loss of function of β1,3-galactosyltransferase 6 (β3GalT6) is partially compensated by β1,3-glucuronosyltransferase 3 (GlcAT-I), the next enzyme in the GAG biosynthetic pathway. In addition, results from transcriptomics, collagen analysis and biophysical experiments revealed that impaired collagen maturation, including defective glycosylation of collagen XII, contributes to altered tissue structure and biomechanics, the hallmarks of spEDS. Our findings unravel a new pathogenic mechanism of spEDS, and bring us one step closer to therapeutic strategies, including cell and tissue engineering.

overall_design: Gene expression profiling of cultured dermal fibroblasts isolated from spondylodysplastic Ehlers-Danlos syndrome patients (B3GALT6 mutations - 3 homozygous and 3 compound heterogygous samples) versus six control individuals (CTRL).

first: Sébastien

first: Catherine

last: Bui

first: Sylvie

last: Fournel-Gigleux


title: TCR repertoire analysis of donor-derived and iTEC-supported thymocytes

city: Kyoto

first: Yann

last: Pretemer

address: 53 Kawahara-cho, Shogoin, Sakyo-ku

country: Japan

institute: Center for iPS Cell Research and Application, Kyoto University

summary: We analyzed the TCRb repertoires of CD4 and CD8 single-positive thymocytes isolated from a pediatric donor, as well as CD4 and CD8 single-positive thymocytes matured in vitro from the double-positive stage in 3D organoid co-culture with iPSC-derived thymic epithelial cells (iTECs). Our analysis shows that iTECs are capable of positively selecting thymocytes with diverse TCR repertoires in vitro.

overall_design: CD4/CD8 double-positive thymocytes were isolated from a pediatric donor and co-cultured with iTECs in 3D organoid culture for two weeks. The resulting CD4 and CD8 single-positive thymocytes were subjected to TCRb repertoire analysis using RNA-seq. CD4 and CD8 single-positive thymocytes isolated from the same donor were used as controls.

first: Yoko

last: Hamazaki


title: Response gene to complement 32 promotes tumorigenesis by mediating DNA damage repair and inhibits CD8+ T cells infiltration in diffuse large B-cell lymphoma

status: Public on Jul 09 2025

city: Jinan

first: xiyuan

last: zhang

state: Shandong

address: No.324, Jingwu Road

institute: Shandong Provincial Hospital, Shandong University

summary: Background: Response gene to complement 32 (RGC32), a complement activation-inducible factor broadly expressed in normal human tissues, has been implicated in tumorigenesis through its dysregulated expression in various malignancies and its involvement in critical oncogenic processes. Despite its established roles in cancer biology, RGC32 remains uncharacterized in diffuse large B-cell lymphoma (DLBCL). This study provides the first comprehensive investigation of RGC32 expression patterns and functional contributions to DLBCL pathogenesis, elucidating its potential as a novel therapeutic target or prognostic biomarker in this disease.  Methods: Immunohistochemical (IHC) staining of RGC32 was performed on specimens from 32 Reactive hyperplasia lymphoid (RHL) patients and 80 DLBCL patients. To evaluate the role of RGC32 in DLBCL, lentivirus vectors either encoding shRGC32 or shControl were transfected into DLBCL cell lines. RNA-sequencing (RNA-seq) analysis was performed between shRGC32 and shControl stably transfected OCI-LY1 cells and functional enrichment analyses used gene ontology (GO) and kyoto encylopaedia of genes and genomes (KEGG). In order to explored its functions in vivo, xenograft models were established by subcutaneously injecting shRGC32 and shControl transfected DLBCL cells into SCID beige mice.  Results: Immunohistochemical analysis revealed RGC32 overexpression in DLBCL tissues contrast with RHL, and was associated advanced Ann Arbor stage (p = 0.043), B symptoms (p = 0.020), and poor progression-free survival (p = 0.015) and overall survival (p = 0.035). Functional studies demonstrated that RGC32 knockdown via shRNA significantly suppressed DLBCL cell proliferation in vitro and in vivo, with xenograft models showing reduced tumor growth and Ki-67 expression. RNA-seq analysis linked RGC32 depletion to downregulation of cell proliferation and impaired DNA damage repair (DDR) mechanisms. Western blot showed RGC32 knockdown could suppress ATM/ATR/CHK1 pathway and increase the tumor mutational burden (TMB). Furthermore, after inhibition of RGC32, infiltration of CD8+ T cells was increased in DLBCL tumor microenvironment (TME).  Conclusions: This study highlights that RGC32 is a novel molecule in DLBCL progression and might be a potential therapeutic target for DLBCL therapy.

