title: Impact of lepidopteran oral secretions on the transcriptome of Arabidopsis thaliana

city: Lausanne

first: Philippe

last: Reymond

address: Biophore building

department: Department of Plant Molecular Biology

institute: University of Lausanne

summary: Plants respond to attack by chewing insects through the recognition of herbivore-associated molecular patterns (HAMPs) that are present in oral secretions (OS) and released at the wound site, leading to appropriate deployment of plant immune responses. Because insect feeding is accompanied by severe wounding of the leaf tissue, the specific contribution of HAMPs to defense is not well characterized. In addition, OS contain effectors that interfere with activation of defenses, including the suppression of wound-induced genes. Here, we analyze the transcriptome of Arabidopsis thaliana leaves in response to wounding and application of OS from Spodoptera littoralis or Pieris brassicae. We report that OS amplify wound-induced responses and specifically promote the activation of hormonal pathways, as well as pathogen- and cell wall-related responses. Furthermore, application of OS on wound sites extensively suppresses the expression of genes involved in the regulation and biosynthesis of aliphatic glucosinolates. Also, OS suppress the expression of genes involved in wound-healing processes and callus formation, including ERF114, DOFs and CYCD3s, in addition to genes encoding cell-wall modifying enzymes, whose activation completes wound sealing. Altogether these results highlight the contribution of OS components to defense and unveil the potential role of conserved OS-derived effector(s) in inhibiting the production of defense compounds and interfering with wound healing processes.

overall_design: Three leaves of each 5-week-old Arabidopsis thaliana plants, except for the unwounded controls, were wounded by piercing four holes of 1 mm each, avoiding the midvein. Two μl of either H2O, Pieris brassicae oral secretions (OS) or Spodoptera littoralis OS were applied to each hole. Samples were collected either 3h after wounding or 24h after wounding. Unwounded controls were collected 3h after start of the treatments. Leaf discs of 1 cm diameter around the wound site were collected, frozen in liquid nitrogen and stored at -80°C.  RNA was then extracted for RNAseq analyses. Three to four our independent biological replicates were carried out using the same procedure.

first: Angel

last: Fernandez Martin


title: RNF126 Promotes Endoplasmic Reticulum Stress in Fetal Growth Restriction via Ubiquitination-Mediated Degradation of the MYH9/MYH10 Complex

status: Public on Jun 20 2025

city: Guangzhou

first: Jing

last: Li

state: Guangdong

address: Jingxi Street

department: Department of Obstetrics and Gynecology

country: China

institute: Southern Medical University Nanfang Hospital

type: Expression profiling by high throughput sequencing

summary: Fetal growth restriction (FGR) stands as a prominent cause of neonatal morbidity and mortality, yet its underlying mechanisms remain elusive. Through a multi-omics analysis of the human placentas, including quantitative proteomics and ubiquitination-modified proteomics, our team find that the E3 ligase Ring finger protein 126 (RNF126) might be a potentially pivotal protein in the development of FGR. Here, we have discovered that RNF126 can induce endoplasmic reticulum stress (ERS) in placental trophoblasts through RNA sequencing, leading to an increase in apoptosis rates. Subsequent studies have confirmed that RNF126 promotes the degradation of the MYH9/MYH10 complex via the ubiquitin-proteasome pathway, thereby contributing to ERS and inducing trophoblast dysfunction. Meanwhile, Our RNF126 placenta-specific knockout mouse model (cKO) validates these findings in vivo. These events significantly contribute to the occurrence and progression of FGR. This study provides new insights and highlights the promising potential of RNF126 as a therapeutic target for FGR treatment.

overall_design: We conducted RNA-seq on BeWo cells that were stably overexpressed with empty vector (OE-NC) or RNF126 (OE-RNF126) using lentiviruses. n = 3 biologically independent experiments.

first: Lilin

last: Lu

first: Xiaomei

last: Ye

first: Jiawen

last: Lan

first: Shuxiu

last: Xu

first: Manyu

last: Cheng

first: Chenlin

last: Lv

first: Jun

last: Zhou


title: LINE-1 transposable elements regulate the exit of human pluripotency and early brain development [long-read RNA and DNA sequencing]

city: Lund

first: Johan

last: Jakobsson

address: Sölvegatan 17

department: Wallenberg Neuroscience Center

country: Sweden

institute: Lund University

summary: The mechanisms underlying primate-specific genetic programs during early human development remain poorly understood. Long interspersed nuclear element 1 (L1) is the most abundant transposable element in the human genome and represents a vast source of divergent genetic information in hominoid genomes, yet its contribution to human development is largely unknown.  Using multiomics profiling, we show here that thousands of hominoid-specific L1 loci are expressed in human induced pluripotent stem cells and cerebral organoids. The transcription of unique L1 elements correlates with the absence of DNA methylation and the presence of an active epigenetic state. CRISPRi silencing of L1s revealed the presence of nearly a hundred co-opted L1-derived chimeric transcripts, and silencing of these transcripts results in altered transcription of many genes involved in neural differentiation, leading to a reduction in cerebral organoid size, implicating L1s in hominoid-specific developmental processes. In conclusion, our results show that L1-derived transcripts provide a layer of primate- and human-specific transcriptome complexity that contributes to early human developmental processes.

overall_design: In this study we characterized the expression profile of evolutionary young (L1HS-L1PA4), full-length L1s in hiPSCs and unguided cerebral organoids (STEMCELL cerebral organoids diff kit). We combined bulkRNA-seq, CUT&RUN, and long-read RNA and DNA sequencing to trace the promoter activity of L1s in hiPSCs (n= 3 technical replicates for bulkRNA-seq; n= 1 technical replicate for H3K4me3 and H3K9me3 CUT&RUN and long-read sequencing) and cerebral organoids (n=3 technical replicate, 3-4 organoids per replicate for bulkRNAseq; n=3 replicate, 4-5 organoids per replicate for snRNAseq; (n= 1 replicate, 5 organoids per replicate). We also performed L1 CRISPRi (via lentiviral transduction) in hiPSCs and investigated the L1 expression profile and the downstream phenotypic effects with the aforementioned technologies. Control cell line was established through lentiviral transduction using a non-targeting (LacZ) gRNA. We also differentiated these cell lines into unguided cerebral organoids and investigated the phenotype.

first: Raquel

last: Garza

first: Anita

last: Adami

first: Patricia

last: Gerdes

first: Pia

middle: A

last: Johansson

first: Fereshteh

last: Dorazehi

first: Symela

last: Koutounidou

first: Laura

last: Castilla-Vallmanya

first: Diahann

last: Atacho

first: Yogita

last: Sharma

first: Jenny

middle: G

first: Oliver

last: Tam

first: Molly

last: Gale-Hammell

first: Christopher

middle: H

last: Douse


title: LINE-1 transposable elements regulate the exit of human pluripotency and early brain development [bulkRNA-seq]


title: LINE-1 transposable elements regulate the exit of human pluripotency and early brain development [CUT&Run]

type: Genome binding/occupancy profiling by high throughput sequencing


title: LINE-1 transposable elements regulate the exit of human pluripotency and early brain development [snRNA-seq]

first: Garza

last: Raquel

first: Adami

last: Anita

first: Gerdes

last: Patricia

first: Johansson

last: Pia

first: Dorazehi

last: Fereshteh

first: Koutounidou

last: Symela

first: Castilla-Vallmanya

last: Laura

first: Atacho

last: Diahann

first: Sharma

last: Yogita

last: Jenny

first: Tam

last: Oliver

first: Gale-Hammell

last: Molly

first: Douse

last: Christopher

first: Jakobsson

last: Johan


title: Prenatal stress alters mouse offspring dorsal striatal development and placental function in sex-specific ways

city: Iowa City

first: Benjamin

last: Hing

state: IA

address: 51 Newton Road, BSB 6-509

country: USA

institute: University of Iowa

summary: Prenatal stress is a risk factor for neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD). However, how early stress modification of brain development contributes to this pathophysiology is poorly understood. Ventral forebrain regions such as dorsal striatum are of particular interest: dorsal striatum modulates movement and cognition, is altered in NDDs, and has a primarily GABAergic population. Here, we examine effects of prenatal stress on adult movement, cognition, and dorsal striatum neurobiology in mice using striatal-dependent behavioral assays, immunohistochemistry, embryonic ventral forebrain transcriptomics, and placental transcriptomics. We found prenatal stress affected adult procedural, habit, and reversal learning in sex-specific ways. Stress also increased adult dorsal striatal GABAergic neurons – an effect largely driven by males. We sought to examine the developmental origins of these adult brain changes. We found similar sex-specific dorsal striatal cellular changes in earlier points of development. The dorsal striatum primordium--embryonic ventral forebrain—showed that prenatal stress increased DNA replication and cell cycle pathways in male but not female transcriptomics and cellular biology. Unique signatures may have arisen from male-female placental differences. Stress-induced placental transcriptomics showed upregulated morphogenesis pathways in males while females downregulated morphogenic, hormonal, and cellular response pathways. Our findings suggest that prenatal stress could affect placenta function and also alter the GABAergic population of dorsal striatum differentially between the sexes.

overall_design: RNA-Seq of E13 placenta

first: Sara V.

last: Maurer

first: Benjamin W.Q.

first: Stephanie

last: Lussier

first: Sreya

last: Radhakrishna

first: Jada L.B.

last: Davis

first: Parker W.

last: Abbott

first: Jacob J.

last: Michaelson

first: Hanna E.

last: Stevens


title: Granzyme K+ CD8 T cells slow tauopathy progression by targeting microglia a

city: Bethesda

first: Kory

middle: R

last: Johnson

state: MD

address: 10/3B01, 9000 Rockville Pike

department: DIR IT & Bioinformatics

institute: NINDS/NIH

summary: Neurodegenerative diseases trigger innate and adaptive immune responses that can either slow or accelerate disease progression. How immune cells contribute to such divergent disease outcomes is not entirely clear. Here, we sought to define beneficial immune pressure that emerged during development of tauopathies in mice and humans. Using mice that express mutant human tau in neurons, we observed that microglia slowed tauopathy development by controlling the spread of tau throughout the CNS and into the blood. However, over time microglia converted into distressed antigen presenting cells, acquired neuronal transcripts, and were targeted by resident CD8+ T cells. We detected clonally expanded CD8+ T cells in the CNS and draining lymph nodes of tauopathy mice that expressed granzyme K, but not traditional effector molecules (e.g., IFN, TNF, granzymes a/b/c), which was deposited onto the microglia they targeted. In fact, engagement of microglia by granzyme K expressing CD8+ T cells was a signature of tauopathy development in mice as well as humans with tau rich brain lesions linked to age, Alzheimer’s disease, or chronic traumatic encephalopathy. Deletion of CD8+ T cells in mice promoted the appearance of distressed microglia containing neuronal transcripts, markedly enhanced tau spread, and accelerated neurological decline. These data highlight a beneficial immune reaction involving microglia and granzyme K expressing CD8+ T cells that can slow tauopathy progression. Enhancement of this coordinated response offers the potential to improve outcomes in tauopathy patients.

