title: Thre impact of Akkermansia muciniphila on Group B Streptococcus gene expression during infection of human vaginal epithelial cells.

city: Aurora

first: Kelly

middle: S.

last: Doran

department: Immunology and Microbiology

institute: University of Colorado Anschutz Medical Campus

summary: Group B Streptococcus (GBS) is an opportunistic pathogen that colonizes the vaginal tract and can be transmitted to the fetus or newborn resulting in infection. Previously we identified that Akkermansia muciniphila alters the dynamics of GBS vaginal colonization. Here we determine that A. muciniphila promotes GBS aggregation and attachment to human vaginal epithelial cells (hVECs). RNA-sequencing analysis revealed that A. muciniphila changed expression of 258 unique GBS genes during hVEC colonization, with many involved in cell wall/membrane/envelope biogenesis. We demonstrate that A. muciniphila-mediated increases in GBS aggregation and attachment to hVECs are dependent on GBS capsule and pili, respectively. Lastly, we found that A. muciniphila promoted GBS aggregation in the murine vaginal lumen and continual treatment with A. muciniphila reduced GBS vaginal persistence. Our results highlight the dynamic impact of a commensal organism on GBS colonization, as well as demonstrate the probiotic potential of A. muciniphila in the vaginal environment.

sample_organism:
Streptococcus agalactiae
Homo sapiens
Akkermansia muciniphila

overall_design: RNA-seq profile of Streptococcus agalactiae or Group B Streptococcus  (Strain: COH1) during mono- and co-infection of human vaginal epithelial cells.

first: Stephanie

last: Marroquin

first: Shirli

last: Cohen

first: Melody

middle: N

last: Neely

middle: S


title: Widespread Cap-Unmethylated mRNAs Revealed by Metabolic Stress

status: Public on Apr 15 2026

city: Dallas

first: Zheng

last: Xing

state: TX

address: 5323 Harry Hines Blvd.

country: USA

institute: UT Southwestern

type: Expression profiling by high throughput sequencing

summary: RNA polymerase II transcripts are capped with N7-methylguanosine (m⁷G), a conserved modification essential for mRNA function. Although traditionally viewed as constitutive, we developed a mass spectrometry-based method to demonstrate that in both yeast and mammalian cells, a substantial population of mRNAs lack cap methylation in response to SAM-limiting conditions. Through developing two transcriptome-wide approaches, we found that methylation is enriched on specific transcripts and uncovered an unexpected connection between histone H3K36me3 and cap methylation. Remarkably, cap-unmethylated mRNAs exhibit features of canonical mRNAs—they are polyadenylated, exported to the cytosol, and translated. Enforced cap methylation reduces cell growth under SAM limitation, suggesting that unmethylated mRNAs confer an adaptive advantage during stress. These findings reveal mRNA cap methylation as a dynamic, regulated modification and a previously underappreciated layer of gene expression control.

overall_design: RNA-sequencing of input and m7G-IP samples from S. cerevisiae (CEN.PK) grown in rich (YPL) medium and after 1h switch to minimal medium (SL), with two biological replicates each.

first: Anna

middle: V

last: Freitas

first: Benjamin

middle: M

last: Sutter

first: Ngoc-Khoi

last: Dang

first: Nicholas

middle: T

last: Ingolia

middle: P

last: Tu


title: The differentially expressed genes after overexpression of TYMP in HaCaT cells

city: Shiyan

first: Qin

last: Shanshan

address: Renmin Road 30, Maojian District

country: China

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

summary: This study aimed to explore the downstream signal pathways by TYMP in keratinocyte hyperproliferation.

overall_design: The HaCaT cells were seeded into 6-well plates and were transfected with stable overexpression-lentivirus to estabilish TYMP overexpression cell lines. The differentally expressed genes by TYMP overexpression were screened by RNA sequencing. The transcriptome sequencing studies were performed by deep sequencing, using Illumina NovaSeq 6000.

first: Shanshan

last: Qin

first: Dandan

last: Li


title: Cohesin-mediated loop extrusion and enhancer-associated factors additively contribute to Sox2 looping with its distal enhancer.

