title: Age and cell type specific specific effects of histone variant H2BE in the brain

city: Philadelphia

first: Sean

last: Louzon

state: PA

address: 3400 Civic Center Blvd

institute: University of Pennsylvania


title: Efficacy of longevity interventions in C. elegans is determined by early life activity of RNA splicing factors II

status: Public on Nov 07 2025

city: Boston

first: William

middle: B

last: Mair

state: MA

address: 677 Huntington Avenue

department: Molecular Metabolism

country: USA

institute: Harvard TH Chan School of Public Health

type: Expression profiling by high throughput sequencing

summary: Geroscience aims to target the aging process to extend healthspan. However, even isogenic individuals show heterogeneity in natural aging rate and responsiveness to pro-longevity interventions, limiting translational potential. Using in vivo mini gene reporters in isogenic C. elegans, we show that alternative splicing of mRNAs related to lipid metabolism in young animals is coupled to subsequent life expectancy. Further, activity of RNA splicing factors REPO-1 and SFA-1 early in life modulates effectiveness of specific longevity interventions via POD-2/ACC1 and regulation of lipid utilization.  In addition, early inhibition of REPO-1 renders animals refractory to late onset suppression of the TORC1 pathway. Together these data suggest that activity of RNA splicing factors and the metabolic landscape early in life can modulate responsiveness to longevity interventions and may explain variance in efficacy between individuals.

overall_design: RNA-seq of wild type N2, eat-2(ad1116), raga-1(ok386), clk-1(qm30) and age-1(hx546) C. elegans +/- repo-1 RNAi from hatch collected at day 1 of adulthood

first: Sneha

last: Dutta

first: Maria

middle: C

last: Perez-Matos

first: Caroline

last: Heintz

first: Mary

last: Piper

first: Meeta

last: Mistry

first: Arpit

last: Sharma

first: Hannah

last: Smith

first: Porsha

last: Howell

first: Rohan

last: Sehgal

first: Anne

last: Lanjuin

first: Meng

last: Wang


title: PLAMseq enables the simultaneous proteo-genomic characterization of chromatin-associated proteins and protein interactions in a single workflow.

city: Sevilla

first: Román

last: González-Prieto

address: Americo Vespucio 24

country: Spain

institute: CABIMER

summary:
Chromatin Immunoprecipitation (ChIP) and Co-Immunoprecipitation (CoIP) assays are the most common approaches to characterize the genomic localization and protein interactors, respectively for a protein of interest. However, these approaches require the use of specific antibodies, which are costly reagents that often face sensitivity and specificity issues. Based on TurboID, we developed PLAMseq (Proximity Labelled Affinity-purified Mass spectrometry plus sequencing), after a short biotin pulse, DNA-protein crosslinks are induced by formaldehyde and the interactors of a protein of interest together with their associated DNA sequences are purified simultaneously and identified by mass spectrometry-based proteomics and Next Generation Sequencing, respectively.
To validate PLAMseq, we performed the proteo-genomic characterization of two proteins which genomic loci are very well characterized, namely, RNA polymerase II and CTCF with excellent robustness and reproducibility. Next, we applied PLAMseq to characterize Histone H1 SUMOylation, a histone post-translational modification which study has remained elusive due to the lack of specific reagents. SETDB1 binds to SUMOylated histone H1 and, accordingly, SUMOylated histone H1 colocalize with H3K9me3 at repetitive regions of the genome.

overall_design: PLAMseq (Proximity Labelled Affinity-purified Mass spectrometry plus sequencing) was performed in CTCF-TurboID, POL2RI-TurboID, TurboID-H1.2, TurboID-H1.4, TurboID-H1.0, NTurboID-H1.2 + CTurboID-SUMO1, NTurboID-H1.2 + CTurboID-SUMO2, NTurboID-H1.4 + CTurboID-SUMO1, NTurboID-H1.4 + CTurboID-SUMO2, NTurboID-H1.0 + CTurboID-SUMO1, NTurboID-H1.0 + CTurboID-SUMO2, TurboID-only and Wild Type HeLa cell lines after 10 minutes biotin 1x exposure. All experiments were done in triplicate.

first: Lourdes

last: González-Vinceiro

first: Carmen

last: Espejo-Serrano

first: María Eugenia

last: Soler-Oliva

first: María Luisa

last: Mateos-Martín

first: Daniel

last: Rico

first: Cristina

last: González-Aguilera


title: Single cell (sc) RNAseq reveals transcriptional states of transgenic MAGE-A1 specific TCR-T CD4+ and CD8+ cells in NSG tumor model

city: Seattle

first: Aude

last: Chapuis

state: WA

address: 1100 Fairview Ave

institute: Fred Hutchinson Cancer Center

summary: We have studied the efficacy of MAGE-A1 specific transgenic T cells against A375F NSG model by flow cytometry and IHC analysis. We then employed a scRNAseq approach to characterize the transcriptional states of transgenic CD4+ and CD8+ TCR-T cells that infiltrated into A375F tumor by extracting these cells from tumors. This scRNAseq study allow us to compare the transcriptional differences between our groups ( T-TCR-MA1-CD8ab, T-TCR-MA1-CD8/28)

overall_design: CD4+ and CD8+ T-TCR-MA1-CD8ab, T-TCR-MA1-CD8/28 were infused into in vivo murine models with A375F tumor cell line as described in methods.  Four  of the following group were compared: CD4+  T-TCR-MA1-CD8ab only , CD8+  T-TCR-MA1-CD8ab only, CD4+ and CD8+ T-TCR-MA1-CD8ab combo, and  CD4+ and CD8+ T-TCR-MA1-CD8/28 combo. Tumors (n=6) were digested and CD4+ and CD8+ T cells were sorted from single cell suspension.  CD4+ only and CD8+ only T-TCR-MA1-CD8ab (pooled as one sample) (NSG_CD8_4), CD4+ and CD8+ T-TCR-MA1-CD8ab combo(NSG_WT), and CD4+ and CD8+ T-TCR-MA1-CD8/28 combo(NSG_G) were then continued for scRNA seq library prep.

first: Shihong

last: Zhang

first: Tzu-Hao

last: Tang

first: Sinead

last: Kinsella

first: Francesco

last: Mazziotta

first: Lauren

last: Martin

first: Bo

last: Lee


title: Location and etiology modulate fibroblast activation in the failing human heart

status: Public on Nov 08 2025

city: Leuven

first: Hywel

middle: Llewelyn

last: Roderick

address: Herestraat 49

department: Cardiovascular Sciences

country: Belgium

institute: Katholieke Universiteit Leuven

summary: Cardiac fibrosis is a major contributor to heart failure (HF), yet its therapeutic targeting remains limited due to the complexity of fibrosis types and distributions. This study investigates fibroblast heterogeneity and spatial organization in the left ventricle of human hearts from non-failing donors and HF patients with ischemic or dilated cardiomyopathy. Using single-nucleus RNA sequencing and spatial transcriptomics, distinct fibroblast subpopulations were identified, with resident fibroblasts being depleted in HF and replaced by disease-associated states. Differences in activation ligands, transcriptional trajectories, and spatial localization revealed divergent fibroblast transitions between scar and interstitial fibrosis, and between HF subtypes. These results provide insight into fibroblast dynamics and offer potential targets to modulate fibrosis in heart failure.

overall_design: Nuclei from snap frozen human cardiac tissue was sequenced using 10x technology in 3 batches. 4 non-failing samples included (each 2 in one 10x lane). 6 samples from DCM, 5 samples from ICM (non-scar), and 5 samples form ICM-scar were included.

first: Mohamad

last: Youness

first: Samaneh

last: Ekhteraei-Tousi

first: Rosa

last: Doñate Puertas

first: Chandan

middle: K

last: Nagaraju

first: Karin

middle: R

last: Sipido

middle: L


title: Survival factors for human microglia

city: Lucknow

first: Shailendra K

last: Saxena

state: UP

address: Chowk

department: Centre for Advanced Research

country: India

institute: King George's Medical University

summary: Microglia is a type of neuroglia (glial cell) located in entire brain and spinal cord playing a crucial role in microglial-associated disorders, immunity, homeostasis of brain and neuronal recovery. Except few growth factors, no drugs are available to enhance the microglial cell survival. Therefore, identification of factors inducing microglia survival is a cost effectove therapeutic intervention which may be utilized in various microglia associated disorders. Cells were treated with drugs (muscarinic receptor antagonists) that may have a role in cell survival and total RNA was isolated from three idenpendent exprements and pooled for whole-transcriptome sequencing. The gene expression  analysis suggested that drugs exhibits microglia survival properties by reducing the caspase activation and other pro-apoptotic factors. In addtion, the anti-apoptotic genes were found to be significanlty upregulated. Furthermore, microglia associated diorders genes were analyzed and was found that the drug may be effective for the treatment of range of neurological disorders.

overall_design: Total RNA was isolated from control and drug treated (muscarinic receptor antagonists) human microglia. Total RNA of 1000 ng with RNA integrity number (RIN) of 9.0 and above was used for library preparation using TruSeq RNA Sample Preparation Kit, Illumina. Approximately, 150-300 ng of each samples were used for generating sequencing libraries using TruSeq RNA Library Prep Kits for Illumina®. cBot Cluster Generation System was used to perform clustering of the index-coded samples using the TruSeq PE Cluster Kit v3-cBot-HS (Illumina). Sequencing was performed using Illumina Hi-Seq platform 2500 sequencing system, as per the standard protocol.

first: Swatantra

last: Kumar

first: Shailendra


title: Efficacy of longevity interventions in C. elegans is determined by early life activity of RNA splicing factors

first: William

last: Mair

overall_design: RNA-seq of KH2235 C. elegans (ret-1 mini gene splicing reporter) separated at day 6 by fluorescence (mostly GFP versus mostly mCherry). Comparison of the two groups, each with 6 replicates.

first: Sneha

last: Dutta

first: Maria C.

last: Perez-Matos

first: Caroline

last: Heintz

first: Mary

last: Piper

first: Meeta

last: Mistry

first: Arpit

last: Sharma

first: Hannah

last: Smith

first: Porsha

last: Howell

first: Rohan

last: Sehgal

first: Anne

last: Lanjuin

first: Meng C.

last: Wang

first: William B.


title: Modulation of Inflammatory Pain by Myeloid FABP5

city: Stony Brook

first: Martin

last: Kaczocha

address: Health Sciences Center

institute: Stony Brook University

summary: The initiation and maintenance of pain involves complex neuroimmune interactions, with myeloid cell output finetuning the balance between pronociceptive and antinociceptive signaling. Fatty acid binding protein 5 (FABP5) is a lipid chaperone whose inhibition produces antinociceptive effects in models of inflammatory pain. While FABP5 is highly expressed in myeloid cells that are recruited to sites of inflammation, the contribution of myeloid FABP5 to nociception is unknown. Utilizing myeloid-specific FABP5 conditional knockout (cKO) mice, we demonstrate that FABP5+ myeloid cells infiltrate into the paw following the onset of carrageenan-induced inflammation. However, myeloid cell recruitment was unaffected by FABP5 deletion. FABP5 cKO were characterized by attenuated development of inflammatory thermal hyperalgesia, which was observed throughout the experimental time course and was evident in both sexes. Transcriptomic profiling of myeloid cells obtained from carrageenan injected paws identified numerous differentially expressed genes between FABP5 cKO mice and Flox controls. Notably, FABP5 cKO myeloid cells featured elevated expression of interleukin-10 (IL-10), consistent with previous findings demonstrating that FABP5 deletion polarizes myeloid cells towards an M2-like anti-inflammatory phenotype. Collectively, this study ascribes a new role to myeloid FABP5 in pain modulation and provides additional evidence that the regulation of nociception by FABP5 involves distinct mechanisms across multiple anatomical loci and cell populations.