overall_design: 4 scRNA-Seq samples representing CD8 or CD4 T cells flow cytometrically sorted from the spinal cords and mediastinal lymph nodes of six homozygous P301S homozygous mice at 28-30 weeks

first: Hannah

middle: D

last: Mason

first: Yvonne

middle: L

last: Latour

first: Christopher

middle: T

last: Boughter

first: Dragan

last: Maric

first: Cayce

middle: E

last: Dorrier

first: Vivian

last: Guedes

first: Chen

last: Lai

first: Patrick

middle: C

last: Duncker

first: Alexis

middle: M

first: Monica

last: Manglani

first: Jessica

last: Gill

first: Daniel

middle: P

last: Perl

first: Martin

last: Meier-Schellersheim

first: Dorian

middle: B

last: McGavern


title: Transcriptome profiling of developing testes in the horse [Small RNA-seq]

city: Madrid

first: Alfonso

last: Gutiérrez-Adán

address: Av. Puerta de Hierro 28

department: Animal Reproduction

country: Spain

institute: INIA

type: Non-coding RNA profiling by high throughput sequencing

summary: The mammalian testis is a highly heterogeneous tissue with a vast array of functional and regulatory RNA molecules that participate in the timely control of the spermatogenesis. This process remains largely unexplored in stallions. We utilized transcriptomic analysis to explore gene expression across various stages of testicular development in horses, from infancy to adulthood, including sperm. The analysis aimed to explore the regulatory networks involving messenger RNAs (mRNAs), long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs). High-throughout RNA sequencing revealed dynamic changes in gene expression. The study identified key genes complex interactions between mRNAs, lncRNAs, circRNAs and miRNAs, and biological pathways associated with each developmental stage that drive the spermatogenesis in stallions and provide new insights into the regulatory mechanisms of horse testis spermatogenesis. This could aid in the improvement of the reproductive health and fertility management in horses.

overall_design: RNA-seq from 5 stages of the spermatogenesis

first: Paula

last: Navarrete-López

first: Cristina

last: García-Merino

first: Eva

last: Pericuesta


title: Combined Flt3L and CD40 agonism restores dendritic cell driven T cell immunity in mouse models and patients with pancreatic cancer [human]

city: St. Louis

first: David

last: DeNardo

state: Missouri

address: 425 S Euclid Ave

institute: Washington University

summary: T cell directed immunotherapies have largely failed to demonstrate clinical efficacy in patients with pancreatic ductal adenocarcinoma (PDAC). This broad resistance may result from poor tumor antigenicity and an immunosuppressive tumor microenvironment (TME). We hypothesize that tumor immunity in pancreatic cancer patients is further limited by systemic and tumor-intrinsic suppression of conventional dendritic cells (cDC). Here, we find that low tissue expression of Flt3L may in part underly cDC deficits in PDAC tissues. We show in both autochthonous murine models and samples from a clinical trial, that treatment with systemic Flt3L and CD40 agonists can restore cDC number and function in the PDAC TME. Alone, CD40 agonism failed to fully engage cDC activity; yet when combined with Flt3L, the dual therapy triggered a cDC driven type-I immune response characterized by CD8+ T cell infiltration, interleukin-12 production, and a reciprocal interferon (IFN) response. In mice, type-1 cDCs (cDC1) were directly responsible for the influx of CD8+ T cells, which in-turn supported cDC1 survival via IFN-γ, resulting in a synergistic feed-forward loop. Lastly, while we find that combination Flt3L and CD40 agonism improve tumor immunity, they also increase the number and effector phenotype of FOXP3+ regulatory T cells (Tregs) in a process dependent on type-2 cDCs. Tregs were found to limit therapeutic efficacy by inhibiting mature cDC subsets, and concurrent Treg depletion led to improved tumor control. These data support the continued investigation of combined Flt3L and CD40. agonism, which represent a promising strategy to engage anti-tumor immunity in advanced human malignancies.

overall_design: Consenting patients diagnosed with resectable PDAC at Washington University and Siteman Cancer Center underwent neoadjuvant treatment with CDX-1140 (anti-CD40 IgGs) +/- CDX-301 (Flt3L). Both drugs were provided by Celldex Therapeutics. Patients received either an i.v. injection of CDX1140 (1.5mg/kg) 7-12 days prior to surgery, or 5-subcutaneous doses of CDX-301 (75 mcg/kg/day) followed by CDX1140 on day 8 +/- 1 day, with surgery 7-12 days thereafter.

first: Graham

last: Hogg


title: Transcriptomes of UFMylation gene knockdown in mouse embryonic fibroblast cell (MEF) treated with hypoxia for 24 hours [mouse]

city: Dongguan

first: Zhou

last: Junzhi

address: Xincheng Road 1#, Songshan Lake

institute: Guangdong Medicine University

summary: To investagate the gene expression profiling of dysUFMylation in MEF under hypoxia, we constructed Ufl1  konckouted-MEF using CRISPR-Cas9 and couducted RNA-seq. mRNAs were isolated and purified using RNeasy Plus Mini Kit (Qiagen). Samples were prepared from three biological replicates.

overall_design: Total RNA transcriptomes of Ufl1-KO MEF cells  were profiled by RNA-seq.

first: JUNZHI

last: ZHOU


title: Transcriptomes of UFMylation gene knockdown in human breast cancer cell treated with hypoxia for 6 hours [human]

summary: To investagate the gene expression profiling of dysUFMylation in breast cancer under hypoxia, we constructed UFL1  konckouted-MDA-MB-231 using CRISPR-Cas9 and couducted RNA-seq. mRNAs were isolated and purified using RNeasy Plus Mini Kit (Qiagen). Samples were prepared from three biological replicates.

overall_design: Total RNA transcriptomes of UFL1 or UFM1 KO MDA-MB-231 cells  were profiled by RNA-seq.


title: Granzyme K+ CD8 T cells slow tauopathy progression by targeting microglia c

first: Kory

last: Johnson

overall_design: 9 bulk RNA-Seq samples representing total RNA isolated from the spinal cords of three different mouse genotypes (WT, P301S heterozygous, and P301S homyzgous).

first: Hannah

last: Mason

first: Yvonne

last: Latour

first: Christopher

last: Boughter

first: Dragan

last: Maric

first: Cayce

last: Dorrier

first: Vivian


title: RNA transcripts regulate G-quadruplex landscapes through G-loop formation

city: Utrecht

first: Jeroen

last: van den Berg

state: Utrecht

address: Uppsalalaan 8

country: Netherlands

institute: Hubrecht Institute

summary: G-quadruplexes (G4s) are epigenetic DNA structures that regulate transcription but also threaten genome stability when dysregulated. It remains unknown how G4 dynamics is organized in a cell-specific manner. Here, we report that RNA transcripts govern G4 landscapes through homology-directed invasion opposite the G4 strand, forming ‘G-loops’. G-loops are disassembled via DHX36-FANCJ-mediated G4 unwinding and subsequent nucleolytic incision by XPF-ERCC1, leading to hybrid strand renewal through DNA synthesis. G-loop disassembly requires stochiometric invading RNAs, by contrast, excess of which stabilizes G-loops against disassembly. Defects in G-loop disassembly accumulate G-loops predominantly in gene regulatory regions, leading to transcriptional dysregulation, replication stress, and DNA damage throughout the cell cycle. These findings establish nuclear RNAs as pivotal G-loop regulators, linking the transcriptome to gene regulation and genome maintenance.

overall_design: Wild-type, DHX36KO, FANCJKO or DHX36/FANCJKO were subjected to scEdU-seq as previously described by van den Berg 2024


title: m6A-modified RNAs in human amniotic epithelial stem cells derived-insulin-producing cells: Wild type vs. overexpressed METTL3 plasmid transfected

city: Nanchang

first: yunfei

last: Luo

address: No. 1 Min De Road

institute: nanchang university

type:
Non-coding RNA profiling by array
Expression profiling by array

summary:
m6A-modified RNAs expression profiles of human amniotic epithelial stem cells differentiation into insulin-producing cells and comparing Wild type with overexpressed METTL3 plasmid transfected.
Goal was to determine the effects of METTL3 transfection on mature insulin-producing cells gene expression.

overall_design: Two-condition experiment, WT vs. OE cells. We assessed the expression profiles of  m6A-modified RNAs by microarray

first: Yunfei

first: Jianping

last: Liu


title: Next Generation Sequencing Facilitates Quantitative Analysis of WT and Glut10ko CD8+ T cells lymphoma

city: Beijing

first: Ying

address: Tiantan street, Tiantan Xili 2rd

department: Institute of Medicinal Biotechnology

institute: Chinese Academy of Medical Sciences

summary: Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to analysis the differiational genes and pathways in  WT and Glut10 ko CD8+ T lymphoma cells  by using NGS-derived lymphoma transcriptome profiling (RNA-seq).

overall_design: WT and Glut10ko CD8+ T cells' mRNA profiles were generated by deep sequencing, in triplicate, using Illumina NovaSeq 6000.

first: Ke

last: Li

first: Feng

last: Wang


title: Molecular signatures and spatial distribution of disease-associated cellular populations in early-onset Alzheimer's disease mouse brain

city: Hangzhou

first: Tianhao

state: Zhejiang

address: Yuhangtang Road, 866

institute: Zhejiang University

summary: Alzheimer's disease (AD) is a multifaceted neurodegenerative disorder. Grasping the pathological transformations in early-phase AD is important. Integrating single-cell and spatial transcriptomics with the pathophysiology of AD from the same origin permits to delineate molecular characteristics and spatial arrangement of cellular populations without individual differences, however, such experimental designs have been ignored in current studies. Here, we use a single-source experimental framework to create a multimodal dataset of disease-susceptible region in early-onset Alzheimer's Disease (EOAD) mouse. Predicated on amyloid-beta (Aβ) immunopathology, a profile of disease-associated alterations is discerned. Mature myelinating oligodendrocytes within fiber tracts exhibit compromised fatty acid synthesis and energy-related processes. Region-specific glutamatergic neurons demonstrate impaired synaptic formation, coupled with transcriptomic modifications that encompass energy homeostasis, lipid metabolism and cellular adhesion. Disease-associated astrocytes, aggregating around Aβ deposits, exhibit neuron-related changes in oxidative phosphorylation (OxPhos) and metal ion responses. This investigation serves as a resource for exploring disease signature across multimodal, which provides a basis for finding the progression mechanisms of AD.

overall_design: The experimental design consists of three phases: mouse preparation, tissue processing and molecular detection. The mice are divided into two groups: the wild-type (WT) group (C57bl/6, n= 12, 6 months) and the 5×FAD group (5×FAD, n= 12, 6 months). All mice are euthanized and their brains are isolated for further analysis. A subset of WT group (n=3) and 5×FAD group (n=3) is selected and dissected into two hemispheres. Single-nucleus RNA sequencing (snRNA-seq) is performed on the right hemisphere. Owing to the well-known involvement of the hippocampus in AD, one left hemisphere from each group is chosen for coronal sectioning around the hippocampus. Three slices are obtained from each group, representing the large (L), middle (M) and small (S) regions of the hippocampus. These slices effectively capture changes in the anterior, middle and posterior areas of disease-prone region. Subsequently, the sections are subjected to immunofluorescence staining and spatial transcriptomics sequencing.

