title: Transcriptomic Analysis of the Candida albicans Response to Treatment with Cinnamaldehyde

city: Hefei

first: Wenqian

address: Longzihu Road

institute: Anhui University of Chinese Medicine

summary: Natural product cinnamaldehyde has significant antifungal activities, and its inhibitory activity against Candida albicans has been reported. Up to now, there are few reports on the changes in the transcriptome of Candida albicans after cinnamaldehyde treatment. Here, RNA sequencing analysis of samples obtained from Candida albicans cells grown in the presence or absence of cinnamaldehyde was performed. A total of 123 differentially expressed genes were identified, of which 15 genes were up-regulated and 108 genes were down-regulated.

overall_design: Candida albicans strain SC5314 was grown in YPD medium overnight, washed with PBS and cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum at 2 × 10^5 CFU/mL and incubated at 37 ℃ for 24 hours in the presence of cinnamaldehyde at 31.25 μg/mL. Considering that cinnamaldehyde was solubilized using DMSO, 5% DMSO treatment was used as a control group. Total RNA was extracted and mRNA enriched by magnetic beads with oligo (dT). The mRNA was randomly broken by adding fragmentation buffer. Short fragments of double-stranded cDNA generated by reverse transcription were subjected to end-repair, phosphorylation and ‘A’ base addition according to Illumina’s library construction protocol. Libraries were size selected for cDNA target fragments of 300 bp on 2% Low Range Ultra Agarose followed by PCR amplified using Phusion DNA polymerase for 15 PCR cycles. After quantified by Qubit 4.0, paired-end RNA-seq sequencing library was sequenced with the NovaSeq 6000 sequencer (2 × 150 bp read length). Three biological replicates were obtained for each condition (control or cinnamaldehyde treated).

first: Zhaoling

last: Shi

first: Kelong

last: Ma


title: Comparison of the three-dimensional chromatin structures of adolescent and adult peripheral blood B cells: implications for the study of pediatric autoimmune diseases

status: Public on Jun 04 2025

city: Oklahoma City

first: Patrick

middle: M

last: Gaffney

state: OK

address: 825 NE 13th Street

department: Genes and Human Disease

country: USA

institute: Oklahoma Medical Research Foundation

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Knowledge of the 3D genome is essential to elucidate genetic mechanisms driving autoimmune diseases. The 3D genome is distinct for each cell type, and it is uncertain whether cell lines faithfully recapitulate the 3D architecture of primary human cells or whether developmental aspects of the pediatric immune system require use of pediatric samples. We find that the the 3D chromatin architecture in B cells is similar across pediatric, adult, and EBV-transformed cell lines.    This conservation of 3D structure includes regions encompassing autoimmune risk haplotypes.  Thus, even for pediatric autoimmune diseases, publicly available adult B cell and cell line datasets may be sufficient for assessing effects exerted in the 3D genomic space.

overall_design: We isolated B cells from four healthy individuals, ages 9-17.  HiChIP was performed using a CTCF antibody, and CTCF peaks were called within each sample separately. Peaks observed in all four samples were identified. CTCF loops were called within the pediatric samples using three CTCF peak datasets: 1) self-called CTCF consensus peaks called within the pediatric samples, 2) ENCODE’s publicly available GM12878 CTCF ChIP-seq peaks, and 3) ENCODE’s primary B cell CTCF ChIP-seq peaks from two adult females. Differential looping was assessed within the pediatric samples and each of the three peak datasets.

first: Kaiyu

last: Jiang

first: Yao

last: Fu

first: Jennifer

middle: A

last: Kelly

first: Lucy

middle: C

last: Holmes

first: James

middle: N

last: Jarvis


title: High-resolution Profiling of RNA-Protein Interaction in Living Cells

city: Beijing

first: Zonggui

last: Chen

state: Beijing

address: No.5 Yiheyuan Road Haidian District

department: Academy for Advanced Interdisciplinary Studies

country: China

institute: Peking University

type: Expression profiling by high throughput sequencing

type: Non-coding RNA profiling by high throughput sequencing

summary: RNA-protein interactions play essential roles in regulating a wide range of cellular processes. Profiling the protein interactome of specific RNA loci enables understanding the underlying molecular mechanisms of RNA regulatory processes. Here we describe an RNA-centric proximity labeling approach for profiling the protein interactome of particular RNA sequences in living cells. In this method, CIRTS3-miniTurbo fusion proteins assemble with specific gRNAs to bind to target RNA and subsequently covalently tag the interacting proteins of target RNA in situ. We first profiled the protein interactome of circRNA mCherry and found that HNRNPK modulates the expression level of circmCherry and some endogenous circRNAs. We then employed our method to in-situ capture the interacting proteins of the rG4 structure in the BCL-2 transcript. We validated the interaction between RBM12 and BCL-2 rG4 structure and showed that RBM12 modulates the translation of the BCL-2 transcript by recruiting ribosomal proteins. Our studies provide a generally applicable strategy for profiling the protein interactome of specific RNA sequences in living cells.

overall_design: To investigate the effect of HNRNPK on the production of endogenous circRNAs,  we overexpressed the HNRNPK protein, and the circRNA expression levels were quantified by circRNA-seq.

first: Jing

last: Mo


title: Gut Microbiota-Butyrate-PPARγ Axis Modulates Adipose Regulatory T Cell Population

city: Shanghai

first: Lizhi

last: Guan

address: 573 Xujiahui Road

department: Department of Endocrine and Metabolic Diseases

institute: Ruijin Hospital, Shanghai Jiao Tong University School of Medicine

summary: Immune cells in visceral adipose tissue are critical for regulating metabolic homeostasis. In addition, gut microbiota is an important regulator of the immune system. We used single-cell RNA sequencing (scRNA-seq) to analyze the relationship between gut microbiota and immune cells in visceral adipose tissue.

overall_design: Visceral adipose tissue CD45+ cells of 15-week-old mice with normal water or antibiotic treatment were sorted using Magnetic-activated cell sorting (MACS) separation according to the manufacturer's protocol (CD45 MicroBeads, Miltenyi Biotec) and analyzed using single-cell RNA sequencing.

first: Banru

first: Ruixin

last: Liu


title: Gastruloids enable modeling of the earliest stages of human cardiac and hepatic vascularization

city: Stanford

first: Oscar

last: Abilez

state: CA

address: Clark Center E276, 318 W Campus Dr

department: Cardiothoracic Surgery

institute: Stanford University

summary: Here we show that spatially micropatterned human pluripotent stem cell (hPSC)-derived gastruloids enable in vitro modeling of the earliest developmental stages of cardiac vascularization, roughly corresponding to the first three weeks of in vivo human development (Carnegie Stages 9 and 10). Using clues from developmental biology, we identified a growth factor/small molecule cocktail, that when added to micropatterned hPSCs, generated a spatially organized, branched, and lumenized vascular network within a multi-lineage cVO comprising endocardial, myocardial, epicardial, and neuronal cell types.

overall_design:
Our single cell RNA-seq (scRNA-seq) data includes one (1) Control (standard cardiac differentiation) and four (4) groups of cVOs (standard cardiac differentiation + vascular factors).

Our bulk RNA-seq (bRNA-seq) includes data for cardiac and hepatic systems. In the cardiac system, there are three groups and a total of 39 samples: 1. hESC-3R at D0 only (3 replicates/timepoint x 1 timepoint = 3 total samples); 2. Control at Days 2, 5, 8, 10, 12, and 16 of differentiation (3 replicates/timepoint x 6 timepoints = 18 total samples); 3. cVO at Days 2, 5, 8, 10, 12, and 16 of differentiation (3 replicates/timepoint x 6 timepoints = 18 total samples). In the hepatic system, there are four groups and a total of 12 samples: 1. hESC-3R at D0 only (3 replicates/timepoint x 1 timepoint = 3 total samples) *Note: this group/replicates were used both for cardiac and hepatic systems; 2. Control at Day 20 of differentiation (3 replicates/timepoint x 1 timepoint = 3 total samples); 3. hVO-D3 at Day 20 of differentiation (3 replicates/timepoint x 1 timepoint = 3 total samples); 4. hVO-D6 at Day 20 of differentiation (3 replicates/timepoint x 1 timepoint = 3 total samples).

Our single cell RNA-seq (scRNA-seq) data includes one (1) Control (standard cardiac differentiation) and four (4) groups of cVOs (standard cardiac differentiation + vascular factors).

middle: J

first: Joseph

last: Wu

first: Ioannis

last: Karakikes


title: Resident memory T cells in regional lymph nodes sustain immunity to cancer

city: St Louis

first: Jichang

last: Han

state: MO

address: 4905 Children's PI

institute: Washington University in St Louis

summary: While immune responses against primary tumors are critically important, T cells must also be capable of functioning at sites where cancers metastasize. Here we investigated how resident memory (TRM) and circulating memory (TCIRCM) CD8 T cells potentiate immunity to cancer in diverse tissue microenvironments. Based on a mouse model of immunity to melanoma with associated autoimmune vitiligo, we show that tumor-specific memory T cells form a widespread network of transcriptionally distinct subsets throughout lymphoid tissues and visceral organs. Among these, we discovered a population of TRM cells that reside durably within LNs, where they protect against invading melanoma cells. These LN-resident memory (LN TRM) cells adopt a transcriptional program that is distinct from TRM cells in other tissues, and which uniquely predicts survival in melanoma patients with regional LN metastases. This work reveals a novel role for TRM cells in durable immunity to cancer at crucial sites of metastasis.

overall_design:
Long-term melanoma survivor and four tissues including blood, tumor lymph node and skin.
NOTE FROM SUBMITTER: since it's human data, the raw files will be uploaded to dpGAP

first: Aleksey K

last: Molodtsov

first: Nikhil

last: Khatwani

first: Jennifer L

last: Vella

first: Kathryn

last: Lewis

first: Yanding

last: Zhao

first: Delaney

middle: E

last: Sullivan

first: Tyler

last: Searles

first: Nicholas

middle: K

last: Preiss

first: Tamer

middle: B

last: Shabaneh

first: Peisheng

last: Zhang

first: Aaron

last: Hawkes

first: Brian

middle: T

last: Malik

first: Fred

last: Kolling IV

first: Edward

last: Usherwood

first: Sandra

middle: L

last: Wong

middle: D

last: Phillips

first: Keisuke

last: Shirai

first: Christina

middle: V

last: Angeles

first: Shaofeng

last: Yan

last: Curiel

first: Yina

middle: H

last: Huang

first: Chao

last: Cheng

first: Mary

last: Turk


title: Microbial Product Cocktails for Personalized Cancer Immunotherapy

status: Public on Jun 03 2025

city: University Park

first: Pak kin

state: State College

address: 513 Chemical and Biomedical Engineering Building

institute: the Pennsylvania State university

summary: Microbial product cocktails induce a cytokine secretion profile in bladder cancer.

overall_design: The cytokine secretion profiles of three human bladder tumor samples (PPS 1–3), treated with or without microbial product cocktails, were compared using the RayBiotech Q1200 Array for Human Microbial Product-Induced Cytokine Detection.