overall_design: CD45+/CD11b+/Ly6G- cells were isolated from paws of FABP5Flox and FABP5Flox/LysM-Cre mice 4 hours after intraplantar injection of saline (vehicle control) or carrageenan. Samples were collected from both Flox and myeloid-specific FABP5 conditional knockout (LysMCre) mice. For each of the 12 total samples, cells from 3-4 mice were pooled to ensure sufficient RNA yield. RNA was extracted using the PUrelink Micro RNA kit, and RNA-seq libraries were prepared using Lexogen protocols. Sequencing was performed on the Illumina NovaSeq platform.

first: Faniya

last: Doswell


title: The methyl-CpG-binding protein 2 inhibits cGAS-associated signaling

city: Montpellier

first: Nadine

last: LAGUETTE

address: 1919 Rte de Mende

country: France

institute: Institut de Génétique Moléculaire de Montpellier

summary: We analyzed the impact of dsDNA stimulation on transcriptomics and retrotranscriptomics profiles in murine cell lines (Mouse Embryonic Fribroblasts and RAW264.7).

overall_design: WT-RAW264.7  and WT-MEF were transfected (or not: Mock) with dsDNA prior to RNA or DNA extraction respectively.  WT and Mecp2 KO RAW264.7 cells were subjected to RNA extraction. All experiemtns were performed in triplicates.

first: Hanane

last: Chamma

first: Soumyabrata

last: Guha

first: Roger Junior

last: Eloiflin

first: Adeline

last: Augereau

first: Pierre

last: Le Hars

first: Moritz

last: Schüssler

first: Yasmine

last: Messaoud-Nacer

first: Mohammad

last: Salma

first: Joe

last: McKellar

first: Joanna

last: Re

first: Morgane

last: Chemarin

first: Arnaud

last: Carrier

first: Michael

middle: A

last: Disyak

first: Clara

last: Taffoni

first: Robin

last: Charpentier

first: Zoé

last: Husson

first: Emmanuel

last: Valjent

first: Charlotte

last: Andrieu-Soler

first: Eric

last: Soler

first: Maria

middle: H

last: Christensen

first: Søren

last: Paludan

first: Florian

middle: I

last: Schmidt

first: Daniela

last: Tropea

first: Karim

last: Majzoub

first: Isabelle

last: Vila

last: Laguette


title: Non-canonical functions of UGT2B17 promote castrate-resistant prostate cancer progression

city: Vancour

first: Xuesen

last: Dong

address: 276 - 2660 Oak Street

country: Canada

institute: Vancour Prostate Cancer

summary: When prostate cancer (PCa) overcomes the androgen receptor (AR) target therapy and progresses to the castrate-resistant prostate cancer (CRPC) stage, it becomes curable. UDP glucuronosyltransferase 2B17 (UGT2B17) is the key enzyme determining androgen bioavailability to AR inside PCa cells. However, whether UGT2B17 promotes CRPC progression remains poorly understood. Here, we report that anti-AR therapy increases UGT2B17 protein stability. UGT2B17 is localized in both the cytoplasm and nucleus to exert multiple non-enzymatic functions. In the cytoplasm, UGT2B17 activates unfolded protein response (UPR) to counteract endoplasmic reticulum (ER) stress for cell survival. UGT2B17 can exert its nuclear functions by stimulating c-Src kinase to activate AR in the absence of androgens. The UGT2B17-Src axis confers PCa cells resistant to DNA damage and promotes cell cycling by passing the G2 checkpoints through de-activating ATM and ATR kinases. We conclude that these non-enzymatic functions of UGT2B17 activate multiple survival pathways to allow CRPC progression.

overall_design: RNA-seq analysis comparing the transcriptome between LNCaP95(UGT2B17 KO) and LNCaP95(UGT2B17 KO) transfected with UGT2B17WT UGT2B17Mut SRCK259M or SRCY530F


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

city: La Jolla

first: Jeffrey

last: Reina

state: CA

address: 10010 N Torrey Pines Rd

institute: Salk Institute for Biological Studies

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

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

first: Queralt

last: Vallmajo-Martin

first: Jia

last: Ning

first: Aubrey

last: Michi

first: Kay

last: Yeung

first: Geoffrey

middle: M

last: Wahl

first: Tony

last: Hunter


title: Cannabis Use and Cannabidiol Modulate HIV-Induced Alterations in TREM2 Expression: Implications for Age-Related Neuropathogenesis

first: Jerel

middle: Adam

last: Fields

address: 5320 La Jolla Hermosa Ave

department: Psychiatry

institute: University of California, San Diego

summary: The study investigates the modulation of TREM2 and related gene expression in HIV- and HIV+ individuals with varying cannabis use patterns. RNA-seq data were obtained from monocyte-derived macrophages exposed to CBD, IL1B, and CBD+IL1B. This study aims to identify mechanisms by which CBD may alter neuroinflammatory processes relevant to TREM2, aging, and neuropathogenesis in people living with HIV.

overall_design: Peripheral blood mononuclear cell (PBMC) isolation was performed on blood collected from HIV+ and HIV- individuals with different cannabis use patterns. Monocytes were cultured in human-serum-supplemented media and differentiated into monocyte-derived macrophages (MDMs) over 7 days. Treatments with vehicle, IL1B, cannabidiol (CBD), and CBD+IL1B (C+I) occurred for 6 hours before RNA isolation. This experiment includes gene expression profiling analysis of RNA-seq data from treated MDMs isolated from HIV- Naïve, HIV+ Naïve, HIV+ Moderate, and HIV+ Daily cannabis users.

first: Bryant

last: Avalos


title: Alteration of Autophagy and Glial Activity in Nilotinib-Treated Huntington’s Disease Patients

city: Washington, DC

first: Max

last: Stevenson

state: DC

address: 3970 Reservoir Rd. NW

institute: Georgetown University

type: Non-coding RNA profiling by high throughput sequencing

summary: We explored the effects of a low dose of nilotinib (150 mg) on behavioral changes and motor symptoms in manifest HD patients and examined the effects of nilotinib on several brain mechanisms, including dopamine transmission and gene expression via cerebrospinal fluid (CSF) miRNA sequencing. Nilotinib, 150 mg, did not result in any behavioral changes, although it significantly attenuated HVA levels, suggesting reduction of dopamine catabolism. There was no significant change in HTT, phosphorylated neuro-filament and inflammatory markers in the CSF and plasma via immunoassays. Whole miRNA genome sequencing of the CSF revealed significant longitudinal changes in miRNAs that control specific genes associated with autophagy, inflammation, microglial activity and basal ganglia neurotransmitters, including dopamine and serotonin.

overall_design: We performed whole genome miRNA sequencing in the CSF (n = 5) collected at baseline and 3 months from each individual patient to allow us to measure longitudinal miRNA changes. miRNAs inversely regulate mRNA, and they do not necessarily require large changes to affect their targets, therefore, we assessed all miRNA that met p < 0.05 between 3 months and baseline

first: Rency

last: Varghese

first: Charbel

last: Moussa


title: Endogenous production of nitric oxide by iNOS in human cells restricts inflammatory activation and cholesterol/fatty acid biosynthesis

city: Burnaby

first: Jonathan

last: Choy

state: BC

address: 8888 University Dr W

department: Molecular Biology and Biochemistry

institute: Simon Fraser University

summary: Nitric oxide (NO) is a bioactive gas that is known to control many physiological processes. In human parenchymal cells, the function of iNOS-derived NO is incompletely understood. Here, we used RNA-seq to examine the role of iNOS-derived NO in the control of gene expression in a human lung epithelial cell line treated with inflammatory cytokines. iNOS-derived NO restricted the expression of genes involved in immune signaling, including the immune-related genes CXCL9 and E-selectin that were not previously known to be inhibited by iNOS. We also determined that iNOS-derived NO inhibits the expression of genes needed for cholesterol/fatty acid biosynthesis in response to cytokine stimulation, a process not previously known to be affected by NO. These findings establish the regulation of immune activation and cholesterol/fatty acid biosynthesis as main functions of iNOS in human parenchymal cells.

overall_design: Our aim is to understand how iNOS-derived NO impacts cytokine-induced gene expression in A549 cells. To achieve this, cells were untreated, treated with 1400W (a selective iNOS inhibitor) alone, treated with cytokines or treated with cytokines and 1400W in quadruplicates for 16 hours. Our main findings were established by comparing cytokine-treated and cytokine+1400W-treated cells.

first: Franklin

middle: F

last: Tam

first: Jenice

last: Dumlao

first: Amy

last: Lee


title: Small RNA-seq of exosomes derived from fetal (55d) skin epithelial cells of Inner Mongolia cashmere goats

city: Hohhot

first: Hai

last: erhan

state: Inner Mongolia

address: Inner Mongolia Key Laboratory of Sheep & Goat Genetics Breeding and Reproduction

country: China

institute: Inner Mongolia Agricultural University

summary: Small RNA-seq of exosomes derived from epithelial cells of skin tissue on the side of the body of Inner Mongolia cashmere goats at 55 days of fetal development


title: Single cell transcriptional analysis of human adenoids identifies molecular features of airway microfold cells

city: Dallas

first: Samuel

last: Alvarez-Arguedas

state: Texas

address: 5323 Harry Hines Blvd

department: Internal Medicine

institute: University of Texas Southwestern Medical Center

summary: The nasal, oropharyngeal, and bronchial mucosa are the initial contact points for airborne pathogens like Mycobacterium tuberculosis (Mtb), SARS-CoV-2, and influenza virus. While mucosal surfaces can function as both entry points and barriers to infection, mucosa-associated lymphoid tissues (MALT) facilitate early immune responses to mucosal antigens. MALT contains a variety of specialized epithelial cells, including a rare cell type called a microfold cell (M cell) that functions to transport apical antigens to basolateral antigen-presenting cells, a crucial step in the initiation of mucosal immunity. M cells have been extensively characterized in the gastrointestinal (GI) tract in murine and human models. However, the precise development and functions of human airway M cells is unknown. Here, using single-nucleus RNA sequencing (snRNA-seq), we generated an atlas of cells from the human adenoid and identified 16 unique cell types representing basal, club, hillock, and hematopoietic lineages, defined their developmental trajectories, and determined cell-cell relationships. Using trajectory analysis, we found that human airway M cells develop from progenitor club cells and express a gene signature distinct from intestinal M cells. Surprisingly, we also identified a heretofore unknown epithelial cell type demonstrating a robust interferon-stimulated gene signature. Our analysis of human adenoid cells enhances our understanding of mucosal immune responses and the role of M cells in airway immunity. This work also provides a resource for understanding early interactions of pathogens with airway mucosa and a platform for development of mucosal vaccines.

