title: TMPRSS11B promotes an acidified microenvironment and immune suppression in squamous lung cancer

city: Dallas

first: Hari Shankar

last: Sunil

state: TX

address: NA6 300A, 6000 Harry Hines Blvd.

department: Molecular Biology

institute: UT Southwestern Medical Center

summary: Lung cancer is the leading cause of cancer-related deaths worldwide. Existing therapeutic options have limited efficacy, particularly for lung squamous cell carcinoma (LUSC), underscoring the critical need for the identification of new therapeutic targets. We previously identified the Transmembrane Serine Protease TMPRSS11B as a novel gene that promotes transformation of human bronchial epithelial cells and enhances lactate export in LUSC. To determine the impact of TMPRSS11B activity on the host immune system and the tumor microenvironment (TME), we evaluated the effect of Tmprss11b depletion in syngeneic and autochthonous mouse models. Tmprss11b depletion significantly reduced tumor burden in immunocompetent mice and triggered an infiltration of immune cells. RNA FISH analysis and spatial transcriptomics in the Rosa26LSL-Sox2-IRES-GFP; Nkx2-1 fl/fl; Lkb1fl/fl (SNL) model revealed an enrichment of Tmprss11b expression in LUSC tumors, specifically in Krt13+ hillock-like cells. Ultra-pH sensitive nanoparticle imaging and metabolite analysis identified regions of acidification, elevated lactate, and enrichment of macrophages in LUSC tumors. These results demonstrate that TMPRSS11B promotes an acidified and immunosuppressive TME and suggests a potential to therapeutically target this enzyme in LUSC.

overall_design: Rosa26LSL-SOX2-IRES-GFP; Nkx2-1fl/fl ;Lkb1fl/fl (SNL) mice were intratracheally administered Cre expressing adenovirus virus to initiate tumorigenesis. At around 11-12 months post-infection , the mice were euthanized and lungs were inflated and perfused through the trachea with 4% paraformaldehyde (PFA), fixed overnight, washed in 1xPBS for 24-48h, then transferred to 70% ethanol and subsequently embedded in paraffin. Sections were cut and stained with H&E. Spatial transcriptomic analysis was then performed on these sections to investigate the gene expression patterns among the heterogeneous tumors (LUSC, Adenosquamous, and LUAD) formed in these lungs.

first: Jean

last: Clemenceau

first: Isabel

last: Barnfather

first: Tae Hyun

last: Hwang

first: Kathryn

last: O'Donnell


title: Genomic Profiling of Sirt6 binding sites in the neuroblastoma cell line ShSy-5y under normal culture conditions.

status: Public on Nov 01 2025

city: Beer sheva

first: Debra

last: Toiber

state: Beer sheva

address: David Ben Gurion Blvd 1

department: Life Sciences

country: Israel

institute: Ben Gurion University of the Negev

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Histone deacetylases are important regulators of gene expression and chromatin conformation. Sirt6 is a histone deacetylase that regulates gene expression by deacetylating histone H3 on the specific lysine residues K9 and K56. Notably, Sirt6 expression and activity negatively correlate with biological aging and the onset of age-related diseases, such as Alzheimer’s disease. Moreover, Sirt6 also binds to DNA double-strand breaks, as a DSB-sensor protein, and regulates the DNA damage response, promoting non-homologous end-joining (NHEJ) or homologous recombination (HR) pathways. Therefore, Sirt6 functions as a stress signaling epigenetic regulator capable of coordinating the cellular response to several cytotoxic stimuli, including DNA damage, as one of its main regulatory outputs. We performed Chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq) to investigate the Sirt6 genomic-binding profile in the neuroblastoma cell line ShSy-5y under normal culture conditions. This experiment allows the scientific community and us to identify the Sirt6 targets at the gene level, and predict a possible regulatory role on its expression. The study on Sirt6 binding to specific genes was further confirmed and analyzed by ChIP-qPCR under specific experimental conditions.

overall_design: For the ChIPseq experiments, we did three independent biological replicates of the next experiment, including input samples and negative controls. We transduced Sh-Sy5y cells with a Myc-tagged Sirt6 protein. After transduction and puromycin selection, we performed the Chromatin Immunoprecipitations. The cells were plated for all the experimental conditions at an equal confluence, fixed with 1% formaldehyde for 10 minutes, quenched, and collected. After cell pellet resuspension in RIPA buffer, the lysates were sonicated using a vibracell needle sonicator (Sonics & Materials Inc, USA) to break the chromatin. Chromatin immunoprecipitations were carried out using anti-myc antibodies coated magnetic beads (MedChemExpress, Cat# HY-K0206) to isolate Sirt6-bound DNA. The negative controls consisted of untransduced ShSy-5y cells used for the same ChIP procedure, and the input samples were taken from the Sirt6-transduced samples used for Sirt6 ChIPs. The entire experiment was repeated on three independent occasions, and each one was validated by ChIP-qPCR using known Sirt6 target sequences. Immunoprecipitated DNA was then sequenced on a Novaseq 6000 sequencer (Illumina) using an SP 100 cycles kit, allocating 20M reads per sample, paired-end sequencing. Peaks were called using the MACS2 software, and the resulting peak files are included as processed data.

first: Alfredo

last: Garcia-Venzor

first: Shai

last: Shai Kaluski-Kopatch

first: Nili

last: Tickotsky-Moskovitz


title: Mapping CMV-Related Immune Signatures in Blood, Aorta, and Adipose Tissue

city: Nashville

first: Lindsey

middle: "Joey"

last: Stolze

state: TN

address: 1211 Medical Center Dr

country: USA

institute: Vanderbilt University Medical Center

type: Expression profiling by high throughput sequencing

summary: Cytomegalovirus (CMV) is a chronic herpes virus infection humans have co-evolved with. CMV infects immune and non-immune cells and alters the immune cell repertoire. CMV seropositivity has been associated with diseases of aging, including cardiovascular diseases. This study aims to deeply phenotype immune cell changes in blood, large arterial blood vessels, and perivascular adipose tissue to understand the role of CMV in cardiovascular disease.

overall_design: Thoracic aorta were obtained from patients undergoing cardiothoracic surgery. Blood and adipose tissue was also collected at the time of surgery. CMV antibody titers were measured in the plasma of all participants. Single cells isolated from aorta, adipose tissue and peripheral blood mononuclear cells were anlyzed using scRNA-seq.

first: Celestine

middle: N

last: Wanjalla


title: An isodecoder‑resolved map of mouse tRNAs, tRNA‑derived small RNAs, and RNA modification signatures across 19 tissues

city: Santa Cruz

first: Aidan

middle: Christian

last: Manning

state: CA

address: 2125 Delaware Ave. Suite B

institute: RealSeq Biosciences

type: Non-coding RNA profiling by high throughput sequencing

summary: Transfer RNAs (tRNAs) and their derived small RNAs (tDRs) vary across mammalian tissues, but the . We applied Ordered Two-Template Relay sequencing (OTTR-seq) to profile small RNAs in 19 tissues from adult mice, quantifying mature tRNAs and tDRs at isodecoder resolution and inferring select base‑modification signatures from reverse‑transcriptase misincorporations. We observe tissue‑biased expression of many isodecoders and identify tDRs with greater tissue specificity than their parent tRNAs. Modification‑associated mismatch profiles are largely consistent across tissues, with notable isodecoder‑specific differences at canonical sites (e.g., A34→I, G37→m1G/wybutosine, C47d→m3C). Because RT‑based signatures do not capture all modifications without chemical pretreatments, our modification inferences represent a subset of the tRNA epitranscriptome. These data provide an isodecoder‑resolved reference for tissue‑biased tRNA and tDR regulation in mice and a framework for exploring disease‑associated remodeling of the tRNA pool. Recent studies have begun to illustrate that transfer RNA (tRNA) expression, processing, and modification can vary among different mammalian tissues and cell types. The full scope of these differences and the regulatory mechanisms that modulate production of a wide variety of tRNAs and tDRs (tRNA-derived small RNAs) across tissues, cell types, and changing cellular conditions is poorly understood. Dysregulation of these transcripts has increasingly been implicated as a critical factor in disease progression; thus, a deeper understanding of the homeostatic variance across somatic tissues is vital. Here, we systematically profile the relative changes in abundance and key sites of base modification within tRNAs, tDRs, and other small RNAs using a powerful small RNA sequencing method, Ordered Two-Template Relay sequencing (OTTR-seq), across a panel of 19 mouse tissues. By analyzing a diverse range of healthy tissues, we can better recognize tissue-biased regulation of tRNAs and identify tDRs that exhibit significantly greater tissue specificity than their corresponding source tRNAs. Furthermore, we leveraged reverse transcriptase-associated base misincorporations to construct an isodecoder-specific map of select nucleotide modifications across all mouse tRNAs. Differentially modified isodecoders can alter their translation functionality, stability, and basis for production of unique tDR profiles. This dataset provides the most comprehensive view to date of the dynamic relationships between tRNAs, their modifications, and tDRs in a mammalian model, offering an important knowledgebase for understanding tissue-specific regulation and the role of these molecules in disease.

overall_design: Small RNA sequencing of 19 tissues from 3 adult, female C57BL/6J mice.

middle: C

first: Todd

middle: M

last: Lowe

first: Patricia

middle: P

last: Chan


title: transcriptomic differences between ACMs stimulated with a high LCAC C16 concentration and control

city: Beijing

first: Rui

last: Lin

address: Chaoyang District

country: China

institute: Capital Medical University Affiliated Anzhen Hospital

summary: About 20% of acute myocardial infarction (AMI) patients with multivessel disease experience adverse outcomes after complete revascularization. We aim to investigate the underlying metabolic mechanism of ischemia-reperfusion injury responsible for abnormal hemodynamic stresses of in high-risk patients undergoing complete revascularization. Elevated preoperative serum levels of long-chain acylcarnitine (LCAC) 16:1 was associated with an increased risk of poor prognosis following complete revascularization. Multi-omics analyses revealed reperfusion injury activates fatty acid degradation and carnitine palmitoyltransferase 1A (CPT1A) was identified as a key regulator of LCACs in the interaction network in the porcine models. In the early stages of reperfusion injury in non-culprit lesions, the release and prolonged elevation of circulating LCACs primarily depend on the activation of endothelial CPT1A through hemodynamic injury, which can be reduced using inhibitor (etomoxir). Excess LCACs entered cardiomyocytes via the organic cation transporter 2, leading to imbalanced mitochondrial quality control and causing cardiomyocyte death.

overall_design: To determine how LCACs affect mitochondrial dysfunction in cardiomyocytes, we investigated the transcriptomic differences between ACMs stimulated with a high LCAC C16 concentration (150 µM) and control cells by transcriptome sequencing.

first: Yuan

last: Wang


title: Fat sensory cues in early life program central response to food and obesity

city: Cologne

first: Sophie

last: Steculorum

address: Gleueler Straße 50

department: Metabolism Research

country: Germany

institute: Max Planck Institute

summary: Maternal obesity predisposes offspring to metabolic diseases. Here, we show that non-nutritive sensory components of high-fat diet (HFD), beyond its hypercaloric, obesogenic effects, are sufficient to alter metabolic health in the offspring. To dissociate the caloric and sensory components of HFD, we feed dams a bacon-flavored diet isonutritional to a normal chow diet but enriched with fat-related odors. Offspring exposed to these fat-related odors during development display metabolic inflexibility and increased adiposity when fed HFD in adulthood independently of maternal metabolic health. Developmental exposure to fat-related odors shifts mesolimbic dopaminergic circuits and Agouti-related peptide (AgRP) hunger neurons' responses to phenocopy those of obese mice, including a desensitization of AgRP neurons to dietary fat. While neither neonatal optogenetic activation of sensory circuits nor passive exposure to fat-related odors is sufficient to alter metabolic responses to HFD, coupling optogenetic stimulation of sensory circuits with caloric intake exacerbates obesity. Collectively, we report that fat-related sensory cues during development act as signals that can prime central responses to food cues and whole-body metabolism regulation.