first: Yue

first: Hawhan

last: Yen

first: Mike

last: Mao


title: JMJD1C facilitates long distance genomic interactions by promoting condensates formation of key leukemic transcription factors in multiple AML cells [4C-seq]

first: Qian

last: Chen

address: Qinghuayuan Stress

institute: Tsinghua University

summary: Dysregulation of transcriptional programs that establish and maintain specific cell identities can lead to various diseases, especially cancer. Acute myeloid leukemia (AML) is an extremely heterogeneous malignancy with frequent genetic mutations such as transcription factors (TFs) and epigenetic factors, resulting in gene dysregulation, differentiation blockade and aberrant proliferation of immature clonal myeloid cells. Various AML subtypes usually involve in distinct genetic alterations, and most studies and therapeutic drugs are focused on specific AML genetic abnormalities. However, whether these seemingly different AML subtypes share a universal transcriptional programs and regulation mechanism is not clear. Identification of such program could help finding of common vulnerabilities and thus future therapeutics against multiple AML subtypes. In this study, we set out to elucidate the underlying mechanism that explains the general dependency towards JMJD1C by AML with different genetic backgrounds. Towards this goal, we first identify RUNX1 as a transcription factor that recruits JMJD1C to chromatin in multiple types of leukemia. Second, we show that JMJD1C directly interacts with RUNX1 at the N-terminus and they co-regulate a set of genes required by leukemic cells. Finally, we found that the N-terminus of JMJD1C could form liquid-like biomolecular RUNX1-containing condensates that are independent of its enzymatic activity, to mediate promoter-enhancer interactions to activate downstream gene expression.

overall_design: The circularized chromosome conformation capture assay combined with high-throughput sequencing (4C-seq) was performed in MOLM13 cells to identify cis regulatory elements interacted with EGR1 promoter (GRCh37/hg19: Chr5: 137,798,978-137,800,396).

first: Mo


title: Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease

city: Ann Arbor

first: Benjamin

middle: H.

last: Singer

state: Mi

address: 109 Zina Pitcher Place

department: Internal Medicine Division of Pulmonary and Critical Care Medicine

institute: University of Michigan

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

overall_design: Refer to individual Series


title: Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease II

summary: Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease. 72 post-mortem perfused brain tissue samples from male and female mice (5xFAD and C57BL/6) with and without sepsis, 25 days post CLP infection.

overall_design: 72 post-mortem perfused brain tissue samples from male and female mice (5xFAD and C57BL/6) with and without sepsis, 25 days post CLP infection.Treatments are CLP, Anesthesia, and unoperated. Groups are 5xFADCLP, 5xFADAnesthesia, 5xFADUnoperated, WtCLP, and WtUnoperated

first: Angela

last: Bustamante

first: Marc

last: Padilla

first: Zhuoer

last: Zeng

first: Michael

middle: W

last: Newsteadt


title: Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease I

summary: Synergistic behavioral and neuroinflammatory effects of amyloid neuropathology and sepsis survival in a murine model of Alzheimer’s disease. 40 post-mortem perfused brain tissue samples from both male and female mice (5xFAD and C57BL/6) with and without sepsis, 5 days post CLP infection.

overall_design: 40 post-mortem perfused brain tissue samples from both male and female mice (5xFAD and C57BL/6) with and without sepsis, 5 days post CLP infection.Treatments are CLP and Anesthesia.  Groups are 5xFADCLP, 5xFADAnesthesia, WtAnesthesia, and WtCLP.


title: Mechanical confinement governs phenotypic plasticity in melanoma [ChIP-seq SKMEL5]

city: New York

first: Miranda

last: Hunter

state: NY

address: 418 E 68th St

institute: Memorial Sloan Kettering Cancer Center

summary: Phenotype switching is a form of cellular plasticity in which cancer cells reversibly move between two opposite extremes - proliferative versus invasive states. While it has long been hypothesised that such switching is triggered by external cues, the identity of these cues has remained elusive. Here, we demonstrate that mechanical confinement mediates phenotype switching through chromatin remodelling. Using a zebrafish model of melanoma coupled with human samples, we profiled tumour cells at the interface between the tumour and surrounding microenvironment. Morphological analysis of these rare cells showed flattened, elliptical nuclei suggestive of mechanical confinement by nearby adjacent tissue. Spatial and single-cell transcriptomics demonstrated that the interface cells adopted a gene program of neuronal invasion, including acquisition of an acetylated tubulin cage that protects the nucleus during migration. We identified the DNA-bending protein HMGB2 as a confinement-induced mediator of the neuronal state. HMGB2 is upregulated in confined cells, and quantitative modelling revealed that confinement prolongs contact time between HMGB2 and chromatin, leading to changes in chromatin configuration that favour the neuronal phenotype. Genetic disruption of HMGB2 showed that it regulates the trade-off between proliferative and invasive states, in which confined HMGB2high tumour cells are less proliferative but more drug resistant. Our results implicate the mechanical microenvironment as a mechanism for phenotype switching in melanoma.

overall_design: ChIP-sequencing targeting HMGB2 in SKMEL5 human melanoma cells expressing V5-tagged HMGB2.

first: Hunter

last: Miranda V


title: Transcriptomics of Thy-Tau22 mice (12 month-old) treated with CSP-TTK21

city: strasbourg

first: Charles

last: DECRAENE

address: 12 rue Goethe

department: UMR 7364 CNRS

country: France

institute: CNRS

summary: This project aims to assess the transcriptomic signature in the dorsal hippocampus of 12 month-old Thy-Tau22 mice in basal conditions and treated with the vehicle CSP (n=4) or CSPTTK21 (n=3), compared to CSP-treated WT (n=4) mice.

overall_design: RNA-Seq

first: Anne-Laurence

last: Boutillier

first: Isabel

last: Paiva


title: Valproic acid inhibits Burkitt lymphoma by downregulating PFN2 expression to modulate the PI3K/AKT pathway

city: Xi'an

first: Yongliang

last: Zheng

address: 157, West 5 Road, Department of Hematology, The Second Affiliated Hospital of Xi

institute: Xi'an Jiaotong University Second Affiliated Hospital

summary: Burkitt lymphoma (BL) is a type of B-cell non-Hodgkin's lymphoma, which commonly occurs in children. At present, chemotherapy is the main treatment for BL, but CHOP treatment regimen has limited effectiveness, requiring precautions against central nervous system involvement and tumor lysis syndrome. Therefore, it is urgent and necessary to find effective and low toxic drugs for the treatment of BL. Valproic acid (VPA), a commercial antiepileptic drug, has been reported to have an inhibitory effect in some tumors, but whether it is effective against BL is unclear. Using CCK-8 test and flow cytometry analysis, we found that VPA could inhibit the proliferation, cell cycle, and promote apoptosis of BL cell lines (Daudi, Raji and Namalwa). Moreover, VPA had a significant inhibitory effect on Namalwa cell line-derived xenograft (CDX) in vivo, and we successfully constructed three BL patient-derived xenograft (PDX) models, and found that VPA had significant inhibitory effects on BL PDX models in vitro and in vivo. Finally, we used RNA-seq, qPCR and Western blotting to verify that VPA could inhibit the growth of BL by down-regulating PFN2 and inhibiting PI3K/AKT pathway. In conclusion, our study demonstrated that VPA was a promising candidate for BL treatment by inhibiting PFN2/PI3K/AKT pathway.

overall_design: RNA-seq of PDX tumor tissue in Control and VPA-treated experiment group


title: Human umbilical cord MSCs prime monocytes to recruit and activate eosinophils for enhanced host defence against Klebsiella pneumoniae

city: Kaifeng

first: yue

last: ming

address: Henan University

institute: Henan University

summary: The global rise of antibiotic-resistant Klebsiella pneumoniae (KP) underscores an urgent need for novel preventive strategies. Although human mesenchymal stem/stromal cells (hMSCs) exhibit immunomodulatory and antimicrobial properties in preclinical model, their clinical efficacy remains limited. We hypothesized that early prophylactic hUC-MSCs administration in high-risk populations could prime the pulmonary immune microenvironment, conferring protection against KP infection. This study evaluated the efficacy and mechanisms of hUC-MSC-based prophylaxis in a murine KP lung infection model.

overall_design: Lung tissues were harvested from KP-infected mice with or without hUC-MSCs pretreatment at 24 hpi, and analyzed using RNA-seq.

first: Ting

last: Yu

last: Ming

first: Yu

last: Gong


title: Adipocyte-Specific IGF1R Knockout Activates the β-Catenin/Apelin Axis to Combat Diet-Induced Obesity

city: Dalian

first: Haoan

last: Wang

address: No. 9, West Section, Lvshun South Road

institute: Dalian Medical University

summary: Obesity, driven by complex genetic and environmental interactions, remains a global health crisis with limited therapeutic options. The insulin-like growth factor 1 receptor (IGF1R) plays dual roles in metabolism and growth, but its tissue-specific functions in adipose biology are controversial. This study investigates how adipose-specific IGF1R knockout impacts systemic metabolism under high-fat diet (HFD) stress and explores the underlying mechanisms.

overall_design: Adipose-specific IGF1R knockout mice (AdIGF1RKO) were generated by crossing Igf1rfl/fl mice with Adipoq-Cre transgenics. Littermate Igf1r-Floxed (Flox) mice were used as controls. Mice were fed a normal chow diet (NCD) for 24 weeks. RNA was isolated from inguinal white adipose tissue.

first: Liyuan

last: Ran

first: Yingjie

last: Wu


title: Mechanical confinement governs phenotypic plasticity in melanoma [ChIP-seq A375]

overall_design: ChIP-sequencing targeting HMGB2 in A375 human melanoma cells, in HMGB2KO cells relative to NT control.

first: Miranda V


title: Thy-Tau22 mice


title: Evaluate of transcriptomic alternation  with Berberine and RPS6KB1 depletion that sensitizes prostate tumors to radiation

city: San Antonio

first: Yidong

last: Chen

state: Texas

address: 8403 Floyd Curl Drive, MSC 7784

department: Population Health Sciences

institute: UT Health Science Center at San Antonio

summary: Transcriptomic analysis of androgen responsive LNCaP cells depleted (RPS6KB1 KO), overexpressing for RPS6KB1 (RPS6KB1 OE) and treated with berberine (24h treatment with 5 microg/ml prior to radiation) in combination with radiation.  Results provide insight into the role of RPS6KB1 in response to radiation.

overall_design: Logarithimically growing parental, RPS6KB1 KO and RPS6KB1 OE LNCaP cells cells (2 10 cm dishes per sample in triplicate) at 70-80% confulency were harvested for preparation of total RNA for use in transcriptomic analysis. LNCaP cells pre-treated with vehicle control (methanol) or berberine (5 microg/ml) for 24h were exposed to ionizing radiation (2Gy for 6h). In addition cells exposed to radiation alone (2Gy) were also included. Cells were harvested for total RNA preparation 6h post-radiation. Additionally, to identify transcripts shared between berberine treatment and RPS6KB1 depletion, transcriptomic data from RPS6KB1 depleted cells and was integrated with LNCaP cells treated with berberine.