first: Menglei

first: Kaiyu

last: Jin

first: Jie

last: Liao

first: Penghui

last: Yang

first: Yao

last: Shen

first: Xiaoyan

last: Lu

first: Zhiyong

last: Zhao

first: Dan

last: Wu

first: Xiaohui

last: Fan


title: Transcriptome profiling of developing testes in the horse [RNA-seq]

first: Alfonso

last: Gutiérrez-Adán

overall_design: Total RNA-seq from 5 stages of the spermatogenesis (adult)

first: Paula

last: Navarrete-López

first: Cristina

last: García-Merino

first: Eva

last: Pericuesta


title: Neuronal differentiation requires BRAT1 complex to remove REST from chromatin

city: Miami

first: Ramin

last: Shiekhattar

state: Florida

address: 1501 NW 10th Avenue

department: Department of Human Genetics

institute: University of Miami - Sylvester Comprehensive Cancer Center

summary: Repressor element-1 silencing transcription factor (REST) is required for the formation of mature neurons. REST dysregulation underlies a key mechanism of neurodegeneration associated with neurological disorders. However, the mechanisms leading to alterations of REST-mediated silencing of key neurogenesis genes are not known. Here, we show that BRCA1 Associated ATM Activator 1 (BRAT1), a gene linked to neurodegenerative diseases, is required for the activation of REST-responsive genes during neuronal differentiation. We find that INTS11 and INTS9 subunits of Integrator complex interact with BRAT1 as a distinct trimeric complex to activate critical neuronal genes during differentiation. BRAT1 depletion results in persistence of REST residence on critical neuronal genes disrupting the differentiation of NT2 cells into astrocytes and neuronal cells. We identified BRAT1 and INTS11 co-occupying the promoter region of these genes and pinpoint a role for BRAT1 in recruiting INTS11 to their promoters. Disease-causing mutations in BRAT1 diminish its association with INTS11/INTS9, linking the manifestation of disease phenotypes with a defect in transcriptional activation of key neuronal genes by BRAT1/INTS11/INTS9 complex. Finally, loss of Brat1 in mouse embryonic stem cells leads to a defect in neuronal differentiation assay. Importantly, while reconstitution with wild-type BRAT1 restores neuronal differentiation, the addition of a BRAT1 mutant is unable to associate with INTS11/INTS9 and fails to rescue the neuronal phenotype. Taken together, our study highlights the importance of BRAT1 association with INTS11 and INTS9 in the development of the nervous system.

overall_design: Total RNA-seq of NT2 cells depleted for BRAT1 using shRNA in duplicates (day 0 and day 28 post-differentiation with ATRA treatment).

first: Sadat

last: Dokaneheifard

first: Helena

last: Gomes Dos Santos

first: Monica

last: Valencia

first: Harikumar

last: Arigela


title: Terminal nucleotidyl transferases govern secondary siRNA production at distinct steps in plants [RACE]

city: København N

first: Peter

last: Brodersen

address: Ole Maaløes Vej 5

country: Denmark

institute: University of Copenhagen

summary: In this study, we aim at understanding the contributions from TUTases, HESO1 and URT1, in miRNA-targeted secondary siRNA production in Arabidopsis thaliana. We have produced 3'RACEseq libraries from various T-DNA insertation single mutants and one double mutant, and compared their capability of uridylating AFB2 and MYB33 5'cleavage fragments. We also compared their uridylyl transfer activity of the AFB3 3' end extremity. Here, we have sequenced biological replicates from Col-0 WT, urt1-1, heso1-4, urt1-1/heso1-4 (set1 and set3) and biological replicates from Col-0 WT, urt1-1, mir393b and rrp4 (set2).

overall_design: 3'RACE sequencing data from mutant lines (urt1-1, heso1-4, urt1-1/heso1-4, rrp4-2, mir393b) and wild type. All lines are ecotype Col-0. The number of biological replicates for each genotype varies from 2-6. The raw fastq files  are submitted here as well as txt files of the end extremities from each transcript included in the manuscript. The tissue that has been sequenced is inflorescences.

first: Maria

last: Vigh

first: Axel

last: Thieffry

first: Laura

last: Arribas-Hernández


title: Epigenetic reprogramming of the mesenchymal state by SUV39H1/H2

city: Boston

first: Gracia

middle: M.

last: Bonilla

state: MA

address: 185 Cambridge St

department: Molecular Biology

institute: Massachusetts General Hospital

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

overall_design: Refer to individual Series


title: Epigenetic reprogramming of the mesenchymal state by SUV39H1/H2 [ChIP-Seq]

summary: Emergence of chemotherapy resistance is a major clinical challenge resulting in large number of deaths yearly. One mechanism involves epigenetic reprogramming through which cancer cells acquire mesenchymal (M) properties akin to cancer stem cells. How cells epigenetically establish resistance to chemotherapy is largely unknown. Here, we show that the two human lysine 9 histone H3 (H3K9) methyltransferase proteins (SUV39H1 and SUV39H2) play a central role in maintaining mesenchymal, chemotherapy resistant state in several cancer models. More importantly, a transient inhibition of these enzymes results in an epigenetic change, triggering a mesenchymal-to-epithelial transition and sensitizing these cells to chemotherapy. These data expand the functional repertoire of SUV39H family of proteins in eukaryotes and expose new therapeutic targets for neutralizing chemotherapy resistance in cancers.

overall_design: H3K9me3 ChIP-seq of HMLE and HMLE-TWIST1 cells  treated DMSO or 80nM chaetocin for two days, after which the cells were washed and incubated in chaetocin-free media for an additional two days (n=3). Also, H3K9me3 ChIP-seq of HMLE and HMLE-TWIST1 cells in which SUV39H1/H2 were knocked down using DsiRNAs for two after which the cells were incubated for an additional two days (n=3). Next generation high throughput sequencing libraries were then generated.

first: Junichi

last: Hanai

first: Noriko

last: Ide

first: Alex

middle: O

last: Gulka

first: Jingyu

last: Zhang

first: Ruslan

last: Sadreyev

first: Toshi

last: Shioda

first: Mo

last: Motamedi


title: RNA-Seq reveals the role of miR-199a-3p in regulating inflammation of bovine mammary epithelial cells

city: Yinchuan

first: Xing-Ping

last: Wang

state: Ningxia

address: No. 489, Helan Shanxi Road, Xixia District

department: College of animal science and technology

institute: Ningxia University

summary: Purpose: to detect expression profile of differentially expressed mRNAs during bovine mammary epithelial cells transfected with miR-199a-3p mimic or negative control (NC) mimic in vitro.  Methods: bovine mammary epithelial cells were transfected with miR-199a-3p mimic or negative control (NC) mimic to assess the expression profiles of mRNAs using RNA-seq.  Results:  there were 140 DEGs (109 up-regulated and 31 down-regulated) in the miR-199a-3p overexpression group compared with the negative control group.  Conclusion: the overexpression of miR-199a-3p resulted in differential expression of 140 genes in bMECs. The functional annotation results of these DEGs suggested that miR-199a-3p may be involved in the inflammatory and immune responses of bMECs by regulating PI3K-Akt signaling pathway, TGF-beta signaling pathway and IL-17 signaling pathway.

overall_design: Bovine mammary epithelial cells were inoculated and cultured in 6-well cell culture plates. When cell confluence reached 60-70%, miR-199a-3p mimic and NC mimic (final concentration 50nM) were transiently transfected into cells. Subsequently, all samples were used to perform the RNA-seq.

first: Yu-Hang

last: Li

first: Qian-Qian

last: Ren

first: Jin-Peng

first: Zhuo-Ma

last: Luoreng

first: Yun

last: Ma

first: Da-Wei

last: Wei


title: Granzyme K+ CD8 T cells slow tauopathy progression by targeting microglia b

first: Kory

last: Johnson

overall_design: 4 scRNA-Seq samples representing single cells isolated from the spinal cords of four different mouse groups: P301S homozygous CD8 KO (30 weeks), P301S homozygous CD8 WT (30 weeks), P301S homozygous CD8 WT (33 weeks), & P301S negative CD8 WT (30 weeks),

first: Hannah

last: Mason

first: Yvonne

last: Latour

first: Christopher

last: Boughter

first: Dragan

last: Maric

first: Cayce

last: Dorrier

first: Vivian

last: Guedes

first: Chen

last: Lai

first: Patrick

last: Duncker

first: Alexis

first: Monica

last: Manglani

first: Jessica

last: Gill

first: Daniel

last: Perl

first: Martin

last: Meier-Schellersheim

first: Dorian

last: McGavern


title: Epigenetic reprogramming of the mesenchymal state by SUV39H1/H2 [RNA-Seq]

first: Gracia

last: Bonilla

overall_design: Transcriptome of HMLE and HMLE-TWIST1 cells  treated with DMSO, different doses of chaetocin, or in which SUV39H1/H2 were knocked down for two or four days were generated using next-generation high-throughput sequencing in triplicates.

first: Junichi

last: Hanai

first: Noriko

last: Ide

first: Alex

last: Gulka

first: Jingyu

last: Zhang

first: Ruslan

last: Sadreyev

first: Mo

last: Motamedi


title: The methylation rate of the promoter and first exon of RELB in esophageal squamous cell carcinoma and para-carcinoma tissues

city: Wuhan

first: Lijuan

last: Gao

address: Luojiashan

institute: Wuhan University

type: Methylation profiling by high throughput sequencing

summary:
To illustrate the molecular mechanism of the overexpression of RELB in esophageal squamous cell carcinoma compared with para-carcinoma tissues
We then calculated bismark analysis using data obtained from bisulfite target sequencing data of six paires of esophageal squamous cell carcinoma and para-carcinoma tissues

overall_design: Comparative methylation rate analysis of Bisulfite target Sequencing data for the promoter and first exon of RELB of six paires of esophageal squamous cell acrcinoma and para-cacinoma tissues

first: Yongshun

last: chen


title: Genome-wide distribution of Spindlin1 and C11orf84

city: Hong Kong

first: Chengmin

last: Qian

address: L3-68, Laboratory Block, 21 Sassoon Road

department: School of Biomedical Sciences

country: Hong Kong

institute: The University of Hong Kong

summary: Spindlin1 is a unique multivalent epigenetic reader that facilitates ribosomal RNA transcription. In this study, we first identified that C11orf84 is a Spindlin1 bona fide binding partner. We performed ChIP-seq in U2OS cells to examine the genome-wide distribution of Spindlin1 and C11orf84. The ChIP-seq data indicates there is approximately 90% overlap in Spindlin1 and C11orf84 target genes.

overall_design: Examination of the genome-wide distribution of Spindlin1 and C11orf84 in U2OS.


title: Culture conditions differentially regulate the inflammatory niche and cellular phenotype of tracheobronchial basal stem cells

city: Duarte

first: Crystal

middle: N

last: Marconett

email: cmarcone@usc.edu, cmarconett@coh.org

state: CA

address: 1500 E Duarte Rd

department: Integrative Translational Sciences

institute: City of Hope

summary: Bronchial epithelial cells derived from the tracheobronchial regions of human airways (HBECs) provide a valuable in vitro model for studying pathological mechanisms and evaluating therapeutics. This cell population comprises a mixed population of basal cells (BCs), the predominant stem cell in airways capable of both self-renewal and functional differentiation. Despite their potential for regenerative medicine, BCs exhibit significant phenotypic variability in culture. To investigate how culture conditions influence BC phenotype and function, we expanded three independent BC isolates in three media: airway epithelial cell growth medium (AECGM), dual-SMAD inhibitor (DSI)-enriched AECGM, and PneumaCult Ex plus (PEx+). Analysis through RNA sequencing, immune assays, and impedance measurements revealed that PEx+ media significantly drove cell proliferation and a broad proinflammatory phenotype in BCs. In contrast, BCs expanded in AECGM and displayed increased expression of structural and extracellular matrix components at higher passage. AECGM increased expression of some cytokines at high passage, whereas DSI suppressed inflammation implicating the involvement TGF-β in BC inflammatory processes. Differentiation capacity of BCs declined with time in culture irrespective of expansion media. This was associated with an increase in PLUNC expressing secretory cells in AECGM and PEx+ media consistent with the known immune modulatory role of PLUNC in the airways. These findings highlight the profound impact of media conditions on inflammatory niche established by, and function of, in vitro expanded BCs. The broad proinflammatory phenotype driven by PEx+ media, in particular, should be considered in the development of cell-based models for airway diseases and therapeutic applications.NEW & NOTEWORTHY Airway basal cells, vital for airway regeneration and potential therapies, show significant changes based on culture conditions. Our study reveals that media composition and culture duration greatly affect basal cell properties with profound changes in the proinflammatory phenotype and extracellular matrix deposition driven by changes in growth conditions. These results underscore the critical impact of culture conditions on BC phenotype, influencing cell-based models for airway disease research and therapy.