overall_design: Phosphorylated ribosome pulldown for the identification of olfactory receptor activation was adapted from previous protocols31. Following 1 h of odor exposure, the olfactory epithelium was dissected on ice in buffer containing 1×HBSS (Gibco, with Ca2+ and Mg2+), 2.5 mM HEPES (pH 7.4), 35 mM glucose, 100 μg/mL cycloheximide, 5 mM sodium fluoride, 1 mM sodium orthovanadate, 1 mM sodium pyrophosphate, 1 mM beta-glycerophosphate. 4 epithelia were pooled and processed

first: Laura

last: Casanueva Reimon

first: Ayden

last: Gouveia

first: André

last: Carvalho

first: Joscha

last: Schmehr

first: Mouna

last: El Mehdi

first: Rolando

last: Moreira-Soto

first: Carlos

last: Ardanaz

first: Janice

last: Bulk

first: Lionel

last: Rigoux

first: Paul

last: Klemm

first: Anna Lena

last: Cremer

first: Frederik

last: Dethloff

first: Yvonne

last: Hinze

first: Heiko

last: Backes

first: Patrick

last: Giavalisco


title: Machine learning–driven decoding of maternal immune signatures in repeated pregnancy loss

city: Daejeon

first: Tae Lyun

last: Ko

address: 245, Daehak-ro, Yuseong-gu

country: South Korea

institute: Korea Institute of Science and Technology Information

summary: Repeated pregnancy loss (RPL) is a multifactorial condition with incompletely understood immunological mechanisms, particularly the immune disruptions contributing to RPL independent of fetal aneuploidy. To dissect this immune dysregulation, we performed single-cell RNA sequencing of decidual tissues from RPL patients and controls. Our analysis revealed that in RPL, fetal immune cells increased while fetal trophoblasts were reduced, and notably, RPL immune cells displayed transcriptional signatures resembling acute transplant rejection. Using machine learning and foundation models, we identified broad T-cell–derived transcriptomic signatures that distinguish RPL immune cells. To prioritize these candidates, we integrated network analysis and assessed their potential for therapeutic reversal using drug response data. After this rigorous filtering, we then controlled for biological confounding factors, a process which robustly identified CXCR4 and JUN in maternal T cells as the key RPL-associated signatures. The drug response analysis also highlighted three specific compounds as candidates for repurposing. Together, our approach identifies critical maternal immune signatures in RPL and links them to potential therapeutic opportunities, thereby providing both mechanistic insights and new avenues for treatment.

overall_design: First-trimester decidual tissues were collected via dilation and curettage from women undergoing elective termination of uncomplicated pregnancies (Norm) and from patients with repeated pregnancy loss (RPL). Decidual samples were dissociated into single-cell suspensions and subjected to droplet-based scRNA-seq on the 10x Genomics Chromium platform with sequencing on Illumina HiSeq-X and NovaSeq 6000.

first: Tae-Lyun

first: Hyojung

last: Paik

first: Sung-Ki

last: Lee


title: KROX20-Notch1 Network Transcriptionally Regulates Meibomian Gland Stem Cells for Its Development and Homeostasis [ChIP-Seq]

city: Charlottesville

first: Yumeng

last: Zhang

state: Virginia

address: 1726 Webland Park

institute: University of Virginia

summary: Meibomian gland dysfunction is the leading cause of Evaporative Dry Eye Disease (EDED), and accounts for approximately 90% of dry eye disease cases worldwide. The transcription factor Krox20 has been shown to mark stem cells that play a critical role in Meibomian gland (MG) development and homeostasis, however, the molecular mechanisms underlying these processes are not well understood. In this report, we used multiple Krox20 lineage tracing and ablation studies to investigate the process that governs lineage commitment during MG morphogenesis and homeostasis. Krox20 marks MG stem/progenitor cell pools, and it regulates cellular contributions to the glands, as loss of Krox20 leads to MG atrophy, while its overexpression results in MG enlargement. We also found that Notch1 signaling is regulated by KROX20 and that ablation of the Notch1 gene in KROX20-expressing cells leads to MG atrophy, while Notch1 overexpression partially rescues MG atrophy caused by the loss of Krox20. Together, these results reveal a critical KROX20-Notch1 regulatory pathway in MG stem/progenitor cells. Activation of Notch1 signaling may offer a novel approach to preventing and treating EDED caused by the depletion of the MG stem cell pool that can occur with aging.

overall_design: ChIP-seq of transcription factor KROX20 binding sites in IHMGECs infected by pLenti-Krox20.

first: Edem

last: Tchegnon

first: Elnaz

last: Ghotbi

first: Zhiguo

last: Chen

first: Stefanie

last: Moye

first: Yi

last: He

first: Renee

last: McKay

first: Lu

middle: Q

last: Le


title: Role of STAT3 in Human Esophageal Epithelial Development

city: New York

first: Yosuke

last: Mitani

state: New York

address: 1130 St Nicholas Ave, 3rd floor

department: HICCC

institute: Columbia University

summary: The transcription factor STAT3 plays broad roles in epithelial biology, yet its function in human esophageal development remains undefined. Using 2D and 3D human induced pluripotent stem cell (hiPSC)-derived platforms, we investigated how STAT3 regulates esophageal epithelial differentiation.

overall_design: We established CRISPR/Cas9-engineered STAT3-knockout (KO) hiPSCs (BU3 NGST). These cells, along with control hiPSCs, were differentiated into esophageal epithelial progenitor cells (EPCs) using a previously reported protocol (Zhang et al., Cell Stem Cell, 2018). After 16 days on the differentiation protocol, the resulting human EPCs were harvested, and total RNA was extracted. The RNA samples were submitted to Azenta for RNA sequencing.

first: Secunda

middle: W

last: Kariuki

first: Joel

last: Gabre

first: Ricardo

last: Cruz-Acuña


title: Mpox virus replicates in lung organoids without significantly affecting their cellular function

city: Kyoto

first: Kazuo

last: Takayama

state: Kyoto

address: Shogoin Kawaharacho 53, Sakyo-ku

department: Center for iPS Cell Research and Application

country: Japan

institute: Kyoto University

summary: Patients with mpox may present with a skin rash and mild respiratory symptoms, including sore throat and cough. The genome of the mpox virus (MPXV) has been detected in throat swab specimens from some mpox patients, indicating potential involvement of the respiratory tract. In this study, we used lung organoids to investigate the effects of MPXV infection on the respiratory system by evaluating the viral replication and the infection-mediated host response. MPXV infection resulted in the accumulation of high levels of viral genomes within the cells. H&E staining showed almost no histological differences between MPXV-infected lung organoids and uninfected lung organoids. In addition, RNA-seq analysis revealed that MPXV infection did not significantly alter the gene expression levels of various lung markers. MPXV infection did not change the production of proinflammatory cytokines, including interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interferon-beta (IFN-β). These findings suggest that MPXV can replicate in lung organoids without significantly affecting their cellular function.

overall_design: Total RNA was collected from MPXV-infected lung organoids, and then RNA-seq was performed.


title: Sequencing data of AQP2-specific inhibitor Steviol against colorectal cancer

city: JiangSu

first: Zhang Meiqi

address: 59 Cangwu Road, Haizhou District, Lianyungang City

institute: 江苏海洋大学

summary: In order to explore the mechanism of Steviol, we used RNA-seq technology to extract and analyze the total RNA of cells treated with DMSO ,Steviol, MG132 and Steviol+MG132 and analyzed the RNA data.

overall_design: After reaching 80% density, HCT116 cells were divided into four groups, with no less than 5×10^6 cells in each group. One group was treated with 80µM Steviol drug,One group was treated with 2µM MG132 drug One group was treated with 80µM Steviol drug +2µM MG132 drug and the other group was treated with DMSO as a control. Both groups of cells were incubated at 37°C. One day later, the original culture medium was removed and washed with 2 mL PBS using an RNaseA-free pipette tip. 1 mL of total RNA extraction reagent (Biyuntian, China) was added to the culture dish until the cells were completely covered. The culture dish was gently shaken and allowed to stand for 2-3 minutes. Mixed by blowing with an RNaseA-free pipette tip and aspirated into an RNaseA-free cryovial. Quickly frozen in liquid nitrogen and stored in a -80°C freezer. Subsequent RNA sequencing analysis was performed by Sangyo Bioengineering (Shanghai).

first: Meiqi

first: Wenhao


first: Hari Shankar

last: Sunil

overall_design: RNA-seq profiling of KLN205 syngeneic tumors expressing scrambled shRNA or shRNAs targeting Tmprss11b. Briefly KLN205 cells expressing scrambled shRNA or Tmprss11b shRNA were injected subcutaneously into the right flanks DBA/2 female mice. Tumor volumes were measured every 3 days using calipers. When the average tumor volume across all the study groups reached 100 mm3, mice were maintained on doxycycline water to induce the expression of the shRNAs for the duration of the experiment. At the terminal timepoint of Day 50 post-injection, the tumors were resected for downstream analysis.Total RNA was isolated from tumor tissues using Trizol, followed by additional cleanup and DNase digestion using RNeasy Mini Kit and subsquently used for RNA-seq profiling.

first: Kathryn

middle: A

last: O'Donnell


title: Immune Checkpoint PD-L1 Modulates Retinal Microglial Activation to Alleviate Vascular Leakage in Choroidal Neovascularization via ERK

city: Shanghai

first: Yue

last: Zou

address: Shanghai

institute: Eye & ENT Hospital, Fudan University

summary: Neovascular age-related macular degeneration (NVAMD) is a common retinal disease causing vision loss in the elderly. Neuroinflammation significantly contributes to NVAMD's etiology. This study explores the role of PD-L1, an immune checkpoint in microglia, known for limiting neuroinflammation in neurodegenerative diseases, and its potential function in NVAMD. We found increased PD-L1 expression in retinal microglia following laser injury. PD-L1 knockout or inhibitory PD-L1 antibody treatment worsened vascular leakage and neoangiogenesis in a laser-induced NVAMD mouse model, effects reversible by microglia depletion with PLX5622. Blocking PD-L1 elevated pro-inflammatory factors and p-ERK levels, indicating microglial overactivation in NVAMD. Conversely, enhancing PD-L1 signaling reduced neuroinflammation and neovascularization via ERK. These findings highlight PD-L1's role in neoangiogenesis and neuroinflammation in NVAMD, suggesting its potential as a target for immunomodulatory treatment in NVAMD.

overall_design: To investigate the PD-L1 function in regulation CNV fomation,we used a PD-L1 knockout (KO) mouse line.