first: Alison

last: Clark

first: Michelle

last: Villarreal

first: Rita

last: Ghosh

first: Addanki

middle: P

last: Kumar

first: Zhao

last: Lai


title: Phenotypic screens for SIRPA expression reveal RAB21 as a general regulator of macrophage surface identity

city: Toronto

first: Jason

last: Moffat

state: Ontario

address: 686 Bay Street

department: Genetics and Genome Biology

country: Canada

institute: Hospital for Sick Children

summary: Factors influencing the macrophage surfaceome define macrophage identity and behaviour. Here, we use genome-wide phenotypic screens to identify genes affecting the accessibility and surface expression of macrophage SIRPA. Our data are consistent with previous evidence but also implicate QPCTL in cis CD47-SIRPA interactions. We also identify endolysosomal factors encoded by RAB21 and members of the CCC and WASH complexes as modulators of SIRPA expression. Surface immunophenotyping and surfaceome profiling show that inactivation of either Sirpa or Rab21 remodels cell surface protein expression. In contrast to Sirpa, Rab21 appears to be a general regulator of established macrophage cell surface markers. Perturbation of RAB21/Rab21 reduced Fc gamma receptor expression, leading to decreased uptake of antibody-nanoparticle conjugates and impaired phagocytosis of opsonized cells. To summarize, our study describes circuitry controlling SIRPA expression on macrophages and reveals a conserved RAB21-dependent trafficking pathway that has a role in modelling the cell surface of macrophages.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: FACS-based selection of modulators of surface SIRPA/Sirpa expression and nanoparticle uptake

first: Adrian

last: Granda Farias

first: Kevin

middle: R

last: Brown


title: RESTORATION OF NOX4 SIGNALLING REVERSES ENDOTHELIAL COLONY-FORMING CELL ANGIOGENIC DYSFUNCTION ASSOCIATED WITH EXPERIMENTAL AND CLINICAL DIABETES

city: Belfast

first: Karla

middle: M

last: O'Neill

address: 97 Lisburn Rd

department: Wellcome Wolfson institute for Experimental Medicine

country: United Kingdom

institute: Queens University Belfast

summary: Progenitor endothelial colony forming cells (ECFCs) are critical for vascular homeostasis and hold therapeutic potential for ischaemic cardiovascular disease (CVD). As angiogenic capacity and efficacy within diseased tissues is particularly impacted in diabetic patients, who show high incidence of ischaemic CVD, targeting of critical ECFC pathways in this setting represents an innovative focus towards enhancing intrinsic vasoreparative function. We previously reported that NADPH oxidase 4 (NOX4)-derived reactive oxygen species promote cord blood-derived ECFC (CB-ECFC) pro-angiogenic response, whilst NOX4 overexpression (OE) enhances revascularisation capacity. Here, we aimed to investigate specific influence of NOX4-dependent signalling on CB-ECFC angiogenic dysfunction observed upon exposure to both experimental and clinical diabetes to define whether NOX4 may represent a viable therapeutic target in this context.

overall_design: RNA sequencing profiling of Cord blood derived progenitor Endothelial Colony Forming Cells obtained from healthy and diabetes donors

last: Madishetti

first: Edoardo

last: Pedrini

middle: S

last: Edgar

last: Pun

first: Reinhold

last: Medina

first: David

last: Grieve


title: Impact of microbiota-derived extracellular vesicles on liver transcriptome

city: Camperdown

first: Jian

last: Tan

state: NSW

address: D17 Charles Perkins Centre, The University of Sydney

country: Australia

institute: The University of Sydney

summary: The gut microbiota plays a critical role in regulating numerous host processes through diverse mechanisms, including metabolite production and direct interactions with host cells. In this study, we explored how extracellular vesicles derived from the gut microbiota impact the host hepatic transcriptome.

overall_design: RNAseq of liver tissue collected from germ-free mice that was either administered PBS or microbiota-derived extracellular vesicles from control SPF mice.


title: Germline-somatic liaison dictates cancer subtype via de novo steroid biosynthesis

city: Trento

first: Francesca

last: Demichelis

state: TN

address: Via Sommarive, 9

department: Department for Cellular, Computational and Integrative Biology - CIBIO

country: Italy

institute: University of Trento

summary: This study investigates the cooperation between germline genetic variants and somatic mutations in prostate cancer. Specifically, we dissected the interplay between a germline variant at the 7p14.3 locus (rs1376350, G>A) and early recurrent prostate cancer-specific mutation in the Speckle-Type POZ protein (SPOP) gene across human prostate adenocarcinomas. The transcriptomes of multiple edited models pointed to Gli3 and the Hedgehog signaling pathway in a genotype-specific manner.

overall_design: RNA-seq profiling of PC3 and LnCaP cellines with single-nucleotide, macrodeletion, microdeletion, and distruption of binging motifs at genomic site 7p14.3 (rs1376350)

first: Paola

last: Gasperini

first: Blerta

last: Stringa

first: Yari

last: Ciani

first: Orsetta

last: Quaini


title: Multi-omics Integration Identifies NK Cell-Mediated Cytotoxicity as a Therapeutic Target in Systemic Lupus Erythematosus

city: Nanjing

first: Jingjing

last: Zhang

state: Jiangsu

address: 321 Zhongshan Road

institute: Nanjing University

summary: Systemic lupus erythematosus (SLE) is an autoimmune condition that impacts various organs. Given the intricate clinical progression of SLE, it is imperative to explore novel avenues for precise diagnosis and treatment.Peripheral blood mononuclear cells (PBMC) were isolated from 6 SLE patients before and after treatment, 7 healthy controls and 7 disease controls. Assay for Transposase Accessible Chromatin with high throughput Sequencing (ATAC-seq) was used to analyze the chromatin accessibility signatures and RNA-seq was used to identify the differentially expressed genes, mRNA, lncRNA, circRNA, miRNA. Then ATAC-seq and RNA-seq were integrated to further analyze hub genes and pathways. Finally, we validated gene expression levels and examined changes in key genes after treatment through in vitro experiments.

overall_design: Peripheral blood mononuclear cells (PBMC) were isolated from 6 SLE patients before and after treatment, 7 healthy controls and 7 disease controls。RNA-seq was used to identify the differentially expressed genes, lncRNA, circRNA, miRNA.

first: Ling

last: Ma

first: Hanyin

last: Deng

first: Wenqian

last: Yi

first: Alim

last: Tohtihan

first: Xiaojun

last: Tang

first: Xiudi

last: Wu

first: Xuebing

last: Feng


title: C-terminal binding protein 2 in macrophage inflammation [RNA-seq]

city: Freising

first: Franziska

last: Greulich

address: Gregor-Mendel-Str. 2

department: Metabolic Programming

country: Germany

institute: TU München

summary: Acute inflammation is critical for survival, but chronic immune mediated inflammation is a leading cause for disease and mortality worldwide , while our understanding of the pathogenesis and precise treatments are still limited. Here we investigate the role of the transcriptional corepressors CTBP 1 and 2 in murine and human macrophage inflammation using loss of function models to show that CTBP2 but not CTBP1 controls inflammatory gene expression . We find that CTBP2 binds to cis-regulatory elements of inflammatory genes together with the transcription factors NFκB and AP-1 and forms a corepressor complex. Rescue of Ctbp1/2 double knockout cells with full length CTBP2 potently represses inflammatory responses while a monomeric mutant does not. Differential profiling of CTBP2’s wild type and monomeric interactome confirms oligomer-specific interactions with multiple repressors including the NuRD complex, WIZ and KDM1A. Conversely, monomers retain their ability to interact with inflammatory transcription factors and polymerase 2, boosting transcription of inflammatory genes. Our findings point to an important function for CTBP2 in the resolution of inflammation, which may contribute to the progression of inflammatory disorders  and which may offer therapeutic targets in the future.

overall_design: Polyadenylated mRNA expression in either bone marrow-derived macrophages (BMDMs) with control siRNA, Ctbp1 siRNA or Ctbp2 siRNA knockdown or the macrophage cell line J774.1 with wildtype or Ctbp1/2 double-knockout was profiled by RNA-seq after stimulation with vehicle control (PBS) or 4h 100 ng/ml LPS. The effect of Ctbp1 and/or 2 on inflamamtory gene expression was analyzed.

first: Benjamin

middle: A

last: Strickland


title: C-terminal binding protein 2 in macrophage inflammation [ChIP-seq]

overall_design: ChIP-seq for CTBP2 in vehicle (PBS) or LPS (3h, 100 ng/ml) treated murine bone marrow-derived macrophages.


title: C-terminal binding protein 2 in macrophage inflammation

overall_design: Refer to individual Series


title: RNA-seq Analysis of Dental Pulp in Rats Under Different Sleep conditions

city: BEIJING,CHINA

first: SIQI

last: HUANG

institute: Capital of china medical university

summary: This study aims to investigate genes from dental pulp tissue regulated by sleep deprived

overall_design:
Twelve eight-week-old male Sprague-Dawley rats (specific pathogen-free grade) were randomly assigned to either sleep deprivation group or control group (n=6 per group). Under sterile conditions in a laminar flow hood, the complete dental pulp tissues were aseptically extracted from the mandibular first molars.

Preliminary experiments revealed that the rat dental pulp tissues had limited mass (approximately 4–5 mg per tooth) and yielded insufficient RNA quantities (<200 ng per sample) for individual library preparation. To address this, we employed an intra-group equal pooling strategy, combining six independent biological replicates per group into a single pooled sample (1 pool per group). Subsequent paired-end sequencing was performed using the Illumina NovaSeq 6000 platform.

first: Siqi

last: Huang

first: Ying

last: Zheng

first: Qian

last: Wang

first: Yumeng

last: Guo


title: ChIP-seq and RNA-seq analysis reveals the association between thyroid hormone receptor α and skeletal muscle aging in mice（RNA-seq）

first: Shi

last: Runqing

address: Department of Gerontology 300 Guangzhou Road

institute: The First Affiliated Hospital of Nanjing Medical University

summary: In the current situation of the aging of the global population, primary sarcopenia is gradually attracting attention because of its potential risk to the elderly, high occult incidence and serious prognosis. As one of the most important hormones affecting skeletal muscle, the aging changes of thyroid hormone have been proved to be closely related to sarcopenia. Thyroid hormone exerts its effects locally in skeletal muscle by binding to thyroid hormone receptor. TRα is the main distribution type of thyroid hormone receptor in skeletal muscle. We have previously found the potential role of TRα in the aging process of skeletal muscle. As a nuclear transcription factor, TRα exerts subsequent biological effects by targeting regulatory genes. However, in the process of skeletal muscle aging, the target regulation map of TRα is still unclear.In this study, we constructed natural aging mouse models of different ages, combined ChIP-seq and mRNA-seq to explore the aging changes of TRα targets in skeletal muscle.

overall_design: Gene expression profiling of RNA-seq data in gastrocnemius muscle tissues of 6, 15, and 21 month old mice. Three mice from each age group were selected for analysis.

first: Duan

last: Yu


title: ChIP-seq and RNA-seq analysis reveals the association between thyroid hormone receptor α and skeletal muscle aging in mice（ChIP-seq）

overall_design: Chromatin immunoprecipitation DNA-sequencing  (ChlP-seq) for thyroid hormone receptor α, TRα in gastrocnemius muscle tissues of 6, 15, and 21 month old mice. Two mice from each age group were selected for analysis.


title: FTO SUMOylation regulates the differentiation of bone marrow mesenchymal stromal cells in Inflammatory Bowel Disease-Induced Bone Loss

city: Hangzhou

first: Putao

last: Yuan

address: No. 3, Qingchun Road East

department: Department of Orthopaedic Surgery

institute: Sir Run Run Shaw Hospital, Zhejiang University School of Medicine

type: Methylation profiling by high throughput sequencing

summary: Gut-bone axis is critical for body homeostasis, but bone loss often complicates inflammatory bowel disease (IBD) with unclear mechanisms. Here, we found that IBD mice showed reduced bone formation, with bone marrow mesenchymal stromal cells (BMSCs) favoring adipogenesis over osteogenesis. Altered m6A modifications of BMSCs were confirmed in IBD mice, and further investigation revealed that the SUMOylation of FTO was involved. Nude mice with FTO-K216/357/365R mutation exhibited increased bone sizes and volumes versus control mice. Tocilizumab, an IL-6R monoclonal antibody, combined with AAV-FTO-3KR, mitigated bone loss and enhanced bone formation in IBD mice. Our findings reveal that SUMOylation of FTO is involved in the differentiation of BMSCs in mice with IBDs. The outcome could be blocked by redirecting differentiation toward osteoblasts treatment with AAV-FTO-3KR and the clinical-stage inhibitor, tocilizumab.