overall_design: Human adenoid samples collected from 6 donors (age 2 – 14; 3 males and 3 females) from elective adenoidectomy for obstructive sleep apnea. All samples were obtained at the Children’s Medical Center of Dallas.

first: Khadijah

last: Mazhar

first: Andi

last: Wangzhou

first: Ishwarya

last: Sankaranarayanan

first: Gabriela

last: Gaona

first: John

middle: T

last: Lafin

first: Ron

last: Mitchell

first: Theodore

middle: J

last: Price

first: Michael

middle: U

last: Shiloh


title: Cannabidiol exerts anti-inflammatory effects but maintains T effector memory cell differentiation: A Single-Cell Study in Humans [scRNA-seq]

city: Indianapolis

last: Eadon

state: IN

address: 950 West Walnut Street Room 402 Room 402

institute: Indiana University School of Medicine

summary: Cannabidiol is widely available and often used for pain management. Individuals with kidney disease or renal allografts  have limited analgesia options. We conducted a Phase 1 healthy volunteer study to compare the peripheral immune cell  distribution before (pre-cannabidiol) and after exposure to cannabidiol at steady state (post-cannabidiol).  This study included specimens from  12 participants who received oral cannabidiol (up to 5 mg/kg twice daily)  for 12 days. Lymphocytes were isolated and stimulated with anti-CD3/CD28 antibodies, with or without tacrolimus.  Understanding the clinical safety of cannabidiol use is important given the paucity of pain control options available for  immunocompromised transplant populations. Each individual has three conditions that are sequenced for the phase No CD3/CD28, CD3/CD28 and CD3/CD28 +Tacrolimus across two phases: pre-CBD and post-CBD.

overall_design:
PBMCs were collected from each participant at Day 1 (pre-CBD) and Day 12 (post-CBD). Cells were cultured ex vivo for 72 h under six conditions that combine T-cell stimulation (±CD3/CD28), cannabidiol (±CBD), and tacrolimus (±TAC). After culture, cells were processed for single-cell RNA-seq using the 10x Genomics Chromium 3′ v3.1 workflow and sequenced on an Illumina NovaSeq 6000. In total, 59 libraries (6 conditions × 2 time-points × participants) capture transcriptomic effects of CBD, TAC, and T-cell activation:
1 - No CD3/CD28, No CBD, No Tacrolimus;
2 - CD3/CD28, No CBD; No Tacrolimus;
3 - CD3/CD28, No CBD, Tacrolimus;
4 - No CD3/CD28, CBD; No Tacrolimus;
5 - CD3/CD28, CBD; No Tacrolimus;
6 - CD3/CD28, CBD; Tacrolimus;

first: Debora

last: Gisch


title: ISR inhibition prolongs the lifespan of a Pelizaeus-Merzbacher disease mouse model by increasing oligodendrocyte survival

city: Chicago

first: Brian

last: Popko

state: IL

address: 7601 Morton Medical Research Building, 320 East Superior Street

department: Neurology

institute: Northwestern Feinberg School of Medicine

summary: The leukodystrophy Pelizaeus-Merzbacher disease (PMD) is caused by myelin protein proteolipid protein (PLP) gene mutations.  PMD is characterized by oligodendrocyte death and CNS hypomyelination; thus, increasing oligodendrocyte survival and enhancing myelination could provide therapeutic benefit.  We used the PMD mouse model Jimpy to explore the impact of the integrated stress response (ISR) on the oligodendrocyte response to mutant PLP expression.  Jimpy animals in which the ISR-triggering eIF2 kinase PERK is inactivated have an extended lifespan that correlates with increased oligodendrocyte survival and enhanced CNS myelination.  Inactivation of the downstream components of the ISR pathway CHOP and GADD34, in contrast, did not rescue oligodendrocytes or myelin.  Phosphorylated eIF2 inhibits the exchange factor eIF2B, resulting in diminished protein synthesis.  Treatment with small molecule eIF2B activators 2BAct and ISRIB dramatically increased oligodendrocyte survival, CNS myelination, and doubled the lifespan of Jimpy mice.  These results suggest that ISR modulation could provide therapeutic benefit to PMD patients.

overall_design: We have two distinct sets of samples. One is from mice in which the ISR gene Perk is inactivated specifically in oligodendrocytes: we have samples from WT mice (control and Perk mutants) as well as Jimpy mice (control and Perk mutants). The other set of samples is from WT and Jimpy mice treated with the ISR inhibitor 2BAct at three different developmental time points P7, P14, and P21.

first: Yanan

last: Chen

first: Rejani

last: Kunjamma

first: Karin

last: Lin

first: Caitlin

last: Connellly

first: Carmela

last: Sidrauski


title: UMP functions as an endogenous regulator of NR4A1 to control gastric cancer progression [ChIP-Seq]

city: Guangzhou

first: Guodi

last: Cai

state: Guangdong Province

address: 132, Waihuandonglu, Daxue Cheng

department: School Of Pharmaceutical Sciences

institute: Sun Yat-Sen university

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Nucleotide metabolism reprogramming drives tumor progression, yet how tumor cells sense nucleotide levels remain unclear. Here we identified UMP as an endogenous regulator of the orphan nuclear receptor NR4A1 in gastric cancer (GCa). Under UMP-sufficiency, UMP directly binds to NR4A1, inhibiting its tumor-suppressive function and promoting GCa progression. Conversely, UMP deficiency resulting from disrupted pyrimidine biosynthesis derepresses NR4A1, which suppresses GCa cell survival and progression by both increasing NR4A1 occupancy at super‑enhancers to reprogram survival‑gene expression and enhancing NR4A1’s pro‑apoptotic activity at the mitochondria. NR4A1 loss was sufficient to rescue the effects of pyrimidine nucleotide stress on GCa cells in vitro and in vivo. NR4A1 agonists suppressed the pyrimidine salvage pathway triggered by de novo pyrimidine biosynthesis (DNPB) inhibition. Co-targeting DNPB and NR4A1 induced synergistic tumor lethality in GCa xenograft models. Together, our results establish UMP as an endogenous regulator of NR4A1 and provide an effective therapeutic strategy for GCa.

overall_design: AGS cells were treated with vehicle, BAY (5 nM) or BAY (5 nM) plus Uridine (100 μM) for 24 h before harvested. Cell preparation, crosslinking, nuclei preparation and chromatin shearing was following truChIP® Chromatin Shearing Kit (Covaris), according to the manufacturer’s instruction. Chromatin fragments were precipitated by using specific antibodies and Protein G beads, washed, and treated with Proteinase K and RNAse A. Purified ChIP DNA was then used for library generation. Libraries were quantified with the Bioanalyzer 2100 (Agilent) and sequenced in single-end 50-bp mode on the MGISEQ2000 (BGI, Wuhan, China). Antibodies used were against H3K27ac (Abcam; ab4729).

first: Junjian

last: Wang

first: Zhenhua

last: Zhang


title: scRNA-seq of mouse prostate 2D and 3D organoids

city: Würzburg

first: Alexander

middle: M.

last: Leipold

address: Josef-Schneider-Str. 2

country: Germany

institute: Helmholtz Institute for RNA-based Infection Research

summary: scRNA-seq of mouse prostate 2D,  3D organoids and ex-vivo prostate units

overall_design: We performed single-cell RNA-seq analysis of organoids and organoid-derived monolayers of mouse prostates treated with 5α-DHT and Ctrl.

first: Carmen

last: Aguilar

first: Antoine-Emmanuel

last: Saliba

first: Maria

last: Guedes

first: Alexander M.


title: UMP functions as an endogenous regulator of NR4A1 to control gastric cancer progression

overall_design: AGS cells were treated with vehicle or DHODH inhibitors BAY (5 nM) or Ach-A (0.75 μM), or the combination of BAY (5 nM) and uridine (100 μM), or NR4A1 agonists Csn-B (40 μM) for 48 h before RNA extraction. RNA-seq libraries from 1 μg total RNA were prepared using Illumina Tru-Seq RNA Sample, according to the manufacturer’s instructions. Libraries were validated with an Agilent Bioanalyzer (Agilent Technologies, Palo Alto, CA). Sequencing was performed on the BGISEQ platform at BGI Tech (Wuhan, China). The FASTQ-formatted sequence data were analyzed by using a standard BWA–Bowtie–Cufflinks workflow. Sequence reads were mapped to GRCh38/hg38 assembly with BWA and Biotie software. The Cufflinks package was used for transcript assembly, quantification of normalized gene and isoform expression, and analysis of different expression. Gene Set Enrichment Analysis (GSEA v.3.0) was applied to rank genes based on the shrunken limma log2 fold changes. The GSEA tool was used in “pre-ranked” model with default parameters.


title: Aerial root growth mechanism of Prunus subgenus Cerasus × Incisa 'Gotenba zakura' and its waterlogging tolerance

city: Beijing

first: Feng

last: Xiaoxuan

address: No. 35 Qinghua East Road, Haidian District

institute: Beijing Forestry University

summary: Prunus subgenus Ceresus is a renowned ornamental wooden plant for its landscape applications and economic value in gardens. However, waterlogging during the rainy season in some areas cause deaths and heavy losses. Fortunately, we have found that a variety of Prunus subgenus Ceresus × Incisa 'Gotenba zakura' could generate aerial roots when suffering from heavy rains and sustainable floods. In this study, we conducted an associated analysis to explore the core regulating network of aerial root growth mechanism in Prunus subgenus Ceresus × Incisa 'Gotenba zakura' by combining phenological observations, physiological assays, and transcriptome comparisons across five separate stages. By analyzing the heatmap of DEGs and gene co-expression network (GCN), we have recognized genes that may play very critical roles under waterlogging stress. Gene network indicates that aerial roots can improve the tolerance under waterlogging by ROS degradation, endogenous hormone induction, as well as energy production. This discover provides a valid foundation of waterlogging tolerance of Prunus subgenus Ceresus, and molecular evidence for selecting promising rootstocks.

overall_design: Comparative gene expression profiling analysis of genes related to the growth of the aerial roots and the waterlogging tolerance of Prunus subgenus Ceresus × Incisa 'Gotenba zakura'. Six samples in total.

first: Xiaoxuan

last: Feng


title: Single-cell analysis reveals the epigenetic remodeling and key effectors of non-cardiomyocytes during heart regeneration.