overall_design: This study employed a multifaceted approach to investigate the role of RGC32 in diffuse large B-cell lymphoma (DLBCL). The core design included: Human Samples: Retrospective analysis of 80 FFPE tumor specimens from DLBCL patients (treated with R-CHOP, 2011-2022) compared to 32 reactive hyperplasia control tissues. Histological diagnosis adhered to WHO Classification (5th edition). Ethical approval and informed consent were obtained (Shandong Provincial Hospital Medical Ethics Committee). Peripheral blood mononuclear cells (PBMCs) from 8 healthy volunteers served as additional controls. Pathological & Molecular Characterization: H&E Staining & Immunohistochemistry (IHC): Performed on FFPE sections using a validated scoring system (intensity x % positive area) with key antibodies including anti-RGC32. Specimens were stratified into low/high RGC32 expression groups. Western Blot: Analyzed RGC32 and associated signaling pathway proteins (e.g., c-myc, p-ATM, p-ATR, PD-L1) in DLBCL cell line lysates. RGC32 Poly(A) Tail (PAT) Length Assay: Quantified mRNA stability/post-transcriptional regulation using a specific kit and RGC32-targeted primers. Functional Analysis (In Vitro): Genetic Manipulation: DLBCL cell lines (OCI-LY1, OCI-LY10) were transfected with RGC32-specific siRNA or control plasmids (validated by Western blot). Proliferation Assay: Monitored cell growth kinetics post-transfection using CCK-8. Cell Cycle Analysis: Performed via propidium iodide staining and flow cytometry (Beckman Coulter Navios). In Vivo Validation: Xenograft Models: shRGC32-transfected or control OCI-LY1 cells were subcutaneously injected into beige SCID mice (n per group). Tumor growth was monitored by caliper measurement for 3-4 weeks. Ethical approval was obtained (Shandong Provincial Hospital Animal Committee). Tumor-Infiltrating Lymphocytes (TILs) Analysis: TILs were isolated from digested tumors, stained for CD8a and CD3, and analyzed by flow cytometry. Transcriptomic Profiling: RNA-Sequencing: Compared global gene expression profiles of shRGC32 vs. shControl OCI-LY1 cells (biological triplicates). Differential expression was analyzed using DESeq2, followed by GO and KEGG pathway enrichment. Target Validation: Quantitative Real-time PCR (qRT-PCR): Quantified gene expression changes (validating RNA-Seq targets/nominated genes) using SYBR Green chemistry and normalized to GAPDH. Statistical Analysis: Data are presented as mean ± SD. Analyses employed Student's t-test, one-way ANOVA, Kaplan-Meier survival curves (log-rank test), using SPSS 24.0 and GraphPad Prism 5.0 (significance: *p<0.05, **p<0.01, ***p<0.001).

first: Xiyuan

last: Zhang

first: Tiange

last: Lu

first: Chunlei

last: Shi

first: Mengfei

last: Ding

first: Ling

last: Wang

first: Xinting

last: Hu

first: Xin


title: Intestinal CD4-CD8αβ-TCRαβ+ T cells function as tolerogenic antigen presenting cells in mice

city: Kamakura

first: Satoshi

last: Kondo

state: Kanagawa

address: Tebiro 6-10-1

department: New Projects Development Division

institute: Toray Industries,Inc.

summary: To distinguish harmless from harmful antigens (Ag), anatomic, cellular and molecular mechanisms operate in the intestinal tract to acquire, process, present and interpret luminal Ags. The intestinal mucosa is populated by many T cell types in the intraepithelial lymphocytes (IEL) and lamina propria lymphocytes (LPL) populations, including double negative CD4-CD8αβ-TCRαβ+ T (double-negative T/DNT) cells. Here we show that murine DNT cells in the small intestine reach across the epithelial barrier to capture luminal Ags. A sizeable fraction of DNT cells in Peyer’s patches and mesenteric lymph nodes express MHC-II, but little or no classical co-stimulatory molecules. Indeed, DNT cells acquire, process and present antigenic proteins to tolerize Ag-specific CD4+ T cells. Conditional genetic ablation of MHC-II in T cells disable this tolerogenic function and rendered mutant mice hypersusceptible to intestinal inflammation. Intriguingly, intestinal T cells in patients with Crohn’s disease express lower levels of HLA-DR than those from controls. Our findings thus suggest that MHC-II+ DNT cells may regulate intestinal immune homeostasis and their dysfunction may contribute to the pathogenesis of inflammatory bowel disease.