overall_design: Basal cells were isolated from donors using established protocols and grown to 80% confluency in the specified media. Total RNA was isolated and underwent PE150 sequencing using the Illumina NovaSeq S2 at Azenta (formerly Genewiz). Data was parsed to ~43M reads per sample and pseudoaligned to the hg38 genome using Kallisto which is contanined in the processed data. Kallisto-generated BAM files were converted to .Bigwidg (processed data files).

first: Shuba

last: Murthy

first: Denise

last: Seabold

first: Lalit

last: Gautam

first: Adrian

last: Caceres

first: Rosemarie

last: Sease

first: Amy

last: Ryan


title: Effect of depletion of the transcriptional factor FoxP1 on gene expression in mouse normal adult hematopoietic stem and progenitor cells.

city: Paris

first: Evelyne

last: LAURET

address: 22 rue Méchain

country: France

institute: INSERM

summary: Transcription factor Forkhead box P1 (FOXP1) is a key regulator of various immune cell functions, including monocyte differentiation, B cell terminal differentiation and CD4+ or CD8+ T cell quiescence. In previous studies, we have shown that FOXP1 contributes to human hematopoietic stem progenitor cell (HSPC) and acute myeloid leukemia (AML) cell growth. Here we investigated the in vivo role of Foxp1 in early adult murine hematopoiesis. We showed that hematopoietic-speciﬁc loss of Foxp1 expression leads to attrition of the medullar HSC/Multipotent progenitor (MPP)-1 compartment in parallel with an enhancement of the myeloid-biased MPP3 compartment, without impact on MPP2 or MPP4 compartments. Foxp1-deﬁcient HSCs exhibited a reduced self-renewal capacity in competitive hematopoietic reconstitution assays, and HSC and all MPP compartments showed enhanced proliferation with a G0 phase reduction. To further investigate the role of Foxp1 in the regulation of HSC and MPP compartments, we performed gene expression profiling analysis of HSC/MPP1 and MPP3 compartments from WT and Foxp1-deficient mice using data obtained from RNASeq of 3 different cell populations.

overall_design: We developed a conditional knock-out (KO) mice model by crossing Foxp1-floxed mice to Vav1-iCre mice which constitutively express the codon-improved Cre (iCre) driven by Vav-1 regulatory elements. WT and Knockout mice (8-12 weeks old) were sacrificed, bone marrow was harvested, lineage neg cells were enriched and Lin-Sca+Kit+CD150+CD48- (HSC/MPP1) cells and Lin-Sca+Kit+CD150-CD48+CD135- (MPP3) cells were purified on AriaIII cytometer. For each cell population, 4 different samples were obtained.

first: Françoise

last: Levavasseur

first: Samia

last: Oussous

first: Alessandro

last: Framarini

first: Ismael

last: Boussaid

first: Panhong

last: Gou

first: Tuerdi

last: Zubaida

first: Iman

last: Litchy Boueya

first: Hélyette

last: Hoffner

first: Marta

last: De Almeida

first: Morgane

last: Legall

first: Haley

last: Tucker

first: Stéphane

last: Giraudier

first: Didier

last: Bouscary

first: Michaela

last: Fontenay

first: Diana

last: Passaro

first: Isabelle

last: Dusanter-Fourt

last: Lauret


title: RNA binding protein IMP1/ZBP1 drives mRNA localization and local translation in microglial peripheral processes and mediates morphological changes, motility  and phagocytosis in response to inflammation.

status: Public on Jun 19 2025

city: Leioa

first: Jimena

last: Baleriola

address: Science Park UPV/EHU. Sede Building, 3rd Floor

institute: Achucarro Basque Center for Neuroscience

summary: Polarized cells in the brain, such as neurons and glia, rely on the asymmetric distribution of their proteins compartmentalizing the function of dendrites, axons, glial projections and endfeet. Subcellular proteomes can be assembled either by the transport of proteins synthesized in the cell soma or by the delivery of mRNAs to target  compartments where they are locally translated into protein. This latter mechanism is known as local protein synthesis or local translation, and it has been best studied in neurons. Increasing evidence suggest it is also required to maintain local protein homeostasis in glial cells, however, in microglia, local translation remains largely unexplored. Given the scant evidence, we aimed at exploring the existence of local translation in microglial peripheral processes (PeMPs) and unravel its functional significance. We report that local translation indeed happens in PeMPs and it is enhanced by triggering a microglial inflammatory response with bacterial lipopolysaccharides (LPS) suggesting a functional relevance of this molecular mechanism in response to inflammation. We found that Actb mRNA polarizes to PeMPs and is locally translated upon LPS exposure. Interestingly, downregulation of the Actb binding protein IMP1/ZBP1 impaired Actb mRNA polarization and its localized translation, and led to defects in filopodia distribution, PeMP motility, lamellar directed migration and phagocytosis in microglia. Thus, our work contributes to recent findings that mRNA localization and localized translation occur in microglia and gives a mechanistic insight into the relevance of this molecular mechanism in fundamental microglial functions in response to inflammation.

overall_design: RNA-seq profiling of wild type microglial peripheral processes and their knockdown derivatives (IMP1 KO) with and without LPS treatment

first: Josune

last: Imaz-Iruretagoyena

first: Maite

last: Blanco-Urrejola

first: Irene

last: Núñez-García

last: García-Toledo

first: Luis

last: Fernández-Beltrán

first: Mar

last: Márquez

first: Silvia

last: Corrochano

first: Amanda

last: Sierra


title: Rbpj  deletion in hepatic progenitor cells attenuates endothelial responses and fibrosis in DDC-fed mice

city: CINCINNATI

first: Soona

last: Shin

state: OH

address: 3333 Burnet Avenue

institute: Cincinnati Children's Hospital Medical Center

summary: Background: As the role of hepatic progenitor cells (HPCs) constituting ductular reactions in pathogenesis remains ambiguous, we aimed to establish the in vivo cause-and-effect relationship between HPCs and chronic liver disease progression. We previously demonstrated that peritumoral ductules are associated with angiogenesis in liver tumors and forkhead box L1 (Foxl1)-expressing murine HPCs secrete angiogenic factors in vitro. Therefore, we hypothesized that HPCs are capable of remodeling the portal vascular microenvironment and regulating overall liver disease progression, and this function of HPCs is dependent on recombination signal binding protein for immunoglobulin kappa J region (RBPJ), a key effector of the Notch signaling pathway. Methods and Results: We generated HPC-specific Rbpj conditional knockout mice (CKO) using Foxl1-Cre and treated them with the DDC diet to induce chronic liver disease. CKO mice exhibited a significant reduction in serum levels of liver injury markers, ductular reactions, vascular and fibrotic areas, and hepatic expression of fibrosis and inflammation markers compared to control mice (WT). Single-nucleus RNA sequencing comparing CKO and WT livers detected transcriptome changes across multiple cell types, including endothelial cells, hepatic stellate cells, and cholangiocytes. Expression of several reactive cholangiocyte markers, including vascular cell adhesion molecule 1 (VCAM1), in HPCs was significantly downregulated in response to anti-Rbpj shRNAs in vitro. Immunofluorescence analysis indicated that the percentage of VCAM1+ cells was reduced in both HPC and cholangiocyte populations in CKO compared to WT in vivo. Conclusions: Our findings reveal Rbpj-dependent expression of reactive cholangiocyte markers in HPCs and demonstrate that Rbpj deletion in HPCs attenuates not only endothelial responses but also liver injury, fibrosis, and VCAM1 expression in cholangiocytes, highlighting the crucial role of HPCs in pathogenic progression.

overall_design: Single-nucleus RNA sequencing (sNuc-seq) analysis was performed using the livers of hepatic progenitor cell-specific Rbpj knockout (CKO) mice and wild-type (WT) mice treated with the DDC diet for 4 weeks.

first: Sanghoon

last: Lee

first: Lu

last: Ren

first: Weiwei

last: Li

first: Aditi

last: Paranjpe

first: Ping

last: Zhou

first: Andrew

last: Potter

first: Stacey

middle: S

last: Huppert


title: Galactose changed the transcriptome of endometrial epithelial cells after E. coli infection

city: Changchun

first: Jiapei

last: Cai

state: Jilin

address: Xi‘an Road 5333

institute: Jilin University

summary: To elucidate the mechanism of galactose preventing endometritis, we treated mice with or without galactose and subsequently employed flow sorting to isolate endometrial epithelial cells.

overall_design: We then performed SMART-seq to analyze the mRNA expression of 2 groups.Comparative gene expression profiling analysis of SMART-seq data for endometrial epithelial cells.

first: Xinyu

last: Zhang


title: Exosome-like nanovesicles from Peucedanum japonicum directly regulate inflammatory cytokines via small RNAs

city: Yayoi, Bunkyo-ku

first: Tomoatsu

last: Hayashi

state: Tokyo

country: Japan

institute: The University of Tokyo

summary: Inflammation plays a key role in the pathogenesis of various diseases, including inflammatory bowel diseases such as ulcerative colitis and Crohn's disease. Similar to animals, plant cells produce exosome-like nanovesicles (ELNs) that play a role in transmitting biological signals from specific types of cells or tissues to other cells or tissues. Here we show that ELNs derived from Peucedanum japonicum (PjELNs) exhibit potent anti-inflammatory effects on macrophages and are effective in a mouse colitis model induced by dextran sodium sulfate (DSS). RNA sequence analysis reveals that PjELNs suppress multiple inflammatory cytokine-mediated signaling pathways in LPS-stimulated macrophage cell lines. We further show that PjENLs promote the differentiation of goblet cells, thereby enhancing mucin production and providing a protective effect on mucosal damage in a DSS-induced murine model of colitis. We also demonstrate that PjELNs inhibit the DSS-induced reduction in the number of transit amplifying cells. PjELNs exhibit anti-inflammatory properties, partly due to the presence of miRNA-like small RNAs that directly regulate the expression of the inflammatory cytokine IL6. Importantly, these small RNAs exhibit cross-species effects in both humans and mice. These findings reveal the mechanism by which plant-derived ELNs modulate inflammatory responses, suggesting their potential as a preventive and therapeutic strategy for inflammatory diseases of the colon.

overall_design: Profiling of gene expression in non-stimulated Raw-Blue cells (None, n = 3), LPS-stimulated Raw-Blue cells (LPS, n = 3), and Raw-Blue cells pre-treated with PjELNs before LPS stimulation (LPS-PjELNs, n = 3).