first: Yage

last: Nie

address: No.74 Zhongshan Rd.2, Guangzhou

institute: Sun Yat-sen University

summary: The restricted regenerative potential of adult hearts poses a significant barrier to effective repair following injury. In contrast to numerous vertebrates, mammalian hearts exhibit only transient neonatal renewal capacity during the initial days of life. Beyond cardiomyocytes, understanding the diverse compositions of non-cardiomyocytes (non-CMs) is imperative for maintaining heart microenvironment homeostasis during neonatal heart regeneration. Here, we conducted single-cell ATAC sequencing (scATAC-seq) on neonatal hearts at varying time points post-apical resection to profile the epigenetic landscape. Intriguingly, fibroblasts and endothelial cells, as the most abundant populations in the heart, exhibited the most dynamic chromatin remodeling as the heart loses its regenerative potential. Our application of scATAC-seq unveiled key regulatory elements such as Cebpd in fibroblast activation and proliferation, while highlighting the essential role of AP-1 in endothelial cell angiogenesis, migration, and proliferation. Additionally, we uncovered active engagement of regulatory elements identified by non-CMs in regulating the behavior of cardiomyocytes, inhibition of which impaired cardiac function post-injury. Collectively, our study delineates the cellular identity of non-CMs at the epigenome level using single-cell approaches, offering insights into cell-type-targeted interventions for heart regeneration.

overall_design: The epigenomic landscape of non-CMs of 7 and 14-day old mice in response to injury.

first: Zihao

first: Liying

last: Huang


title: Receptor kinase heterodimers refine cambium activity in Arabidopsis

city: Durham

first: Wenbin

last: Wei

address: Stockton Road

department: Biosciences

country: United Kingdom

institute: Durham University

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

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

first: Qing

last: He

first: Ehmke

last: Pohl

first: Changyin

last: Wu

first: Raymond

last: Wightman

first: Peter

last: Etchells


title: Convergent evolution of scavenger cell development at vertebrate brain borders

city: Melbourne

first: Michelle

last: Meier

address: 305 Grattan Street

country: Australia

institute: Peter MacCallum Cancer Centre

summary: The vertebrate central nervous system (CNS) is protected by the blood brain barrier (BBB) and meningeal membranes, which ensure immune privilege. In the mammalian brain, microglia and border associated macrophages (BAMs) provide immune surveillance and scavenge wastes, yet how evolution shaped immune-cell diversity and function is not understood. In zebrafish, a vascular-derived mural lymphatic endothelial cell (muLEC) lineage fulfils scavenger cell functions at CNS borders. Here, we identify the transcription factor odd-skipped related 2 (osr2) as a specific marker and regulator of muLEC differentiation and maintenance. osr2 controls the transition of muLECs from interconnected endothelial cells to individual scavenger cells in part via control of cadherin-6 (cdh6). muLECs are more transcriptionally similar to BAMs than to other mammalian meningeal cells and share several functions in tissue homeostasis. However, BAMs are absent from zebrafish and muLECs from mice and humans. Analysis of osr2, LEC and BAM markers in diverse vertebrate species reveals muLECs as an ancient lineage and BAMs a recent mammalian specialisation. muLECs and BAMs share functional analogies but are not homologous, providing an example of convergent evolution. This highlights the physiological importance of meningeal scavenger cells and the developmental plasticity of LECs in generating specialised cell types throughout evolution.

sample_organism:
Danio rerio
Mus musculus

platform_organism:
Danio rerio
Mus musculus

overall_design: This study contains three datasets from two species (zebrafish and mouse). 1. Cells of transgenic WT zebrafish heads (7dpf) were isolated using fluorescence activated cell sorting (FACS) according to the presence or absence of kdrl (+). 2. Cells of transgenic WT and osr2-/- zebrafish heads (30dpf) were isolated using fluorescence activated cell sorting (FACS) according to the presence or absence of fli1a (+) and lyve1b (+) 3. Cells of 488acLDL uptake enriched cells of the mouse meningeal layer (3 months) were isolated using FACS, according to presence of absence of 488acLDL. scRNA-seq analysis was performed both within and across species and datasets.

first: Andrea

last: U Gaudi

first: Oguzhan

last: Baltaci

first: Sayali

last: Chowdhary

first: Frank

last: Tulenko

first: Stefanie

last: Dudczig

first: Sebastian-Alexander

last: Stamatis

first: Scott

last: Paterson

first: Hujun

last: Yu

first: Maria Cristina

last: Rondon Galeano

first: Elizabeth

last: Mason

first: Lee

last: Miles

first: Robert

last: Bryson-Richardson

first: Andrew

last: Pask

first: Jana

last: Vukovic

first: Anne

last: Lagendijk

first: Kelly

last: Smith

first: Jan

last: Kaslin

first: Michael

last: Harrison

middle: D

last: Currie

first: Neil

last: Bower

first: Benjamin

last: Hogan


title: Interphase chromosome conformation is specified by distinct folding programs inherited via mitotic chromosomes or through the cytoplasm [SLAM-seq]

status: Public on Nov 06 2025

city: Worcester

first: Allana

last: Schooley

address: 368 Plantation St

department: Systems Biology

institute: UMass Medical School

summary: Identity-specific interphase chromosome conformation must be re-established each time a cell divides. To understand how interphase folding is inherited, we developed an experimental approach that segregates chromosome-intrinsic factors from those inherited through the cytoplasm during the establishment of G1 nuclear architecture. Endogenous RanGAP1 or Nup93 proteins were degraded in pro-metaphase arrested DLD-1 cells to prevent the establishment of nucleo-cytoplasmic transport during mitotic exit and isolate the decondensing mitotic chromatin of G1 daughter cells from the cytoplasm. Using this approach, we uncovered a transient folding intermediate entirely driven by chromosome-intrinsic factors. In addition to conventional compartmental segregation, this chromosome-intrinsic folding program leads to prominent genome-scale microcompartmentalization of mitotically bookmarked and cell type-specific cis-regulatory elements. The microcompartment conformation is formed during telophase and subsequently modulated by a second folding program driven by factors inherited through the cytoplasm in G1. The nuclear import-dependent folding program includes cohesin and factors involved in transcription and RNA processing. The combined and inter-dependent action of chromosome-intrinsic and cytoplasmic inherited folding programs determines the interphase chromatin conformation as cells exit mitosis.

overall_design: SLAM-seq profiling of total and nascent RNA in control or RanGAP1-depleted DLD-1 cells during mitosis. Time course experiment in which cells were labeled with 1mM 4-thio-uridine (4sU) in 1-hour, non-overlapping intervals comprising the final hour of culture for each time point. Unlabeled controls were included at pro-metaphase arrest (hour 0) and at the end of the 5-hour time course. Each experiment was performed in triplicate.

first: Athma

last: Pai

first: Job

last: Dekker

first: Jesse

middle: W

last: Lehman


title: Interphase chromosome conformation is specified by distinct folding programs inherited via mitotic chromosomes or through the cytoplasm [CUT&Run]

overall_design: Cut&Run libraries for RanGAP1-AID DLD-1 cells arrested in prometaphase or released to G1 for 5h. Replicate samples for control and Auxin-treated RanGAP1-AID cells were generated for IgG, H3K4me3, H3K27ac, H3K27me3, and CTCF.

first: Vasilisa

last: Aksenova


title: Alcohol Dependence-Induced Astrocyte Immune Activation in the Nucleus Accumbens

city: Portland

first: Marina

last: Guizzetti

state: OR

address: 3710 SW US Veterans Hospital Rd

department: Behavioral Neuroscience

institute: Oregon Health & Science University; Portland VA Research Service

summary: Astrocytes play many physiological roles in the brain including maintenance of brain homeostasis, modulation of synapse formation and function, and regulation of the blood brain barrier permeability. Upon brain exposure to noxious stimuli, astrocytes can become reactive and activate neuroimmune responses. The nucleus accumbens (NAc) is a critical region involved in reward processing and is integrally involved in the establishment and maintenance of alcohol (ethanol, EtOH) dependence. Here we used the chronic intermittent ethanol – two-bottle choice (CIE-2BC) drinking model to induce EtOH dependence in Aldh1l1-eGFP/Rpl10a mice, which allow the pull-down of astrocyte specific RNA using translating ribosome affinity purification (TRAP) procedure. NAc astrocyte translating RNA and bulk-tissue RNA was analyzed by RNA-Seq to identify genes altered by EtOH dependence or EtOH drinking in astrocytes and the bulk NAc. The number of differentially regulated genes was greater in the astrocyte-specific analysis compared to the bulk-tissue suggesting the cell-type specific approach enables greater resolution of the effects of EtOH. In the astrocyte-specific translatome of EtOH dependent animals, genes related to neuroimmune activation were highly enriched with overall activation of pathways related to interferon and interleukin signaling. In addition, pathways relating to oxidative stress and glutathione related responses were enriched in NAc astrocytes from dependent animals. In contrast, the astrocyte response to EtOH drinking identified pathways related to homeostatic changes. These findings highlight the profound immune activation in NAc astrocytes during EtOH dependence which are distinct from the response to lower levels of EtOH exposure. This study identifies astrocyte pathways and genes involved in the transition from alcohol drinking to alcohol dependence and identify potential novel cell type-specific targets that underlie vulnerability to alcohol use.

overall_design: Male and female mice CIE-2BC treated (dependent), 2BC controls (non-dependent), and ethanol naïve nucleus accumbens. Each brain sample from an individual mouse was fractionated into astrocyte translating RNA (IP) and bulk-tissue RNA (input).

first: Hashimoto

middle: G

last: Joel

first: Mangieri

last: Regina

first: Roberts

last: Amanda

first: Lime

last: Turner

first: Davis

last: Brett

first: Carbone

last: Lucia

first: Roberto

last: Marisa

first: Guizzetti

last: Marina


title: Bovine host transcriptomics to evaluate how markets and vaccines influence health and disease

city: Canyon

first: Matthew

last: Scott

state: TX

address: 3201 Russell Long Blvd

department: Large Animal Clinical Sciences

institute: Texas A&M University

summary: To evaluate how commercially available vaccines and marketing strategy affect the host transcriptome of commercial beef cattle overtime, we sequenced the whole blood RNA of 73 commercial beef bull calves enrolled in a split plot study. Calves were randomized to one of four groups, having received a commercially available vaccine during the cow-calf phase or not, and placed in a commercial salebarn system after weaning (auction) or directly shipped to backgrounding (direct). Samples were acquired from six time points: T1 (modified live viral (MLV) vaccination; age: ~107 d.), T2 (seven days post-vaccination; age: ~114 d.), T3 (revaccination; age: ~183 d.),  T4 (abrupt weaning; age: ~230 d.), T5 (arrival to backgrounding after marketing decision; age: ~233 d.), and T6 (45 days post-arrival to backgrounding; age: ~278 d.). Further evaluation was made based on whether calves were clinically diagnosed with bovine respiratory disease (BRD) after weaning.

overall_design: Whole blood from 73 randomly selected individuals with relative equal allocation across study group and disease acqusition were used for gene expression profiling and differential analysis across six time points (T1-T6).