overall_design: PP cells were collected from pool of 3-5 C57BL/6 mice (10-week-old, male and female), stained with anti-CD8β-PE, anti-CD4-APC, anti-TCRβ-APC-Cy7, and anti-γδTCR-PE-Cy7, and then sorted by the MofFlo-XDP as the following fractions: γδTCR+TCRβ- (γδ), γδTCR-TCRβ+CD4-CD8β- (DN), γδTCR-TCRβ+CD4+CD8β (CD4), and γδTCR-TCRβ+CD4-CD8β+ (CD8). More than 98% purity of each fraction was confirmed by analysing post-sorted cells with the FACS Canto II. Total RNA was collected from each fraction with a RNeasy Mini Kit (QIAGEN# 74106). RNA collection was repeated 3 times. Microarray analysis including PCA plots and gene expression analysis was outsourced to KAMAKURA TECHNO-SCIENCE INC. Samples were analysed as triplicated with a 3D gene chip (Mouse oligo 24k).

first: Yasuhiro

last: Nemoto

first: Ulrich

last: von Andrian


title: Enhancing Non-Small Cell Lung Cancer Treatment Utilizing Natural Killer Cell-Derived Extracellular Vesicles (NKEVS) As A Novel Adoptive Cellular Therapeutic [tumor]

city: Phoenix

first: Eric

last: Alsop

state: AZ

address: 445 N 5th St

institute: TGen

summary: An established mechanism contributing to Immune Checkpoint Inhibitor (ICI) therapy failure is tumor evasion of T-cell responses via downregulation of human leukocyte antigen (HLA). Conversely, the effector function of Natural Killer (NK) cells is enhanced in the absence of HLA expression, making NK-based cellular therapies an attractive option for tumors that are resistant to ICIs. We investigated the preclinical efficacy of using selective isolation of NK cells and harvesting of NKEVs in NSCLC. Single-cell RNAseq (scRNAseq) was used to examine the cellular landscape in PBMCs and tumor tissue. NK cells were isolated from PBMCs, expanded in vitro, and NK-derived EVs (NKEV) were collected and the EV RNA and protein cargo was characterized using proteomics and transcriptomics. The functional capabilities of patient derived NKEVs were assayed with 3-dimensional organoid-like structures derived from patient tumor cells.  This work described the cellular landscape in NSCLC circulating and tumor infiltrating immune cells. Additionally, it demonstrated that NKEVs can be successfully harvested from patient derived, expanded NK cells, and highlighted their anti-tumor properties in combination with standard-of-care therapies.

overall_design: Samples from NSCLC patients (n=10) enrolled in the study were collected at Baylor Scott and White, by trained medical personnel. Specifically, a blood sample was collected pre- and post- tumor resection surgery, and PBMCs were isolated via density gradient separation. From the tumor resection, whatever tissue was left behind after pathology and diagnostic tests, was snap frozen in preparation for scRNAseq. Everything was collected, and kept frozen at Baylor Scott and White, and shipped to the Translational Genomics Research Institute for analysis.

first: Ronan

last: Kelly

first: Kendall

last: Van Keuren Jensen

first: Joanna

last: Palade


title: Epigenomic signatures of accelerated epigenetic aging are associated with congenital heart disease in newborns

city: Washington

first: Kristen

last: Kocher

state: DC

address: 111 Michigan Ave NW

institute: Children's National Hospital

summary: Background: Congenital heart disease (CHD) lesions are the most common birth defects and are associated with life-long neurodevelopmental risks. The exact mechanism by which CHD and neurodevelopment are linked remains unclear; exploring the epigenome in these cases may provide novel insights into predictive biomarkers contributing to outcomes. The present study characterizes the impact of CHD on the newborn epigenome and uncovers potential differences in epigenetic age that may underpin long-term neurodevelopmental disabilities in this high-risk population.  Methods: This is a prospective, single-site case-control study conducted at Children’s National Hospital with subjects enrolled from the Washington DC Metropolitan area. Genomic samples were collected between 2018 and 2024 and analyzed using the Illumina MethylationEPIC BeadChip array platform. PedBE was used to assess infant biological age acceleration.  Results: Using a methylation array approach, analysis of 33 newborns with complex CHD requiring neonatal cardiac surgery and 26 healthy controls. There was a significant accelerated epigenetic age in newborns with CHD compared to newborns from uncomplicated pregnancies (p < 0.001). Further subgroup analysis within the CHD cohort revealed that both single- and two-ventricle CHD displayed significant accelerated epigenetic age, with transposition of the great arteries (TGA) cases specifically having the greatest accelerated age (107.2 days, p = 0.0001). Further analysis of the CHD group revealed significant age acceleration associated with low blood oxygen saturation.  Conclusions: The present study reveals novel epigenomic signatures newborns with CHD. The functional significance of these findings, specifically accelerated epigenetic age, should be the focus of future analyses to uncover correlations associated with related outcomes. These studies aim to advance our understanding of mechanisms underlying long-term neurodevelopmental and behavioral impairment in these patients.