city: Amsterdam

first: Elzo

last: de Wit

address: Plesmanlaan 121

country: Netherlands

institute: Netherlands Cancer Institute

type: Genome binding/occupancy profiling by high throughput sequencing

type: Methylation profiling by high throughput sequencing

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

overall_design: Refer to individual Series


title: Cohesin-mediated loop extrusion and enhancer-associated factors additively contribute to Sox2 looping with its distal enhancer [TT-seq]

summary: Sox2 expression is regulated by a distal enhancer cluster known as the Sox2 Control Region (SCR). Although Sox2 and the SCR exhibit strong interactions in chromosome conformation capture experiments, acute depletion of cohesin only mildly affects Sox2 transcription. Here we show that continuous loop extrusion, but not stalling of cohesin at CTCF sites is involved in the maintenance of the Sox2-SCR loop. While depletion of cohesin or CTCF has only a mild impact on Sox2 gene expression, stabilizing cohesin on the DNA by depleting the cohesin release factor WAPL results in a rapid decrease in expression. Furthermore, using genome editing we show that a weak enhancer located downstream from the Sox2 gene renders Sox2 expression insensitive to the loss of cohesin stalling at CTCF sites. Finally, through targeted and pleiotropic inhibition of the SCR we demonstrate that the Sox2-SCR loop is a multi-component system that depends on cohesin-mediated loop extrusion and enhancer-associated factors. Together, our findings highlight the intricate interplay between enhancer activity and loop extrusion in the establishment and maintenance of chromatin loops in the Sox2 locus.

overall_design: TT-seq was performed on sorted Sox2 SCR 129/CAST F1 hybrid methylation reporter populations (Song et al. 2019) based on which allele the SCR is methylated (DP = unmethylated on both alleles, GFP = unmethylated CAST, RFP = unmethylated 129).

first: Moreno

last: Martinovic

first: Koen

middle: D

last: Flach

first: Hans

last: Teunissen


title: Cohesin-mediated loop extrusion and enhancer-associated factors additively contribute to Sox2 looping with its distal enhancer [ATAC-seq]

overall_design: ATAC-seq was performed on sorted Sox2 SCR 129/CAST F1 hybrid methylation reporter populations (Song et al. 2019) based on which allele the SCR is methylated (DP = unmethylated on both alleles, GFP = unmethylated CAST, RFP = unmethylated 129).

first: Michela

last: Maresca


title: Variant U1 snRNAs contribute to cell cycle and differentiation control of human iPS cells

city: Göttingen

first: Argyris

last: Papantonis

address: Robert-Koch-Str. 40

department: Institute of Pathology

country: Germany

institute: University Medical Center Göttingen

summary: Maintenance of stem cell identity as well as differentiation of stem cells into the various lineages requires intricate regulation of gene expression. Despite intensive research, our understanding of these regulatory networks remains incomplete. Here, we focus on the understudied paralogs of the U1 small nuclear RNA (snRNA) gene known as variant U1 (vU1) snRNAs. By generating isogenic knockout lines of human induced pluripotent stem cells for two different vU1s, we show that their loss profoundly changes both hiPSC gene expression and cell cycle profiles. These changes appear to manifest at the level of alternative splicing choices, including those at recursive splicing sites, and lead to the differential availability of stem cell regulators. Together, our results shed new light on the function of vU1 snRNAs and further our understanding of the programs controlling human pluripotency.

overall_design: We generated the two CRISPR-knockout hiPSc lines of vU1.3 and vU1.8 snRNA genes, sequenced their transcriptomes, and quantified differential gene expression, alternative and recursive splicing. We also immunoprecipitated RNAs interacting with either the vU1.8 or the vU1.3 snRNA (stabilised via crosslinking), followed by total RNA-seq.

first: Yajie

last: Zhu

first: Konstantinos

last: Sofiadis


title: Cohesin-mediated loop extrusion and enhancer-associated factors additively contribute to Sox2 looping with its distal enhancer [4C-Seq]

overall_design: High-resolution 4C-seq was performed on AID-tagged (RAD21, CTCF, WAPL, WAPL/CTCF) cell lines, RAD21-FKBP cell lines with and without BET inhibitors, and sorted Sox2 SCR 129/CAST F1 hybrid methylation reporter populations (Song et al. 2019) based on which allele the SCR is methylated (DP = unmethylated on both alleles, GFP = unmethylated CAST, RFP = unmethylated 129). DpnII and Csp6I (NEB) were used as the primary and secondary restriction enzymes respectively. For allele-resolved 4C-seq in SCR methylation populations, a reverse reading primer that amplifies a single nucleotide variant was used.


title: PGC-1alpha pathway dysregulation disrupts myofiber specification in a mouse model of SBMA [ChIP-Seq]

city: Ann Arbor

first: Andrew

last: Lieberman

state: MI

address: 1150 W Medical Center Dr.