first: Junliang

last: Jiang

first: Yunqin

last: Li

first: Ling

last: chen

first: Lei

last: Xiao


title: RNAPII and DNA supercoiling regulate cohesin engagement in neurons [ChIP-Seq]

first: Morgan

last: Crewe

address: 2201 Inwood Road, NC6.506

department: Psychiatry

institute: University of Texas Southwestern Medical Center

summary: Chromatin looping by CTCF and cohesin is thought to be crucial for chromosome organization and gene transcription. Yet the precise relationships between CTCF, cohesin, and transcription in neurons are still poorly understood. To address this issue, we compared the occupancy of CTCF and the cohesin subunit, SMC1, relative to transcriptionally engaged RNAPII and as a function of stimulus-dependent transcription in cultured mouse cortical neurons. We show that CTCF and cohesin are enriched at transcription start sites (TSS) and that their levels increase with the level of transcriptionally engaged RNAPII, suggesting that RNAPII facilitates the engagement of CTCF and cohesin. Unexpectedly, while neuronal stimulation causes widespread transcriptional activation, it resulted in the rapid genome-wide loss of SMC1 signals, including at the TSS of genes, loop anchors, and TAD boundaries. Activity-dependent reductions in cohesin were independent of CTCF but were mimicked by inhibiting topoisomerase IIb (TOP2B), which resolves torsional stress from DNA supercoiling. We show that neuronal stimulation elevates DNA supercoiling and that increasing torsional stress triggers the dissociation of SMC1 from chromatin. Overall, these results suggest that modulation of torsional stress could be a physiologically relevant mechanism of regulating cohesin engagement and chromatin architecture in neurons.

overall_design: ChIP-seq in mouse primary cortical neurons

first: Ilse

last: Delint-Ramirez

first: Lance

last: Heady

first: Ram

last: Madabhushi


title: RNAPII and DNA supercoiling regulate cohesin engagement in neurons [RNA-Seq]

overall_design: RNA-seq in mouse cortical neurons


title: Gene expression-based, profiles characterizing recurrence sites in surgically treated pancreatic cancer patients

city: Kamakura

first: Satoshi

last: Kondo

state: Kanagawa

address: Tebiro 6-10-1

department: New Projects Development Division

institute: Toray Industries,Inc.

summary: Gene expression characteristics associated with different recurrence patterns were successfully identified through expression profiling of a total of 8,644 genes in 16 pancreatic cancer cases, which had been consecutively operated on within a defiend short period of time

overall_design: In the study presented here, a consecutively operated, well-defined cohort of 16 pancreatic cancer cases, followed up more than two years, was used to acquire expression profiles of a total of 8,644 unique genes, leading to the successful construction of supervised models

first: S

last: Miyahara

first: Y

last: Tomimaru

first: H

last: Takahashi

last: Eguchi


title: VRK1 can be a novel therapeutic target in small cell neuroendocrine carcinoma of the uterine cervix

city: Suita

last: Nakagawa

state: Osaka

address: 2-15 Yamadaoka

department: Osaka University

institute: Department of Obstetrics and Gynecology

summary: Small cell neuroendocrine carcinoma of the uterine cervix (SCNEC) is a rare and highly aggressive cancer. In this study, we aimed to investigate the potential of vaccinia-related kinase 1 (VRK1) as a therapeutic target for SCNEC and to elucidate its functional mechanisms. VRK1 expression was found to be higher in SCNEC than in other histological types of cervical cancer. In both 3D cell culture and subcutaneous mouse models, shRNA-mediated VRK1 knockdown (shVRK1) exhibited significant antitumor effects. Gene Set Enrichment Analysis of RNA-seq data from the subcutaneous mouse models indicated that the effects of VRK1 are related to responses to external stimuli and mitochondrial pathways. In vitro, mitochondrial membrane potential was significantly decreased under hydrogen peroxide stimulation in shVRK1 cells compared to controls, suggesting that VRK1 knockdown induces mitochondrial dysfunction under external stimuli. In summary, VRK1 may be a promising therapeutic target for SCNEC, particularly through its role in mitochondrial responses to external stimuli.

overall_design: To investigate the function of VRK1, we established HCSC-1 and TC-YIK cells with VRK1 knockdown via shRNA (shVRK1) and corresponding control cells (shCont). These cells were transplanted subcutaneously into mice, and the resulting tumors were excised. Gene Set Enrichment Analysis was then performed on RNA-seq data obtained from these tumors.

first: Mariya

last: Kobayashi

first: Yuji

last: Kamei


title: Small intestinal  lymph node identity is defined by medullary stromal cells in humans

city: Philadelphia

first: Aliia

middle: R

last: Fatkhullina

state: Pennsylvania

address: 3400 Civic Center Blvd Bldg 421

institute: University of Pennsylvania

summary: Lymph nodes (LNs) along the murine gastrointestinal tract are immunologically distinct. Here, we investigated what defines gut LN identity at large in humans and mice and drives their regional differences. Using transcriptional profiling and imaging, we found that stromal cells in the LN medulla and sinus are susceptible to location along the intestine, with high conservation between human and mouse. Specifically, the medulla of small intestine-draining LNs was enriched for fibroblastic reticular cell subpopulations implicated in extracellular matrix remodeling and stromal cell replenishment, lymphatic endothelial cells, and macrophages compared to LNs draining colon and other sites like lung. In mice, this unique medullary cellular network was established around weaning age by Vitamin A, while the gut microbiota regulated the effect’s amplitude. Our study posits the LN medulla as a location for tissue-specific immune responses and uncovers privileged access to lipid-soluble vitamins as a pivotal driving force for small intestinal LN properties.

overall_design:
To uncover what the biggest transcriptional differences between lymph nodes (LNs) along the human intestine are, we performed bulk RNAseq on whole LNs from organ donors. In addition to small (superior central, mesenteric, juxta-intestinal, ileocolic) and large (caecum, ascending colon) intestine draining LNs, we included LNs of four different lung stations (4R - lower paratracheal (right), 7 - subcarinal, 10R - hilar (right), 14R - subsegmental (right)) from the same donors to assess whether tissue compartmentalization was a unique feature of the gut and, in case all gut LNs were the same, whether LNs draining different organs were perhaps distinct.

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first: Fatkhullina

last: Aliia R


title: Small intestinal  lymph node identity is defined by medullary stromal cells in humans and mice [Sorted_lns_macrophages_RNAseq]

overall_design:
To address the role of lymph node (LN) macrophages in the regional specificity of gut-draining lymph nodes, we sorted subcapsular sinus macrophages (SCM, CD169+F4/80-), medullary sinus macrophages (MSM, CD169+F4/80+), medullary cord macrophages (MCM, CD169-F4/80+) from duodenum (Duo), jejunum (Jej), ileum (Ile), ceco-colonic (Col), and inguinal (Ing, as non-gut reference) LNs and performed bulk RNAseq analysis.

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title: Small intestinal  lymph node identity is defined by medullary stromal cells in humans and mice

overall_design:
To identify region-specific gene signatures of gut-draining lymph nodes (LNs) and microbiome role in this, we analyzed duodenum (Duo), jejunum (Jej), ileum (Ile), ceco-colonic (Col) and skin-draining inguinal (Ing, as non-gut reference) LNs RNA from specific pathogen-free (SPF) and germ-free (GF) mice.
**** Submitters state that raw data files have been lost and thus are not provided***


title: Small intestinal  lymph node identity is defined by medullary stromal cells in humans and mice [Rag1KO_lns_RNAseq]

overall_design:
To examine the transcriptional differences between gut-draining lymph nodes (duodenum (Duo), jejunum (Jej), ileum (Ile), ceco-colonic (Col), and inguinal (Ing, skin-draining, as non-gut reference)) with a lack of adaptive immune cells (mature T and B cells), we performed bulk RNAseq on whole LNs from Rag1-/- (B6.129S7-Rag1tm1Mom/J) mice.

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title: RNA seq of liver cancer cells treated with different concentration gradients of Thapsigargin (TG), Tunicamycin (TM), and FCCP

city: Lianyungang

first: yuzien

last: yu

state: Jiangsu

address: 59 Cangwu Road, Haizhou District

department: College of Pharmacy

institute: Jiangsu Ocean University

summary: To investigate the effects of TG, TM, and FCCP treatments with different concentration gradients on liver cancer cells.

overall_design: HCCLM3 cells were treated with TG (0, 0.5, 1, 2 μM), TG (2 μM) + melatonin (10 μM), TG (2 μM) + ISRIB (0.5 μM), TG (2 μM) + 4μ8c (20 μM), TG (2 μM) + MG132 (10 μM), TM (0, 0.5, 1, 2 μM), TM (2 μM) + melatonin (10 μM), TM (2 μM) + ISRIB (0.5 μM), TM (2 μM) + 4μ8c (20 μM), TM (2 μM) + MG132 (10 μM), FCCP (0, 1.25, 2.5, 5 μM), FCCP (5 μM) + 3-MA (5 μM), and FCCP (5 μM) + MG132 (10 μM) for 24 hours. Two biological replicates were prepared for each condition.

first: Bin

last: Liu


title: Pathogen-derived glyoxylate inhibits Tet2 DNA dioxygenase to facilitate bacterial persister formation

first: Zixin

last: Wang

address: Siping Road

institute: Tongji University

summary: Resistance, tolerance and persistence enable pathogenic bacteria to survive antibiotic treatment and are associated with an elevated risk of treatment failure and relapsing infections. The mechanism underlying bacterial antibiotic persister formation is not well understood. Here, we show that glyoxylate, a metabolite originally evolved to allow bacteria to utilize alternative carbon sources for optimal growth and pathogenicity, also serves as a signaling molecule to alter host gene expression and support persister formation. Specifically, we discovered glyoxylate interacting with TET2 DNA dioxygenase through an in-silico screen of human metabolome. We further show that Salmonella-produced glyoxylate inhibits the activity of Tet2 to suppress the expression of pro-inflammatory genes and attenuate host immune defense. Catalytic inactivation of Tet2, by genetic knock-in mutation, glyoxylate production by Salmonella, or exogenous glyoxylate treatment, facilitates bacterial persister formation in both murine and human macrophages. Conversely, stimulating TET2 with vitamin C or blocking Salmonella production of glyoxylate counters bacterial antibiotic resistance and improves the infection treatment outcomes. In conclusion, our study reveals a novel signaling function of glyoxylate in gene regulation beyond energetic and biosynthetic metabolism. Our findings also suggest that stimulating TET activity within host cells represents a potential therapeutic strategy to combat bacterial persistence.

overall_design: We performed ACE-seq in BMDMs infected with different S. Tm strains to investigate the role of  glyoxylate-Tet2 in regulating 5hmC level of genes. The reads passed the quality check were aligned to the mouse mm39 genome.

first: Zhouli

last: Cheng

first: Faying

last: Chen

first: Jiejun

last: Shi


title: Effect of knockdown of STXBP6 on SKOV3 ovarian cancer cells

city: Chongqing

first: Min

address: No. 1 Yixueyuan Road

institute: Chongqing Medical University

summary: To investigate the function of STXBP6 in the regulation of ovarian cancer, we established SKOV3 cell lines in which STXBP6 gene has been knocked down by shRNA.

overall_design: We then performed gene expression profiling analysis using data obtained from RNA-seq of SKOV3 cells.

first: Qinke

last: Li

first: Hang

last: Xu

first: Fengzhen

last: Jin


city: 上海

first: Zhou-Li

address: dong'an road 131

institute: Fudan University

overall_design: We performed RNA-seq in BMDMs infected with different S. Tm strains to investigate the role of  glyoxylate-Tet2 in regulating transcription. The reads passed the quality check were aligned to the mouse mm10 genome. In this study, samples for each condition were collected in biological triplicates.