first: Takuya

last: Kojima

first: Tomoatu

first: Yasunari

last: Kageyama

first: Tsutomu

last: Nakamura

first: Tetsu

last: Akiyama


title: Tumors with active microenvironmental type-I interferon response are sensitive to inhibitors of heme degradation

city: London

first: Dominika

last: Sosnowska

state: Please select...

address: King's College London Guy's Campus, New Hunt's House, Newcomen St

department: Comprehensive Cancer Centre

country: United Kingdom

institute: King's College London

summary: The tumor microenvironment (TME) is highly heterogeneous and plays a critical role in determining the success of therapeutic interventions. Identifying TMEs that are susceptible to specific therapies enables the development of more personalized and effective treatments. In this study, using a spontaneous murine model of breast cancer, we characterize a TME that is sensitive to inhibitors of the heme degradation pathway mediated by heme oxygenase (HO) activity, leading to CD8+ T- and NK-cell-dependent tumor control. A key feature of this TME is a chronic type-I interferon (IFN) signal, which is crucial in orchestrating an anti-tumor immune response. Notably, similar TMEs are found in human breast cancer and are associated with patient prognosis. Leveraging these insights, we demonstrate that combining a STING agonist, which induces type-I IFN responses, with an HO inhibitor results in a synergistic effect, enhancing tumor control. This study identifies HO activity as a potential resistance mechanism to type-I IFN responses, providing a novel strategy for overcoming immune evasion in cancer therapy.    As part of this investigation, multiplex gene expression analysis was performed on 770 genes, including 40 housekeeping genes, from RNA extracted from MMTV-PyMT tumors. The samples were processed using the nCounter® platform, with RNA isolated, quantified, and assessed for integrity following standardized protocols, allowing for detailed molecular characterization of the TME.

overall_design: This study conducted a gene expression analysis to explore the tumor microenvironment (TME) in MMTV-PyMT mouse model. Tumor tissues were obtained from Prf1+/+ and Prf1-/- mice, each treated with either a vehicle or SnMP for 36 hours, totaling 12 samples (3 per condition). RNA was isolated from these tissues, quantified, and assessed for integrity. The NanoString nCounter® platform, utilizing the Pan-Cancer Immune Profiling Panel, was used to profile the expression of 770 genes, including 40 housekeeping genes.

first: Sosnowska

last: Dominika

first: Arnold

last: James

first: Opzoomer

middle: W

first: Buus

last: Richard

first: Grigoriadis

last: Anita


title: (re)freezing PBMC

city: Gent

first: Eufra

last: Van Damme

address: Technologiepark 75

department: CMB

country: Belgium

institute: VIB-UGent

summary: This study investigates the impact of cryopreservation and freezing media on RNA quality and gene expression profiles of peripheral blood mononuclear cells (PBMC). No significant difference in cell viability or RNA quality was observed between freshly isolated and cryopreserved cells, even after two freeze-thaw cycles. Transcriptome analysis revealed no significant differences in alignment rates or read counts across various conditions. Differential gene expression analysis identified changes between fresh and thawed samples, with a consistent downward trend of mRNA abundance in the frozen samples, but minimal changes were observed between the first and second freeze-thaw cycles. Gene set enrichment analysis showed only minor significant differences, and stress-related gene sets were not upregulated. Freezing medium appears to be the safer option compared to freezing in trizol. These results confirm that cryopreservation and thawing processes do not compromise RNA integrity or sequencing reliability in PBMC, supporting the use of cryopreserved samples for gene expression studies.

overall_design:
Study samples  Blood was collected from three healthy donors (one male and two female adults) following informed consent with Ethical Committee approval of the University Hospital of Ghent (reference number 2017/1207). Blood samples were collected in K2 EDTA-tubes (BD Vacutainer) and four 10mL tubes were processed per donor.  PBMC isolation, cryopreservation and thawing  Within one hour after blood collection, PBMC isolation was performed simultaneously for all three donors. The PBMC were isolated by density gradient centrifugation using Ficoll-Paque PLUS density gradient media. Samples were centrifuged at 800g for 18min without brake at room temperature. Isolated PBMC were washed twice in PBS at 400g for seven minutes at room temperature. The cells were resuspended in 0,5mL PBS and concentration was determined using the BioRad TC20 Automated Cell Counter in combination with trypan blue staining. PBMC were aliquoted at 5 million cells per vial. One vial per donor was directly processed for RNA extraction (these samples will be named “fresh”). For cryopreservation, the remaining PBMC were diluted in freezing medium (RPMI + 1% penicillin/streptomycin + 10% FCS plus 10% dimethyl sulfoxide). PBMC were transferred to isopropanol containers (Mr. Frosty™ Thermo-Fischer Scientific) and stored at -80 °C for 24 h, before being transferred to -150°C freezers for one week. PBMC were thawed at room temperature before transferring to warm (37°C) complete medium (RPMI + 1% penicillin/streptomycin + 10% FCS plus 10% dimethyl sulfoxide). After centrifugation at 400g for 7min the supernatant was discarded, and the cells were resuspended in PBS. One vial was directly processed for RNA extraction (these samples will be named “defrosted”), the cells from one other vial was transferred to complete freezing medium (these samples will be named “FM” or “freezing mix”) and from a third vial the cells were directly refrozen in trizol reagent (these samples will be named “trizol”). These two refrozen samples per donor (FM and trizol) were preserved for an additional week in -150°C before thawing, and subsequent RNA extraction was performed. A graphical summary of the workflow is provided in Figure 1. The viability of the cells was assessed using the BioRad TC20 Automated Cell Counter in combination with trypan blue staining.RNA extraction and RNA sequencing.  RNA from PBMC was extracted using the trizol-based miRNeasy Mini kit (Qiagen, Hilden, Germany) following the manufacturers’ instructions, including the on-column DNase digestion step. RNA concentrations were quantified using Nanodrop (ThermoFisher Scientific, Waltham, MA, USA) spectrophotometry. Further characterization and quality assessment was carried out using the Fragment Analyzer (Agilent Technologies, Santa Clara, CA, USA). RNA sequencing was performed after library preparation according to the TruSeq mRNA protocol (Illumina, San Diego, CA, USA) in a single flowcell on the NovaSeq 6000 instrument following these parameters: Illumina NovaSeq 6000 v1.5 sequencing kit 100 cycles single-end reads (101-10-10-0), 1%PhiX. Sequencing yielded high-quality data, with 94.02% of bases exceeding Q30 and 85.38% of clusters passing the quality filter and a mean read depth of 27,8 million reads (18,4M to 32,7M).   RNA sequencing preprocessing  To achieve a uniform sequencing depth for all samples, allowing a fair comparison, random subsampling was performed using setqk (version 1.4) and adjusted to the minimum read count (18 million). Pseudo-alignment and transcript quantification was obtained by Kallisto13 (version 0.48.0) using a GRCh38 Ensembl v 100 index. The length of reads was set to 200 base pairs, and 20 bootstraps were set as parameters during the (pseudo-)alignment.  Plots, statical analysis, differential expression analysis and GSEA  All analyses were performed using the R statistical software (version 4.4.1). For statistical comparisons between different sample conditions, the Mann-Whitney U test was performed, and data visualization was conducted using the ggplot2 package (version 3.5.1). Before performing the differential expression analysis, transcript-based counts were summed up to gene counts whereafter genes were filtered to retain those with minimum sum of 100 over all samples. The DESeq2 package (version 1.44.0) was used, and genes were considered to be significantly differentially expressed when the adjusted p-value was below 0.05 and the absolute value of the log2 fold change was larger than 2.  For the gene set enrichment analysis (GSEA), fgsea14 package (version 1.30.0) was used to perform the analysis. Firstly, a list of marker genes for each cell type was constructed on Azimuth scRNA-seq database15 by using “FindMarkers” function in Seurat package (version 5.1.0) with the following parameters: logFC > 0.25, min.pct > 0.25. Additionally, Wilcoxon Rank Sum test was selected to identify differentially expressed genes for one cell type versus the rest of the cell types. Subsequently, the Cell Type Signature (C8) pathways were retrieved from the Molecular Signatures Database (MSigDB), and the immune-related gene sets were selected for analysis. For stress specific pathways, chemical stress, fluid shear stress, oxidative stress, osmotic stress, stress in general and stress response signaling signatures were selected from the biological process ontology gene sets (C5, subcategory = GO:BP).  Deconvolution of RNA sequencing data  To estimate the cell type fractions and compositions from the transcriptome data, reference-based deconvolution was performed using the Dampened Weighted Least Squares (DWLS) (v.0.1.0) method16. We selected the method based on our previous benchmarking studies on RNA-seq based deconvolution approaches17. As reference, we used a publicly available scRNA-seq data generated on PBMC from healthy donors (EGAS00001004571)18. The scRNA-seq data labelled with seven different cell types (T cells, B cells, neutrophils, natural killer (NK) cells, monocytes, erythrocytes, and eosinophils) were used to construct a signature matrix, that was subsequently used as an input for deconvolution. The signature matrix for the different cell types was built in R (v4.3.2) using the function ‘buildSignatureMatrixMAST’ with default parameters. Afterwards, common genes between the bulk data and the signature matrix were filtered with the function ‘trimData’. Subsequently, deconvolution was performed using the function ‘solDWLS’, resulting in inferred cell type proportions from the bulk data.  To assess significant differences in deconvolved proportions between the fresh condition and the freezing conditions, paired t-tests were performed, and the FDR method was used for the multiple hypothesis testing.

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Raw files for human/patient samples are being made available in EGA (https://www.ebi.ac.uk/ega/) for controlled access to the personally identifiable sequence data.
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title: Bcl11a is essential for B-1a cell maintenance during aging (scRNA-seq)

city: shanghai

first: Yong

last: Yu

address: 1239 Siping Road

department: School of Life Sciences and Technology

institute: Tongji University

summary: B-1a cells are important immune cells and are the first line of defence against pathogens. During aging, B-1a cells undergo a series of changes that reduce their protective effects on the body. However, the characteristics of B-1a cells during aging are not fully understood. In this study, we transcriptionally and epigenetically characterised B-1a cells from 3-month-old and 24-month-old mice. Interestingly, we found that the expression of the transcription factor Bcl11a was positively correlated with the number of B-1a cells in old male and old female mice. We performed single-cell sequencing from C57BL/6 young female mice (3 months of age), middle-aged female mice (15 months of age) old female mice (26 months of age) to characterise the senescence transition in female mice.

overall_design: scRNA-seq were performed on the B-1a isolated from young female mice (3-month-old),middle female  (15-month-old mice),old female mice (26-month-old mice)of C57BL/6.

first: Shasha

last: Xu

first: Liangfeng

last: huang

first: Linlin

first: Yifeng

last: Hu


title: Small RNAs in Exosome-like nanovesicles from Peucedanum japonicum (PjELNs)

first: Tomoatsu

overall_design: Profiling of small RNAs, including miRNAs, in Exosome-like nanovesicles from Peucedanum japonicum (PjELNs)

first: Takuya


title: Bcl11a is essential for B-1a cell maintenance during aging (RNA-Seq)

summary: B-1a cells are important immune cells, serving as the first line of defense against pathogens. B-1a cell undergo a series of alterations during aging and decrease the protection to our body. However, the characteristics of B-1a cells during the aging process are not fully understood. In this study, we discrible transcriptional and epigenetic profiles of B-1a from 3-month-old and 24-month-old mice across both genders. Interestingly，We found that the expression of the transcription factor Bcl11a was positively correlated with the number of B-1a cells in aged male and aged female mice.To further characterize senescent B-1a cells and the mechanisms of Bcl11a regulates B-1a. ATAC-seq and RNA-seq were performed on the B-1a isolated from young male mice (3-month-old),old male mice (24-month-old mice), young female mice (3-month-old),old female mice (24-month-old mice) of C57BL/6,and Bcl11a delated young male mice. CUT&tag was performed on the B-1a isolated from young male mice. Collectively, we provide a comprehensive resource to decode the aging process of B-1a, shedding light on how Bcl11a regulate B-1a cells maintenance.