institute: University of Michigan

summary: Skeletal muscle pathology is a critical but poorly understood contributor to neuromuscular degeneration in spinal and bulbar muscular atrophy (SBMA), a CAG/polyglutamine (polyQ) expansion disorder caused by mutation in the androgen receptor (AR). Using a gene-targeted SBMA mouse model, we applied single-nucleus RNA sequencing to identify a previously unrecognized, disease-specific population of skeletal muscle myonuclei that replace normal myonuclear subtypes. This transition was driven by dysregulation of the PGC-1α pathway, a central regulator of myofiber specification and metabolic identity. PGC-1α dysfunction in SBMA muscle was age-, hormone-, and polyQ length–dependent and was partially rescued by subcutaneous delivery of AR-targeted antisense oligonucleotides. Integrated ChIP-seq and RNA-seq analyses revealed that aberrant PGC-1α activity promoted the expression of a distinct set of myofiber specification genes while downregulating those defining healthy Type IIb and Type IIx myonuclei. We propose a model in which this dysfunction arose downstream of polyQ-mediated sequestration of PGC-1α cofactors MEF2, CREB, and CBP, leading to transcriptional reprogramming and cellular dysfunction. These findings implicate PGC-1α dysregulation as a key event linking AR polyQ expansion to skeletal muscle degeneration and suggest a shared mechanism for polyQ-mediated muscle pathology across related neurodegenerative diseases.

overall_design: Chromatin was extracted from pooled tibialis anterior, totaling 200 mg per genotype, from WT and AR113Q. This was then immunoprecipitated with an antibody against PGC-1alpha (Novus NBP1-04676) and peaks were identified by ChIP-seq.

first: Curtis

middle: J

last: Kuo

first: Laura

middle: B

last: Chopp

first: Zhigang

last: Yu

first: Luhan

last: Ni

first: Hien

last: Zhao

first: Janghoo

last: Lim


title: PGC-1alpha pathway dysregulation disrupts myofiber specification in a mouse model of SBMA [AR113Q RNA-Seq]

overall_design: RNA from tibialis anterior was extracted and sequenced from mice at 5, 26, or 52 weeks comparing WT and AR113Q knock-in tissue at each age. For the 52 week cohort, an additional included group of AR113Q mice received weekly subcutaneous injections of an anti-sense oligonucleotide directed against AR starting at 26 weeks.


title: Single-cell profiling reveals RAB13+ endothelial cells and profibrotic mesenchymal cells in aged human bone marrow

city: Pamplona

first: Itziar

last: Cenzano

state: Navarra

address: Avenida de Pio XII, 55

country: Spain

institute: CIMA Universidad de Navarra

summary: The bone marrow (BM) microenvironment plays a crucial role in regulating hematopoiesis, yet the molecular changes associated with aging in humans remain poorly understood. Using single-cell RNA sequencing, we uncovered transcriptional shifts in BM endothelial cells (EC) and mesenchymal stem cells (MSC) during aging. Aged sinusoidal EC exhibited a prothrombotic phenotype with compromised mitochondrial and vascular function. Additionally, we identified a novel arterial EC subset, emerging in aged individuals, characterized by RAB13 expression and associated with transcriptional regulatory processes. MSC from aged subjects displayed impaired matrix remodeling and epithelial-mesenchymal transition, driven partly by a subpopulation of THY1+ profibrotic cells absent in younger individuals. Finally, immunofluorescent imaging and spatial transcriptomics confirmed the presence of these aging-associated cells in BM samples from aged individuals. In summary, this work provides a comprehensive view of the transcriptional landscape, cellular interactions, and spatial organization of aged EC and MSC, offering novel insights and potential targets that could be exploited for preventing age-associated changes in humans.

overall_design: We performed single-cell RNA sequencing (scRNA-seq) on prospectively isolated endothelial cells (EC) and mesenchymal stromal cells (MSC) from bone marrow (BM) samples of healthy young (28–48 years) and aged (58–79 years) donors of both sexes undergoing orthopedic surgery.