first: Robert

last: Valeris-Chacin

first: Sarah

last: Capik

first: Bradly

last: Ramirez


title: eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by small molecules

city: Aurora

first: Neelanjan

last: Mukherjee

state: Colorado

address: Research Complex 1 South, 12801 E 17th Ave

department: Biochemistry and Molecular Genetics

institute: University of Colorado School of Medicine

summary: Exposure to hypoxia is linked to increased cellular plasticity and enhanced metastasis; effects which are primarily attributed to the transcriptional activation of large gene programs downstream of hypoxia inducible factors (HIFs). However, translational effects in hypoxia, that likely precede transcriptional effects, have remained largely unexplored. Using ribosome-profiling, we uncovered a selective translational response in acute hypoxia that is eIF3d/eIF3e-dependent and controls downstream hypoxic responses including HIF1a accumulation and cellular invasion. We further demonstrated that eIF3e copy number and eIF3e- and eIF3d-expression signatures are associated with worsened outcomes for breast cancer patients. Finally, we identified a class of novel small molecules that target eIF3e specifically, reducing the translational response to hypoxia and to ER stress, another stressor that is dependent on eIF3d/eIF3e-mediated translation. Our data uncover critical functions for eIF3d/eIF3e in the hypoxic response and identify a potential means to inhibit stress-induced translation, and potentially plasticity and metastasis, mediated by eIF3e.

overall_design: Ribosome profiling and RNA-sequencing from MCF7-SIX1 cells and MDA-MB-231 cells. Cells were treated with etiher 1 hour hypoxia or normoxia and sictrl, si3d, si3e, DMSO, a209 or 8430.

first: Stephen C.

last: Purdy

first: Kate

last: Matlin

first: Christopher

last: Alderman

first: Amber

last: Baldwin

first: Natasha

last: Shrivastava

first: Goksu

last: Sarioglu

first: Somnath

last: Dutta

first: Kristofor J.

last: Webb

first: Arthur

last: Wolin

first: Dillon P.

last: Boulton

first: Annika

last: Gustafson

first: Jyoti

last: Kapali

first: John D.

last: Landua

first: Michael T.

last: Lewis

first: M. Cecilia

last: Caino

first: James C.

last: Costello

first: William

last: Old

first: Xiang

last: Wang

first: Rui

last: Zhao

first: Heide L.

last: Ford


title: Genome-wide CRISPR Knockout Screen in HAP1 MTHFD1-K56R cells to identify genes which confer to resistance to adenosine toxicity

city: Vienna

first: Stefan

last: Kubicek

address: Lazarettgasse 14

country: Austria

institute: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences

summary: This dataset contains sequencing data from a pooled CRISPR knockout screen performed in HAP1 MTHFD1K56R (i.e. harbouring a K56R mutation in MTHFD1) cells. Cells were transduced with a lentiviral genome-wide sgRNA knockout library (Brunello, Addgene #73179) followed by puromycin selection. The screen was then performed in IMDM medium with dialysed FBS supplemented with 50µM adenosine (ADE). Under these conditions, HAP1 MTHFD1K56R usually die. Dialysed medium (DIA) was used as control conditions. Cells were expanded for 14 days and surviving cells were collected for subsequent sequencing analyses. The screen aimed to identify genes whose loss would confer to adenosine resistance in HAP1 MTHFD1-K56R cells. Sequencing was performed to identify sgRNA abundances between adenosine treatment and control. Data was analyzed using PinAPL-Py.

overall_design: MTHFD1-K56R cells were transduced with Brunello sgRNA KO library (MOI approx. 1, >500x sgRNA coverage), selected for puromycin and cultured for 14days in total in dialysed media -+ 50µM adenosine. Experiments were performed in duplicates (2x DIA = CTRL, 2x ADE)

first: Jung-Ming George

last: Lin


title: A chromatin-linked CPL2–PHD2/3 module sustains multiple DNA methylation pathways and Polycomb silencing [WGBS]

city: Shenzhen

first: Jian-Kang

last: Zhu

state: Guangdong

address: 1088 Xueyuan Blvd, Nanshan

department: Institute of Advanced Biotechnology, Institute of Homeostatic Medicine, and School of Medicine

institute: Southern University of Science and Technology

type: Methylation profiling by high throughput sequencing

summary: While multiple chromatin-based epigenetic pathways are well characterized, their genome-wide coordination and hierarchical interplay remain poorly understood. We previously identified the BAH–PHD–CPL2 complex, where AIPP3 binds H3K27me3 via its BAH domain and, in concert with PHD2 and PHD3 (PHD2/3), recruits CPL2 to repress transcription by dephosphorylating RNA Polymerase II. Here, we show that CPL2 and PHD2/3 form a distinct module (CPL2–PHD2/3) that safeguards CHH DNA methylation and silences CHH-methylated sites at transposable elements (TEs) through engagement of multiple DNA methylation pathways. The CPL2–PHD2/3 module physically associates with SUVH4 and SUVH5 (SUVH4/5) to preserve SUVH4/5–CMT2-mediated CHH methylation at a subset of H3K9me2-marked regions. Chromatin enrichment of PHD3 likewise enables the module to sustain RNA-directed DNA methylation (RdDM)-mediated CHH DNA methylation at sites bearing H3K9me2, H3K27me3, or neither. Thus, CPL2–PHD2/3 emerges as a previously underappreciated, multifunctional regulator of plant DNA methylation networks. Unexpectedly, its gene repression function is uncoupled from DNA methylation. CPL2–PHD2/3 represses Polycomb-marked genes by interacting with LHP1 or recognizing hypomethylated H3K4. While it cooperates with LHP1 at a subset of targets, it also independently silences many more genes that LHP1 alone cannot repress, both sets of genes being critical for proper development. This dual, yet largely LHP1-insufficient, repression mode singles out CPL2–PHD2/3 as the essential executor of Polycomb silencing. Together, our findings establish CPL2–PHD2/3 as a chromatin-responsive integrator that spans DNA methylation and Polycomb-associated repression, providing a unifying mechanism for epigenetic control of both TEs and genes across diverse chromatin landscapes.

overall_design: To investigate whether the CPL2–PHD2/3 module regulates DNA methylation and how it interacts with SUVH–CMT-mediated methylation maintenance loops and/or RdDM-dependent de novo pathways, we generated single-base resolution DNA methylome maps for Col-0, cpl2-2, phd2-1, phd3-1, as well as CRISPR (C) knockout lines of the double mutants phd2/3C11 (hereafter referred to as phd2phd3C11 in library names) and phd2/3C19 (phd2phd3C19). To further assess transcriptional consequences associated with DNA methylation or Polycomb silencing, we performed RNA sequencing on the same set of genotypes.

first: Lingrui

last: Zhang

first: Kai

last: Tang


title: Synaptic proteins that aggregate and degrade slower with aging accumulate in microglia

city: Stanford

first: Ian

last: Guldner

address: 290 Jane Stanford Way

department: Neuro

institute: Stanford University

summary: As part of our study, we sorted CD11b+ cells (microglia) from the brain. To assess the purity of the sorted cells, we performed RNA-seq on them. As a relative comparison, we also performed RNA-seq on whole brain homogenate.

overall_design: 400,000 CD11b+ cells (microglia) from the mouse brain were sorted and subjected to preparation for RNA-seq. Hemi brains were also subjected to preparation for RNA-seq. All samples were obtained from young male C57BL/6 mice.

first: Wyss-Coray

last: Tony


title: A chromatin-linked CPL2–PHD2/3 module sustains multiple DNA methylation pathways and Polycomb silencing [RNA-seq]


title: Female- or Male-biased Offspring Generated by Targeted Distortion of Sex Chromosome Transmission

city: Berlin

first: Frederic

last: Koch

address: Ihnestraße 63-73

department: Developmental Genetics

institute: Max Planck Institute for Molecular Genetics

summary: In animal breeding, female or male progeny is preferred depending on the use of the animals. Especially in livestock, offspring with undesired sex is of low economic value and often culled. Here we achieve targeted sex ratio distortion in the mouse, leveraging components of a selfish supergene, the t-haplotype. Utilizing its central element, the t-responder, we generate a highly “selfless” genetic element disabling transgenic sperm. When integrated on the X or Y chromosome it results in a high prevalence of non-transgenic offspring of the desired sex. Our strategy overcomes key limitations of existing strategies, including compromised animal health, reduced fertility, and fully transgenic breeding stocks, which might foster acceptance of its application to livestock. The efficacy of our approach marks a groundbreaking advance in animal breeding.

overall_design: Total RNA-Seq and ChIP-seq (H3K27Ac) samples from whole testis of WT C57BL/6J mice at different ages p.p. (d12, d16, d24 and adult stage).

first: Hermann

last: Bauer

first: Bettina

last: Lipkowitz

first: Jürgen

last: Willert

first: Gaby

last: Bläß

first: Manuela

last: Scholze-Wittler

first: Sandra

last: Währisch

first: Lars

last: Wittler

first: Bernhard

last: Herrmann


title: A chromatin-linked CPL2–PHD2/3 module sustains multiple DNA methylation pathways and Polycomb silencing.

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

overall_design: Refer to individual Series


title: Sprint interval exercise drives a unique transcriptional mitochondrial stress response in humans

first: Javier

last: Botella

address: Ballarat road

institute: Victoria University

summary: The molecular mechanisms by which different exercise prescriptions dictate mitochondrial remodelling are poorly understood in humans. Here, we show that, compared to moderate-intensity continuous exercise (MICE), sprint-interval exercise (SIE) – a known time-efficient high-intensity exercise – leads to mitochondrial stress and transcriptionally activates the mitochondrial unfolded protein response (UPRmt).

overall_design: Baseline (Pre), post-exercise (+2.5h), post-recovery (+24h)

first: David

last: Bishop


title: Endothelial Cells retain inflammatory memory through chromatin remodeling [ATAC]

city: Albany

first: Ramon

last: Bossardi Ramos

state: Ny

address: 43 New Scotland Avenue

department: Department of Molecular and Cellular Physiology

institute: Albany Medical College

summary: Sepsis survivors exhibit long-term endothelial dysfunction, increasing susceptibility to secondary infections such as pneumonia. To investigate the molecular basis of endothelial inflammatory memory, we performed transcriptomic profiling of lung and kidney endothelial cells isolated from a murine two-hit sepsis model. This model incorporates cecal ligation and puncture (CLP) as the primary inflammatory event, followed by a secondary intranasal challenge with Streptococcus pneumoniae.

overall_design: Kidney endothelial cells isolated from mice subjected to a two-hit model of sepsis. The first hit involved cecal ligation and puncture (CLP) or sham surgery, followed by recovery. The second hit consisted of a secondary intranasal challenge with Streptococcus pneumoniae (SP) or PBS.