last: Huang


title: Digital reconstruction of spatiotemporal atlas unveils the cellular origins and signaling networks underlying early mouse organogenesis

city: nanjing

first: yi

last: yang

address: sipailou 2

institute: southeast university

summary: Spatiotemporal gene expression and signaling orchestration are pivotal for shaping the patterns of early embryonic development. Here we profiled 360 serial sections (10-mm thickness) across 6 whole embryos during early organogenesis to generate a comprehensive spatial transcriptomic map at single-cell resolution. We developed SEU-3D to reconstruct "digital embryos", providing a virtual representation and investigation of regionalized gene expression in its native spatial context. By combining these measurements with space-informed gene-cell co-embedding analysis, we have systematically characterized the spatial atlas of endoderm and mesoderm over time, elucidating the intricate networks of cell signaling that traverse germ layers and cell types. Furthermore, we observed regionalized identity of cells along the anterior boundary between embryonic and extra-embryonic tissues of the cardiac crescent, which reflects their cellular origins, and the coordinated signaling further patterning these cells into cardiac-specific territories. Collectively, the reconstruction of single-cell resolution whole “digital embryo” provides significant insights into early mouse organogenesis, offering a unique platform for future investigations into the mechanisms underlying embryonic development.

overall_design: Stereo-seq on whole mouse embryos at E7.5, E7.75 and E8.0 stages (replicates per stage). Replicates were OCT-embeded and sequenced together.  Samples were collected by sereal coronal sections of 10-µm thickness.

first: Yi

last: Yang


title: Bcl11a is essential for B-1a cell maintenance during aging (CUT&Tag)

overall_design: CUT&tag was performed on the B-1a isolated from young male mice

last: Zhang


title: Iron Drives Eosinophil Differentiation in Allergic Airway Inflammation through Mitochondrial Metabolic Adaptation

city: Hangzhou

first: Fei

last: Li

address: 866 Yuhangtang Road

department: Department of Medicine

institute: Zhejiang University

summary: Understanding the metabolic mechanisms driving eosinophil differentiation in allergic airway inflammation is imperative for developing effective asthma therapies. Despite iron's well-established involvement in various cellular processes, its role in eosinophil differentiation remains elusive. This study observed elevated intracellular iron levels during eosinophil differentiation in the context of allergic airway inflammation. Through experiments involving iron-related compounds and specific diets, we demonstrated iron's indispensable role in promoting eosinophil differentiation, both in vitro and in vivo. Remarkably, an iron chelator effectively suppressed eosinophil differentiation and alleviated allergic airway inflammation. Mechanistically, iron maintains mitochondrial metabolic activities, mTORC1 signaling, and the expression of transcription factors that enforce eosinophil differentiation. Notably, iron influx rewires specific metabolic shifts in Krebs cycle, with succinate promoting eosinophil differentiation. Overall, this study highlights the significance of understanding the regulatory role of iron and underlying metabolic mechanisms in eosinophil differentiation, providing potential metabolic intervention strategies for asthma treatment.

overall_design:
We conducted a comparative analysis of bone marrow Granulocyte-Macrophage Progenitors (GMPs) and eosinophils to pinpoint the transcriptional programs driving iron pool expansion.
Additionally, we performed RNA sequencing to contrast cytokine-stimulated eosinophils, which simulate an allergic response, with resting eosinophils through transcriptome profiling.
To deepen our comprehension of how intracellular iron levels affect eosinophil differentiation, we assessed the transcriptional profile of Bone Marrow-Derived Eosinophils (BMDEs) on the seventh day following the induction of iron deficiency or iron overload.

first: Haoyu

last: Tang

first: Yuejue

last: Wang


title: Genetic tuning of ipRGC subtype identity to shape visual behavior

city: Evanston

first: Yue

state: IL

address: 2200 Campus Dr

department: Neurobiology

institute: Northwestern University

summary: The distinct blend of molecular and cellular features that define neuronal subtype identity are central to shaping how individual subtypes impact animal behavior. The diversity of the mammalian nervous system is vast — the retina alone contains over 100 neuronal subtypes. Yet, the genetic processes giving rise to this stunning structural and functional diversity remain poorly understood. Here, we uncover a graded expression pattern of the transcription factor Brn3b that tunes and maintains multiple, subtype-defining transcriptional and morphophysiological features of the melanopsin-expressing, intrinsically photosensitive retinal ganglion cells (ipRGCs). Disruption of this Brn3b gradient causes the transcriptional and morphophysiological identity of ipRGC subtypes to begin to converge, leading to dysfunction in multiple ipRGC-dependent behaviors. These findings show that a single transcription factor gradient can tune a diverse array of features to shape neuronal identity and circuit function to drive behavior.

overall_design: Retina from Brn3b conditional knockout (Brn3bcKO) mice expressing Rpl22-HA in ipRGCs or control mice were subjected to translating ribosome affinity purification (TRAP) followed by library preparation using the Smart-seq3 protocol. RNA libraries were sequenced on the Illumina NextSeq 550 platform to obtain 37 bp paired-end reads. Two to four biological replicates were performed for all conditions.

first: Marcos

last: Aranda

first: Jacob

last: Bhoi

first: Omar

middle: A

last: Payán Parra

first: Seul

middle: K

last: Lee

first: Tomoko

last: Yamada

first: Tiffany

last: Schmidt


title: SMN1 orchestrates the global transcriptome profile associated with neuropathic pain development in SHSY5Y cells

first: Jun

last: Zhou

address: No.9 Zhangzhidong Road

institute: Renmin Hospital of Wuhan University

summary: Survival of motor neuron 1 (SMN1) acts as an RNA-binding protein, exerts multiple biological effects, participates in the production of small ribonucleoproteins (snRNPs), and regulates RNA metabolism through post-transcriptional regulation. Previous studies have reported that SMN1 mediates neuronal death through the classical apoptotic pathway; however, the mechanism by which it regulates neuropathic pain (NP) remains unknown. In this study, we used transcriptome sequencing, observed that SMN1 overexpression significantly impacted gene expression, and obtained functional clusters of differentially expressed genes (DEGs) highly enriched in NP-related terms. These genes were mainly enriched in biological pathways related to cell adhesion, inflammatory response, and signal transduction. In addition, the overexpression of SMN1 also regulated the alternative splicing (AS) of genes related to biological pathways such as DNA damage stimulation and DNA repair. Our study showed that SMN1 might be involved in the occurrence and development of NP by regulating the transcriptional and AS levels of related genes.

overall_design: We constructed a smn1 overexpression model in SHSY5Y cell line, coupled with RNA-seq sequences, to comprehensively reveal the biological function of SMN1 in SHSY5Y cell and analyze the alterations of transcriptional profiles upon SMN1 overexpression.

first: Zhongyuan

last: Xia

first: Qinqin

last: Yin


title: Effect of knockdown of KIAA1429 on gene expression in HepG2 cells

city: CHONG QING

first: HUA

middle: MEI

last: SHAN

address: 30 Gaotanyan, Shapingba

institute: Army Medical University

summary: Total RNA was extracted from HepG2 cells with si-NC (N=2) or si-KIAA1429 (N=2). To investigate the global genes which were regulated by KIAA1429, high-throughput mRNA sequencing (RNA-Seq) was performed to compare the expression profile in HepG2 cells.

overall_design: RNA-seq was performed in HepG2 cells after control siRNA or KIAA1429 siRNA transfection

first: Meihua

last: Shan


title: Whole blood gene expression data of thrombotic and non-thrombotic critically ill COVID-19 patients

status: Public on Jun 18 2025

city: Amsterdam

first: Cosimo

last: Cristella

address: Meibergdreef 9

department: Medical microbiology and infection prevention

institute: Amsterdam University Medical Centers

summary:
Background: COVID-19 has revealed novel pathological mechanisms, particularly hypercoagulability leading to increased thrombotic risk in critically ill patients. This study investigates transcriptional signatures associated with thrombosis development in COVID-19 intensive care unit (ICU) patients and evaluates their predictive potential.
Methods: We performed whole blood transcriptional profiling of 57 mechanically ventilated COVID-19 patients, comparing those with thrombotic complications (TC, n=36) to those without (non-TC, n=21) using differential gene expression and machine learning approaches.
Results: TC patients showed greater transcriptome disruption and 283 differentially expressed genes compared to non-TC patients. Key features included enhanced neutrophil activation, inflammatory responses, and monocyte activation alongside suppressed lymphocyte function. An OPLS-DA model achieved excellent classification performance (AUC=0.961, 95% CI: 0.905-0.997). The maltase-glucoamylase gene (MGAM) was the top discriminatory biomarker outperforming traditional clinical markers like D-dimer and C-reactive protein (AUC=0.94).
Conclusions: Thrombotic complications in critically ill COVID-19 patients are characterized by distinct transcriptional signatures reflecting heightened neutrophil activation and inflammatory dysregulation. MGAM represents a novel potential biomarker that outperforms traditional clinical markers for identifying patients at high thrombotic risk, offering new opportunities for personalized risk stratification and management in severe COVID-19.

overall_design: This was a retrospective, observational study conducted at Erasmus medical center, The Netherlands, during the first wave of COVID-19 pandemic and precisely between 2nd March 2020 and 20th of April 2020. In brief, 77 patients with COVID-19 admitted to the ICU with ARDS were included in a biobank study (CIUM). If indicated by clinician, patients underwent computed tomographic pulmonary angiography, which was subsequently repeated 7 days after admission, or if the patient’s clinical condition abruptly deteriorated. Whole blood samples were available from 57 subjects at day 2 of ICU admission and were used in the presented research. Healthy controls were obtained from convalescent subjects enrolled as part of the MERMAIDS-ARI clinical observational study and were matched with cases based on age, gender, pulmonary, cardiovascular and metabolic disease infromation.

first: Matthijs

last: Raadsen

first: Karen

last: de Haan

first: Sarah

last: van Leeuwen

first: Mohammad

middle: R

last: Toliat

first: Nina

last: Dalibor

first: Marion

last: Koopmans

first: Menno

last: de Jong


title: Cell layer-specific modification of cell wall is associated with  exo-mesocarp split in pistachio (Pistacia vera L.)

city: Davis

first: Shuxiao

last: Zhang

address: One Shields Ave

department: Plant Sciences

institute: UC Davis

summary: Pistachio (Pistacia vera) is a drought and salinity-tolerant perennial whose fruit features a fleshy exo-mesocarp, or “hull,” that protects the kernel. Hull development and degradation are key to kernel quality, yet the anatomy and mechanisms driving hull breakdown during late-stage development remain largely unknown. Here, we show that the hull contains anatomically distinct layers of hypodermal parenchyma and filler parenchyma. Using a combination of transcriptome analyses and immunohistochemistry, we show that changes in pectin associated gene expression and modification of this polysaccharide are involved in hull cell size increase, loss of cell-cell adhesion, and softening. Anatomical analysis shows that filler parenchyma expands during late-stage hull development while hypodermal parenchyma remains constant in size. Field data suggest that irrigation and humidity affect pistachio hull split, implicating a role for water status in cell expansion. In summary, the complex interplay between molecular, cellular, and environmental changes suggests that cell layer–specific modifications of the cell wall are linked to exo-mesocarp splitting, forming a model for understanding the mechanism of fruit split during ripening in non-berry fruit crops.