first: Dan

last: Ye


title: Small intestinal  lymph node identity is defined by medullary stromal cells in humans and mice [CD169_RPL22HA_lns_RNAseq]

overall_design: RiboTag mice were crossed to a CD169-Cre recombinase-expressing mouse to activate the Rpl22HA allele in all tissues. Homozygous CD169RPL22HA mice lymph nodes were collected and used for the RiboTag immunoprecipitation. RNA was extracted using the Arcturus PicoPure RNA isolation kit (Applied Biosystems) according to the manufacturer’s instructions.


title: Global transcriptions upon MAZ knockdown HUDEP-2 cells

city: Guangzhou

first: Bo

last: Yang

state: Guangdong

address: Guangzhou, 510150, Guangdong Province, China.

institute: The Third Affiliated Hospital of Guangzhou Medical University

summary: Hemoglobinopathies, such as sickle cell disease and β-thalassemia, are common genetic disorders remaining significant global health challenges due to their associated morbidity and mortality. Increasing fetal hemoglobin (HbF) levels has emerged as a promising therapeutic strategy for these disorders. In this study, we report MAZ as a repressor of γ-globin expression in human erythroid cells. Depletion of MAZ in HUDEP-2 and patient-derived β-thalassemia cells leads to significant inductions both of γ-globin mRNA and protein levels, resulting in increased HbF percentages and HbF+ erythroid cells. We demonstrate that MAZ occupies at the MYB promoter. MAZ depletion reduced MYB and BCL11A levels. Restoration of MYB re-silenced the γ-globin levels in MAZ depleted cells. Our findings uncover the MAZ-MYB axis in γ-globin regulation, highlighting MAZ as a potential target to enhance HbF levels in patients with hemoglobin disorders.

overall_design: To investigate the role of MAZ in γ-globin regulation, we employed shRNAs to knockdown MAZ in a human adult-type erythroid cell line HUDEP-2. We performed RNA-seq to measure global transcriptions upon MAZ knockdown HUDEP-2 cells.

first: Dian

last: Lu

first: Yinghong


title: RNA seq of breast cancer cells treated with different concentration gradients of Thapsigargin (TG), Tunicamycin (TM), and FCCP.

summary: To investigate the effects of TG, TM, and FCCP treatments with different concentration gradients on breast cancer cells.

overall_design: MDA cells were treated with FCCP (0, 0.5, 1, 2 μM), FCCP (5 μM) + MG132 (10 μM), FCCP (5 μM) + 3-MA (5 μM), TG (0, 1.25, 2.5, 5 μM), TG (2 μM) + MG132 (10 μM), TG (2 μM) + ISRIB (0.5 μM), TG (2 μM) + melatonin (10 μM), TG (2 μM) + 4μ8c (20 μM), TM (0, 0.5, 1, 2 μM), TM (2 μM) + MG132 (10 μM), TM (2 μM) + ISRIB (0.5 μM), TM (2 μM) + melatonin (10 μM), TM (2 μM) + 4μ8c (20 μM) for 24 hours. Two biological replicates were prepared for each condition.


title: Small intestinal  lymph node identity is defined by medullary stromal cells in mice

first: Aliia

overall_design: To study the role of Vitamin A on gut-draining lymph nodes regionalization, 7-8 weeks old C57BL/6J females were placed on a vitamin A deficient (TD.86143, Inotiv) or ingredient matched control with vitamin A added back at 20 IU/g (TD.91280, Inotiv) 3 weeks before breeding set up. Second and third litters were sacrificed at 8 (postnatal day 56) weeks old.


title: FSTL1 Promotes Macrophage M2 Polarization and Its Role in Allergic Rhinitis

city: taizhou

first: qian

last: zhu

address: gaoxinarea

institute: qian

summary: Allergic rhinitis (AR) is a prevalent inflammatory condition characterized by an overactive immune response to allergens. Recent studies have highlighted the role of macrophage polarization in modulating immune responses. This study investigates the role of Follistatin-like 1 (FSTL1) in promoting macrophage M2 polarization and its implications in AR. Using in vitro and in vivo models, we demonstrate that FSTL1 significantly enhances the expression of M2 macrophage markers, including Arg1, CD206, and IL-10, while concurrently reducing M1 markers such as iNOS and TNF-α. Furthermore, FSTL1-treated macrophages exhibited increased anti-inflammatory properties, contributing to the attenuation of allergic inflammation in a murine model of AR. Our findings suggest that FSTL1-mediated M2 polarization plays a crucial role in mitigating allergic responses, providing a potential therapeutic target for AR management.

overall_design: The aim of this study is to investigate the effects and mechanisms of FSTL1 on the polarization of THP-1-derived macrophages.Experimental Design: THP-1 cells were differentiated into M0 macrophages using phorbol 12-myristate 13-acetate (PMA). The cells were then divided into three groups: a blank control, a negative control (transfected with si-NC or pcDNA3.1 (+)-NC), and an experimental group (transfected with FSTL1 or pcDNA3.1 (+)-FSTL1). M1 polarization was induced in all groups using LPS, IFN-γ, and IL-6, while M2 polarization was achieved with IL-4, IL-13, and IL-6. Flow cytometry was used to assess CD206 and CD86 expression levels in each group.Vector Construction Method:The FSTL1 overexpression construct was generated by amplifying cDNA via PCR and inserting it into the pcDNA3.1 (+) vector.The small-interfering RNA (siRNA) targeting FSTL1 along with a scrambled negative control siRNA, were synthesized as single-stranded primers and annealed to form double-stranded RNA, which was subsequently cloned into the pLKO.1-puro vector.High-throughput sequencing design: RNA-seq analysis was performed on M0 macrophages transfected with si-FSTL1 and M0 macrophages transfected with pcDNA3.1(+)-FXTL1.


title: Fluoxetine promotes recovery from noise-induced Hippocampus  degeneration

city: Seongnam

first: Hyun-Ju

last: An

state: --- Select One ---

address: Seongnam-si, 13496

institute: CHA university

summary: Fluoxetine treatment after noise exposure restored hippocampus synaptic expression of brevican and decreased low-frequency hearing thresholds. In cochlear nuclei, fluoxetine treatment decreased the expression of PNN and was predicted to upregulate the neuropeptide signaling pathway

first: Hyunju


title: KROX20-Notch1 Network Transcriptionally Regulates Meibomian Gland Stem Cells for Its Development and Homeostasis

first: Yumeng

last: Zhang

overall_design: RNA-seq profiling of widetype IHMGECs and their derivatives (pLenti-GFP and pLenti-Krox20 infected cells) after 18 hour, 42 hour and 66 hour infection.

first: Edem

last: Tchegnon

first: Elnaz

last: Ghotbi

first: Zhiguo

first: Stefanie

last: Moye

first: Yi

last: He

first: Renee

last: McKay

first: Lu

last: Le


title: chrna3 modulates alcohol response in zebrafish

city: Singapore

first: Ajay

last: Mathuru

state: Singapore

address: 28 Medical Drive, #5-COR

department: Physiology

country: Singapore

institute: NUS

summary: Alcohol use disorders (AUDs) are complex phenomena governed by genetics, neurophysiology, environment, and societal structures. New methods to understand the underlying neurogenetics are valuable for designing personalised interventional strategies. Here, we used a novel, two-choice self-administration zebrafish assay (SAZA) to isolate the function of nicotinic acetylcholine receptor (nAChR) subunit alpha3 (chrna3) in alcohol response. Juvenile zebrafish exhibited a biphasic response when self-administering alcohol that transitioned from attraction to aversion within minutes, suggesting they can regulate exposure to alcohol. This inverted U-shaped self-administration mirrored the effect alcohol has on shoaling behaviour. Exposure to low concentration of alcohol reduced anxiety-like behaviours, while sedative effects became prominent at higher concentrations resulting in reduced locomotion and uncoordinated swimming. In contrast, these responses are blunted in chrna3 mutants. They exhibit prolonged alcohol self-administration, and increased gregariousness. Transcriptomic analyses suggest that glutamatergic and GABAergic neurotransmission alongside cholinergic signalling is impacted in the mutant brains. Our results thus suggest that chrna3 dysfunction has a systemic change with an increase in alcohol tolerance being one effect. These findings also highlight the use of non-rodent alternatives to understand the neurogenetics of development of AUD.

overall_design:
We generated CRISPR/Cas-9 mutants in the gene chrna3 called chrna3C246X. For analysis of trancriptomic changes in adult brains, homozygous mutants chrna3C246X and WT were raised to adulthood.
RNA-seq analysis performed on whole brains in triplicates. The quality of each sample was verified by gel electrophoresis and bio-analyser. Samples that passed QC were sent for sequencing by Novogene AIT. An mRNA cDNA library made up of Paired-end sequencing reads of 150 bp in length was generated on the Illumina HiSeq instrument.

first: Joshua

last: Raine

first: Caroline

last: Kibat

middle: S


title: Elucidating the Role of Prefrontal Cortex Damage in Persistent Cognitive Impairment Following Traumatic Brain Injury: Behavioral and Molecular Insights

city: Kunming

first: Yifei

last: Dong

state: Yunnan Province

address: No. 374, Dian Burma Avenue

institute: Dept. of Rehabilitation, The 2st Affiliated Hospital of Kunming Medical University

summary: RNA-seq was performed on PFC tissues to identify differentially expressed genes (DEGs) between pCI and tCI groups. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, along with protein-protein interaction (PPI) network examinations, were used to explore the biological functions of DEGs.

overall_design: On day 35 post-TBI, animals were deeply anesthetized, and the brains were carefully extracted (n=6 per group). The PFC was immediately dissected under RNase-free conditions and placed in RNAsolid™ tissue stabilization solution (Servicebio, Wuhan, China), stored at 4°C overnight for infiltration, and then preserved at −80°C until RNA extraction. Total RNA was extracted using Trizol reagent (ThermoFisher, 15596018) following the manufacturer's standard protocol. The quantity and purity of the extracted RNA were assessed using a NanoDrop ND-1000 spectrophotometer (NanoDrop, Wilmington, DE, USA), and RNA integrity was evaluated with a Bioanalyzer 2100 (Agilent, CA, USA). Only high-quality RNA samples with RIN values greater than 7.0 were used for library construction. The RNA-seq library was constructed according to the manufacturer's instructions using Dynabeads Oligo (dT), the NEBNext® Magnesium RNA Fragmentation Module, Invitrogen SuperScript™ II Reverse Transcriptase (cat.1896649, CA, USA), E. coli DNA polymerase I, and dUTP Solution (Thermo Fisher, cat. R0133, CA, USA).At last, we performed the 2×150bp paired-end sequencing (PE150) on an Illumina Novaseq™ 6000 (LC-Bio Technology CO., Ltd., Hangzhou, China) following the vendor's recommended protocol.

first: Jiaxin

last: Fan

first: Yongmei

last: Li


title: Loss of METTL3 potentiates transposable element expression and drives inflammation-induced cell plasticity in the mammary epithelium [scRNA-seq]

city: Boston

first: Xintao

last: Qiu

state: MA

address: 440 brookline ave

institute: Dana Faber Cancer Institute

summary: Sustained proliferation and aberrant cellular plasticity are the hallmarks of breast premalignancy, yet the mechanisms driving this process remain unclear. Using CRISPR knockout screens, we systematically characterized the regulators of cellular fitness in the normal mammary epithelium. We found that loss of RNA methyltransferase METTL3 initiates mammary epithelial proliferation and reprograms gene expression, which depends on its catalytic activity. Single-cell analysis in normal breast organoids revealed that METTL3 ablation causes disruption of the mammary cellular hierarchy through increased aberrant luminal differentiation. Mechanically, METTL3 loss reduces the RNA m6A modification of transcribed transposable elements leading to their increased expression and upregulating interferon-STAT signaling. This inflammatory response leads to the crosstalk between STAT and GATA3 transcription factors, resulting in transcriptional activation of luminal genes in the mammary epithelium. These findings identify a cell-intrinsic epigenetic loop contributing to mammary epithelial plasticity and highlight a potential role of METTL3-dependent m6A modification during neoplastic transformation.