last: Bossardi-Ramos


title: The murine meninges is a resilient B cell lymphopoietic reservoir conferring protection against infections [BCR-seq]

city: Manchester

first: Matthew

middle: Christopher

last: Sinton

state: Greater Manchester

address: Core Technology Facility

department: Division of Immunology, Immunity to Infection and Respiratory Medicine

institute: University of Manchester

summary: It is now recognised that under homeostasis the dura meninges host a wide array of resident early haematopoietic precursors including those responsible for de novo B cell lymphopoiesis. The vascular connections between the skull bone marrow in the calvaria and the underlying meningeal layers provide an anatomical bridge connecting these two structures, and most of the early precursor populations are likely to originate from the calvaria before seeding the dura meninges. However, the impact of chronic, non-sterile challenges such as infections on these resident precursor populations remains to be determined. Furthermore, it is unclear whether the mechanisms providing local tolerance to infection result in the same outputs as those generated in conventional lymphoid organs such as the spleen. Trypanosoma brucei parasites, the causative agents of sleeping sickness, successfully colonise a myriad of tissues during the chronic stages of the infection, including the central nervous system (CNS) borders and the brain parenchyma. In the periphery, T. brucei infection results in severe B cell lymphopenia, including NK- and neutrophil mediated killing of conventional B-2 B cells in the spleen, compromising subsequent humoral responses necessary to control the infection. This begs the question of whether alternative tissue sites are also capable of supporting B cell lymphopoiesis when canonical lymphoid tissues such as the bone marrow and the spleen are severely compromised. We recently identified that the dura meninges acquire properties typically associated with ectopic lymphoid clusters resulting in the generation of high affinity antibodies during the chronic stages of the infection. Critically, the presence of these dura-associated lymphoid tissues under homeostasis was interdependently reported in mice and humans, highlighting conservation of these immunological hubs across species. In this study, we asked whether chronic T. brucei infection also disrupts meningeal B cell development, as it is recognised to take place in bona fide lymphopoietic organs such as the bone marrow and the spleen in response to T. brucei infection resulting in B cell lymphopenia. Thorough a combination of approaches, we show that the dura meninges support B cell lymphopoiesis when peripheral B cell lymphopoiesis is impaired. Mechanistically, we report that meningeal stroma, in particular signals derived from fibroblasts, endothelial, and sensory neurons provide environmental cues for the survival and development of these cells locally in a process dependent of IL-7 and STAT5 signalling resulting in sustained B cell replication capacity in this anatomical compartment. Critically, we show that the repertoire of B cells developing in the dura meninges undergo extensive clonal selection that is distinct from those found in the spleen. These B cells predominantly express various members of the Ighv1 family, including Ighv1-15, Ighv1-26, and Ighv1-76, that we proposed to be polyreactive and able to recognise a wide range of CNS antigens with various degrees of specificity, providing further evidence of tissue-specific B cell responses operating at the CNS borders. Lastly, through adoptive transfer experiments, we demonstrate that the B cells located in the meninges during infection, but not those from the spleen, protect B cell-deficient mice from infection for a longer period and are able to produce anti-T. brucei IgG. Collectively, our data demonstrate, for the first time, that the dura meninges independently support the development and selection of a a distinct reservoir of B cells when peripheral lymphopoietic organs are compromised, highlighting the meninges as a critical source of humoral responses against pathogens that highjack the peripheral immune system to promote chronicity.

overall_design: BCR sequencing of the dura mater and spleen from naive or chronically infected (25DPI) female C57BL/6 mice

middle: C

first: Alice

last: Costain

first: Chloe

last: Barnes

first: Olivia

last: Shorthouse

first: Katrine

last: Wonsbek

first: Anmoyul

last: Mohon

first: Jessica

last: Costa

first: Neil

last: Mabbott

first: Cecile

last: Benezech

first: Juan

last: Quintana


title: Inhibition of heme biosynthesis triggers cuproptosis in acute myeloid leukemia

first: Emily

last: Gruber

state: VIC

address: 305 Grattan St

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus


title: SCFA producing capabilities of the gut microbiota enhance tumor-specific CD127+CD8+ T cell immunity against melanoma

first: Lachlan

last: Dryburgh

state: Victoria

address: 792 Elizabeth Street

department: The Department of Microbiology and Immunology,  The University of Melbourne

institute: The Peter Doherty Institute for Infection and Immunity

summary: Gut microbiota modulate cancer control but how the different bacteria impact tumor-specific CD8+ T cell immunity remains unclear. Here, we identified that spontaneous control of cutaneous melanoma in mice correlated with microbiome-encoded metabolic pathways required for short-chain fatty acid (SCFA) synthesis. Diet-induced enforcement of microbial SCFA production reduced tumor progression and enriched tumor-specific CD8+ T cells in the tumor draining lymph node (tdLN) that lacked features of exhausted T cells. The SCFA butyrate promoted a FOXO1-dependent stemness program in these CD8+ T cells, enhanced the differentiation of CD127+CD8+ T cells and induced immune checkpoint blockade (ICB) responsiveness. Consistent with these experimental studies, metabolic modelling predicted enhanced microbial production of the SCFA butyrate in ICB-responsive melanoma patients and butyrate induced transcriptional features of ICB-responsiveness in CD8+ T cells. Collectively, these data identify the effects of microbial metabolic pathways on tumor-specific CD8+ T cell differentiation as critical components of how the gut microbiome regulates cancer immunity.

overall_design: In vitro activated gBT-I cells were treated with 0.5 mM sodium butyrate from d3 to d5 and sort-purified cells were sequenced on d6 post activation.

first: Annabell

last: Bachem

first: Michele

last: Clarke

first: Geraldine

last: Kong

first: Ilaryia

last: Tarasova

first: Lindsay

last: Kosack

first: Ariane

middle: R

last: Lee

first: Lewis

last: Newland

first: Teagan

last: McGivern

first: Emma

last: Bawden

first: Kah

last: Yap

first: Michael

last: Wilson

first: Sven

last: Engel

first: Brendan

middle: E

last: Russ

first: Kshitij

last: Tandon

first: Grant

last: McArthur

first: Vanessa

last: Marcelino

first: Paul

last: Beavis

first: Stephen

last: Turner

first: Jason

last: Waithman

first: Timothy

middle: P

last: Stinear

first: Shahneen

last: Sandhu

first: Jan

last: Schroeder

first: Thomas

last: Gebhardt

first: Sammy

last: Bedoui


title: Suprachiasmatic nucleus regulation of brown fat thermogenesis via ADRB3-S100B axis

city: suzhou

first: Yizhun

last: Zeng

address: renai road NO.199

institute: schoow university

summary: The suprachiasmatic nucleus (SCN), the central circadian pacemaker, orchestrates daily metabolic rhythms, yet its role in substrate selection and thermogenic adaptation remains insufficiently understood. Here, we show that SCN lesioning abolishes the adaptive suppression of brown adipose tissue (BAT) thermogenesis typically observed during time-restricted feeding in subthermoneutral environments (TRF-STE), a condition that imposes concurrent nutrient and thermal challenges. Contrary to wild-type responses, SCN-lesioned mice maintain elevated BAT thermogenic activity, driven by enhanced sympathetic tone and β3-adrenergic receptor (ADRB3) signaling. This compensatory response promotes a shift from lipid oxidation to glucose utilization, enabling heat production despite impaired lipolysis. Mechanistically, we identify a SCN-regulated ADRB3-S100B signaling axis underlying this metabolic reprogramming. S100B, a nutrient-sensitive protein calcium-binding protein, is upregulated in BAT following SCN disruption, where it enhances thermogenic capacity by stimulating brown adipocyte proliferation and suppressing senescence. Functional studies reveal that S100B is both necessary and sufficient for sustaining BAT thermogenesis under TRF-STE. Furthermore, diverse SCN disruption models, including light-induced circadian arrhythmia, N - Methyl - D - aspartic acid (NMDA) excitotoxicity, and Caspase-3-mediated ablation, consistently elevates S100B expression in BAT, reinforcing its role as a convergent effector of SCN-regulated metabolic adaptation. These findings uncover a previously unrecognized role of the SCN in coordinating thermogenic flexibility and fuel partitioning under stress. The identification of the ADRB3-S100B axis as a key mediator of this adaptation provides new mechanistic insight into the neural regulation of energy balance, with potential therapeutic relevance for circadian misalignment, obesity, and resistance to diet-induced weight loss.

overall_design: After two days of TRF or ad libitum at 21℃ for both sham and SCNx mice, their interscapular brown adipose tissue was collected at ZT4 and ZT16 on day two for RNA-seq.

first: Ying

last: Xu

first: Qi

last: Chen

first: Xiaopeng

last: Song

first: Yue

last: Gu

first: Antonio

last: Vidal-Puig

first: Jie

last: Zhang


title: Inhibition of interleukin-1 receptor-associated kinase (IRAK)-4 provides partial rescue of interleukin-1 beta induced functional and gene expression changes in equine tendon cells.

city: Hatfield

first: Debbie

last: Guest

state: Hertfordshire

address: Royal Veterinary College, Hawkshead Lane, North Mymms

department: Clinical Science and Services

institute: Royal Veterinary College

summary: We investigated if the daily application of the interleukin-1 receptor-associated kinase (IRAK)-4 inhibitor PF-06650833 could rescue the effect of interleukin-1 beta on equine tendon cells cultured in 3D

overall_design: Five lines of adult equine tenocytes (from different donors) were cultured in 3D in the presence of PF-06650833 alone, or IL-1β plus PF-06650833 for 14 days. Gene expression profiles were generated by RNA sequencing on an Illumina Novaseq 6000. Quality control was perfromed using FASTQC and reads were aligned to the Equus Caballus transcriptome using the pseudoaligner Salmon. Differential expression was quantified using DESeq2.

first: Ross

last: Beaumont

first: Deborah


title: GW9662 , a Peroxisome proliferator-activated receptor γ (PPARγ) inhibitor, impairs early embryonic development in zebrafish

city: Clemson

first: Subham

last: Dasgupta

state: South Carolina

address: 142 Long Hall

department: Biological Sciences

institute: Clemson University

summary: Peroxisome proliferator-activated receptor γ (PPARγ) functions as a nuclear transcription factor with primary roles in lipid and glucose metabolism and adipocyte differentiation. Despite intensive research in metabolic contexts, its role during early vertebrate development remains underexplored. Our study focused on understanding PPARγ's developmental role by administering a PPARγ antagonist called GW9662 (GW) to block its activity in zebrafish embryos during early development from 6 hours post-fertilization (hpf) to 24 hpf. The first phenotypic screening found that ventralization occurred along with an expanded blood island region, a structure that is involved in early blood cell development. Transcriptomic analysis demonstrated that exposure to GW led to dysregulation of multiple biological pathways, including cytoskeletal organization, lipid biosynthesis, and epithelial-to-mesenchymal transition (EMT). Immunohistochemistry further validated these findings, demonstrating increased lipid accumulation, cytoskeletal disruption, and altered EMT markers. Our findings suggest that PPARγ plays a crucial role in multiple processes  during early embryogenesis, and this disruption can lead to profound morphological and molecular alterations.

overall_design: Zebrafish embryos were exposed to GW-9662, followed by phenotyping, RNA seq, immunohistochemistry and Nile Red stain

first: Sunil

last: Sharma

first: Kanchaka

last: Pathiraja

first: Tyler

last: Johnson

first: Jabez

last: Battu


title: Impact of Electric Potential on the Transcriptome of Paracoccus denitrificans in denitrification Conditions

city: Mexico

first: Leticia

last: Vega

state: Mexico

address: Circuito Ext s/n

country: Mexico

institute: Universidad Nacional Autonoma de Mexico

summary: This study aimed to evaluate the transcriptomic response of Paracoccus denitrificans PD1222 exposed to an applied electric potential of +200 mV under aerobic denitrification conditions. RNA-seq analysis was conducted on five biological samples: three independent replicates under 200 mV and two control samples at 0 mV. Differential gene expression changes revealed genes associated with amino acid metabolism, carbohydrate metabolism, membrane transport, and energy metabolism.