overall_design: 33 CHD cases and 26 newborn controls were analyzed via Illumina MethylationEPIC BeadChip array (both version 1 and 2). DNA was extracted from Genotek OC-175 buccal swabs.

first: Kocher

last: Kristen

first: Ngwa

last: Julius

first: Bhattacharya

last: Surajit

first: Donofrio

last: Mary

first: Limperopoulos

last: Catherine

first: Andescavage

last: Nickie


title: Single-cell RNA-seq of Atg7 knockout mice reveals ATG7’s role in antimicrobial immunity against nontuberculous mycobacteria

city: Seoul

first: Yeonju

last: Lee

address: 500-1 Anam-dong, Seongbuk-gu

institute: Sungkyunkwan University

summary: We performed single-cell RNA sequencing (scRNA-seq) using the 10X Genomics platform to investigate the role of the autophagy-related protein ATG7 in the context of nontuberculous mycobacterial (NTM) infection. ATG7 in innate immune cells plays a critical role in controlling NTM infection and protecting lung tissue from pathological inflammation.  This study represents single-cell analysis of Mice deletion of Atg7 in innate immune cells and reveals the importance of ATG7 in mediating antimicrobial responses during infection and its essential role in host defense mechanisms against NTM.

overall_design: Following the resection of lungs from Mav-infected Atg7 wild type and knock out at 21 dpi. Tissues were dissociated by Liberase TL

first: Eunkyeong

last: Jo

first: Woongyang

last: Park

first: Sangmin

last: Jeon


title: Spatial transcriptomics of Atg7 knockout mice reveals ATG7’s role in antimicrobial immunity against nontuberculous mycobacteria

summary: We performed Spatial transcriptomics (Visium) using the 10X Genomics platform to investigate the role of the autophagy-related protein ATG7 in the context of nontuberculous mycobacterial (NTM) infection. ATG7 in innate immune cells plays a critical role in controlling NTM infection and protecting lung tissue from pathological inflammation.  This study represents single-cell analysis of Mice deletion of Atg7 in innate immune cells and reveals the importance of ATG7 in mediating antimicrobial responses during infection and its essential role in host defense mechanisms against NTM.


title: The spatial landscape of glial pathology and T-cell response in Parkinson’s disease substantia nigra [ST]

first: Osama

last: Al Dalahmah

address: 622 West 168th Street

department: Pathology & Cell Biology

institute: Columbia University Irving Medical Center

summary: Recent evidence, including identification of specific peripheral T-cell receptor sequences, indicates the adaptive immune response is associated with disease pathogenesis. However, the properties of T-cells in the brain regions where neurons degenerate are uncharacterized. We have analyzed the identities and interactions of T-cells in PD in post-mortem brain tissue using single nucleus RNA sequencing, spatial transcriptomics and T-cell receptor sequencing. We found that T-cells in the substantia nigra of PD brain donors exhibit a CD8+ resident memory phenotype, increased clonal expansion, and altered spatial relationships with astrocytes, myeloid cells, and endothelial cells. We also describe regional differences in astrocytic responses to neurodegeneration. Our findings nominate potential molecular and cellular candidates that allow a deeper understanding of the pathophysiology of neurodegeneration in PD. Together, our work represents a major single nucleus and spatial transcriptional resource for the fields of neurodegeneration and PD

overall_design: Analysis of human brain samples using snRNAseq, spatial transcriptomics, and TCR sequencing merged with computational techniques to analyze glial pathology and T-cell response in PD

first: Maxwell

last: Ma

first: Fahad

last: Paryani

first: Kelly

last: Jakubiak

first: Shengnan

last: Xia

first: Susumu

last: Antoku

first: Adithya

last: Kannan

first: Jaeseung

first: Nacoya

last: Madden

first: Juncheng

last: Li

first: David

last: Chen

first: Gunnar

last: Hargus

first: Aayushi

last: Mahajan

first: Xena

last: Flowers

first: Ashley

last: Harms

last: Sulzer

first: James

last: Goldman

first: Peter

last: Sims

last: Al-Dalahmah


title: Serine-Driven Metabolic Plasticity Drives Adaptive Resilience in Pancreatic Cancer Cells [PANC-1]