overall_design: m6A transcriptomics assay was performed for investigating the downstream signaling pathways of BMSCs treated with AAV-FTO-WT or AAV-FTO-3KR.

first: Haoming

first: Jiandong

first: Lijun

last: Li

first: Zhiwei

last: Jie

first: Shunwu

last: Fan

first: Ziang

last: Xie


title: Sucrose metabolism and hormone interaction determine the fate of different florets within central spikelet of wheat

city: Beijing

first: SUN

last: WAN

address: o. 2 Yuanmingyuan West Road, Haidian District

institute: China Agricultural University

summary: In the central spikelet, floret primordia proximal to rachis typically develop into fertile florets, while those distal ones tend to abort. However, the mechanisms driving these divergent outcomes remain unclear. To elucidate these differences, a two-year field experiment was conducted, analyzing the differences between fertile (floret 1) and abortive florets (floret 5) at phenotypic, physiological, cellular, and transcriptional levels. Our results showed that floret 1 (F1) developed earlier than floret 5 (F5), evidenced as distinct floret and anther cell morphology. This developmental difference was associated with distinct metabolic strategies: F1 prioritizes starch biosynthesis by enhancing photosynthetic efficiency and reducing thermal dissipation, while F5 diverts carbon to trehalose metabolism under resource constraints. Transcriptomic profiling revealed 17,711 differentially expressed genes, predominantly enriched in carbohydrate metabolism. Key starch-related genes (WAXY, SS, GBE1) were upregulated in F1, while trehalose synthesis genes (TPS, TPP) dominated in F5, reflecting a metabolic trade-off between growth and survival. Hormonal profiling revealed elevated indole-3-acetic acid (IAA) levels in F1, driven by upregulated genes encoding enzymes of TDC and YUCCA, whereas abscisic acid (ABA) level increased in F5, mediated by NCED. Specially, tissue-specific regulation in fertile floret was clarified: lemma tissues enriched in photosynthesis genes supplied localized carbon, anthers relied on sucrose cleavage genes to sustain pollen development, and ovaries activated lipid biosynthesis genes for embryogenesis. Collectively, we propose a model where IAA-starch synergy in proximal florets establishes a competitive metabolic sink, whereas ABA-T6P interplay in distal florets enforces developmental arrest, thereby optimizing resource allocation and reproductive success. The proposed regulatory framework provides novel views for improving floret fertility through carbohydrate partitioning and hormone signaling.

overall_design: To investigate the transcriptional difference of fertile floret and abortive floret within central spikelets and the function of lemma, anther and ovary within fertile floret,  transcriptome analysis was conducted at 21 days after terminal  spikelet stage

first: Wan

last: Sun

first: Jie

last: Ren

first: Xuechen

last: Xiao

first: Wanqing

last: Zhang

first: Haoran

first: Zhimin

first: Zhigan

last: Zhao

first: Zhencai

first: Xubo

first: Yinghua


title: Multigenerational Proteolytic Inactivation of Restriction Upon Subtle Genomic Hypomethylation

city: Chicago

first: Chang

last: Ye

state: Illinois

institute: University of Chicago

summary: In Pseudomonas aeruginosa, restriction inactivation upon growth at high temperatures was previously described, however, which system is being inactivated, the underlying mechanism, as well as the timing of recovery, remain unknown. Here, we report that P. aeruginosa Type I methyltransferase (HsdMS) and restriction endonuclease (HsdR) components are degraded by two Lon-like proteases when replicating above 41 °C, which induces partial genome hypomethylation and simultaneously prevents self-targeting, respectively. Interestingly, upon return to 37 °C, methyltransferase activity returns gradually, with restriction activity not fully recovering for over 60 bacterial generations, representing the longest bacterial memory to our knowledge. Forced expression of HsdR over the first 45 generations is toxic, demonstrating the fitness benefit of HsdR inactivation.

overall_design: 6mA modification sequencing for  Pseudomonas aeruginosa samples.


title: Dynamic properties of enhancer and promoter during DNA damage in hepatocellular carcinoma [ChIP-Seq]

city: Temporarily undisclosed

first: Temporarily undisclosed

last: Temporarily undisclosed

address: Temporarily undisclosed

institute: Temporarily undisclosed

summary: DNA damage is a critical factor contributing to tumorigenesis, however, the dynamic changes in multi-omics signatures of enhancers and promoters during the DNA damage response (DDR) remain poorly understood. In this study, we discovered that the expression levels, chromatin accessibility, and element activity of distal/proximal enhancers and promoters exhibited obvious dynamic similarity and duality of characteristics at different stages of DNA damage in hepatocellular carcinoma (HCC). Furthermore, we found that the pre-damage accessibility and activity status of enhancers and promoters played an important role in determining their regulatory features following DNA damage in HCC. Finally, we identified transcription factors (TFs) with significantly altered activity in response to DNA damage, with notable differences between p53 activity in enhancers and promoters during the DDR. Overall, these findings reveal the complex dynamic changes within cis-regulatory elements in response to DNA damage.

overall_design: HepG2 cells were cultured in DMEM (Gibco, USA) supplemented with 10% fetal bovine serum (FBS) and 1% penicillin–streptomycin. When the cell spreading rate reached 80%, the cells were cultured with complete medium containing DOX at a final concentration of 0.5μg/mL. Subsequently, the cells were treated for various durations (0h, 4h, 8h, 12h, 16h, 24h, 36h, and 48h) before samples were extracted for additional experimental validation.


title: Dynamic properties of enhancer and promoter during DNA damage in hepatocellular carcinoma [RNA-Seq]


title: LILRB4 regulates multiple myeloma development through STAT3-PFKFB1 pathway

city: Shanghai

first: Wei

last: Yusheng

state: New York

address: 227,South Road of Chongqian,Shanghai,China

institute: Shanghai Jiao Tong University of Medicine

summary: To explore the cancdidate targets of LILRB4 in MM

overall_design: Comparative gene expression profiling analysis of RNA-seq data for LILRB4-knockdown and scrambled MM cells

first: Chiqi

last: Chen

first: Junke

last: Zheng


title: Plant U-Box 4 regulates chloroplast stress signaling and programmed cell death via Salicylic acid modulation

city: Tucson

first: Jesse

middle: Daniel

last: Woodson

state: AZ

address: 1140 E. South Campus Drive, 303 Forbes Hall

department: School of Plant Sciences

institute: University of Arizona

summary: In response to environmental stress, chloroplasts generate reactive oxygen species, including singlet oxygen (1O2), which regulates nuclear gene expression (retrograde signaling), chloroplast turnover, and programmed cell death (PCD). Yet, the central signaling mechanisms and downstream responses remain poorly understood. The Arabidopsis thaliana plastid ferrochelatase two (fc2) mutant conditionally accumulates 1O2 and involves Plant U-Box 4 (PUB4), a cytoplasmic E3 ubiquitin ligase, in propagating these signals. To gain insights into 1O2 signaling pathways, we compared transcriptomes of fc2 and fc2 pub4 mutants. The accumulation of 1O2 in fc2 plants broadly repressed genes involved in chloroplast function and photosynthesis, while 1O2 induced genes and transcription factors involved in abiotic and biotic stress, the biosynthesis of jasmonic acid (JA), and Salicylic acid (SA). Elevated JA and SA levels were observed in stressed fc2 plants, but were not responsible for PCD. pub4 reversed the majority of 1O2-induced gene expression in fc2 and reduced the JA content, but maintained elevated levels of SA even in the absence of 1O2 stress. Reducing SA levels in fc2 pub4 restored 1O2 signaling and light sensitivity. Together, this work demonstrates that SA plays a protective role during photo-oxidative stress and that PUB4 mediates 1O2 signaling by modulating its levels.

overall_design: To investigate the molecular mechanisms underlying chloroplast singlet oxygen stress signaling in Arabidopsis thaliana, we grew wt and fc2 plants under permissive constant light and singlet oxygen-producing diurnal light cycling conditions. To understand the role of Plant U-Box 4 (PUB4) in signaling, we also included fc2 pub4 mutants under both conditions.

first: Snigdha

last: Rai

first: Matthew

last: Lemke

first: Anika

last: Arias

first: Maria

middle: F

last: Gomez Mendez

first: Katayoon

last: Dehesh


title: Dynamic properties of enhancer and promoter during DNA damage in hepatocellular carcinoma [ATAC-Seq]


title: piRNA expression profiling for 6 human samples

first: Wentao

address: Rd Yanchang

institute: Shanghai tenth people‘s hospital

summary: To further define the role of piRNAs in the development of renal cancer, we employed piRNA microarray expression profiling as a discovery platform to identify differentially expressed piRNAs. Radical nephrectomy was performed on 3 patients with renal cancer, and the postoperative pathology was clear cell renal cell carcinoma. The cancer tissues and adjacent normal tissues of the patients were taken for piRNA sequencing. And the differentially high-expressed and differentially low-expressed piRNAs were analyzed by bioinformatics.

overall_design: Radical nephrectomy was performed on 3 patients with clear cell renal cell carcinoma, and the expression of piRNA in renal cancer tissue and adjacent tissue was measured.

last: Li


title: An integrated transcription factor framework for Treg identity and diversity

status: Public on Jun 02 2025

city: Boston

first: CBDM

last: Lab

state: MA

address: 77 Avenue Louis Pasteur

department: Microbiology and Immunobiology

institute: Harvard Medical School

summary: Vertebrate cell identity depends on the combined activity of scores of transcription factors (TF). While TFs have often been studied in isolation, a systematic perspective on their integration has been missing. Focusing on FoxP3+ regulatory T cells (Tregs), key guardians of immune tolerance, we combined single-cell chromatin accessibility, machine learning, and high-density genetic variation, to resolve a validated framework of diverse Treg chromatin programs, each shaped by multi-TF inputs. This framework identified previously unrecognized Treg controllers (Smarcc1) and illuminated the mechanism of action of FoxP3, which amplified a pre-existing Treg identity, diversely activating or repressing distinct programs, dependent on different regulatory partners. Treg subpopulations in the colon relied variably on FoxP3, Helios+ Tregs being completely dependent, but RORγ+ Tregs largely independent. These differences were rooted in intrinsic biases decoded by the integrated framework. Moving beyond master regulators, this work unravels how overlapping TF activities coalesce into Treg identity and diversity.

overall_design: We isolated CD4 T cells from mouse spleen and LNs, and used CRISPR-Cas9 ribonucleoprotein complexes to engineer Tregs carrying Smarcc1 deletions (and corresponding non-targeting gRNA controls), which were then parked in vivo in Treg-dpeleted hosts (Foxp3-DTR mice) for 1 wk in vivo before isolation for bulk ATAC-seq.

first: Kaitavjeet

last: Chowdhary

first: Diane

last: Mathis

first: Christophe

last: Benoist


title: The oncogenic mechanisms of FUS-CREB3L2

first: Xinyu

last: Wang

address: 15 Datun Road

institute: Institute of Biophysics

summary: FUS-CREB3L2 is reccurently identified in low-grade fibromyxoid sarcoma (LGFMS). To explore how FUS-CREB3L2 activate LFGMS target genes, we performed RNA-seq and CUT&Tag assay.

overall_design: In order to explore how FUS-CREB3L2 affects the transcription profiles, we performed RNA-seq and CUT&Tag in cells overexpressing FUS-CREB3L2, CREB3L2, TDP43-CREB3L2, FUS-CREB3L2 mutants (12E and del-bZIP).