overall_design: To systematically understand the cellular and molecular changes that associated with aberrant mammary epithelial differentiation upon METTL3 loss, we performed single-cell RNA sequencing in the normal breast organoids with or without METTL3 sgRNA-mediated depletion


title: Comparison between Arabidopsis WT plants exposed to mVOCs and control plants

city: Turin

first: Massimo

middle: E

last: Maffei

state: Italy

address: Via Quarello 15/a

department: Life Sciences and Systems Biology

country: Italy

institute: University of Turin

summary: ArabidopsisCol0 plants are exposed to Pseudomonas syringae pv tomato DC3000 Volatile Organic Compounds and compared to Arabidopsis Col0 plants not exposed and grown in the same conditions

overall_design: Control DC3000: Arabidopsis Col 0 grown for 8 days on agar plates (Controls) (cRNAs labelled with Cy3-green) versus DC 3000: Arabidopsis Col 0 grown for 8 days on agar plates and exposed to Pseudomonas syringae DC3000 for 12 hours (cRNA labelled with Cy5-red)


title: Position-Specific Methylation of Benzo[a]pyrene Drives AHR-Dependent Fin Duplication in Zebrafish

city: Corvallis

first: Robyn

middle: Leigh

last: Tanguay

state: Oregon

address: 28645 east hwy 34

department: Environmental and Molecular Toxicology

institute: Oregon State University

summary: Polycyclic aromatic hydrocarbons (PAHs) are an environmental contaminant class characterized by fused aromatic rings. PAHs are released through the incomplete combustion of organic materials as well as petrogenic sources like oil and gas. Benzo[a]pyrene (BaP) is one of the most well-studied PAHs and is known to cause cancer through the formation of DNA adducts and strand breaks. In larval zebrafish exposed from 6 hpf, BaP caused behavioral effects by 4 µM but no morphological effects up to 50 µM by 120 hours post-fertilization (hpf). In contrast, 8-methylbenzo[a]pyrene caused a distinct fin duplication phenotype by 0.26 µM and severe edema and mortality 1 µM. Alkyl substitutions in different positions (7-, 6-, 9-, and 10-MBaP) did not elicit morphological effects at similar concentrations. Utilizing knock-out lines, we determined that the effects of 8-MBaP were Ahr2 dependent and that Cyp1a served a protective role. To identify transcriptomic changes underlying the observed phenotypic effects, larvae were exposed to three concentrations of BaP, 6-MBaP, and 8-MBaP. Whole larvae were collected at 48 and 72 hpf which was before and during phenotype onset, respectively. A systematic approach allowed us to identify the concentration-dependent transcriptional responses linked to the downstream morphological phenotypes unique to BaP methylation at the eight position. This study improves environmental and human health hazard assessment by identifying critical structural features and mechanisms of action contributing to the toxicity of PAH mixtures in the environment.

overall_design: Poly-A tail bulk RNA sequencing was performed for three chemicals (8-MBaP, 6-MBaP, and BaP) at three concentrations and two timepoints to elucidate transcriptomic changes unique to 8-MBaP exposure and development of the x-fin phenotype. Embryonic zebrafish were exposed to three concentrations (0.133, 1.33, and 13.3 µM) of 3 chemicals (8-methylbenzo[a]pyrene, 6-methylbenzo[a]pyrene, and benzo[a]pyrene) and a DMSO control at 6 hpf.  Embryos were exposed to chemical in 100µL of embryonic medium in 96-well plates. Pools of 6 embryos were collected at 48 hpf and 72 hpf. RNA sequencing was performed by Alithia Genomics (Epalignes, Switzerland) using their Mercurius™ BRB-SEQ service, which is a multiplexed 3’ RNA sequencing library preparation technique.

first: Mackenzie

middle: L

last: Morshead

first: Lisa

last: Truong


title: Pathogen-derived glyoxylate inhibits Tet2 DNA dioxygenase to facilitate bacterial persister formation [II]

first: Zhou-Li

last: Cheng

overall_design: We performed RNA-seq in WT and  TET2 KO BMDMs treated with IFNb for 6h to investigate the role of  Tet2 in regulating transcription. The reads passed the quality check were aligned to the mouse mm10 genome. In this study, samples for each condition were collected in biological triplicates.

first: Dan

last: Ye


title: Loss of METTL3 potentiates transposable element expression and drives inflammation-induced cell plasticity in the mammary epithelium [ATAC-seq]

overall_design: we performed ATAC-seq in control or METTL3 depleted MCF10A cells to evaluate whether changes in chromatin state are associated with the transcription of mammary epithelial luminal genes.


title: Generation and exosomal non-coding RNAs profiling of down syndrome-specific induced pluripotent stem cells

city: Guilin

first: gengshuo

last: chen

address: No. 212, Renmin Road, Guilin

institute: The Second Affiliated Hospital of Guilin Medical University

summary: Down Syndrome (DS) is a relatively severe chromosomal disorder associated with many significant clinical anomalies. Nowadays, it is still challenging to collect DS samples for studies in clinical settings. In addition, there are no perfect animal models for DS. Therefore, we constructed disease-specific induced pluripotent stem cells（iPSCs）to explore a new modality for non-invasive prenatal diagnosis of DS.

overall_design: To investigate the differential expression of Small RNA in exosomes from Down syndrome induced pluripotent stem cells. We isolated exosomes from cell culture supernatants, extracted RNA from exosomes and performed high-throughput sequencing.

first: Gengshuo

last: Chen

first: Weiwei

last: Gong

first: Yu

last: Sha

first: Minglin

last: Ou


title: Loss of METTL3 potentiates transposable element expression and drives inflammation-induced cell plasticity in the mammary epithelium [ChIP-seq]

overall_design: GATA3 is a critical transcription factor in the mammary epithelium, which coordinately regulates ESR1 and FOXA1 mediated transcription, and drives luminal epithelial differentiation and breast cancer progression. We therefore performed GATA3 ChIP-seq to examine GATA3-bound DNA regions in MCF10A cells upon METTL3 depletion.


title: PINK1 Deficiency Aggravates Age-related Bone Loss

first: Hyun-Ju

last: An

summary: In this study, we aimed to explore the impact of PINK1 deficiency on MSC differentiation and bone health within the context of age-related bone loss, with a particular focus on the mechanisms regulating the balance between osteogenesis and adipogenesis. By examining how PINK1 influences bone health in both young and aged mice, we hope to gain a deeper understanding of the age-specific roles of PINK1 in skeletal bone maintenance and explore the possibility of targeting PINK1 to mitigate osteoporosis in the aging population.

overall_design: 3T3-L1 cells treated with sipink1 and sicontrol

first: Hyunju


title: Long-read single-cell RNA sequencing analysis of key genes and isoforms during corneal wound healing in Macaca fascicularis

city: guangzhou

first: ming

last: zhou

address: jinsui road 7

institute: Sun Yat-sen University,

summary: The repair of corneal damage is crucial for maintaining clear vision. When the corneal epithelium is damaged, epithelial cells at the corneal limbus quickly initiate a series of complex biological processes, including cell migration, extracellular matrix remodeling, and cell proliferation and differentiation, to promote repair and wound healing. However, comprehensive studies on the transcriptional heterogeneity of corneal limbal cell populations during migration, proliferation, and differentiation in the context of corneal epithelial injury repair are still lacking. In this study, we conducted a systematic analysis of five major cell types in the corneal limbus, including terminally differentiated cells of corneal epithelium (TDCE), basal cells (BC), transit-amplifying cells (TAC), limbal stem cells (LSC), and conjunctival cells (CC ), using high-throughput long-read single-cell RNA sequencing of corneal limbal tissues from Macaca fascicularis. The corneal epithelium was examined at three time points: before injury (0 days) and after injury (1 day and 3 days). The study focused on the migration, proliferation, and differentiation dynamics of these cells during different stages of corneal injury repair. Additionally, key regulatory genes and their RNA isoforms were investigated to uncover their roles in these processes. The results revealed that LSCs and BCs play pivotal roles in corneal epithelial healing, highlighting the regulatory functions of several key genes and their RNA isoforms in cell migration, proliferation, and differentiation. These include growth factors (e.g., IGF2), extracellular matrix components (e.g., FN1 and LAMC2), integrins (e.g., ITGB1 and ITGAV), and Keratin (e.g., KRT3, KRT12 and KRT6A). The study provides novel insights into the transcriptional landscape at the single-cell level during corneal epithelial damage repair, identifying important cell types and key regulatory genes with corresponding RNA isoforms.

overall_design: we extracted corneal epithelial cells from corneal tissues on days 0, 1, and 3 after corneal injury in cynomolgus monkeys (2 replicate samples were taken at each time point), and obtained single-cell full-length cDNAs using the 10× Genomics platform, and then used the HIT-scISOseq method for library construction and sequencing.

first: Hu

first: Qiy

last: Dai

first: Ming

first: Zhuo-Xing

last: Shi


title: Ribosomal RNA synthesis by RNA polymerase I is regulated by premature termination of transcription II

city: Toulouse

first: olivier

last: Gadal

address: 169 av. Marianne Grunberg_Manago

department: UMR5087 CNRSS

country: France

institute: centre de biologie integrative (CBI)

summary: The synthesis of the large rRNA precursors is achieved by the RNA polymerase I (Pol I) enzyme. During elongation, Pol I exhibits a highly discontinuous process with a high rate of pauses. Here, we propose that Pol I Premature Termination of Transcription (PTT) is a major regulatory step limiting rRNA production in vivo. We previously isolated a mutant of Pol I carrying the RPA135-F301S mutation. This mutant (hereafter called SuperPol) is able to produce 1.5-fold more rRNA than wild-type (WT). Combining crosslinking and analysis of cDNAs (CRAC) and rRNA analysis we could show that increased rRNA production in SuperPol is associated with a reduced premature release of nascent transcripts and a shift of the polymerase distribution toward the 3’ end of rDNA genes. In vitro, SuperPol shows a defect in nascent transcript cleavage combined with an increased ability to resume elongation after a pause, to the detriment of transcriptional fidelity. SuperPol is resistant to high concentrations of BMH-21, a drug that severely impairs Pol I elongation and triggers the proteasome-mediated degradation of the largest subunits of Pol I, in both human and yeast. Compared to WT, SuperPol retains subunits stability and maintains high levels of Pol I transcription upon BMH-21 treatment. These results show that PTT is both alleviated in SuperPol and targeted by BMH-21 in WT Pol I.

overall_design: CRAC protocol performed on samples containing HTP-tagged proteins: Rpa135(WT)-HTP, Rpa135(F301S)-HTTP s were analyzed and in presence of BMH-21.