first: Felipe

last: Prosper


title: Mutation of Tubgcp6 induces hematopoietic stem and progenitor cell exhaustion in zebrafish

city: Guangzhou

first: Zhibin

last: Huang

state: Guangdong Province

address: 382 Waihuan E Rd, Panyu District

department: School of Medicine

institute: South China University of Technology

summary: Hematopoietic stem and progenitor cells (HSPCs) sustain blood cell production by balancing self-renewal and differentiation. While regulatory networks of transcription factors are well established during development of these cells, intrinsic cytoskeletal elements remain unclear. Here we show that the gamma-tubulin ring complex (γ-TuRC), a key regulator of microtubule nucleation, is essential for HSPC expansion in zebrafish. Forward genetic screening identifies the zebrafish smu1347 mutant, which exhibits HSPC exhaustion during definitive hematopoiesis. Positional cloning reveals a nonsense mutation in the tubgcp6 gene, encoding a core component of γ-TuRC, as responsible for the smu1347 phenotype. Mutation of Tubgcp6 causes mitotic arrest, disorganized spindle formation, and increased p53-dependent apoptosis. Time-lapse imaging and lineage tracing further demonstrate that Tubgcp6-deficient HSPCs preferentially undergo symmetric differentiation rather than self-renewal. Disrupting other γ-TuRC subunits (Tubgcp3, Tubgcp4, Tubgcp5) produces similar hematopoietic defects, underscoring the importance of intact microtubule nucleation for stem cell maintenance. These findings identify γ-TuRC-mediated microtubule organization as a critical regulator of HSPC fate and suggest that Tubgcp6 may represent a potential therapeutic target for bone marrow failure syndromes and stem cell exhaustion disorders.

overall_design: RNA-seq analysis of sibling and tubgcp6 mutant zebrafish embryos .

first: Yuxian

last: Zhang

first: Li

last: Li

first: Wei

last: Liu

first: Wenqing


title: NEAT1-driven ceRNA network in multiple myeloma

city: MILAN

first: Luca

last: Agnelli

address: Venezian 1

department: Department of Advanced Diagnostics

country: Italy

institute: IRCCS Istituto Nazionale dei Tumori

summary: The lncRNA NEAT1 is overexpressed in multiple myeloma (MM) plasma cells and plays a key role in MM pathogenesis. NEAT1 is involved in ceRNA network in several cancers; however, data in MM are virtually absent. This study identified a NEAT1-driven ceRNA network involving 96 miRNAs and 40 target genes, selected as concurrently downregulated in NEAT1-KD AMO1 cells and upregulated in NEAT1-overexpressing AMO1 cells (AMO1-OVX). The co-expression of NEAT1 and the targets was validated in MM patients (GSE116294, GSE13591, GSE6477, CoMMpass), and in NEAT1-KD NCI-H929, LP1, and KMS27 cell lines, showing for all targets a consistent downregulation, resembling that of NEAT1. The functional implication of the ceRNA network was explored by functional enrichment analyses of the 40 targets, identifying 78 significant gene sets, 17 of which found significantly enriched by GSEA analysis in at least one experimental condition among NEAT1-KD LP1, NCI-H929, and KMS27 cells, AMO1-OVX cells, or the extreme quartiles of NEAT1 expression in the CoMMpass dataset. Noteworthy, the cell cycle gene set was validated in 5 out of 6 conditions tested, suggesting that in MM the impact of NEAT1 upregulation on the cell cycle, experimentally demonstrated in our earlier publications, may be attributable, at least partially, to ceRNA mechanisms.

overall_design: AMO1, LP1, and NCI-H929 human multiple myeloma cell lines were silenced for NEAT1 expression by the use of specific Gapmers. Global transcript expression was investigated by RNA sequencing analyses, comparing data from NEAT1-KD cell lines with the relative control condition (SCRgapmer) at 48 days.

first: Domenica

last: Ronchetti

first: Valentina

last: Traini

first: Ilaria

last: Silvestris

first: Giuseppina

last: Fabbiano

first: Andrea

last: Devecchi

first: Federica

last: Torricelli

first: Noemi

last: Puccio

last: Craparotta

first: Marco

last: Bolis

first: Roberto

last: Piva

first: Antonino

last: Neri

first: Francesco

last: Passamonti

first: Niccolò

last: Bolli

first: Elisa

last: Taiana


title: Folate Receptor Beta Regulates Macrophage NLRP3 Inflammasome Activation and Pyroptosis in a Folate-Independent Manner