first: Dong


title: Dynamics of microcompartment formation at the mitosis-to-G1 transition

city: Cambridge

first: Viraat

middle: Yogi

last: Goel

state: Massachusetts

department: Biological Engineering

institute: Massachusetts Institute of Technology (MIT)

summary: As cells exit mitosis and enter G1, mitotic chromosomes decompact and transcription is  reestablished, with prior studies showing that essentially all interphase 3D genome features including A/B-compartments, TADs, and CTCF loops are lost during mitosis. Microcompartments, nested focal interactions between cis-regulatory elements (CREs), can now be resolved using Region Capture Micro-C (RCMC), though the dynamics of their formation remain unknown. We therefore applied Region Capture Micro-C to G1E-ER4 cells across five mitosis-to-G1 stages: prometaphase, ana/telophase, early G1, mid G1, and late G1, along with an asynchronous condition. Five mouse loci ranging from 1-2 Mb in size were selected for capture: Id1, Klf1, Cdt1, Dag1, and Myc. Follow-up RCMC experiments were also performed at these loci in an SMC2 (condensin) degron G1E-ER4 subline, in which cells were arrested in prometaphase and auxin-treated for five tested depletion conditions: 0h, 0.5h, 1h, 4h, and 8h. We find that microcompartments form early in the M-to-G1 transition but weaken as cells enter G1, suggesting that microcompartmentalization is distinct from A/B-compartmentalization and loop extrusion.

overall_design: Region Capture Micro-C was performed in G1E-ER4 cells arrested to different stages of the mitosis-to-G1 transition and varying degrees of condensin depletion

middle: Y

first: Nicholas

middle: G

last: Aboreden

first: James

last: Jusuf

first: Haoyue

last: Zhang

first: Luisa

last: Mori

first: Leonid

last: Mirny

first: Gerd

last: Blobel

first: Edward

middle: J

last: Banigan

first: Anders

last: Hansen


title: Human adipose-derived mesenchymal stem cell-derived exosomes induce epithelial remodeling and anti-scar healing revealed by single-cell RNA sequencing

city: shanghai

first: Jing

state: Shanghai

address: No. 389 Xincun Road, Shanghai

institute: tongji university

summary: Effectively managing skin wounds to achieve quick and scarless healing is a significant clinical challenge. Several cell types participate in wound healing, including keratinocytes, fibroblasts, and many others. Human adipose-derived mesenchymal stem cell-derived exosomes (hADSC-Exos) are regarded as promising therapeutic choice. However, a comprehensive understanding of what mechanisms promote regenerative healing respond to hADSC-Exos treatment is still limited. Here, we utilize a high-resolution single-cell RNA sequencing analysis (scRNA-seq) from adult wild-type mice, postoperative day (POD) 14 mice and hADSC-Exos-treated postoperative day (POD) 14 mice. hADSC-Exos influences epithelial cells and fibroblasts, leading to scar-free wound healing. Among epithelial cell subtypes, Lef1high proliferating keratinocytes (prolif KC) are particularly remodeled by hADSC-Exos. Prolif KC exhibit epithelial-mesenchymal plasticity (EMP). The cell-cell communication between keratinocytes and fibroblasts in anti-scar healing is modulated by TGF-β1, which promote EMP transition cascade. hADSC-Exos may inhibit wound fibrosis through the 14-3-3Zeta-YES-associated protein (YAP)-hippo signaling pathway. This study enhances our understanding of epithelial cell diversity and interactions in wound healing, highlighting hADSC-Exos-induced prolif KC as potential reprogramming targets. These epithelial cells present promising therapeutic targets for improving wound healing strategies.

overall_design: scRNA-seq profiling of skin from adult, POD14, POD14-Exo

first: Yu

last: Fu

first: Junling

last: Xie

first: xingliao

last: zhang

first: Guangming

first: Xin-Min

first: Yao-ting

last: Han

first: Meng-meng

last: Xu

first: Jun


title: Myeloid cell METTL1 deletion significantly mitigated CLP-induced multiple organ injury and I/ R-induced kidney injury

city: Hefei

first: Chao

last: Hou

state: Anhui province

address: 81 Meishan Road

institute: Anhui Medical University

summary: 1. METTL1 expression was upregulated in monocytes/macrophages during acute inflammation. 2. Myeloid METTL1 depletion alleviated tissue damage induced by CLP and I/R. 3. METTL1 promoted infiltration and pro-inflammatory differentiation of macrophages. 4. SARM1-induced NAD+ consumption is crucial for the METTL1-induced metabolic reprogramming of macrophages. 5. SA91-0178, a METTL1 inhibitor, effectively alleviated injuries induced by CLP and I/R.

overall_design: m7G meRIP-seq profiling of wildtype THP-1 cells and their knockdown derivatives (shMETTL1)  .

first: Hao

first: Xinru

first: Tong

last: Chen


title: The RNA-seq study of CCL20 in OSCC cell line

city: Shiyan

first: Qin

last: Shanshan

address: Renmin Road 30, Maojian District

institute: Institute of Basic Medical Sciences, School of Basic Medical Sciences, Hubei University of Medicine

summary: This study aimed to explore the underlying molecular mechanism of CCL20 in OSCC progression.

overall_design: The estabilished OSCC cell lines (negative control and CCL20-overexpression) were seeded into 6-well plates and grown overnight. The differentally expressed genes by CCL20 overexpression were screened by RNA sequencing. The transcriptome sequencing studies were performed by deep sequencing, using Illumina NovaSeq 6000.

first: Shanshan

last: Qin

first: Dandan

last: Li


title: Changes in expression of genes +/- CREB3L1 expression

city: Saskatoon

first: Deborah

last: Anderson

state: Saskatchewan

address: 107 Wiggins Road

institute: University of Saskatchewan

summary: Assessing the changes in the expression of genes in the presence of CREB3L1 in human breast cancer cell lines

overall_design: Total RNA isolated from human breast cancer cell lines grown in standard conditions

first: Paul

last: Mellor


title: RG108-Pt(IV) Prodrug as a Potential Antitumor Agent with Hearing Protection Effects in Squamous Cell Carcinoma of the Head and Neck

city: Jinan City

first: Wu

last: Huina

state: Shandong Province

address: No.4, Duanxing West Road, Huaiyin District

department: Department of Pharmacy

institute: Shandong Second Provincial General Hospital

summary: This study developed a novel series of Pt(IV) prodrugs derived from the hearing-protective ligand RG108, including mono- and di-substituted cisplatin and oxaliplatin derivatives, to achieve high therapeutic efficacy with reduced toxicity. Compound 4 emerged as a standout candidate, demonstrating remarkable anti-tumor activity in FADU cells with an IC50 value exceeding 500-fold that of cisplatin. It potently induced apoptosis, suppressed migration, and exhibited robust in vivo anti-tumor efficacy. Mechanistically, the compound was found to enhance platinum accumulation in tumor cells via the EZH2/SLC47A2 regulatory axis, marking the first introduction of this pathway into tetravalent platinum drug research. Notably, the synthesized derivatives significantly mitigated platinum-associated ototoxicity, as evidenced by preserved cochlear hair cell viability, stabilized auditory brainstem response thresholds, and intact cochlear basement membrane morphology, thereby overcoming the hearing loss limitations of conventional platinum chemotherapy. This work establishes a pioneering framework for designing dual-functional platinum-based agents that synergize anti-tumor potency with organoprotective properties, offering both theoretical insights and translational potential.

overall_design: Generate mRNA gene profiles of FaDu cells treated with quadrivalent platinum drugs based on Illumina

first: Jiyong

last: Wu

first: Jing

last: Nie

first: Huina

first: Yong

last: Wang


title: Epstein-Barr virus BOLF1-containing extracellular vesicles promote nasopharyngeal carcinoma metastasis via SPP1+ macrophages

city: guangzhou

first: Ning

last: Meng

state: guangdong

address: 651 Dongfeng East Road

institute: Sun Yat-sen University Cancer Center

summary: Nasopharyngeal carcinoma (NPC) patients with elevated plasma Epstein-Barr virus (EBV) DNA levels are more susceptible to distant metastasis. However, the mechanisms underlying NPC progression mediated by EBV interactions with surrounding immune cells remain poorly understood. In this study, we investigated immune cell subsets within the tumor microenvironment of NPC patients, stratified by EBV-DNA load. We innovatively identified SPP1+ tumor-associated macrophages (TAMs), uniquely associated with EBV, as crucial prognostic indicators in NPC, within a retrospective cohort of 186 patients with a 10-year follow-up. Additionally, utilizing liquid chromatography-tandem mass spectrometry (LC-MS/MS), we confirmed the presence of EBV protein in plasma extracellular vesicles (EVs). Screening revealed that only BOLF1-EVs promote NPC metastasis by upregulating SPP1+ TAMs. Notably, BOLF1-EVs induced significant metabolic alterations in TAMs, characterized by increased glycolysis and spare respiratory capacity. Importantly, we identified the JAK1-STAT3 pathway as a key mediator of BOLF1-EV-induced upregulation of SPP1 in macrophages, a crucial mechanism underlying tumor metastasis promotion. These findings highlight a potential biomarker for predicting patient metastasis and offer valuable insights for therapeutic decision-making.

overall_design: To assess the response of macrophages to BOLF1-EVs, we performed RNA sequencing (RNA-seq) on THP1-derived macrophages co-cultured with either an empty vector control (Vector-EVs) or BOLF1-EVs (100 ng/ml for 48 h)

first: Mu-Sheng

last: Zeng


title: MicroRNA-6084 orchestrates angiogenesis and liver metastasis in colorectal cancer via extracellular vesicles

city: Chengdu

first: Yang

last: Zhang

state: Sichuan

address: No. 37 Guo Xue Alley

institute: West China Hospital of Sichuan University

summary: The prognosis for colorectal cancer (CRC) patients with liver metastasis remains poor, and the molecular mechanisms driving CRC liver metastasis are still not fully understood. Hypoxia-induced extracellular vesicles (H-EVs) derived from tumors have emerged as key players in inducing angiogenesis by transferring non-coding RNAs. However, the specific role of CRC-derived hypoxic EVs (H-EVs) in regulating the formation of the pre-metastatic microenvironment (PMN) by inducing angiogenesis remains unclear. Our study demonstrates that H-EVs induce both angiogenesis and liver metastasis. Through microRNA microarray analysis, we identified a reduction in miR-6084 levels within H-EVs. We found that miR-6084 inhibits angiogenesis by being transferred to endothelial cells via EVs. In endothelial cells, miR-6084 directly targets ANGPTL4 mRNA, thereby suppressing angiogenesis through ANGPTL4-mediated JAK2/STAT3 pathway. Furthermore, we uncovered that SP1 acts as a transcription factor regulating miR-6084 transcription, while HIF1A decreases miR-6084 expression by promoting SP1 protein dephosphorylation and facilitating ubiquitin‒proteasome degradation in SW620 cells. In clinical samples, we observed low expression of miR-6084 in plasma-derived EVs from CRC patients with liver metastasis. In summary, our findings suggest that CRC-derived hypoxic EVs promote angiogenesis and liver metastasis through the HIF1A/SP1/miR-6084/ANGPTL4 axis. Additionally, miR-6084 holds promise as a potential diagnostic and prognostic biomarker for CRC liver metastasis.