first: Chaïma

last: Azouzi

first: Marion

last: Aguirrebengoa

first: Christophe

last: Dez

first: Olivier


title: Next-Generation Sequencing Facilitates Quantitative Analysis of WT and Mpp8/Tasor double knockout Embryonic Stem Cells Transcriptomes

city: Nanjing

first: Yuzhuo

last: Xu

address: 12 Xue-fu Road, Pukou District

institute: Nanjing University

summary: Purpose: The goals of this study are to compare Mpp8/Tasor-dko with wildtype embryonic stem cells transcriptome profiling (RNA-seq) to evaluate the target genes regulated by HUSH complex.

overall_design: mRNA profiles of WT and MPP8/Tasor-dko embryonic stem cells were generated by deep sequencing, in triplicate, using Illumina Novaseq6000.

first: Bowen

last: Wang

first: Jinzhong

last: Qin


title: Multi-omic approach indicates that bacterial volatile organic compounds (VOCs) promote Setaria viridis growth mainly via energy metabolism, cell wall modulation and hormonal signaling

city: Campinas

first: Gabriela

middle: F

last: Persinoti

state: São Paulo

address: Rua Giuseppe Máximo Scalfaro, 10.000

department: Brazilian Biorenewables National Laboratory LNBR

country: Brazil

institute: Brazilian Center for Research in Energy and Materials CNPEM

summary: Some plant growth promoting bacteria (PGPB) do not need to colonize plant roots to trigger the growth promotion mechanisms, as they emit volatile organic compounds (VOCs), which are small gaseous signaling molecules that mediate short- and long-distance interactions between plants and microorganisms. Therefore, VOCs-producing PGPB can be an eco-friendly solution to increase agricultural production. We aimed to understand the mechanisms underlying the VOC-mediated growth promotion effect on Setaria viridis, a model plant of C4 metabolism, by investigating its molecular, cellular, physiological and phenotypical changes triggered by these bioactive compounds. Remarkably, we screened and selected two bacteria, Pseudomonas and Burkholderia, capable of increasing the biomass of S. viridis plants by up to 4-fold in a co-cultivation system, wherein plant and bacteria only share the same atmosphere. A total of 2,871 differentially expressed genes (DEGs) were identified in S. viridis plants when exposed to VOCs from at least one of the three isolates (AI2, CTB and MTS) compared to the mock control. Then, a Gene Ontology analysis was performed. Comparing AI2 and mock treatment, 80 and 26 up- and down-regulated GOs were identified, respectively, while when comparing CTB and mock treatment, 94 up- and 36 down-regulated GOs were identified. Among these differential GOs in at least one of the growth promotion treatments compared to one or both controls we found categories like “aromatic compound biosynthetic process” (GO:0019438), “abscisic acid binding” (GO:0010427), "systemic acquired resistance" (GO:0009627), and “chitin catabolic process” (GO:0006032). Other GOs were only regulated in the treatments containing bacteria, such as “sucrose biosynthetic process” (GO:0005986), “L-phenylalanine metabolic process” (GO:0006558), “cell surface receptor signaling pathway” (GO:0007166), and “regulation of nitrogen compound metabolic process” (GO:0051171). Overall, the enrichment analysis showed a diverse spectrum of categories related to primary and secondary metabolisms, hormone pathways, enzymatic activities, plant defense and resistance, among others. Together with the other omic and target analyses, the study suggests that bacterial VOCs were able to boost photosynthesis, increasing the sugar content, that fuels respiration and cell wall modulation. Besides, VOCs were able to trigger defense response.

overall_design: To investigate the transcriptional profile of S. viridis in response to bacterial VOCs, seedlings were co-cultivated with three bacterial isolates (AI2.2-A, CTB P6B8 and MTS P5D6) and in the abscence of bacteria (mock control) for seven days. Total RNA was extracted from shoots and used to generate RNA-Seq libraries. Differential expression analysis was carried out by pairwise comparisons between all four treatments.

first: Octávio

last: Almeida

first: Maria

middle: J

last: Calderan-Rodrigues

first: Juliana

middle: V

last: Oliveira


title: Gene expressions of primary fibroblasts derived from human right-sided and left-sided colorectal cancer and adjacent normal tissues

city: Kota Bharu

first: Marahaini

last: Musa

state: Kelantan

address: Universiti Sains Malaysia, Health Campus, Kota Bharu

department: Human Genome Centre

country: Malaysia

institute: Universiti Sains Malaysia

summary:
We compared gene expressions between primary fibroblasts from right- and left-sided colorectal cancer and adjacent normal tissue
It is expected that the heterogeneous cancer associated fibroblasts contribute to different biological manifestation in right- and left-sided colorectal cancer. Characterisation of fibroblasts based on their expression profiles via microarray revealed specific markers related to tumour biology and thus elucidate the differentiating mechanism between right- and left-sided colorectal cancer.

overall_design: A total of 8 RNA samples were extracted from primary fibroblasts which are derived from right- and left-sided colorectal cancer and adjacent normal tissues, and epithelial colorectal cancer cell line, SW620. All samples were subjected to microarray analysis. RNA sample from SW620 cell line is included as a negative control. Duplicates were included.

first: Sahira

last: Zawawi


title: Insulin resistance alters cortical inhibitory neurons and microglia to exacerbate Alzheimer’s knock-in mouse phenotypes

city: New Haven

first: Stephen

last: Strittmatter.

state: Connecticut

address: 295 Congress Ave, BCMM Rm433

department: Neurology

institute: Yale University

summary: Clinically, patients with diabetes have a higher risk of suffering from Alzheimer's disease (AD), with increased severity of cognitive decline upon disease onset. Several studies have reported on the metabolic impact of chronic hyperglycemia using various mouse models of AD, with varying results and behavioral outcomes. Furthermore, the underlying cellular mechanisms driving any observable increases in cognitive impairments remain unclear. In this study, we induced either Type-1 (streptozotocin, STZ) or  Type-2 (chronic high-fat diet,  HFD)  diabetes on either wild type or a double knock-in AD mouse model. We found that there was no observable difference in behavioral defect between AD and AD mice with STZ-induced diabetes. However, AD mice on a chronic high-fat diet displayed increased impairments in memory and learning. Histological and transcriptomic analysis of these mice revealed an increase in glial-mediated synapse due to an altered metabolic state of microglia.

overall_design: The impact of chronic elevated glucose levels on synapse loss was tested in homozygous AppNL-G-F/hMapt double knock-in (DKI) mouse model of Alzheimer's Diease. DKI mice on a sustained control diet, containing low sucorse, or high fat diet, were compared to wild type mice under going the same treatment.  Mice in all groups were evaluated for behavioral deficits, synapse loss by immunohistology, tau pathology, gliosis, inflammatory markers, and snRNA-seq transcriptomic profiling.

first: LaShae

middle: K

last: Nicholson

first: Si Jie

last: Tang

first: Tejaswini

last: Karra

first: Habiba

last: Abouelatta

last: Strittmatter


title: Characterization of elongation of the very long chain fatty acid protein 6 (elovl6) gene in male Oreochromis niloticus and its potential regulatory roles in lipid and glucose metabolism

city: wuxi

first: Yi-Fan

last: Tao

state: jiangsu

address: 9 Shanshui East Road

institute: Freshwater Fisheries Research Center

summary: Elongation of very long-chain fatty acids protein 6 (Elovl6) is a crucial enzyme in the synthesis of endogenous fatty acids, which participates in the energy balance and metabolic diseases. The main objective of this study was to explore the molecular characterization of elovl6 and study regulatory mechanism of elovl6 on male Nile tilapia, Oreochromis niloticus. In the present study, the full-length cDNA of Nile tilapia elovl6 was 2255 bp, comprising a 5'-UTR of 193 bp, an ORF of 810 bp, and a 3'-UTR of 1252 bp, encoding 269 amino acids that possesses the characteristic features of Elovl proteins. The transcription expression of elovl6 transcripts showed differential expression in different tissues and fed with different lipid sources diet. Antisense RNA technology was used to knock-down elovl6 in Nile tilapia. Compared with the control treatments (transfected with ultrapure water (control) or the blank expression vector (negative control)), knockdown elovl6 altered hepatic morphology, Long chain fatty acid synthesis, fatty acid oxidation, lead to excess fat deposition in the liver, ultimately cause abnormal glucose/lipid metabolism in male Nile tilapia. Transcriptome analyses (AGPAT2 knock-down vs. negative control) revealed a total of 5877 differentially expressed genes (DEGs). Transcriptome analyses revealed DEGs were greatly involved in some signaling pathways, such as PPAR signaling pathway, fatty acid degradation, glycolysis/gluconeogenesis, and insulin signaling pathway, which were related to lipid and glucose metabolism. We used qRT-PCR to verify the mRNA expression changes of 13 DEGs in related signaling pathways. Our results demonstrate that knock-down of elovl6 in tilapia blocks the synthesis of oleic acid and leads to abnormal glucose/lipid metabolism.

overall_design: In order to study regulatory mechanism of elovl6 on male Nile tilapia, Oreochromis niloticus, we performed gene expression profiling analysis using data obtained from RNA-seq of elovl6 knockdown group and negative control group.

first: Tao

last: Yifan

first: Pan

first: Jiang

last: Bingjie

first: Wang

last: Qingchun

first: Hua

last: Jixiang

first: Lu

last: Siqi

first: Li

last: Yan

first: Dong

last: Yalun

first: Qiang

last: Jun

first: Xu

last: Pao


title: RNA sequencing of human monocyte-derived dendritic cells stimulated with CLEC10A ligand glycodendrimers in the presence of Pam3CysK4

city: Amsterdam

first: Nadia

last: van der Meijs

address: De Boelelaan 1108

department: MCBI

country: Netherlands

institute: Amsterdam UMC

summary: To investigate ligand-specific responses via CLEC10A in human monocyte-derived dendritic cells, five CLEC10A ligands were coupled to dendrimers. The ligands consist of alfa-GalNAc and the GalNAc-containing structures Forssman antigen, blood group A antigen, asialo GM2, and GM2. The human dendritic cells of 4 independent donors were stimulated with these glycodendrimers or a control dendrimer (coupled to C6 chain) for 5 hours in the presence of TLR stimulus Pam3CysK4. Total RNA was isolated and sequenced.

overall_design: Human monocyte-derived dendritic cells of 4 donors were each stimulated with 5 CLEC10A ligand glycodendrimers or a control glycodendrimer as reference. All 24 samples were included in the RNA sequencing.

first: Mike

last: de Kok

first: Sandra

last: van Vliet


title: Ribosomal RNA synthesis by RNA polymerase I is regulated by premature termination of transcription.

first: olivier

last: Gadal

first: Chaïma

last: Azouzi

first: Marion

last: Aguirrebengoa

first: Christophe

last: Dez

first: Olivier


title: Single cell-RNA Sequencing Shows Exercise Protects db/db Mouse Pancreatic Injuries by Regulating Endothelial Cells Homeostasis

city: Ruian

first: Wenya

last: Weng

state: Zhejiang

address: Room 1204, Science and Education Building, No. 168 Ruifeng Avenue, Anyang Street,

institute: the Third affliated hospital of Wenzhou medical University

summary: The prevalence and mortality rates of type 2 diabetes mellitus (T2DM) continue to increase, imposing a significant burden on individuals and nations worldwide. The pancreas plays an important role in T2DM development, while exercise is acrucial nonpharmacological treatment. Although the pancreas comprises various cell types, current studies on the effects of exercise on diabetes have mainly focused on the beta cells. In this study, we aimed to enhance our understanding of the effects of exercise on other pancreatic cell types. This was aimed at facilitating the comprehensive analysis of the processes and principles by which exercise protects and enhances pancreatic function.  Six-week-old male db/db mice were trained on a treadmill at a speed of 9 m/min for 10 weeks (50 min/day, 5 days/week). Single-cell RNA sequencing (scRNA-seq) was performed to analyze cell types in the pancreas.   The results showed that exercise improved the body weight and pancreas profile of db/db mice.The scRNA-seq demonstrated that the pancreas was composed of 12 cell types, with obvious changes in endothelial cells (ECs) among all groups. Further subtype analysis suggested that ECs could be annotated into five subtypes, with capillary ECs presenting remarkable differences among the groups. Additionally, Gene Ontology (GO) enrichment analysis showed the close role of capillary ECs, which are a cell group involved in vascular development and regulation of EC proliferation and migration in blood vessels.  The newly identified capillary ECs may be involved in the protective effect of exercise against pancreatic injury in db/db mice.