overall_design: Triplicate cultures of P. denitrificans PD1222 were grown anaerobically in the presence of 7.5 mM nitrate and 3.5 mM succinate as electron donor and acceptor, respectively. Samples were exposed to 0 mV (control) or +200 mV (treatment) for 6 hours.

first: Francisco

last: Vera Lopez-Portillo

first: Alberto

last: Hernandez-Eligio

last: Vega-Alvarado

first: Raunel

last: Tinoco-Valencia

first: Leobardo

last: Serrano-Carreon

first: Arturo

last: Cadena-Ramirez

first: Katy

last: Juarez


title: Endothelial Cells retain inflammatory memory through chromatin remodeling II

first: Ramon

last: Bossardi Ramos

summary: Sepsis survivors exhibit long-term endothelial dysfunction, increasing susceptibility to secondary infections such as pneumonia. To investigate the epigenetic and transcriptional basis of endothelial inflammatory memory, we performed transcriptomic profiling of primary human endothelial cells exposed to sequential inflammatory stimuli in a two-hit in vitro model. IL-6 priming induced sustained transcriptional reprogramming and heightened responsiveness to a secondary LPS challenge, indicative of a memory-like state. To mechanistically dissect this response, we silenced the AP-1 transcription factor JunB using siRNA during the priming phase and evaluated its role in shaping the inflammatory memory response. These studies provide insight into the molecular circuitry maintaining endothelial memory and identify JunB as a potential regulator of this process.

overall_design: Primary human umbilical vein endothelial cells (HUVECs) were treated with IL-6 (50 ng/mL) or PBS for 72 hours (first hit)

last: Bossardi-Ramos


title: Endothelial Cells retain inflammatory memory through chromatin remodeling [RNA-Seq 2]

overall_design: RNA was extracted from lung and kidney endothelial cells isolated from mice subjected to a two-hit model of sepsis. The first hit involved cecal ligation and puncture (CLP) or sham surgery, followed by recovery. The second hit consisted of a secondary intranasal challenge with Streptococcus pneumoniae (SP) or PBS. Endothelial cells were isolated at defined time points and RNA-seq was performed using the Illumina NovaSeq 6000 platform (paired-end). A total of 54 samples representing various treatment groups across lung and kidney tissues were analyzed to identify gene expression signatures associated with endothelial inflammatory memory.


title: Endothelial Cells retain inflammatory memory through chromatin remodeling [ATAC-seq]

summary: Sepsis survivors exhibit long-term endothelial dysfunction, increasing susceptibility to secondary infections such as pneumonia. To investigate the epigenetic and transcriptional basis of endothelial inflammatory memory, we employed transcriptomic profiling of primary endothelial cells exposed to inflammatory stimuli in a two-hit model. This study reveals persistent transcriptional reprogramming following IL-6 exposure and identifies a primed endothelial state that amplifies responses to secondary challenges.

overall_design: Primary endothelial cells were treated with IL-6 or PBS for 72 hours (first hit), followed by a 48-hour washout phase. Nuclei were isolated for ATAC-seq from cells collected at two timepoints: immediately after the 72-hour treatment (IL6_72h, PBS_72h) and after the 48-hour washout (IL6_72h_W48h, PBS_72h_W48h). Each group included two or three biological replicates


title: CTNNB1 mutations have diverse effects on signalling in Embryonic Stem Cells

city: Leiden

first: Karamjit

middle: Singh

last: Dolt

address: Einthovenweg 20

department: Human Genetics

country: Netherlands

institute: LUMC

summary: Bulk 3' RNA-Seq was performed on Embronic Stem Cells (E14) to explore the diverse effect of CTNNB1 mutation alongside GSK3β inhibition via CHIR99021 serving as a positive control.

overall_design: Genomewide expression profile in E14 ESCs with targetted CTNNB1 mutations and GSK3β inhibition via CHIR99021 for 48 hours. The sequncing libraries contained Read 1 (R1) and Read2(R2) for each sample. Read 1 contained the cDNA information and read 2 only the UMI and sample barcodes. R1 and R2 were combined to build R4 reads file that was alingned to mouse genome build mm10 to calculate the read counts per sample for comparision.

last: S. Dolt

first: Peter

last: Hohenstein


title: The murine meninges is a resilient B cell lymphopoietic reservoir conferring protection against infections

first: Matthew

last: Sinton

overall_design: RNA sequencing of skull bone marrow, femur bone marrow, spleen and meninges from naive or chronically infected (25DPI) female C57BL/6 mice

first: Alice

last: Costain

first: Chloe

last: Barnes

first: Olivia

last: Shorthouse

first: Katrine

last: Wonsbek

first: Anmoyul

last: Mohon

first: Jessica

last: Costa

first: Neil

middle: A

last: Mabbott

first: Cecile

last: Benezech

first: Juan

last: Quintana


title: Endothelial Cells retain inflammatory memory through chromatin remodeling

overall_design: Primary endothelial cells were treated with IL-6 or PBS for 72 hours (first hit), followed by a 48-hour washout phase. Cells were then challenged with either LPS or PBS for 6 hours (second hit). Total RNA was extracted from 18 samples across six experimental conditions: IL6_72h, IL6_72h_W48h, IL672h_W48h_LPS, PBS_72h, PBS_72h_W48h, and PBS72h_W48h_LPS, each with three biological replicates. RNA-seq was performed using the Illumina NovaSeq 6000 platform (paired-end). The resulting data were analyzed to identify genes associated with inflammatory memory.


title: Genome-wide methylation profiles of post-mortem tissue samples (human)

city: Seoul

first: Hwan Young

last: Lee

address: 103, Daehak-ro, Jongno-gu

country: South Korea

institute: Seoul National University College of Medicine

summary: In this study, genome-wide DNA methylation profiling was performed on post-mortem skeletal muscle tissues obtained from three Korean individuals. A total of 250 ng of genomic DNA from each sample was analyzed using the Illumina Infinium MethylationEPIC BeadChip array (Illumina, San Diego, CA, USA) at Macrogen Inc. (Seoul, Korea).

overall_design: DNA methylation profiling of 3 post-mortem muscle tissue samples was conducted using the Infinium MethylationEPIC Beadchip array.

first: Soo Bin

last: Yang


title: MCF7 ChIP-seq

city: Barcelona

first: Toni

last: Celià-Terrassa

address: C/ del Dr. Aiguader, 88, Ciutat Vella,

institute: Hospital del Mar Research Institute

summary: LCOR is a corepressor of activated nuclear receptors that inhibits the transcriptional activity of these proteins. Recently, LCOR was described to act also as a transcription activator by DNA direct binding through its HTH domain of genes involved in antigen presentation. This double transcriptional role of LCOR is determined by the expression of nuclear receptor. Here we performed ChiP-seq analysis of LCOR in MCF-7 cells which expressed the nuclear receptor estrogen receptor. In paralel we treated the cells with an estrogen receptor degrader (fulvestrant) or ectopic expression of the LCOR without the nuclear receptor binding domain (LSKAA). This analysis allows to compare the genome wide distribution of LCOR depending on the presence of nuclear receptor and the ability to interact.

overall_design: MCF7 cells were transduced with control, LCOR and LSKAA inducible overexpressing plasmids. MCF7-LCOR OE cells were induced with 1 ug/ml of doxycycline and treated with vehicle or 1 uM of fulvestrant. MCF7-LSKAA OE were induced with doxycycline. After 24 h, cells were croslinked and chromatin extracts were obtained for immunoprecipitation of LCOR. Isolated DNA bound to LCOR was submitted for sequencing. After alignment and analysis of sequenced DNA, conditions were compared to check the different prefferentially bound motif of LCOR in each condition

first: José Ángel

last: Palomeque


title: Pulsed 980 nm Near-Infrared Photobiomodulation Attenuates OVA-Induced Allergic Asthma by Modulating Th2 Cytokine Responses and Inflammatory Cell Infiltration

city: xiamen

first: Qingxiang

last: Gao

address: Xiang'an south way

institute: Xiamen University

summary: Photobiomodulation (PBM) is a non-invasive therapeutic strategy that uses specific light wavelengths to stimulate cellular processes that promote tissue repair, reduce inflammation, and alleviate pain. In this study, we evaluated the efficacy of a high-intensity 980 nm near-infrared (NIR) pulsed laser in a murine model of ovalbumin (OVA)-induced allergic asthma. In OVA-sensitized mice, typical allergic features were noted, including airway wall thickening, significant peribronchial and perivascular inflammatory cell infiltration, and compressed alveolar spaces. NIR PBM treatment markedly attenuated these histological changes. At the molecular level, PBM significantly downregulated type 2 cytokine gene expression, including IL-4, IL-5 and IL-13, in the lung tissue. Flow cytometry analyses further revealed that PBM reduced the infiltration of pulmonary eosinophils and inflammatory monocytes. Transcriptomic profiling coupled with gene set enrichment analysis (GSEA) indicated that PBM suppressed NF-κB-mediated inflammatory signaling while modulating Th2-related responses. Collectively, our findings demonstrate that high-intensity 980 nm NIR PBM effectively mitigates key features of allergic asthma in a murine model, supporting its potential as a non-pharmacological, non-invasive adjunct therapy for asthma management.

first: Zhengyi

last: Wu

first: Shih-Chin

last: Cheng


title: AT3 RNA-seq

summary: ER+ breast cancer is the most prevalent subtype of the disease with improved prognosis thanks to advances in target therapies against the main driver of proliferation, estrogen receptor (ER). Despite all the advances in the study of this subtype, murine models that allow to study the interaction of tumor cells with the stromal compartment are merely absent. In this study we aimed to ectopically overexpresse the protein ER in AT3 murine cell line and check the ability to resemble ER+ breast cancer cells. We compared the transcriptomic profile of ER-OE cells versus control.

overall_design: AT3 cells were transduced with vector control or ER overexpressing construct. Both cell lines were treated with 10 nm of E2 during 24 h. Cell pellets were lysed and RNA extracted for RNA sequencing. Transcriptomic changes upon ER overexpression together with E2 treatment were analyzed.


title: RNA-seq analysis of canine thyroid carcinomas.