status: Public on Jul 08 2025

city: Segrate

first: Marcella

last: Bonanomi

state: Milan

address: Via Fratelli Cervi 93

department: IBSBC

country: Italy

institute: CNR

summary:
Pancreatic cancer is one of the most lethal malignancies, partly due to its profound metabolic adaptability, which contributes to drug resistance and therapeutic failure. Understanding how pancreatic cancer cells reprogram their metabolism in response to treatment may uncover new therapeutic vulnerabilities. This study investigates the metabolic adaptations underlying resistance to drug treatment in pancreatic cancer using a systems metabolomics approach to explore novel biomarkers and therapeutic strategies.
Methods: Eight human pancreatic cancer cell lines were analyzed to assess metabolic heterogeneity and drug response. Untargeted and isotope-labeled metabolomics were performed to evaluate metabolic rewiring before and after treatment with erastin, a redox-disrupting agent. Differential correlation analysis was applied to identify key metabolic nodes associated with treatment adaptation. Combinatorial treatments using FDA-approved drugs targeting glycolysis and one-carbon metabolism were tested. Multi-omics integration of metabolomics and transcriptomics data was conducted to elucidate mechanisms of resistance.
Results: Pancreatic cancer cell lines exhibited marked metabolic heterogeneity, with differences in nutrient dependency and mitochondrial activity. Erastin treatment revealed metabolic vulnerabilities but failed to sustain long-term growth suppression. Combinatorial treatments of erastin with methotrexate or alpelisib significantly reduced proliferation and induced metabolic alteration. A systems-level analysis identified serine metabolism as a central adaptive pathway activated in resistant mechanism. Metabolic tracing and gene expression analyses revealed increased de novo serine biosynthesis and uptake, coupled with enhanced redox balancing and epigenetic regulation. Notably, cell lines that reactivated growth after drug withdrawal exhibited transcriptional reprogramming involving serine-driven pathways. These adaptations were associated with increased expression of survival, proliferation and migration-related genes.
Conclusions: This study demonstrates that pancreatic cancer cells rewire their metabolism in response to combinatorial drug treatment by activating serine synthesis and uptake. These metabolic adaptations sustain redox homeostasis, biosynthetic processes and transcriptional reprogramming, contributing to resistance mechanism. Serine metabolism emerges as a functional biomarker of metabolic plasticity and drug tolerance. These insights open new avenues for metabolism-based strategies to overcome resistance and advance precision therapy in pancreatic cancer.

overall_design: Drug treatment induced gene expression was measured after 72 hours of multi-stage treatment. 8 independent experiments for wash-out control and 7 independent experiments for re-combinatorial treatment were conducted.

first: Sara

last: Mallia

first: Mariafrancesca

last: Scalise

first: Tecla

last: Aramini

first: Federica

last: Baldassari

first: Elisa

last: Brivio

last: Conte

first: Alessia

last: Lo Dico

first: Matteo

last: Bonas

first: Danilo

last: Porro

first: Cesare

last: Indiveri

first: Christian

last: Metallo

first: Daniela

last: Gaglio


title: The spatial landscape of glial pathology and T-cell response in Parkinson’s disease substantia nigra [snRNAseq]

first: Osama

last: Al Dalahmah

overall_design: Analysis of human brain samples using snRNAseq, spatial transcriptomics, and TCR sequencing merged with computational techniques to analyze glial pathology and T-call response in PD

first: Maxwell

last: Ma

first: Fahad

last: Paryani

first: Kelly

last: Jakubiak

first: Shengnan

last: Tia

first: Susumu

last: Antoku

first: Adithya

last: Kannan

first: Jaeseung

last: Lee

first: Nacoya

last: Madden

first: Juncheng

last: Li

first: David

last: Chen

first: Gunnar

last: Hargus

first: Aayushi

last: Mahajan

last: Flowers

last: Harms

last: Sulzer


title: Gene expression characteristics of sepsis induced muscle atrophy in pigs

city: Nanning

first: Maosen

last: Yang

state: Guangxi

address: No. 100, Daxue East Road

institute: Guangxi University

summary: We generated 364.63 Gb of high-quality bulk RNA sequencing data from the skeletal muscle samples (approximately 6.75 Gb per sample). This dataset provided insightful gene expression information to understand the role of ZBED6 gene on skeletal muscle atrophy in sepsis. In addition, this dataset can be used for heterogeneity analysis between skeletal muscle tissues from multiple species or female pigs.

overall_design: In this study, we performed RNA sequencing for 54 samples of skeletal muscle from nine different anatomical regions from male ZBED6 knockout sepsis model minipigs and control minipigs.