overall_design: To explore the main microRNAs mediating angiogenesis in CRC-derived hypoxic extracellular vesicles, SW620 cells were cultured under normoxic (20% oxygen concentration) or hypoxic conditions (1% oxygen concentration) in DMEM (Cytiva, USA) plus 10% fetal bovine serum (Excell Bio, HK) and 1% penicillin/ streptomycin (Beyotime, China) for 48 hours. Then, SW620 cell supernatant were collected and EVs were isolated by ultrafiltration plus size exclusion chromatography. Next, total RNA was extracted, and an Affymetrix miRNA 4.0 microarray was used for expression profiling analysis. RNA isolation, adding Poly A tail and biotin labeling, hybridization, Washing, staining, and scanning were performed by Echo biotech (Beijing, China) according to the Affymetrix protocol. Scanned signal was processed following a standard instruction of ThermoScientific Affymetrix pipeline. Raw data (CEL files) were generated using AGCC. Signal summarization and normalization were performed using Affymetrix Expression Console™ software with the RMA+DABG algorithm (Robust Multi-array Average with Detection Above Background).

first: Xuyang

last: Yang


title: Dietary fiber inulin enables intestinal microbiome to clear fructose and protect the host

city: Irvine

first: Cholsoon

last: Jang

state: CA

address: 839 Health Sciences Rd

department: Biological Chemistry

institute: University of California Irvine

summary: Excessive consumption of fructose leads to various cardiometabolic diseases. However, inulin, dietary fiber composed of numerous fructose molecules, exerts health-beneficial effects. Here we report that inulin shifts fructose catabolism from the host organs to gut microbiome, reversing fructose-induced hyperlipidemia, hepatic steatosis and systemic glucose intolerance. Both simultaneous and delayed inulin intake enhances fructose clearance by the small intestinal microbiome, effectively reducing fructose dose reaching the liver and colon and thus suppressing hepatic lipogenesis. Inulin also activates the hepatic de novo serine synthesis pathway and cystine uptake to augment glutathione production and reduce oxidative stress. This dual effect of inulin is blocked by antibiotics and transmittable by fecal transplantation.  Moreover, inulin-enriched Bacteroides acidifaciens is protective against HFCS-induced lipogenesis. Our data provide mechanistic insights into how fructose-polymer fiber inulin rewires gut microbial fructose catabolism and protects the host from excessive fructose exposure, paving the way to mitigate fructose-induced metabolic disease.

overall_design: 8–week-old male C57BL/6 mice were fed either control (Research diets, D21050401) or 10% (gm%) inulin diet (Research diets, D21050402) for 30 weeks. To investigate the effect of inulin supplementation with HFCS, mice were assigned into five groups (n = 9): (1) consumed control diet with normal water (C); (2) inulin diet with normal water (I); (3) control diet with HFCS water (CF); (4) inulin diet with HFCS water (IF); (5) switched from control diet to inulin diet with continual provision of HFCS water (CIF). For HFCS water, mice were provided either normal water or 15% (weight/volume) 1:1 mixture of glucose and fructose in water to mimic high fructose corn syrup. After 30 weeks of feeding, liver tissues were quickly dissected and snap-frozen in liquid nitrogen with a pre-cooled Wollenberger clamp and subjected to RNA-sequencing.

first: Sunhee

last: Jung

first: Hosung

last: Bae

first: Won-Suk

last: Song

first: Yujin

last: Chun


title: Bulk RNA-seq of iPSC-derived macrophages exposed to disease-relevant stimuli

city: Ridgefield

first: Aleksandra

last: Ivovic

address: 900 Ridgebury Rd

institute: Boehringer Ingelheim

summary: Monocyte-derived macrophages (MDMs) are widely used to study human macrophage biology in vitro. However, use of MDMs as an experimental system is limited by donor-to-donor variability, the total cell availability and pre-activation effects . Here we generated iPSC- derived macrophages (iDMs) with high yield and low phenotypic and functional variability. We used iDMs to model disease-relevant phenotypes and mapped their transcriptomes to inflammatory conditions (IBD). Using this approach, we found that the transcriptomic phenotypes generated in vitro closely correlate to macrophage phenotypes present in disease.

overall_design: iPSC-derived macrophages (IDMs) from 6 batches were stimulated with TNFa, IFNg, IL1b, and TGFb to compare the downstream signaling induced by these different cytokines and assess the relevance of this in-vitro model for drug discovery purposes.

first: Daniela

last: Schloesser


title: epigenome-wide association analysis on weighted life events in PD patients - MDD cohort

city: Munich

first: Binder

last: Elisabeth

address: Kraepelinstr. 2+10

institute: Max-Planck-Institute Psychiatry

type: Methylation profiling by genome tiling array

summary: DNAm was assessed by the Illumina HumanMethylation450 BeadChip. In a meta-analytic approach, epigenome-wide DNAm changes in association with weighted life events were analyzed in two PD cohorts and afterwards meta-analyzed with MDD cases. This is the data from the MDD cohort

overall_design: Bisulphite converted DNA from the 109 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip

first: Darina

last: Czamara

first: Stella

last: Iurato

first: Angelika

last: Erhardt


title: Unraveling the cohesin-chromatin interface: identifying protein interactions that modulate chromosome structure and function [Micro-C]

city: Chapel Hill

first: Jill

last: Dowen

state: NC

address: 250 Bell Tower Drive

institute: University of North Carolina - Chapel Hill

summary: Cohesin is a plieotropic regulator of genom structure and function with several known interactors that aid in regulation of genome organization. A comprehensive cohesin interactome has yet to be established, and we identify several chromatin regulating complexes that interact with the cohesin complex, including the SWI/SNF chromatin remodeling complex. SWI/SNF and cohesin co-localize to enhancers, promoters, and CTCF binding sites as deteremined by overlapping ChIP-seq data from mESCs for the cohesin subunit RAD21 and the SWI/SNF subunit BRG1, CTCF, H3K27ac, and H3K4me3. To assessthe functional implications of the cohesin-SWI/SNF interaction we treated mESCs with one of three small molecule drugs targeting the BRG1 subunit of SWI/SNF (ACBI1, PFI-3, BRM014) for either degradation of the complex or perturbation of SWI/SNF function, then performed ChIP-seq for the RAD21 subunit of cohesin. Differential RAD21 peaks in cells treated with a small molecule compared to DMSO control were assessed for overlap with DNA loops (Micro-C).

overall_design: Micro-C was performed in duplicate in mESCs treated with a siRNA control (siControl)

first: Natalie

middle: L

last: Rittenhouse

first: Riya

last: Gohil

first: June

last: Arricastres


title: Molecular Determinants of Sotorasib Clinical Efficacy in KRAS G12C–Mutated Non–Small-Cell Lung Cancer

city: Thousand Oaks

first: Abraham

last: Anderson

state: California

address: 1 amgen center drive

institute: Amgen Inc.

summary:
This study describes transcriptional subtypes of non-squamous non–small cell lung cancer (NSCLC).
Baseline tissue samples (fresh/archival) were analyzed using a whole-transcriptome RNA assay (Tempus RS.v2; Tempus Labs, Inc., Chicago, IL, USA).
Objectives included expression characterization of the KRAS G12C subject population with respect to genetic mutation (ATM, SMARCA4, KEAP1, STK11) and transcriptional signatures: KPCL (Skoulidis, Cancer Discov (2015) 5 (8): 860–877) & NRF2 activation (Singh, Clin Cancer Res (2021) 27 (3): 877–888).

overall_design: This data set consists of 234 NSCLC gene expression profiles of baseline tissue samples (fresh/archival), from patients with KRAS G12C‒mutated locally advanced or metastatic NSCLC after progression on prior therapies, who were randomized to the single-arm phase 2 CodeBreaK 100 study and the global randomized phase 3 CodeBreaK 200 study. Tumor specimens were prepared following standard pathology practices. Total nucleic acid (TNA) was extracted from tissue specimens using a Chemagic 360 or similar instrumentation, and the recovered TNA was quantified and qualified, and may have been concentrated if necessary. Extracted TNA that was intended for processing by Tempus|RS was treated with Invitrogen TURBO DNase to degrade DNA. The minimum amount of input total RNA required to perform the test was 50 ng. RNA was fragmented using heat and magnesium, with variable parameters, to yield similar sized fragments from RNA inputs with different starting size distributions. Strand-specific library preparation was performed using the KAPA RNA HyperPrep Kit for Illumina with KAPA single indexed 6 base pair adapters. The libraries were amplified with high fidelity, low-bias PCR using primers complementary to adapter sequences. After library preparation and amplification, targets were captured by hybridization, clean-up of captured targets was performed, and unbound fragments were washed away. The amplified target-captured libraries were sequenced with a 2x76 read length to an average of 50 million total reads on an Illumina HiSeq4000 System using patterned flowcells. Transcript level pseudo-alignment and quantification to the Ensembl GRCh37 Release 97 (July 2019) reference was performed using Kallisto (version 0.44). Raw counts or transcripts per million (TPM) were calculated for 180,253 transcripts in the Ensembl reference. 134,160 transcripts were covered by the Tempus|RS panel.

first: Ferdinandos

last: Skoulidis

first: Bob

middle: T

last: Li

first: Adrianus

last: de Langen

first: David

last: Hong

first: Herve

last: Lena

first: Juergen

last: Wolf

first: Grace

middle: K

last: Dy

first: Alessandra

middle: C

last: Fontecedro

first: Pascale

last: Tomasini

first: Vamsidhar

last: Velcheti

first: Anthonie

last: van der Wekken

first: Christophe

last: Dooms

first: Luis

last: Rodriguez

first: Giannis

last: Mountzios

first: Adrian

last: Sacher

first: Ernest

last: Nadal

first: Sebastien

last: Couraud

first: Sang-We

last: Kim

first: Kenneth

last: O’Byrne

first: Danilo

last: Rocco

first: Ryo

last: Toyozawa

first: Izabela

last: Chmielewska

first: Colin

last: Lindsay

first: Antreas

last: Hindoyan

first: Lata

last: Mukundan

first: Tomasz

last: Wilmanski

first: Christine

last: Ardito-Abraham

first: Amrita

last: Pati

first: Anita

last: Reddy

first: Bhakti

last: Mehta

first: Martin

last: Schuler


title: Inhibition of de novo fatty acid synthesis in Mycobacterium tuberculosis

city: Ithaca

first: Emma

last: Roszkowski

state: NY

address: 930 Campus Rd

department: Microbiology and Immunology

institute: Cornell University

summary: De novo fatty acid synthesis produces the acyl units needed to generate phospholipids, lipoproteins, enzyme prosthetic factors, polyketides, and mycolic acids in Mycobacterium tuberculosis (Mtb). Here, we identifed sALT629, a novel butoxyphenyl-tetrazole-acetamide compound that inhibits de novo lipid synthesis in Mtb. This compound disrupts the Mtb lipidome and prevents incorporation of metabolic tracers into acyl chains of Mtb lipids. Unexpectedly, we also found that sALT629 treatment significantly depleted triacylglycerol (TAG) pools as a metabolic compensation mechanism when de novo fatty acid synthesis was inhibited. Resistance to sALT629 was mediated by loss of function mutations in HadC, the non-essential hydroxyacyl-ACP-dehydratase subunit involved in the synthesis of long-chain oxygenated mycolic acids. Inactivating HadC rescued sALT629-mediated inhibition by sustaining TAG pools to fulfill Mtb’s biosynthetic demand for acyl chains. Lastly, loss of function HadC resistance mutations resulted in cell wall perturbations that confer fitness defects in vitro and in vivo suggesting that this specific resistance mechanism is unlikely to arise in Mtb in a clinical setting.

overall_design: RNA-seq of WT Mtb treated with different antitubercular compounds (sALT629, INH, and ISO) for 4 hours in standard rich medium.