city: Fort Collins

first: Sunetra

last: Das

state: CO

address: 300 W Drake Rd

department: Clinical Sciences

institute: Colorado State University

summary: Thyroid tumors represent 1-3% of canine cancers with most tumors classified as follicular carcinomas and less frequently as medullary carcinomas. A cohort of canine thyroid carcinomas underwent RNASeq exploration (n=30). Clustering of tumor transcriptomes produced 2 groups; T1 and T2 clusters comprised of follicular thyroid carcinomas (FTC) and medullary thyroid carcinomas (MTC), respectively. Tumors were histologically typed as follicular, compact, and follicular-compact on blinded review, with most MTC classified as compact with rare follicular-compact appearance, while FTC displayed all 3 patterns. FTC samples had significantly elevated levels of ERBB2 and HER2 protein and RET signaling was up-regulated in MTC. Elevated HER2 protein staining was associated with shorter progression free survival (PFI). Additional studies are warranted to explore the utility of these biomarkers to improve diagnosis and treatment of thyroid carcinoma in dogs.

overall_design: We ran  gene expression profiling analysis,  hirerchical clustering, and differential expression between in silico clusters, using data obtained from RNA-seq.

first: Dawn

last: Duval


title: ColoStem, a core transcriptional signature that identifies poor prognosis fetal-type colorectal tumors

first: Lluis

last: Espinosa

state: Barcelona

address: Dr. Aiguader 88

department: Institut Municipal d'Investigacions Mèdiques, (IMIM)

institute: Hospital del Mar

summary: We have previously shown that non-curative chemotherapy imposes fetal conversion and high metastatic capacity to cancer cells. Analysis of public colorectal cancer datasets confirms the existence of a fetal signature consisting of 28 upregulated and 8 downregulated genes that stratify patients with worse prognosis. We have analyzed a metacohort generated by the integration of several colorectal cancer datasets and performed qPCR analysis of paraffin-embedded and plasma samples from our in-house cohort of colorectal cancer tumors. We uncovered a core fetal signature, which we have called ColoStem, composed of 5 genes upregulated and 3 genes downregulated that display prognosis value in a multivariate analysis. We also define EpiColostem as a purer epithelial signature with comparable prognosis value as ColoStem. By qPCR analysis of RNA extracted from paraffin-embedded tissues, we demonstrated the actual possibility of using ColoStem and EpiColoStem to refine the prognostication of CRC patients with a simple an affordable method. Initial analysis of plasma samples indicates that both signatures could be adapted for its use in liquid biopsy. Our results reveal ColoStem and EpiColoStem tests as valuable tools for the identification of fetal-type CRC tumors thus refining patient prognosis.

overall_design: We analyzed bulk RNAseq samples obtained from colorectal cancer Patient-Derived Organoids: 3xnon-fetal (PDO4, PDO10 and PDO66) and 3xfetal (PDO5, PDO27 and PDO127B), plus 2xtreated with 5-FU+Irinotecan (PDO66), each in triplicates.

first: Laura

last: Solé

first: Eric

last: Canton

first: María

last: Maqueda

first: Teresa

last: Lobo-Jarne

first: Antonio

last: Barbáchano

first: Ferran

last: Torres

first: Julia-Jié

last: Cabré-Romans

first: Ángela

last: Montoto

first: Lierni

last: Fernández-Ibarrondo

first: Daniel

last: Martínez-Garcia

first: Marta

last: Guix

first: Mónica

last: Larrubia-Loring

first: Clara

last: Montagut

first: Alberto

last: Muñoz

first: Anna

last: Bigas

first: Mar

last: Iglesias

first: Beatriz

last: Bellosillo

first: Lluís


title: Cryptococcus exploits delayed microglial activation, and microglial osteopontin (OPN/Spp1) impairs peripheral host control

city: Durham

first: Mari

middle: L.

last: Shinohara

state: NC

address: 207 Research Dr.

department: Integrative Immunobiology

institute: Duke University School of Medicine

summary: Cryptococcus, a neurotropic fungus and the World Health Organization (WHO) critical-priority pathogen, causes cryptococcal meningoencephalitis (CM), the second leading cause of death in HIV/AIDS patients. Despite the significance, host brain responses during CM remain underexplored. In a non-acute systemic mouse model, Cryptococcus infiltrates the brain within one day from circulation, yet full activation of microglia is delayed until 14 days post-infection. Microglia, regarded as sentinels of the central nervous system (CNS), exhibit slow responses, partly due to limited direct fungal recognition and reliance on T cells as a source of IFNg. Once activated, microglia upregulate Spp1, encoding osteopontin (OPN), a factor highly expressed in neurodegenerative diseases. Our findings demonstrate that microglia-derived OPN negatively impacts the host by altering peripheral immune responses. Thus, Cryptococcus exploits the delayed host response to establish brain infection, with activated microglia producing OPN in a host-detrimental manner.

overall_design: Age-matched female B6 WT and GeneX-/-mice were retro-orbitally infected with 10^6 yeasts/mouse of Cryptococcus neoformans (deneoformans) strain 52D; brains were collected at 0, 4, and 14 days post infection.  Samples from two mice were pooled for each time point, except 14-dpi which only had 1 sample. Brain cells were isolated using the Papain Dissociation Kit (Worthington Biochemical Corporation) and myelin was removed using Myelin Removal Beads II (Miltenyi Biotec). Live cells were enriched using the EasySep™ Dead Cell Removal (Annexin V) Kit (STEMCELL Technologies).

first: Estefany

middle: Y

last: Reyes

first: Jae

last: Yong

first: Devon

last: DiPalma

first: Jonathan

middle: L

last: Messerschmidt

first: Miranda

last: Lumbreras

first: Hana

middle: H

last: Hendi

first: Danira

last: Mukhamedyarova

first: Emily

last: Troutman

last: Wert


title: MCF7 and MDA-MB-231 RNA-seq

first: Toni

last: Celià-Terrassa

summary: LCOR is a corepressor of activated nuclear receptors that inhibits the transcriptional activity of these proteins. Recently, LCOR was described to act also as a transcription activator by DNA direct binding through its HTH domain of genes involved in antigen presentation. This double transcriptional role of LCOR is determined by the expression of nuclear receptor. We overexpressed LCOR and performed RNA-seq in breast cancer cell lines of nuclear receptor positive subtype (MCF7) and nuclear receptor absent (MDA-MB-231). This analysis allows to compare transcriptional regulation of LCOR depending on the presence of nuclear receptors.

overall_design: MCF7 and MDA-MB-231 were transduced with inducible LCOR construct. After antibiotic selection, cells were treated with vehicle or 1 ug/ml of doxycycline. After 24 h of induction, cells were lysed following Qiagen RNA extraction protocol. RNA was submitted for RNA-sequencing and study the transcriptional changes occurring when LCOR is overexpressed in both breast cancer cell lines.

first: José Ángel

last: Palomeque


title: Transcriptional Dynamics and Chromatin Accessibility in the Regulation of Shade-Responsive Genes in Arabidopsis [RNA-Seq]

city: Lausanne

first: Christian

last: Fankhauser

state: Vaud

address: Batiment Genopode

department: Center for Integrative Genomics

country: Switzerland

institute: University of Lausanne

summary: Accessible chromatin regions host DNA regulatory motives and are highly accessible to the transcription factors and transcriptional machinery. In Arabidopsis, responses to light are heavily regulated at the transcriptional level.  Shade, for example, can limit photosynthesis and is rapidly perceived by phytochromes as a reduction of red to far-red light ratio. Under shade, phytochromes inactivate and allow PHYTOCHROME INTERACTING FACTORs (PIFs) to promote a wide scale genome reprogramming. A strong and fast initial regulation of shade responsive genes is followed by an attenuation of this response under prolonged shade. We wanted to determine if transcriptional response pattern to shade depends on chromatin accessibility. For this we used ATAC-seq to profile the chromatin of seedlings exposed to short (1h) and long (25h) simulated shade. Transcription pattern of most acute shade responsive genes correlates with the rapid increase in PIF levels/activity at 1h, and its decrease at 25h of shade exposure. For a set of acute responding genes, PIFs also modulate chromatin accessibility at their binding sites in response to shade. Our results suggest that permanent state of open chromatin conformation allows PIFs to easily access and recognize their binding motifs, rapidly initiating a burst in gene expression triggered by shade. This transcriptional response primarily depends on a transient increase in stability of PIFs and gene occupancy and is followed by a moderate change of chromatin accessibility.

overall_design: RNA-seq profiling of 7 day-old seedlings grown in high red:far-red light ratio (HRFR) or exposed to 1h or 25h of low red:far-red light ratio (LRFR). Three replicates of Col-0 and pif457 for each condition were collected at ZT3.

first: Sandi

last: Paulišić

first: Alessandra

last: Boccaccini


title: Dynamics of the Spanish fir transcriptome in nature: Metabolic pathways and gene networks involved in the response to climate stress

city: Malaga

first: Vanessa

middle: Viviana

last: Castro Rodriguez

state: Malaga

address: Universidad de Malaga

institute: Universidad de Malaga

summary: Mediterranean forests such as those integrated by Spanish firs in southern Spain are extremely sensitive to the effects of climate climate-driven stresses. Recurrent periods of drought and prolonged warming in the last few years are major factors involves in the current vulnerability of local populations. In this work, physiological and transcriptional analyses were combined to assess the response of trees growing in the forest under natural conditions. The results show a modulation of the transcriptome in response to climatic stress with substantial changes in the expression of genes involved in water stress, aromatic amino acid metabolism, and transcription factors associated with the transcriptional regulation of the observed patterns of gene expression. Roots were determined to be the primary organs involved in the transcriptional response to stress which may be mediated by a gene-network including interactions among structural and regulatory genes. Interactive elements comprise genes encoding stress-related proteins of the ApLEA family, ApADH, the first committed enzyme in tyrosine biosynthesis, and root-specific transcription factors implicated in stress regulation belonging to the ApERF, ApYABBY and ApNAC superfamilies. Data provide new insights to understand the response of Spanish firs to current climatic disturbances by the identification of individual genes and gene-networks potentially involved in local adaptation. This new knowledge will facilitate comparative studies of gene variation in the Spanish fir populations using the identified genes as molecular markers for selection of the best adapted genotypes in the response of climate stress.

overall_design: In this study, needles and roots from adult Abies pinsapo trees (30–50 years old) were analyzed. To examine the effect of climatic variations on the tree transcriptome dynamics, tissue samples were collected from two different organs (needles and roots) at both sites (YUN and RON) and during both seasons, spring (SPR) and autumn (AUT). On each occasion, needles and roots were harvested at midday from ten randomly selected adult individuals (30-50 yr-old trees) of A. pinsapo.

first: Irene

last: Blanca-Reyes

first: María

last: Torés-España

first: Víctor

last: Lechuga

first: María Teresa

last: Llebrés

first: Fernando N

last: de la Torre

first: José A

last: Carreira

first: Concepción

last: Ávila

first: Francisco M

last: Cánovas

last: Castro-Rodriguez


title: Transcriptional Dynamics and Chromatin Accessibility in the Regulation of Shade-Responsive Genes in Arabidopsis [ATAC-seq]

overall_design: ATAC-seq profiling of 7 day-old seedlings grown in high red:far-red light ratio (HRFR) or exposed to 1h or 25h of low red:far-red light ratio (LRFR). Three replicates of Col-0; pUBQ10::BirA; pUBQ10::NTF and sav3-2; pUBQ10::BirA; pUBQ10::NTF for each condition were collected at ZT3.