overall_design: To facilitate the comprehensive analysis of the processes and principles by which exercise protects and enhances pancreatic function, six-week-old male db/db mice were trained on a treadmill.Then single-cell RNA sequencing (scRNA-seq) was performed to analyze cell types in the pancreas.

first: Manjuan

last: Li

first: Mengmeng

last: Peng

first: Zixuan

last: Wang

first: Guoyong

last: Fan

first: Shicui

last: Jiang

first: Chi

last: Zhang

first: Xuemian

last: Lu


title: Remodeling of 3D Gene Architecture in Myocardium from Embryonic Development to Early Aging

city: Chengdu

first: Yuwei

last: Gou

address: No. 211, Huimin Road, Wenjiang District

institute: Sichuan Agricultural University

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

overall_design: Refer to individual Series


title: Epigenome analysis of SCC15 and SCC25  exposed to 0.5 μM JQ1 for 48 h compared with DMSO

city: guangzhong

first: yurui

last: liu

address: No. 1023-1063, Shatai South Road, Baiyun District, Guangzhou City, Guangdong Province

institute: Southern Medical University

type: Methylation profiling by genome tiling array

summary: Genome wide DNA methylation profiling of SCC15 and SCC25  exposed to 0.5 μM JQ1 for 48 h compared with DMSO.The Illumina Infinium Methylation EPIC BeadChip assay  was used to DNA methylation assays.

overall_design: Bisulphite converted DNA from the 12 samples were hybridised to the Illumina Infinium Methylation EPIC BeadChip assay

first: Zeting

last: Chen

first: Zixin

last: Hong

first: Huiling

last: Luo

first: Meiqun

first: Yurui

last: Liu


title: Functional Screening and Transcriptomic Analysis Identify Novel Druggable Dependencies and Immunotherapy Targets in Desmoplastic Small Round Cell Tumor

city: New York

first: Madelyn

last: Espinosa-Cotton

state: New York

address: 1275 York Ave

institute: Memorial Sloan Kettering Cancer Center

summary: Desmoplastic small round cell tumor (DSRCT) is a rare, primitive sarcoma most commonly found in the abdominal and pelvic cavities. DSRCT is characterized by a chromosomal translocation that leads to the formation of the EWSR1::WT1 fusion oncogene, which alters gene expression and drives oncogenesis. With the exception of this translocation, few other recurrent mutations have been identified making it challenging to develop targeted therapies. Given this low rate of recurrent mutations, we hypothesize that examining the DSRCT transcriptome may be more successful in identifying novel therapies. However, only limited transcriptomic analysis has been performed on primary DSRCT samples, none with associated outcomes data. Here we report the results of our effort to better characterize DSRCT using RNA-seq on more than 50 tumor samples. We identify pathways and genes not only enriched in DSRCT but associated with poor DSRCT prognosis and which may have important therapeutic implications. We further identify novel immunotherapy targets expressed on the surface of DSRCT and which have a greater specificity for DSRCT than current targets under investigation.

overall_design: RNA was islated from a set of 57 DSRCT tumors and 5 normal tissues with two replicates per sample

first: Nai-Kong

last: Cheung

first: Justin

last: Magrath

first: Sean

middle: B

last: Lee


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

city: Rehovot

first: Arunachalam

last: Sekar

address: Herzl street

department: IRB

institute: Weizmann Institute of Science


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

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

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

first: Eviatar

last: Weizmann

first: Ronnie

last: Blecher-Gonen


title: scRNA-seq of control and Etv1 mutant distal small intestinal organoid cultures

city: Copenhagen N

first: Kim

last: Jensen

address: Belgdamsvej 3B

country: Denmark

institute: University of Copenhagen

summary: To characterize the effect of mutating Etv1 on enteroendocrine cell specification and hormone expression, we performed scRNA-seq experiments analysing cells from control and Etv1 mutant organoid cultures from mouse distal small intestine. We identified 6 transcriptionally distinct clusters, that had a similar cellular contribution from controls and Etv1 mutants. In the cluster identified as enteroendocrine cells, we observed differences in hormone expression between controls and Etv1 mutants.

overall_design: Five samples containing 2 biological replicates from control cultures and 3 biological replicates from mutant Etv1 cultures, subjected to cell sorting and tagged using hashtag oligos. Subsequently, samples were pooled and sequenced with Illumina NovaSeq 6000 platform.

first: Astrid

last: Baattrup

first: Stine

last: Lind Hansen

first: Martti

last: Maimets

first: Cecilia

last: Lövkvist


title: Remodeling of 3D Gene Architecture in Myocardium from Embryonic Development to Early Aging [snRNA-Seq]

first: Yuwei

last: Gou

summary: Heart-related diseases are increasingly attacking the younger population, and getting more prevalent as the population ages. Better understanding of heart development and aging could help decipher the mechanism of associated heart diseases.  In this study, we reported the application of a typical miniature swine -- Tibetan pig, as human heart model, and illustrated the changes in higher-order chromatin structure and transcription regulation from fetal to sexual maturity and early senescence, as well as the role they play in physiological development and aging. We observed altered multi-scale structures of the 3D genome from territories and A/B compartments to TADs and loops/PEIs. Changes in territories and A/B compartments indicate high plasticity and disorganization of chromatin structure for the fetal and senescent stages, respectively, compared to the more ordered conformation for the young adult stage, embodied by Von Neumann Entropy (VNE) and compartmentalization strength indexes. From such coarse scale, we also observed that heterochromatin gradually stacked and relaxed during development and senescence, supported by evidence of change in intensity of B-B interactions and correlation between sequence features and A/B compartment switches, across the three critical stages. A finer examination of TAD and loops/PEIs showed that young adults tend to have more accurate transcription regulation through finer control of chromatin structure dynamics, supported by higher correlation of gene expression and TAD connectivity, more space between dynamic boundaries and their targeted genes, and stronger ‘loop skew’ towards A compartments. Another observation of monotonic increase in long-range interactions and decrease in short-range interactions throughout the development and senescent process indicates the gradual loss of plasticity for chromatin conformation.

overall_design: To investigate the changes in the three-dimensional conformation of chromatin during development and aging, as well as the relationship between its trend and transcriptional expression

first: Qianzi

last: Tang


title: BRD4 Inhibition Sensitizes Head and Neck Squamous Cell Carcinoma to Senescence without Pro-inflammatory Response

first: yurui

last: liu

summary: To investigate the function of JQ1 on head and neck squamous cell carcinoma,we treated SCC15 cells and SCC25 cells with JQ1.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for SCC15 and SCC25 cells before and after JQ1 treatment.

first: Zeting

last: Chen

first: Zixin

last: Hong

first: Huiling

first: Yin

last: Zhu

first: Jiayu

last: Li

first: Haiqiong

first: Qinpeng

first: Yu

first: Lishan

last: Ning

first: Xuan

last: Zhou

first: Shuyao

last: Xu


title: RNA-sequencing analysis of differential expressed genes in TGFβ-treated HK-2 cells after HDAC11 inhibition

city: Shenzhen

first: Han

last: Wu

address: Liuxian Road 1066

institute: Shenzhen University

summary: Renal fibrosis is a pathological damage associated with nearly all forms of kidney disease. Although a recent study has reported an association between upregulation of histone deacetylase 11 (HDAC11) levels in the kidneys and renal fibrosis in several different mouse models, however, the mechanisms remain elusive. Renal fibrosis is characterized by excessive accumulation of extracellular matrix (ECM), which includes type I and IV collagens, fibronectin and α-smooth muscle actin (α-SMA). The tubular epithelial injury and activation of pro-inflammation contribute to excessive collagen deposition in the pathogenesis of renal fibrosis. Here we aim to explore the role and the underlying mechanisms of HDAC11 in the of progression renal fibrosis. we performed RNA transcriptome sequencing to identify the differentially expressed genes (DEGs) between before and after HDAC11 inhibitor (FT895)-intreated HK-2 cells. GSEA analysis showed that the DEGs were highly enriched in the pathways of epithelial mesenchymal transition and inflammatory response, indicating that HDAC11 inhibitor may resistant to TGFβ-induced ECM deposition.

overall_design: To investigate the underlying mechanisms of HDAC11 functions in renal fibrosis, we established TGF-beta treated human renal epitehlial cell line HK-2 cells to mimic renal fibrosis.We performed gene expression profiling analysis using RNA-seq data from HK-2 cells treated with TGFb in the absence or presence of HDAC11 selective inhibitor, FT895.Comparative gene expression profiling analysis of RNA-seq data for HK-2 cells  treated by TGFb with the presence of DMSO as vehicle  (Vehicle+TGFb) and TGFb with the presence of FT895  (FT895+TGFb) for 1h or 12 h.


title: Effect of hypertonicity on chromatin accessibility and contribution of NFAT5

city: Halle

first: Bayram

last: Edemir

address: Ernst-Grube-Str. 20

institute: University Hospital Halle (Saale)

summary: Understanding the mechanisms underlying cell type-specific gene expression in the kidney is essential to elucidate renal function. Using the Assay for Transposase-Accessible Chromatin with high-throughput sequencing (ATAC-seq) we analyzed open chromatin structures and the involvement of epigenetic mechanisms in mediating gene expression differences between the renal cortex (CTX) and inner medulla (IM). We also examined the role of the nuclear factor of activated T cells 5 (NFAT5), a key regulator of hypertonicity. ATAC-seq analysis was performed on CTX and IM samples from both wild-type (WT) and NFAT5 knockout (KO) mice. This study revealed global differences in chromatin accessibility between renal CTX and IM and the impact of NFAT5 loss on open chromatin regions. Furthermore, spatial localization and NFAT5-promoted chromatin accessibility correlate with differential gene expression and altered promoter binding motif enrichment in CTX and IM. Our findings provide new insights into spatial and NFAT5-promoted transcriptional regulation in the kidney, and their importance for renal function and adaptation to osmotic stress.

overall_design: Renal cortex and renal inner medulla from WT (Aqp2-Cre+/-) and NFAT5-KO (NFAT5fl/fl-AQP2-470 CRE+/-) mice were used for ATAC-seq analysis. Mice are deficient in NFAT5 in the principal cells (PC) of the collecting duct. 3 replicate samples per tissue were analyzed.