first: Huan

last: Liu

first: Wen

last: Shi

first: Yanjun

last: Zheng

first: Song

first: Yihui

last: Wang

first: Enqiang

last: Mao

first: Hanbing

last: Shang

first: Erzhen

first: Ying


title: Thor: a platform for cell-level investigation of spatial transcriptomics and histology [Bladder Cancer]

first: Tu N

last: Tran

overall_design:
Archival FFPE tissue blocks from muscle-invasive bladder cancer patients treated at The Houston Methodist Hospital were obtained under IRB protocol PRO00037670 (“Molecular analysis of archived cancer tissues”). FFPE tissue sections were processed using the 10x Genomics Visium HD Spatial Gene Expression platform according to the manufacturer’s protocol (Visium HD Spatial Gene Expression Reagent Kits for FFPE, CG000663). Briefly, 5 µm-thick FFPE sections were mounted onto Visium HD slides and baked at 60°C for 1 hour. Following deparaffinization and heat-induced epitope retrieval, tissue sections were hybridized with probe sets targeting the human transcriptome and subjected to reverse transcription to capture spatial barcodes and unique molecular identifiers (UMIs). .Slides were then permeabilized at 37 °C for 30 minutes to release the barcoded cDNA fragments, which were collected and amplified to generate sequencing libraries. Whole-transcriptome libraries were sequenced on an Illumina platform to a target depth of approximately 200–300 million reads per capture area. Image alignment, UMI counting and spatial mapping were performed using 10x Genomics’ Loupe Browser and Space Ranger (version 3.1.0) pipeline. Quality-control metrics were reviewed to exclude low-quality bins prior to downstream analyses.

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

first: Pengzhi

last: Zhang

first: Weiqing

first: Guangyu

first: Fotis

last: Nikolos

first: Keith

last: Syson Chan


title: Serine-Driven Metabolic Plasticity Drives Adaptive Resilience in Pancreatic Cancer Cells [HPAF-2]

first: Marcella

last: Bonanomi

first: Sara

last: Mallia

first: Mariafrancesca

last: Scalise

first: Tecla

last: Aramini

first: Federica

last: Baldassari

first: Elisa

last: Brivio

last: Conte

first: Alessia

last: Lo Dico

first: Matteo

last: Bonas

first: Danilo

last: Porro

first: Cesare

last: Indiveri

first: Christian

last: Metallo

first: Daniela

last: Gaglio


title: Identification of SRSF9 through pooled shRNA screening links BNIP3 splicing to autophagy and metabolic reprogramming in breast cancer

city: Bhopal

first: Sanjeev

last: Shukla

state: Madhya Prades

address: Bhopal Bypass Road, Bhauri Bhopal 462 066 Madhya Pradesh, INDIA

country: India

institute: Indian Institute of Science Education and Research Bhopal

summary: Autophagy is a catabolic process that facilitates the degradation of toxic molecules and contributes to the maintenance of cellular homeostasis. However, the alternative splicing of genes involved in hypoxia-induced autophagy remains relatively unexplored. Here we performed pooled shRNA screening of multiple RNA binding proteins under hypoxia to mechanistically decipher their role in regulating alternative splicing of autophagy genes in breast cancer cells. We reported reduced SRSF9 expression under hypoxia that when exogenously expressed diminishes autophagosome formation. SRSF9 regulates alternative splicing of BNIP3 generating two functionally distinct isoforms regulating autophagosome formation and cancer progression through Warburg effect.  Mechanistically, SRSF9 directly binds to exon 3 of BNIP3 mRNA inhibiting the truncated BNIP3- Δ3 generation and resultant warburg effect. Moreover, the individual ectopic expression of full length BNIP-FL promotes autophagosome formation. Collectively, our study identifies novel mechanism where SRSF9 mediates the switch between autophagy and Warburg effect via BNIP3 alternative splicing thereby impacting breast cancer progression and chemoresistance.

overall_design: RNA-Seq was performed using RNA extracted from normoxia and hypoxia treated MCF7 cells.

first: Anchala

last: Pandey

first: Jithin

last: Biju

first: Srinivas Abhishek

last: Mutnuru

first: Shukla

last: Sanjeev


title: Control of stem cell activity by CSLD5-mediated cell wall remodelling.

city: Shanghai

first: yangxuan

last: liu

address: 300 Fenglin Road

institute: CAS Center for Excellence in Molecular Plant Science (CEMPS), Chinese Academy of Sciences

summary: To investigate the molecular mechanisms of CSLD5-mediated control of stem cell activity, the inflorescence meristems of wild-type, csld5, and complemented plants grown under the same conditions were dissected for transcriptome analysis.

overall_design: The inflorescence meristems of wild-type, csld5, and complemented plants were dissected for transcriptome analysis.

first: Miao

last: Lan

first: Yangxuan

last: Liu

first: Weibing

last: Yang


title: FTO degrader inhibits acute myeloid leukemia by impairing ribosome biogenesis and translation

city: Chicago

first: Chuan

last: He

state: IL

address: 929 E 57th St

department: Chemistry Department

institute: University of Chicago

summary: The fat mass and obesity-associated protein (FTO), an RNA m6A eraser, has been identified as a critical oncogenic factor in acute myeloid leukemia (AML). We presented the development of an FTO degrader(FP54) that selectively degrades FTO in AML cells, demonstrating superior efficacy both in vitro and in vivo. Mechanistically, FTO degradation increases m6A modifications on ribosome biogenesis related mRNAs and thus promotes YTHDF2-mediated degradation. This process impairs ribosome biogenesis and translation process, ultimately inhibiting AML progression.