overall_design: RNAseq of whole pistachio hull samples for 'Golden Hills' and 'Lost Hills' cultivars with different phenotypes (intact, cracked or tattered) collected 91 and 133 days post anthesis.

first: Minmin

last: Wang

first: Shaina

last: Eagle

first: Alisa

last: Chernikova

first: Kaleigh

last: Bedell

first: Phuong

last: Tran

first: Chaehee

first: Jaclyn

last: Adaskaveg

first: Yiduo

last: Wei

first: Rolando

last: Lopez

first: Annamarie

last: Basco

first: Phoebe

last: Gordon

first: Barbara

last: Blanco-Ulate

first: Grey

last: Monroe

first: Georgia

last: Drakakaki


title: Epigenetic profiles of response to transcranial magnetic stimulation in treatment resistant depression

city: Tampa

first: Jan

last: Dahrendorff

address: 3720 Spectrum Blvd

department: Department of Global, Environmental, and Genomic Health Science

institute: University of South Florida

type: Methylation profiling by genome tiling array

summary: Peripheral blood DNA methylation was profiled in 46 patients with treatment-resistant depression prior to treatment with transcranial magnetic stimulation (TMS). Genome-wide DNA methylation was measured using the Illumina Infinium MethylationEPIC BeadChip (850K array). Following quality control, data from 46 subjects were included in downstream analyses. Treatment outcomes were assessed using the PHQ-9 depression scale and included treatment response (≥50% reduction in PHQ-9), symptom trajectory (ΔPHQ-9), and remission (PHQ-9 score < 5). Methylation data were analyzed to identify differentially methylated regions (DMRs) associated with treatment outcomes. Both raw IDAT files and processed beta-value data are provided.

overall_design: Peripheral blood samples were collected and analyzed from 46 patients with treatment-resistant depression prior to a standardized 36-session course of transcranial magnetic stimulation (TMS) treatment. Genomic DNA was extracted and bisulfite converted for methylation profiling using the Illumina Infinium MethylationEPIC BeadChip (850K array). After sample-level quality control, 46 samples were retained for analysis. DNA methylation data were analyzed in relation to clinical outcomes based on PHQ-9 scores, including treatment response, symptom change, and remission status.

first: Monica

last: Uddin


title: Epigenetic and 3D genome reprogramming during the aging of human hippocampus [CUT&Tag]

city: La Jolla

first: Bing

last: Ren

address: 9500 Gilman Drive

institute: UCSD

summary: Age-related cognitive decline in humans is associated with altered physiology of the hippocampus, a region critical for memory consolidation and spatial navigation. While changes in gene expression have been observed in aging brain cells, our understanding of the regulatory mechanisms underlying these changes and their connection to chromatin structure remains limited. To unravel these complexities, we have applied a comprehensive multi-omics approach, integrating single-nucleus gene expression, chromatin accessibility, DNA methylation, and 3D chromatin architecture data obtained from hippocampal tissues of 40 neurotypical human donors spanning the adult lifespan. We observed a striking loss of astrocytes during aging, including the subset of astrocytes that play a role in maintaining and regulating synaptic transmission. In individuals aged 50-75 years, microglia undergo a dramatic switch from a predominantly homeostatic state to an epigenetically primed inflammatory state that coincides with reprogramming of their DNA methylomes. In the aged cells, we detected erosion of the 3D genome architecture, where local chromatin domains are diminished, trans-chromosomal interactions are strengthened, and CTCF DNA binding is reduced. Importantly, age-related changes in chromatin folding have high correspondence with the aging transcriptome and epigenome in multiple cell types. Our data identifies age-associated changes in cell types/states and gene regulatory features that provide insight into the loss of synapses and cognitive decline that occurs in the human brain during aging.

overall_design: Analysis of CTCF binding using CUT&Tag with 7 samples of human hippocampus tissue from neurotypical donors.

first: Nathan

last: Zemke

first: Seoyeon

last: Lee

first: Emily

last: Hsu


title: A SWEET Challenge: Less Sugar for Rhizospheric Microbiome Under the Successive Wheat Cultivatoin

city: Kiel

first: Zheng

last: Zhou

state: Schleswig-Holstein

address: Hermann-Rodewald-Straße, 9

department: Molecular Phytopathology

country: Germany

institute: CAU Kiel

summary: Considering the crucial role of root exudates, we hypothesized that continuous wheat cultivation would lead to lower glucose release, resulting in lower microbial growth, activity, and biomass. For the first time in situ glucose imaging was optimized for studying the interactions in the first (W1) and third (W3) wheat after break crop plots in the field. Glucose imaging method combined with soil microbial respiration, enzyme kinetics and the quantification SWEET genes expression levels in wheat plants. W3 had the lowest proportion of hotspots for glucose release with 1.35 % of the total soil surface area, indicating a 17.7 % decline compared to W1. Also, the expressions of functional orthologous genes of SWEET1a in wheat roots were significantly upregulated in W3 compared to W1. The growing microbial biomass in the rhizosphere soil of W1 was about five times higher than W3. Differences in SWEET gene expression and shift in glucose release is linked to altered root physiology and exudation processes, potentially reflecting the plant's strategy to create a less favourable environment for opportunistic pathogens. Hence, this study provides novel insights into the complex interactions between continuous wheat cultivation, root exudation, microbial dynamics, gene expression, and enzymatic activities.

overall_design: This study examines the impacts of continuous wheat cultivation on glucose release, microbial growth and activity, and the expression of sugar transporter genes. We propose the following hypotheses: i) continuous wheat cultivation differentially alters sugar transporter gene expression in roots and leaves; ii) reduced SWEET gene expression lowers glucose release, decreasing microbial growth, activity, and biomass in the rhizosphere; and iii) diminished glucose exudation reduces microbial functionality, reflected in lower enzyme activity and efficiency. These hypotheses were tested using root window installations, in situ glucose imaging, gene expression analysis of SWEET genes in roots and leaves, and destructive soil analyses of microbial growth and enzyme kinetics in first- and third-year wheat plots following a break crop at the Hohenschulen field, CAU Kiel.

first: Mehdi

last: Rashtbari

first: Lingyue

last: Han

first: Seyed

last: Hoseini

first: Ahmad

last: Azimi

first: Henning

last: Kage

first: Daguang

last: Cai

first: Bahar

last: Razavi


title: Hepatic transcriptome profiling in beef cattle: effects of rumen-protected niacin supplementation

city: Auburn University

first: Xu

last: Wang

state: AL

address: 273 CASIC Building, Auburn Research Park, 559 Devall Dr

department: Pathobiology, College of Veterinary Medicine

institute: Auburn University

summary: The objective of our study was to assess the effect of rumen-protected niacin supplementation on the overall transcriptomics profile of liver tissue on growing Angus × Simmental steers and heifers. Consequently, the vasodilatory, detoxifying, and immune suppressor effects of niacin were evaluated in hepatocytes. After a 30-day supplementation period with rumen-protected niacin on normal weaned beef calves, we observed a significant list of benefits at the liver transcriptome level. Several metabolic pathways revealed positive effects of administration of rumen-protected niacin; for example, a decrease in lipolysis, apoptosis, inflammatory responses, atherosclerosis, oxidative stress, fibrosis, and vasodilation-related pathways. Therefore, results from this study could potentially promote supplementation of rumen-protected niacin on beef cattle backgrounding operations or new arrivals to a feedlot, especially during the acclimation period when the health status of growing beef cattle is usually compromised.

overall_design: Profile of transcriptome-wide gene expression changes in liver samples from Angus × Simmental cattle supplemented with rumen protected niacin (n=3) compared to control samples (n=3).

first: Sonia

last: Moisa


title: Nanoplastics dysregulate macrophage function by impairing glutathione metabolism

city: Seoul

first: Koung-Min

last: Park

address: 5-26, Sinchon-ro 4-gil

country: South Korea

institute: Yonsei university college of medicine

summary: Micro- and nanoplastics (MNPs) are emerging environmental contaminants increasingly detected in human tissues. However, how MNP-related effector mechanisms that impact the immunological function of macrophages remain elusive. Here, we demonstrated that MNPs disrupt redox homeostasis and induce immune dysfunction in bone marrow-derived macrophages. MNP internalization in macrophages impairs mitochondrial function, inducing excessive and sustained production of reactive oxygen species along with suppressed glutathione metabolism, including the substantial down-regulation of key antioxidant enzymes, such as glutathione peroxidase (GPX) 1, GPX3, and GPX4. These processes cause oxidative imbalance, thereby triggering ferroptosis, compromising cellular integrity, and amplifying inflammatory signaling. Two-photon intravital and three-dimensional imaging in mice confirmed that orally administered MNPs accumulate in multiple organs. Such MNP accumulation exacerbates lung tumor progression, potentially through chronic inflammation and the immune dysregulation of macrophages. These findings reveal a novel mechanism by which MNPs alter innate immunity and promote an inflammatory microenvironment via redox-mediated ferroptosis.

overall_design: Total RNA-seq profiling of mouse bone marrow-derived macrophage and treated or no-treated by polystyrene micro- and nanoplastics.

first: Bora

last: Kim

first: Haerang

first: Young-Min

last: Hyun


title: Bcl11a is essential for B-1a cell maintenance during aging (ATAC-Seq)

first: Yong

last: Yu

overall_design: ATAC-seq were performed on the B-1a isolated from young male mice (3-month-old),old male mice (24-month-old mice), young female mice (3-month-old),old female mice (24-month-old mice) of C57BL/6,and Bcl11a delated young male mice.

first: Shasha

last: Xu

first: Liangfeng

last: Huang

first: Linlin

last: Zhang

first: Yifeng

last: Hu


title: Effects on renal senescence, copper flux and respiration during stem cell-based therapy

city: Beijing

first: Kaiting

last: Zhuang

state: Beijing

address: 28 Fuxing Road, Haidian District

institute: 1st Medical Center of Chinese PLA General Hospital

summary: Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) can reverse senescence after acute kidney injury (AKI) via maintaining mitochondrial homeostasis. Copper accumulation could promote senescence, but its response to MSCs remains unclear. C57 mice with renal unilateral ischemia reperfusion injury (uIRI) were renal capsular transplanted with hUC-MSCs for two weeks then performed mRNA sequencing. Gene correlation analysis revealed that senescence regulation is associated with copper homeostasis and respiratory chain complex IV.

overall_design: RNA-seq profiling of sham, uIRI and MSCs transplantation at Day 14.