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

first: Arunachalam

last: Sekar

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

first: Eviatar

last: Weizmann

first: Ronnie

last: Blecher-Gonen


title: scRNA-seq for E16.5 intestinal epithelial cells grown in conventional organoid cultures or as engineered tissues

first: Kim

last: Jensen

summary: As part of our characterization of cellular complexity within our in vitro cultures, we performed scRNA-seq experiments analysing mouse E16.5 intestinal epithelial cells cultured 1) in conventional organoid cultures 3D or 2) as engineered tissues on microfabricated hydrogel scaffolds. We identified 6 transcriptionally disting clusters of both, fetal and adult identity highlighting the cellular complexity within our in vitro models.

overall_design: Four samples containing 2 biological replicates from 3D cultures and two biological replicates from engineered tissues were collected, subjected to cell sorting and tagged using hashtag oligos. Subsequently, samples were pooled and sequenced with Illumina NovaSeq 6000 platform.

first: Martti

last: Maimets

first: Cecilia

first: Astrid

last: Baattrup

first: Stine

last: Hansen


title: Soybean Foral Whorl Expression Atlas

city: Ithaca

first: Nicole

last: Szeluga

state: NY

address: 236 Tower Road

department: Plant Biology

institute: Cornell University

summary: This Soybean Floral Whorl Atlas is composed of RNA-Seq and ChIP-Seq data collected from individual floral whorls and floral developmental stages in Glycine max.

overall_design: To build a floral whorl atlas, we dissected individual floral whorls from young flower buds (< 1mm) and two developmental stages (flower bud and mature flower) from soybean cultivar Williams 82 for 3' RNAseq analysis. Leaf was used as a control and three replicates were taken from each tissue type.

first: Margaret

last: Frank


title: Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [ATAC-Seq]

city: Cold Spring Harbor

first: Aybuke

last: Alici

address: 1 Bungtown Rd.

institute: Cold Spring Harbor Laboratory

summary: We performed epigenetic profiling to assess the effects of arachidonic acid (AA) on intestinal stem cell regeneration via ATAC-seq and found that AA treatment led to global changes in chromatin accessibility of genes that are associated with stem cell reprogramming.

overall_design: ATAC-seq profiles of  mouse intestinal organoids after treatment with vehicle, arachidonic acid or 6,16-dimethyl PGE2.

first: Onur

last: Eskiocak

first: Semir

last: Beyaz

first: Cem

last: Meydan

first: Vyom

last: Shah


title: Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [CutnRun 2]

summary: We performed epigenomic profiling to evaluate the effects of  arachidonic acid (AA) on intestinal stem cell regeneration via CutnRun and found that AA treatment led to global changes in methylation status of genes that are associated with stem cell reprogramming.

overall_design: Cut&Run was performed from mouse intestinal organoids treated with vehicle, arachidonic acid or 6,16-dimethyl PGE2 for H3K27me3, H3K27ac, H3K4me3.

last: Alici-Garipcan


title: RNA-Seq in undifferentiated and differentiated retinoblastoma

city: Essen

first: Karim

last: Al-Ghazzawi

address: Hufelandstraße 55

department: Ophthalmology

institute: University-Clinic Duisburg-Essen

summary: Contributor to high-risk subgroup were successfully identified with the help of NanoString nCounter platform for digital gene expression analysis with the appurtenant PanCancerProfiling panel, consisting of 770 genes as well as 30 reference genes

overall_design: 23 Retinoblastoma samples divided according to their histopathological classification were analyzed


title: Epigenetic reprogramming of intestinal stemness by dietary arachidonic acid [CutnRun 1]

summary: We evaluated tthe necessity of PGE2-Ptger4 signaling in regulating stemness enhancing effects of arachidonic acid (AA) via CutnRun and found that Ptger4 KO organoids failed to cause  global methylation changes in signature genes that are associated with stem cell reprogramming in response to AA or PGE2.

overall_design: Cut&Run was performed from Ptger KO intestinal organoids treated with vehicle,  25 µM AA or 50 nM 6,16-dimethyl PGE2 for H3K27ac.


title: Loss of METTL3 potentiates transposable element expression and drives inflammation-induced cell plasticity in the mammary epithelium [RNA-seq]

city: Boston

first: Xintao

last: Qiu

address: 440 brookline ave

institute: Dana Faber Cancer Institute

summary: Sustained proliferation and aberrant cellular plasticity are the hallmarks of breast premalignancy, yet the mechanisms driving this process remain unclear. Using CRISPR knockout screens, we systematically characterized the regulators of cellular fitness in the normal mammary epithelium. We found that loss of RNA methyltransferase METTL3 initiates mammary epithelial proliferation and reprograms gene expression, which depends on its catalytic activity. Single-cell analysis in normal breast organoids revealed that METTL3 ablation causes disruption of the mammary cellular hierarchy through increased aberrant luminal differentiation. Mechanically, METTL3 loss reduces the RNA m6A modification of transcribed transposable elements leading to their increased expression and upregulating interferon-STAT signaling. This inflammatory response leads to the crosstalk between STAT and GATA3 transcription factors, resulting in transcriptional activation of luminal genes in the mammary epithelium. These findings identify a cell-intrinsic epigenetic loop contributing to mammary epithelial plasticity and highlight a potential role of METTL3-dependent m6A modification during neoplastic transformation.

overall_design: To identify the regulatory mechanisms that contribute to increased cell fitness in mammary epithelial cells upon METTL3 depletion, we assessed the RNA expression profile in control and METTL3 KO cells.


title: Serine Hydroxymethyltransferase 6 is involved in growth and resistance against pathogens via ethylene and lignin production in Arabidopsis

city: New Delhi

first: Jagadis

middle: Gupta

last: Kapuganti

state: Delhi

address: Indusind bank OMMON CAUSE HOUSE, 5,INSTITUTIONAL AREA, NELSON MANDELA ROAD, VASANT KUNJ, NEW DELHI-110070

country: India

institute: National Institute of Plant Genome Research

summary: Photorespiratory serine hydroxymethyltransferases (SHMTs) are important enzymes of cellular one-carbon metabolism. In this work, we investigated the potential role of SHMT6 in Arabidopsis thaliana. We found that SHMT6 is localized in the nucleus and expressed in different tissues during development. Interestingly the gene is inducible in response to avirulent, virulent Pseudomonas syringae and to Fusarium oxysporum infection. Overexpression of SHMT6 leads to large flowers, siliques, seeds, roots and enhanced biomass. This enhanced growth was accompanied by increased stomatal conductance and photosynthetic capacity as well as ATP, protein, and chlorophyll levels. By contrast, a shmt6 knockout mutant displayed reduced growth. When challenged with Pseudomonas syringae pv tomato (Pst) DC3000 expressing AvrRpm1, SHMT6 overexpression lines displayed a clear hypersensitive response which was characterized by enhanced electrolyte leakage and reduced bacterial growth. In response to virulent Pst DC3000, the shmt6 mutant developed severe disease symptoms and becomes very susceptible, whereas SHMT6 overexpression lines showed enhanced resistance with increased expression of defense pathways. In response to Fusarium oxysporum, overexpression lines showed reduction in symptoms. Moreover, SHMT6 overexpression lead to enhanced production of ethylene and lignin, which are important components of the defense response. Transcriptome analysis of shmt6 mutant and WT showed that several genes involved in defense, ethylene and lignin pathways are suppressed in the mutant. Collectively, our data reveal that SHMT6 plays an important role in development and defense against pathogens.

overall_design: Pseudomonas syringae pv. Tomato (Pst) DC3000 was grown at 28°C in King’s B (KB) medium supplemented with 50 mg/ml rifampicin. After overnight cultivation, a bacterial suspension was prepared in 10 mM MgCl2 at OD600 0.2 (Pst AvrRpm1). Four-week-old soilrite and agropeat grown fully expanded Arabidopsis leaves were infiltrated with suspension of avirulent Pseudomonas syringae pv tomato (Pst) DC3000 in 10 mM MgCl2 at OD600 = 0.04. Control (10 mM MgCl2) and pathogen infiltrated samples were harvested at 6 hours of infection.

first: Pooja

last: Singh

middle: G

first: Priyanka

last: Jain


title: MeRIP-Seq analysis in thyroid cancer cells knocking down METTL3

city: Tianjin

first: Junya

last: Ning

state: -- None --

address: Huanhuxi Road, Hexi District, Tianjin

institute: Tianjin Medical University Cancer Institute & Hospital

type: Methylation profiling by high throughput sequencing

summary: To detect METTL3-mediated m6A methylated transcript in thyroid cancer, we performed MeRIP-Seq of control and METTL3 knockdown BCPAP cells

overall_design: We knocked down METTL3 in BCPAP cells and performed the MeRIP-Seq analysis in order to examine the m6A methylated transcript after METTL3 knockdown

first: Xiukun

last: Hou

first: Jie

last: Hao


title: SRSF1 knockdown alleviates the ribosomal stress-induced inhibition of cell proliferation through the MAPK signaling pathway

city: shanghai

first: Yuxin

last: Zhao

address: 2999 north renmin road

institute: Donghua University

summary: To investigate the regulatory function of the RNA-binding protein SRSF1 in short-term starvation-induced ribosomal stress (RS), we established the 293T starvation model and the SRSF1 knockdown model. We then performed gene expression profiling using the data obtained from RNA-seq of 293T cells from 3 different treatments.

overall_design: Comparative gene expression profiling of RNA-seq data of 293T cells and their KD derivatives (shSRSF1, shSRPK1, and shUPF1).

first: Junhua

last: Xiao


title: MCF7 cells were cultured in pH6.6 medium for 6/12/24h

city: Hangzhou, Zhejiang 310014, P. R. China.

first: zhuazhua

last: Wu

state: ZheJiang

address: 158 Shangtang Road

department: Center of Oncology, Department of Medical Oncology

institute: Zhejiang Provincial People’s Hospital, People’s Hospital of Hangzhou Medical College

summary: Acidosis has been found to have multiple effects on tumor cells and immune cells among the tumor microenvironment. Ferroptosis is a nonapoptotic and iron-dependent form of cell death characterized by the accumulation of lipid peroxidation involved in various cancers. However, recent ferroptosis researches in the breast cancer (BC) acidic microenvironment context remains unrevealed. Acidosis induced ferroptosis in the ZFAND5/SLC3A2 independent manner to suppress tumor growth using in silico and multiple biological experiments. Mechanistically, we demonstrated that acidosis increased total/lipid ROS level, decreased GSH level and induced the morphological changes of mitochondria. Specifically, acidosis restrained the protein stability of SLC3A2 by promoting its ubiquitination process. Furthermore, acidosis combined with metformin or macrophages, could work in a synergistic manner to suppress the proliferation and enhance the ferroptosis of BC cells. This study firstly demonstrated that the ability of combination of acidosis and metformin, macrophages to induce ferroptosis might be a novel mechanism underlying its anti-BC effect.

overall_design: RNA-saq analysis of MCF7 cells cultured in pH6.6 medium for 6/12/24h

first: Hanchu

last: Xiong

first: Liu

last: Yang


title: ChIP-seq analysis in Cal-62 cells treated with Niraparib

address: Huanhu Road

institute: Tianjin Cancer Institute and Hospital

summary:
To assess the function of Niraparib in thyroid cancer, we performed transcriptome analysis through high-throughput CHIP-Seq of PARP1 in DMSO and Niraparib treated Cal-62 cells
Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for PARP1 in DMSO and Niraparib treated Cal-62 cells.

overall_design: Xiukun,Hou

first: Mengran

last: Tian


title: RNA-seq analysis in thyroid cancer cells knocking down METTL3

summary: To assess the function of METTL3 in thyroid cancer, we performed transcriptome analysis through high-throughput RNA-Seq of control and METTL3 knockdown BCPAP cells

overall_design: We knocked down METTL3 in BCPAP cells and performed the RNA-seq analysis in order to exam the transcriptome after METTL3 knockdown