overall_design: We developed an FTO degrader FP54. We performed m6A-seq to identify m6A-hyper genes and found those genes were mostly enriched in ribosome biogenesis. Then we performed polysome-seq to identify which transcripted was influenced during translation process

first: Zhao

last: Yutao

first: Wenlong

last: Li

first: He

last: Chuan


title: Gene expression profile at single cell level of iPSC-derived and primary thymic epithelial cells (TECs)

first: Yann

last: Pretemer

summary: We used single cell RNA sequencing (scRNA-seq) to explore the development of heterogeneous TEC-like populations from iPSCs.

overall_design: iPSC-derived cells from the stages of anterior foregut endoderm up to mature TEC were collected for scRNA-seq in a timecourse series from day 7 to 133. For days 38 and 81, samples from two separate inductions are provided. To compare the similarity of induced TECs to primary TECs, thymic stromal cells were isolated from three donors and used as controls. One sample of co-cultured primary thymocytes and induced TECs is also included to examine the effects of thymocytes on TEC maturation.

first: Yoko

last: Hamazaki


title: Harnessing extracellular vesicles from adipose-derived stem cells for the treatment of 4-vinylcyclohexene diepoxide-induced premature ovarian insufficiency

status: Public on Jul 07 2025

first: Yanquan

last: li

address: 1567#, Jinqian Road, Shanghai, China

institute: International Peace Maternity and Child Health Hospital

summary: Adipose-derived stem cells (ADSCs) demonstrated potential in tissue repair, and their extracellular vesicles (ADSC-EVs) show more safety in clinical translation. This study aims to investigate the protective effects of ADSC-EVs on rat POI models and to explore the potential therapeutic mechanisms. Whole-transcriptome sequencing of ADSC-EVs were performed to identify bioactive molecules.

overall_design: In this study, EVs were extracted and purified from the culture medium of adipose-derived mesenchymal stem cells isolated from rats. A total of three batches of extracellular vesicles were obtained from the cell samples for the exploration of potential active RNA components in ADSC-EVs.

first: Feng

last: Chen

first: Wei

last: Zhao

first: Wen

first: Fanghao

last: Guo

first: Qing

last: Zhang


title: Multi-omics analysis reveals single-cell meiotic hotspot dynamics and epigenomic regulations in female mammals

city: Beijing

first: Jiansen

last: Lu

address: No. 5 Yiheyuan Road, Haidian District

department: Biomedical Pioneering Innovation Center (BIOPIC)

institute: Peking University

summary: Meiotic recombination initiates via DNA double-strand breaks (DSBs) at specialized hotspots, while the regulation of meiotic recombination hotspots in females remain elusive due to the scarcity of embryonic stage germ cells (EGCs). Here, we mapped genome-wide active recombination hotspots and estimated their activities in female EGCs at single-cell resolution, revealing the high variability in hotspot usage frequency among individual germ cells. Further investigation of nucleosome positioning and histone modifications at recombination hotspots revealed that PRDM9-mediated open chromatin and flanking H3K4me3 established earlier at high-frequency hotspots compared with less frequently used ones. Unexpectedly, although recombination hotspots usually distributed outside of heterochromatin, H3K9me3 was clearly enriched around hotspots in females, forming a unique H3K4me3/H3K9me3 bivalent state. And we showed that appropriate H3K9me3 level may be required for downstream DSB repairs. Together, our results provided novel understanding about the landscape and epigenomic regulation of recombination hotspots in females.

overall_design: We used scATAC-seq, ultra-low-Input native ChIP-seq (ULI-NChIP-seq) and low-input MNase-seq to analyse the change of chromatin accessibility and histone modification profiles in  embryonic germ cells and somatic cells in mouse gonads during E13.5 to E16.5.

first: Jingyi

first: Qianzheng

last: Fu


title: The changes of OsTSN1 binding-genes in wildtype, P6-overexpression transgenic plants, SRBSDV-infected rice plants and SRBSDV-uninfected rice plants [CLIP-seq]