first: Kating

first: Wenjuan

first: Guangyan


title: Insulin-degrading enzyme regulates mRNA processing and interacts with the CCR4-NOT complex

city: Paris 15

first: Lamine

last: TOURE

address: 160 Rue de Vaugirad

institute: INEM

summary: Insulin-degrading enzyme is a zinc metallo protease degrading low molecular weight substrates including insulin. Ubiquitous expression, high evolutionary conservation, upregulation of Ide in stress situations, and literature findings suggest a broader function of Ide in cell physiology and protein homeostasis that remains to be elucidated. We used proteomics and transcriptomics approaches searching for leads related to a broader role of Ide in protein homeostasis. We combined an analysis of the proteome and single-cell transcriptome of Ide+/+ and Ide-/- pancreatic islet cells with an examination of the interactome of human cytosolic Ide using proximity biotinylation. We observe an upregulation of pathways related to RNA processing, translation and splicing in Ide+/+ relative to Ide-/- islet cells. Corroborating these results and providing a potential mechanistic explanation, proximity biotinylation reveals interaction of Ide with several subunits of CCR4-NOT, a key mRNA deadenylase regulating gene expression "from birth to death". We propose a speculative model in which human and murine Ide and CCR4-NOT cooperate to control protein expression in proteotoxic and metabolic stress situations through cooperation between their deadenylase and protease functions.

overall_design: Islets were isolated and dissociated into single cell suspensions from the pancreas of 3 Ide-/- and 3 Ide+/+ C57BL/6 mice. Cell capture and cDNA library amplification were carried out using the BD Rhapsody system.

first: Barbara

last: Bertocci

first: Ayse

last: Yilmaz

first: Emmanuelle

last: Waeckel-Énée

first: Chiara

last: Guerrera

first: Kevin

last: Roger

last: Touré

first: Peter van

last: Endert


title: Chronic inflammatory stimulation of endothelial cells

city: Vienna

first: Johannes

middle: A.

last: Schmid

address: Schwarzspanierstr. 17

department: Vascular Biology and Thrombosis Research

country: Austria

institute: Med. Univ. Wien

summary: This study investigates the interplay between cellular senescence and inflammation in human umbilical vein endothelial cells (HUVECs). We employed RNA sequencing to analyze gene expression changes in HUVECs subjected to replicative- or radiation-stress-induced senescence, and compared these profiles with those of cells under acute or chronic TNFα-mediated inflammation. Our findings reveal that both senescence types exhibit significant upregulation of genes associated with epithelial- (or endothelial) mesenchymal transition (EMT) and inflammatory pathways, indicating a shared molecular response. Notably, chronic inflammation led to a pronounced EMT signature as well, while acute inflammation primarily activated classical inflammatory responses. Experimental validation confirmed reduced proliferation and increased secretion of pro-inflammatory cytokines (IL-6 and IL-8) in senescent and chronically inflamed cells and substantiated the upregulation of EMT marker genes. Additionally, we observed impaired wound healing capacity in senescent and chronically inflamed cells, highlighting the functional consequences of these cellular states. Our study underscores the critical role of inflammation in exacerbating senescence-related changes, contributing to the understanding of age-related cardiovascular pathologies. These insights may inform future therapeutic strategies aimed at mitigating the effects of aging and inflammation on endothelial function and cardiovascular health.

overall_design: RNAseq profiling of untreated ("control") and TNFα stimulated human umbilical vein endothelial cells (HUVECs) treated in two dosage regiments (5h or 9d). Experiment performed in technical triplicates.

first: Barbora

last: Belakova

first: José

last: Basílio

first: Manuel

last: Campos-Medina

first: Anna

last: F. P. Sommer

first: Ulrike

last: Resch

last: Breuss

first: Pavel

last: Uhrin

last: A. Schmid


title: Lupus nephritis serum induces changes in gene expression in human glomerular endothelial cells, which is modulated by L-sepiapterin: Implications for redox-mediated endothelial dysfunction

city: Charleston

first: Jeremy

last: Barth

state: SC

address: 173 Ashley Ave, BSB 627

institute: MUSC

summary: Lupus nephritis (LN) is characterized by renal endothelial dysfunction, which contributes to progressive kidney injury. Endothelial nitric oxide synthase (eNOS) plays a modulating role in LN, as genetic ablation of the eNOS enzyme worsens disease. Serum from patients with active LN induces uncoupling of eNOS homodimers, leading to superoxide (SO) rather than nitric oxide (NO) production by eNOS. This uncoupling is reversed with L-sepiapterin (L-Sep). This study was designed to further examine changes in gene expression in glomerular endothelial cells induced by LN serum and whether treatment with L-Sep can ameliorate these changes. Methods Primary human renal glomerular endothelial cells (HRGECs) were cultured with serum from non-lupus controls (HC), LN patients during remission (LN rem), or LN patients during flare (LN flare) with and without L-Sep. Bulk RNA sequencing was performed on RNA isolated from cultured cells. Differential gene expression was determined, and pathway and gene enrichment analyses were performed on differentially expressed genes. Results L-Sep treatment induced differential gene expression after culture in HRGECs cultured with LN flare serum. Addition of L-Sep induced genes involved in promoting endothelial function and  enriched for pathways of NO biosynthetic and metabolic processes, fatty acid and lipid biosynthesis, neurotransmitter biosynthesis, reactive oxygen biosynthesis, vascular endothelial growth factor production, and regulation of smooth muscle contraction. Conclusions These results indicate that glomerular endothelial cells can mount an active inflammatory response in an LN serum environment. More importantly, L-Sep modulates gene expression in a fashion consistent with reduction of oxidative stress and increased NO production. These findings provide the rationale to target endothelial dysfunction to modulate LN with L-Sep as a therapeutic.

overall_design: RNAseq profiling of human renal glomerular endothelial cells cultured with serum from non-lupus controls (HC) and from LN patients during flare (LN flare) with and without L-Sep

first: James

last: Oates

first: Dayvia

middle: L

last: Russell

first: Justin

last: Van Beusecum

first: Margaret

last: Markiewicz

first: Sandra

middle: G

last: Mungaray


title: Engrafted hPSC-Derived Nitrergic Neurons Improve Gut Dysmotility in Mice

city: San Francisco

first: Faranak

last: Fattahi

state: California

department: Cellular and Molecular Pharmacology

institute: University of California San Francisco

summary: We used bulk RNA-seq to compare gene expression profiles of nitrergic (NO) neurons vs other neurons in control hPSC-derived ENS cultures vs cultures that were enriched in NO nuerons by treating their progenitors with PP121.

overall_design: Using H9 NOS1::GFP resporter hPSC cells, we generated enteric nervous system (ENS) cultures treated with or without PP121 which was identified to enriched nitrergic (NO, NOS1+) neruons. We then sorted the neruons (CD24+ cells) into NO (GFP+) vs other (GFP-) and performed bulk RNA-sequencing.

last: Barber

first: Johnny

last: Yu

first: Homa

last: Majd

first: Matvei

last: Khoroshkin

first: Ryan

last: Samuel

first: Hani

last: Goodarzi


title: PTP4A1 alleviates angiotensin II-induced aortic aneurysmal lesions by regulating immature mural neovascularisation

city: ulsan

first: JooChan

last: Lee

state: Gyeongsangbuk-do

address: 0, UNIST-gil, Eonyang-eup, Ulju-gun, Ulsan, Republic of Korea

institute: UNIST

summary: RNA-seq analysis of human endothelial cells overexpressing PTP4A1 and treated with Angiotensin II revealed transcriptional programs involved in angiogenesis and vascular stabilization. Libraries were prepared using QuantSeq 3′ mRNA-Seq and sequenced on Illumina NovaSeq.

overall_design: Human endothelial cells (huECs) were transduced with PTP4A1 or control lentivirus, stimulated with Ang II (1 µM, 24h), and RNA was extracted. Strand-specific libraries were prepared using Lexogen QuantSeq 3′ mRNA-Seq Kit and sequenced with Illumina NovaSeq. Reads were aligned to GRCh38 using STAR and analyzed for DEGs using ExDEGA.

first: Min

last: J Cho

first: Byung

last: T Hwang

first: Joo

last: C Lee

first: Jeong

last: K Min

first: Sung

last: H Park

first: Jong

last: G Park


title: MG53-PPARα Drives Stem Cell Differentiation Easing Intestinal Injury and Inflammation

city: hangzhou

first: Yumeng

last: Pei

state: zhejiang

address: Xihu district Zhuan Tang street

institute: Zhejiang university

summary: Emerging evidence suggests that priming intestinal stem cell (ISC) lineages towards secretory progenitor cells is beneficial for maintaining gut homeostasis against inflammatory bowel disease (IBD). However, the mechanism driving such biased lineage commitment remains elusive. Here we show that MG53, also named as TRIM72, plays and important role in maintaining intestinal epithelium integrity against various insults-induced IBD. Specifically, MG53 deficiency leads to exacerbated IBD manifestations caused by various injuries in mice, whereas MG53 overexpression in ISCs is sufficient to ameliorate intestinal damage.

overall_design: Isolated the intestinal epithelial cells from MG53-TG and WT mice by flow cytometry, on day 7 after 2.5% DSS treatment, and conducted single cell sequncing

first: Meng

last: Fang

first: Xinli

last: Hu

first: Rui-Ping

last: Xiao


title: Repurposing the Memory-promoting Meclofenoxate Hydrochloride as a Treatment for Parkinson’s Disease through Integrative Multi-omics analysis

city: Guangzhou

first: Huasong

last: Zhang

state: Guangdong

address: 63 Duobao Road, Liwan District, Guangzhou

institute: The Third Affiliated Hospital, Guangzhou Medical University

summary: Parkinson’s disease (PD) is a devastating neurodegenerative disorder with growing prevalence worldwide and, as yet, no effective treatment. Drug repurposing is invaluable for detecting novel PD therapeutics. Here, we compiled gene expression data from 1,231 healthy human brain samples and 357 samples across tissues, ethnicities, brain regions, Braak stages, and disease status. By integrating them with multiple-source genomic data, we found a PD-associated gene co-expression module, and its alignment with the CMAP database successfully identified drug candidates. Among these, meclofenoxate hydrochloride (MH) and sodium phenylbutyrate (SP) are indicated to be able to prevent mitochondria destruction, reduce lipid peroxidation and protect dopamine synthesis. MH was validated to prevent the neuronal death and synaptic damage, improve motor function, and reduce anhedonic and depressive-like behaviors of PD mice. The interaction of MH with a PD-related protein, sigma1 was confirmed experimentally. Thus, our findings support MH potentially ameliorating PD by interacting with sigma1.

overall_design: To explore drug repurposing for Parkinson's Disease (PD), we developed a computational framework called iGOLD, which integrates multi-source genomic data with gene co-expression modules (Figure 1). This framework (available at https://github.com/fanc232CO/iGOLD_pipline) was used to identify gene co-expression modules affected by PD-related genes and SNPs. We evaluated the gene co-expression modules that were significantly enriched in PD-associated genes and SNPs through conservation analysis using seven gene expression datasets spanning various ethnicities, brain regions, tissues, Braak stages, and PD disease status. The highly conserved modules were then utilized for drug discovery. Subsequent experiments involved rotenone-induced primary neuronal cells and a mouse model to assess the efficacy of the identified drugs in promoting neuronal survival, enhancing hippocampal function, and modifying PD-related behaviors.

first: Cong

last: Fan

first: Huiying

last: Zhao


title: Ventral hippocampus neurons encode meal-related memory

city: Philadelphia

first: Benjamin

middle: C.

last: Reiner

state: PA

address: 125 S 31st St

institute: University of Pennsylvania

summary: We performed single nuclei transcriptomics of ventral hippocampus from rats that were food deprived for 24 hours, offered a 30 minute feeding or fast, and then sacrificed 90 minutes later.

overall_design: Fresh frozen postmortem rat ventral hippocampus samples were used to generate single nuclei suspensions and the nuclei were processed for the 10x Genomics 3' gene expression assay v3.1.

first: Richard

last: Crist