first: Sarita

last: Charap

last: Montague

first: Paridhi

last: Sukheja

first: Case

last: McNamara

first: Paul

last: Soma

first: M

middle: N

last: Islam

first: Barbara

last: Graham

first: Anna

middle: E

last: Grzegorzewicz

first: Mary

last: Jackson

first: Peter

last: Schultz

first: Anthony

last: Hay

first: David

last: Russell

first: John

last: Belisle

first: Brian

last: VanderVen


title: Heterozygous Kmt2d loss diminishes enhancers to render medulloblastoma cells vulnerable to combinatory inhibition of lysine demethylation and oxidative phosphorylation [RNA-seq]

city: Denver

first: Pluto

last: Bio

state: CO

address: 3575 Ringsby Ct Suite 414

institute: Pluto Bio

summary: The histone methyltransferase KMT2D (alias MLL4) is frequently mutated in medulloblastoma (MB). Heterozygous loss of KMT2D is prevalent in MB. However, the role of heterozygous KMT2D loss remains unknown. Here, we show that heterozygous Kmt2d loss highly promotes Ptch+/–-driven MB genesis in mice. Heterozygous Kmt2d loss upregulated tumor-promoting programs, including oxidative phosphorylation (OXPHOS), in Ptch+/–-driven MB genesis. Heterozygous Kmt2d loss extensively diminished enhancer signals and H3K4me3 signature, including those for transcription-repressive tumor suppressor genes (e.g., Ncor2). NCOR2 repressed the expression of tumor-promoting genes. Combinatory pharmacological inhibition of OXPHOS and the enhancer-decommissioning demethylase LSD1 drastically reduced the tumorigenicity of MB cells bearing heterozygous Kmt2d loss. These findings reveal the mechanistic basis underlying the MB-promoting effect of heterozygous KMT2D loss.

overall_design: To understand the molecular mechanism by which heterozygous Kmt2d loss promotes Ptch+/–-driven MB genesis, we isolated the cerebella from mice and then compared gene expression profiles between Ptch+/– cerebella and NKP (or AKP) cerebella bearing MB using RNA sequencing (RNA-seq).

first: Shilpa

last: Dhar

first: Min

last: Lee


title: ZDHHC5-Mediated BRAF Palmitoylation Drives KRASG12C-Inhibitor Resistance and Sustains Oncogenic MAPK Signalling

first: Li

last: Wang

address: No. 443, Mount Huangshan Road, Shushan District

institute: University of Science and Technology of China

summary: Therapeutic resistance to single-agent targeted therapies (e.g., KRASG12C inhibitors) frequently arises in tumors through adaptive mechanisms such as cellular plasticity and genetic instability. Here, we demonstrated that KRASG12C inhibitors induce BRAF membrane localization, leading to MAPK pathway reactivation in KRASG12C-mutant cancers. The engineered tethering of BRAF to the membrane significantly diminished the antitumour efficacy of the KRASG12C inhibitors. Mechanistically, ZDHHC5-mediated palmitoylation at residues Cys194/195, located within the RAS-binding domain (RBD) of BRAF, governs BRAF membrane recruitment and protein stability. Notably, BRAF palmitoylation sustains oncogenic signalling across diverse cancer types, especially in cholangiocarcinoma, and high ZDHHC5 expression is correlated with aggressive clinical behavior in KRASG12C-mutant and other MAPK-driven malignancies. Depletion of ZDHHC5 or disruption of BRAF palmitoylation at these critical sites suppressed MAPK signalling, restored sensitivity to KRASG12C inhibition, and impaired tumor progression in vitro and in vivo. Our findings identify BRAF palmitoylation as a dual regulator of therapeutic resistance and tumor progression, highlighting ZDHHC5 as a therapeutic target to overcome KRASG12C inhibitor resistance and treat BRAF palmitoylation-dependent cancers.

overall_design: RNA-seg profiling of wildtype RBE cells and their knockdown derivatives (siZDHHC5).

first: Chunxi

last: Li

first: Xiezong

last: Hu

first: Ziqiu

last: Zang

first: Qingsong


title: Newly-diagnosed IDHwt MGMT unmethylated glioblastoma patients treated with standard radiation, nivolumab, and BMS-986205 [bulk RNA-seq]

city: Chicago

first: Derek

last: Wainwright

state: IL

address: 2160 South First Avenue

department: Cancer Biology

institute: Loyola University Chicago Stritch School of Medicine

summary: Improving immunotherapeutic efficacy for patients with glioblastoma (GBM) has been suggested to be limited by a number of factors including indoleamine 2,3 dioxygenease 1 (IDO; IDO1); an enzyme that converts L-tryptophan (Trp) into L-kynurenine (Kyn). Here, we report the results of a first-in-human phase 1 trial for 12 patients with newly-diagnosed IDHwt MGMT unmethylated GBM treated with standard radiation, nivolumab, and BMS-986205 – the latter being a potent IDO1 enzyme inhibitor. The treatment regimen was found to be safe and tolerable when administered at 50mg. Treated patients experienced decreased L-kynurenine levels without changes in L-tryptophan. No other kynurenine-pathway metabolites were altered while on treatment. The median overall survival (OS) was 11.5 months for all patients, with 4 individuals alive at ≥28 months, and 2 patients alive at 5 years post-diagnosis. Analysis of resected tumor at the time of first recurrence revealed intratumoral IDO1 expression to be primarily enriched in myeloid lineage cells. Higher systemic levels of naïve and early effector CD8+ T cells, higher systemic levels of microbial-derived aryl-lactates, lower systemic levels of microbial-derived aryl acetates, higher levels of fecal-derived Massilioclostridium coli, GGB3819-SGB5184, Dysosmobacter welbionis, Phocaeicola plebeius, an age of <65 years old, and patients who underwent subtotal but not gross total tumor resection, were significantly more likely to live past 28 months while on treatment. This study provides a biological rationale for use of RT, PD-1 mAb, and IDO1 enzyme inhibitor treatment in temodar naïve GBM patients who survive well after 2 years while on treatment (ClinicalTrials.gov: NCT04047706).

overall_design: To determine the gene expression regulatory effects of combined therapy evaluated in current clinical trial on peripheral blood leukocytes (PBLs), blood samples were collected from newly diagnoased GBM patients at baseline and different treatment stages during the trial. PBLs were isolated and subject to bulk RNA-Seq analysis.

first: Rimas

middle: V

last: Lucas

first: Lijie

last: Zhai

first: Miri

last: Kim


title: RNA-binding protein Cpeb1 is a marker of healthy adult β cells in mice but is dispensable β cell identity and function

city: Madison

first: Barak

last: Blum

state: Wisconsin

address: 4551 WIMR II, 1111 Highland Ave.

institute: University of Wisconsin-Madison

summary: RNA binding proteins (RBPs) are increasingly being recognized as important regulators of pancreatic β-cells’ identity and function. We identified the poly-A binding RBP, Cpeb1, as a potential new regulator linked to β-cell failure in diabetes based on its enrichment in mature, healthy adult β-cells and its sharp decrease in β-cells in type 1 diabetes (T1D) and type 2 diabetes (T2D). While Cpeb1 is known to regulate an extensive range of biological processes and its involvement in regulating genes involved in insulin signaling and apoptosis in the liver has been reported, Cpeb1 function in β-cells is unknown. Here, we have used two independent genetic models, namely β-cell-specific and whole body Cpeb1 deletions, to assess the role of Cpeb1 in β-cells. We show Cpeb1 function is dispensable for β-cell function and identity. Using bulk RNA sequencing on islets of both models, we also show that Cpeb1 regulates markedly different sets of genes between male and female islets, both at the transcriptional and at the polyadenylation levels.

overall_design: RNA-seq profiling of β cell-specific Cpeb1 knockout primary islets (Cpeb1 βKO: Cpeb1flx/flx; Ins1-Cre) and wildtype control (Cpeb1+/+; Ins1-Cre), and of whole-body knockout of Cpeb1 islets (Cpeb1 KO) and wildtype control.

first: Sutichot

middle: D

last: Nimkulrat

first: Bayley

last: Waters

first: Matthew

middle: R

last: Wagner

first: Maria

last: Mendoza Niemes

first: Cyrus

last: Sethna

first: Hariharan

last: Jayaraaman


title: DNMT3A-dependent DNA methylation shapes the endothelial enhancer landscape

city: Heidelberg

first: Stephanie

last: Gehrs

address: Im Neuenheimer Feld

institute: DKFZ

summary: DNA methylation plays a fundamental role in regulating transcription during development, cell differentiation, and maintenance of cellular identity. However, the functional role of DNA methylation in the regulation of endothelial cell (EC) transcription during state transition, meaning the switch from an angiogenic to a quiescent cell state, has not been determined. Here, we conducted a DNA methylome analysis over a longitudinal postnatal timeline of EC in the murine pulmonary vasculature, revealing two significant observations. First, prominent alterations in DNA methylation patterns occurred during the transition from angiogenic to quiescent EC. Second, once a quiescent state is established, DNA methylation marks remain stable throughout further EC aging. These longitudinal differentially methylated regions correlated with endothelial gene expression and provided evidence for the recruitment of de novo DNA methyltransferase 3a (DNMT3A). Comprehensive loss-of-function studies in mice revealed that the absence of DNMT3A-dependent DNA methylation led to the loss of active enhancers, resulting in mild transcriptional changes, likely due to loss of active enhancer integrity. These results underline the importance of DNA methylation as a key epigenetic mechanism of EC function during state transition. Furthermore, we showed that DNMT3A-dependent DNA methylation appears to be involved in establishing the proper histone landscape required for accurate transcriptome regulation.

overall_design: Sequencing experiments were performed on FACS-sorted lung endothelial cells isolated from 8- and 18-months-old mice.

first: Hellmut

last: Augustin


title: Small Extracellular Vesicles from Radioresistant H3K27M-Pediatric Diffuse Midline Glioma Cells Modulate Tumor Phenotypes and Radiation Response [bulk RNA-seq]

city: Lexington

first: Jessica

middle: S

last: Blackburn

state: Kentucky

address: 741 S. Limestone

institute: University of Kentucky

summary: Pediatric diffuse midline gliomas harboring the Histone 3 lysine 27-to-methionine mutation (H3K27M-pDMG) represent a highly heterogenous group of brain tumors characterized by intrinsic resistance to radiation therapy, the current standard of care. Recent evidence suggests that intratumor small extracellular vesicle (sEV)-mediated signaling plays an oncogenic role among glioma stem cell populations. However, the dynamics and functional roles of H3K27M-pDMG derived sEVs in the context of radiation-induced stress remain unclear. In this study, we characterize sEV uptake dynamics between H3K27M tumor cells, identify potential sEV surface proteins involved in the process, and demonstrate that radioresistant (RR) H3K27M-pDMG-derived sEVs confer radioprotective effects to radiosensitive (RS) H3K27M-pDMG cells at the population level. RR-sEVs induce metabolic and gene expression changes in RS cell populations within the timescale of EV uptake and internalization, leading to improved DNA repair following radiation-induced stress. Furthermore, we identified the proteins, microRNAs (miRNAs), and metabolites present in RR-sEVs, shedding light on the molecular cargo that may be responsible for these effects. Our findings provide insights into the intrinsic radioresistant properties mediated by H3K27M-pDMG-derived sEVs and propose novel targets for disrupting radioresistant intratumoral communication in H3K27M-pDMGs.

overall_design: RNA-seq profiling of 3 bulk cell lines, SF7761, SF8628, and SF7761-Clone#1

first: Viral

last: Oza


title: Glomerular Transcriptome from Experimental Nephrotic Syndrome Model and Treatment with PPARgamma Agonists [ADR]

city: Columbus

first: Amy

last: Hite

state: OH - Ohio

address: 1800 Cannon Drive 250 Lincoln Tower

department: Biomedical Informatics

institute: The Ohio State University

summary: Nephropathy was induced with puromycin amino-nucleoside (PAN) in Wistar rats and treated with daily treatments of Pioglitazone (Pio) and GQ-16. Nephropathy was induced in a separate group of rats with Adriamycin (ADR) in Wistar rats. Total glomerular RNA was isolated, and mRNA libraries were generated and subjected to sequencing using NovaSeq6000 SP. Injury with PAN and ADR resulted in differential expression of genes (DEGs). Many of the PAN-induced DEGs were restored with Pio and GQ16 treatments.