city: Hangzhou

first: Ming

last: Zeng

address: 866 Yuhangtang Road

institute: Zhejiang university

summary: Membraneless biomolecular condensates formed through liquid-liquid phase separation (LLPS) are known to play key roles in plant growth and stress responses. How plant viruses utilize LLPS to escape host immunity remains largely unexplored. Here, we present evidence demonstrating that the P6 protein encoded by southern rice black-streaked dwarf virus (SRBSDV) undergoes LLPS. P6 interacts with OsTSN1 and triggers the assembly of P6-OsTSN1-containing droplets that co-localize with stress granules (SGs). Within these P6-OsTSN1-containing droplets, P6 enhances the nuclease activity of OsTSN1 via promoting its multimerization to degrade transcripts with G-A-rich motifs of two transcription factors (TFs), OsNAC15 and OsLHY. These TFs regulate the transcription of OsJAZ6, OsJAZ12, and OsATG8C, involved in jasmonic acid (JA)- and autophagy-associated defense pathways in plants. Additionally, the degradation of OsNAC15 and OsLHY transcripts in the P6-OsTSN1-containing droplets in SGs weakens JA- and autophagy-mediated defenses in rice, facilitating SRBSDV infection. Interestingly, similar to SRBSDV P6, intrinsically disordered region (IDR)-containing RNA silencing suppressors encoded by other rice viruses such as rice black-streaked dwarf virus and rice stripe virus, also interact with OsTSN1, promoting the degradation of OsNAC15 and OsLHY transcripts to enhance viral infection. Our findings indicate that OsTSN1 acts as a central positive regulator of virus infection in rice, convergently co-opted by viruses. These insights help us to better understand the roles of LLPS and OsTSN1 in virus infection in rice.

overall_design: CLIP-seq profiling of wildtype SRBSDV-infected rice plants and SRBSDV-uninfected rice plants.

first: Shuai

first: Jianxiang

last: Wu


title: Transcriptome analysis unveils multiple reasons behind delayed and slower deposition of intramuscular fat compared to subcutaneous fat in cattle

city: BLACKSBURG

first: Zhendong

last: Tan

state: VA

address: 175 West Campus Drive

institute: Virginia Tech

summary:
Abstract
Background: Intramuscular fat refers to the white adipose tissue deposited between muscle fibers, and its quantity and distribution directly impact the quality and value of beef. Compared to subcutaneous fat, intramuscular fat develops later and accumulates more slowly in cattle. The reasons for the delayed development and slower growth of intramuscular fat in cattle remain unclear.
Results: Histological analysis showed that adipocytes in intramuscular fat were smaller than those in subcutaneous fat from the same mature cattle, indicating a delayed development or slower growth of intramuscular fat compared to subcutaneous fat. Intramuscular fat had a lower capacity for retaining or incorporating long-chain fatty acids into triglycerides than subcutaneous fat. Comparing the transcriptomes of intramuscular and subcutaneous fat by RNA sequencing identified more than 1,000 genes differentially expressed (DEGs) between the two adipose depots. Genes upregulated in intramuscular fat included FOXO6, SLC27A1, HDAC9, WWTR1, and PIK3C2A, which are known to inhibit adipose tissue development and growth. Genes downregulated in intramuscular fat included FABP4, AGPAT2, ADIG, ADIRF, and PLIN2, which are known to promote adipose tissue development and growth. Functional enrichment analyses of these DEGs suggested that intramuscular fat may have a lower capacity for fatty acid binding and adipogenesis compared to subcutaneous fat. Furthermore, genes downregulated in intramuscular fat were enriched in signaling pathways such as the PPAR signaling pathway, whereas genes upregulated in intramuscular fat were enriched in pathways including the Wnt signaling pathway. Stromal vascular fraction (SVF) cells from intramuscular fat exhibited a lower adipogenic potential than those from subcutaneous fat.
Conclusion: Multiple factors may contribute to the delayed and slower deposition of intramuscular fat compared to subcutaneous fat in cattle, including reduced fatty acid binding capacity, lower triglyceride synthesis, and decreased adipogenesis in intramuscular fat. These differences are possibly driven by lower expressions of genes such as AGPAT2, FABP4, and ADIG, higher expression of genes such as FOXO6, HDAC9, and SLC27A1, reduced activation of the PPAR signaling pathway, and increased activation of the Wnt signaling pathway in intramuscular fat.

overall_design: To investigate the molecular basis of the delayed and slower deposition of intramuscular fat (IMF) compared to subcutaneous fat (SF) in cattle, we performed RNA-seq on adipose tissues isolated from the IMF and SF depots of five Angus-crossbred heifers. Total RNA was extracted from each tissue sample, and libraries were prepared and sequenced using paired-end sequencing on the Illumina NovaSeq platform. Differential gene expression analysis was conducted to identify depot-specific gene expression profiles. This transcriptomic dataset was used to explore biological processes and pathways that may explain differences in adipogenic capacity and lipid metabolism between IMF and SF. We then validated the differential expression of key genes and functional differences between these fat depots through cellular experiments.

first: Binod

last: Pokhrel

first: Ziqi

last: Zhou

first: Honglin

last: Jiang