overall_design: 1 group with 4 replicates sequenced over 2 lanes

first: Shipra

last: Agrawal

last: Webb

first: Claire

last: Bryant


title: Single-Cell Profiling of Zebrafish Retinal Ganglion Cells Reveal an Injury Response Mediated by Cell Dedifferentiation and Leukocytes [scRNA-Seq]

city: Austin

first: Anna

last: Battenhouse

state: TX

address: 100 East 24th St., Stop A5000

department: Center for Biomedical Research Support

institute: The University of Texas at Austin

summary: Retinal ganglion cells (RGCs) are the sole projection neurons connecting the retina to the brain and therefore play a critical role in vision. Death of RGCs during glaucoma results in irreversible loss of vision as RGCs do not regenerate after injury in the human eye. There are no FDA approved drugs to prevent RGC death and/or promote RGC survival after injury. There is a critical need to better understand the molecular underpinnings of neuroprotection in vivo that can then be leveraged to develop new therapeutic approaches. Unlike mammals, zebrafish RGCs are resilient to injury and this study characterizes zebrafish retinal ganglion cell injury response to optic nerve transection (ONT) using isl2b:eGFP transgenic fish line, single cell and bulk RNA sequencing and in situ hybridization. We demonstrate that zebrafish RGCs do not show subtype specific resilience to injury but show a distinct temporal injury response which includes an increase in subtype 3, a cell population having progenitor and regenerative identity.

overall_design: Seven single-cell RNA libraries were prepared from FACS-purified retinal ganglion cells (RGC) from pooled tissue from seven sets of adult zebrafish: four libraries from injured tissue after optic nerve transection at 2 timepoints: 1 and 7 days post-injury (dpi), and three libraries from uninjured tissue on the same days.

first: Ashrifa

last: Ali

first: Hannah

last: Schriever

first: Dennis

last: Kostka

first: Taka

last: Kuwajima

first: Kristen

last: Koenig

first: Jeffrey

last: Gross


title: Binding of KAP1 organizes HP1alpha for transcriptional silencing [ChIP-seq]

city: Dallas

first: Laura

last: Banaszynski

address: 5323 Harry Hines Blvd

department: Green Center for Reproductive Biology Sciences

institute: UT Southwestern Medical Center

summary: Constitutive heterochromatin is enriched in repetitive elements, including endogenous retroviral element (ERV) sequences that must be repressed to sustain normal cell developmental programs and prevent chromosomal instability. ERVs are silenced through trimethylation of lysine 9 on histone H3 (H3K9me3) by ESET (also known as SETDB1, SET domain bifurcated 1, or KMT1E) and a co-repressor complex containing KAP1 (KRAB-associated protein 1, also known as tripartite motif-containing protein 28, Trim28) in mouse embryonic stem cells. H3K9me3 then serves as a scaffold for the recruitment of proteins that maintain ERVs in a transcriptionally silent state, including the HP1 proteins that themselves interact with the co-repressor KAP1. In this study, we provide structural insights into the KAP1-HP1 interaction. Further, we demonstrate that this interaction plays a role in maintaining inaccessible chromatin at specific ERV elements in embryonic stem cells (ESCs).

overall_design: ChIP-seq analysis in mouse embryonic stem cell lines. WT mESCs were used for H3K9ac, H3K27ac, and H3K27me3 ChIP-seq

first: Ryan

last: O'Hara

middle: A


title: Small Extracellular Vesicles from Radioresistant H3K27M-Pediatric Diffuse Midline Glioma Cells Modulate Tumor Phenotypes and Radiation Response [smRNA-Seq]

overall_design: sEVs were isolated from 3 cells lines, SF7761, SF8628, and SF7761-Clone#1 using differential ultracentrifugation followed by 100kDa ultrafiltration. Small RNA was extracted from each sEV preparation and sequenced.


title: Unraveling the cohesin-chromatin interface: identifying protein interactions that modulate chromosome structure and function [ChIP-Seq]

first: Jill

last: Dowen

overall_design: ChIP-seq was performed in wildtype mESCs with five replicates for RAD21 and CTCF. ChIP-seq was performed in mESCs treated with BRG1 targeting drugs (ACBI1 PROTAC, PFI-3 bromodomain inhibitor, or BRM014 ATPase inhibitor) or DMSO as a control in duplicate for RAD21.

middle: M

first: Natalie

last: Rittenhouse

first: Riya

last: Gohil

first: June

last: Arricastres


title: Small Extracellular Vesicles from Radioresistant H3K27M-Pediatric Diffuse Midline Glioma Cells Modulate Tumor Phenotypes and Radiation Response [EVtreat_RNA-Seq]

first: Jessica

last: Blackburn

overall_design: RNA-seq of SF7761 cells treated with 1) Control (RR-sEV 100 kDa flow through solution), 2) SF8628-sEV, or 3) SF7761-Clone #1-sEV for 18 hours

first: Viral

last: Oza


title: Newly-diagnosed IDHwt MGMT unmethylated glioblastoma patients treated with standard radiation, nivolumab, and BMS-986205 [scRNA-seq]

first: Derek

last: Wainwright

overall_design: Tumor tissue sample and peripheral blood leukocytes were collected from the patient who developed recurrent GBM during the clinical trial. Single cells wereprepared from the tumor tissue sample. CD45 positive immune cells were further isolated from the tumor single cell suspension and PBLs, respectively.

first: Rimas

last: Lucas

first: Lijie

last: Zhai

first: Brandyn

last: Castro


title: Vostok (CG11504):  A New Looping Factor for the Organization of the Regulatory Genome in the Drosophila Brain

city: Princeton

first: Michael

last: Levine

state: New Jersey

address: Icahn lab, Princeton University

institute: Princeton University

summary: The Drosophila regulatory genome is organized in a hierarchical series of topological associating domains (TADs) and intra-TAD regulatory loops.  High-resolution Micro-C maps identified ~645 such loops in the larval brain of Drosophila, spanning distances of 25 kb to 250 kb.  Many of these loops are associated with genes encoding neural adhesion proteins implicated in the formation of specific synapses, including Dprs, Dips, Sides and Beats.  They are formed by interactions of pairs of tethering elements that contain simple repeated sequence motifs, such as GAGAG.  Approximately 10% (64/645) of the loops are lost or diminished in larval brains obtained from homozygous mutants lacking the GAF (GAGA-associated factor) POZ oligomerization domain.  We also present evidence for a second looping factor, the MADF-containing Vostok protein, which recognizes a GCAACA motif that is over-represented in brain tethering elements.  There is a loss of 47 of the loops (7%) in larval brains obtained from Vostok mutants. These losses are associated with diminished expression of associated genes, suggesting impaired enhancer-promoter interactions.  Only 9 loops are disrupted in both Vostok and GAF mutants, raising the possibility of a combinatorial code for tether-tether interactions.  Support for this possibility stems from the observation that two previously identified meta-loops spanning 6 Mb rely on both GAF and Vostok. We discuss the prospects of using different combinations of looping factors to produce unlimited 3D associations of genetic loci in animal genomes.

overall_design: Micro-C and bulk RNA-seq on Vostok mutant to examine the gene function on chromatin organization and transcription

first: Jie

last: Hu

first: Xiao

last: Li

first: Lomaev

last: Dmitry

first: Nadezhda E.

last: Vorobyeva

first: Maksim

last: Erokhin

first: Darya

last: Chetverina


title: Mucosal effects of tenofovir 1% gel wane over longer-term use but retain pro-proliferative and type I/III interferon pathway signatures [MTN014_Vagina]

city: Seattle

first: Sean

last: Hughes

state: WA

address: 850 Republican St

institute: University of Washington

summary: The nucleotide reverse transcriptase inhibitor (NRTI) tenofovir has been extensively tested as a topical preventative against vaginal and rectal HIV transmission. We sought to determine how use of this product affects gene expression. We used samples from MTN-014, a study of vaginal and rectal gel application. We obtained vaginal biopsies before treatment initiation and after two weeks of daily use of tenofovir 1% gel applied rectally or vaginally. We isolated RNA from vaginal biopsies preserved with RNAlater. Gene expression was measured from all three samples (three time points) from each participant.

overall_design: Gene expression was measured by Illumina HumanHT-12 v4 Expression BeadChips. Samples were paired with samples taken at baseline (pre-treatment) and after two weeks of daily gel use. Vaginal biopsies were preserved with RNAlater at -80 degrees C. Samples were not replicated on the arrays. During quality control assessment, two pairs of samples were determined by gene expression profiles to have been switched. In both cases, the pairs were physically adjacent during sample processing and the sample labeled “rectum” had gene expression consistent with vagina and vice versa. The two pairs are B11 (GSM8520898)/B12 (GSM8520862) and D10 (GSM8520864)/D11 (GSM8520894). The labeling has been corrected here so that the samples match their gene expression profiles.

first: Florian

last: Hladik

first: Claire

last: Levy


title: Mucosal effects of tenofovir 1% gel wane over longer-term use but retain pro-proliferative and type I/III interferon pathway signatures [MTN014_15cmRectum]

summary: The nucleotide reverse transcriptase inhibitor (NRTI) tenofovir has been extensively tested as a topical preventative against vaginal and rectal HIV transmission. We sought to determine how use of this product affects gene expression. We used samples from MTN-014, a study of vaginal and rectal gel application. We obtained rectal biopsies before treatment initiation and after two weeks of daily use of tenofovir 1% gel applied rectally or vaginally. We isolated RNA from rectal biopsies preserved with RNAlater. Gene expression was measured from all three samples (three time points) from each participant.

overall_design: Gene expression was measured by Illumina HumanHT-12 v4 Expression BeadChips. Samples were paired with samples taken at baseline (pre-treatment) and after two weeks of daily gel use. Rectal and vaginal biopsies were preserved with RNAlater at -80 degrees C. Samples were not replicated on the arrays. During quality control assessment, two pairs of samples were determined by gene expression profiles to have been switched. In both cases, the pairs were physically adjacent during sample processing and the sample labeled “rectum” had gene expression consistent with vagina and vice versa. The two pairs are B11 (GSM8520898)/B12 (GSM8520862) and D10 (GSM8520864)/D11 (GSM8520894). The labeling has been corrected here so that the samples match their gene expression profiles.


title: Exploring the binding sites of RBM25 by RIP-seq in the inner ear organoids.

city: Shanghai

first: Mingyu

last: Xia

state: Shanghai

address: No. 83, Fenyang Road, Xuhui District

department: ENT Institute and Otorhinolaryngology Department of the Affiliated Eye and ENT Hospital, Sta

institute: Fudan University

summary: Purpose:  The goals of this study are to ecavate the binding sites of RNA-binding protein RBM25 during inner ear aging. Using the inn er organoids as model, RBM25 incubate with RNA from organois.Then transcriptome profiling (RNA-seq) was performed to analyze the binding genes and sites.

overall_design: Methods: Two replicates of each group from cultured organois were havested, named control1, control2, RBM25 KO1, and RBM25 KO2. RNA were extracted and co-immunoprecipitation (CO-IP) with IIgG and RBM25 antibody, and then  sequenced by RNAseq.

first: MIngyu

first: Yunjie

first: Jiaoyao

last: Ma