city: Indianapolis

first: David

last: Aronoff

state: Indiana

address: 545 Barnhill Dr. EH 305

department: Department of Medicine

institute: Indiana University School of Medicine

summary: Folate receptor beta (FRb), encoded by FOLR2, is selectively expressed in monocytes and macrophages, yet its function in innate immune signaling remains poorly defined. Here, we identify FRb as a novel regulator of NLRP3 inflammasome activation and pyroptosis in human THP-1 macrophages. Using CRISPR/Cas9-mediated gene deletion, we show that loss of FOLR2 impairs caspase-1 activation, gasdermin D cleavage, and IL-1b release in response to multiple NLRP3 stimuli, without altering pro-IL-1 b induction. These defects were not rescued by exogenous folate and were independent of extracellular folate concentrations. Mechanistically, FOLR2 deletion reduced potassium efflux and downregulated multiple potassium channel genes. Single-cell RNA sequencing revealed broad transcriptional repression in FRb-deficient macrophages, including genes involved in inflammasome signaling and ion transport. Genome-wide methylation profiling showed increased CpG hypermethylation in FOLR2-deficient cells, consistent with reduced transcriptional activity. Our findings indicate that FRb promotes NLRP3 activation in a folate-independent manner by regulating transcription and K⁺ efflux in macrophages. These data reveal a previously unrecognized immunoregulatory role for FRb with implications for host defense, autoimmunity, and macrophage function in tissue microenvironments such as the tumor or placenta.

overall_design: Following treatment with phorbol 12 myristate 13 acetate (PMA) THP-1 WT or FOLR2 KO cells were rested at 37C for 24 hours. Cells were then harvested from tissue culture flasks, removed dead cells with magnetic bead based separation and fixed according to 10x Genomics FLEX protocol. Cells were then submitted for scRNA-seq.

first: Lisa

last: Rogers

first: Kyle

last: Firestone

first: Riya

last: Chinni

first: Anna

middle: C

last: Branco

first: Kayla

last: Wrobleski

first: Teresa

last: Chou

first: Jeffery

middle: A

last: Goldstein

first: Xiaoping

last: Gu

first: Emily

last: Mason

first: Shaoyou

last: Chu

first: Michael

last: Rubart-von der Lohe

first: Philip

last: Low


title: RNA-seq of liver biopsies from patients with pediatric autoimmune liver disease

city: Cincinnati

first: Yunguan

last: Wang

state: oh

address: 3333 Burnet Avenue

institute: Cincinnati Children's Hospital Medical Center

summary: Background: Primary sclerosing cholangitis (PSC) is an autoimmune, cholestatic liver disease characterized by inflammation and fibrosis surrounding interlobular bile ducts. The cellular composition and cell-cell-communications driving periductal fibrosis remain ill defined.

overall_design: Paired-end, 50 million read, RNA-seq was performed on cryopreserved whole liver tissue samples from diagnostic liver biopsies (PSC, n= 34; autoimmune hepatitis [AIH], n=30).

first: Alexander

middle: G

last: Mietheke


title: A lncRNA drives developmentally-timed decay of all members an essential microRNA family

city: Bethesda

first: Katherine

last: McJunkin

state: Maryland

address: 50 South Dr, Building 50 Room 3148

institute: NIDDK/ NIH

type: Non-coding RNA profiling by high throughput sequencing

summary: The spatiotemporal expression patterns of microRNAs (miRNAs) are crucial to their function. Target-directed miRNA degradation (TDMD) is an emerging regulatory module that contributes to these expression patterns wherein a specialized RNA (TDMD trigger) drives miRNA decay through base pairing and resulting recruitment of E3 ubiquitin ligase ZSWIM8/EBAX-1. Here we show a long noncoding RNA, tts-2, drives developmentally-timed TDMD of mir-35-42, representing a large-scale resetting of the miRNA pool at the end of embryogenesis in C. elegans. While extensive base pairing to the miRNA seed and 3′ end was thought to be the distinguishing feature of TDMD triggers, a single site in tts-2 drives decay of mir-35-42 through base pairing to the seed region. A second unusual site supports decay of mir-38 with incomplete seed complementarity. The relaxed base pairing requirements of tts-2-induced TDMD demonstrate that alternative cues – not just extensive miRNA 3′ end pairing – can license transcripts to drive TDMD.

overall_design:
small RNA sequencing performed using NEBNext small RNA kit followed with size selection in different mutants of C.elegans.
RNA-sequencing of chimeric eCLIP libraries prepared from C. elegans embryos.

first: Acadia

middle: L

last: Grimme

first: Lu

last: Li

first: Alyshia

last: Scholl

first: Bridget

middle: F

last: Donnelly

first: Neha

last: Channamraju

first: Karl-Frédéric

last: Vieux

first: Lecong

last: Zhou

first: Geraldine

last: Seydoux

first: Mingyi

last: Xie


title: Cohesin-mediated loop extrusion and enhancer-associated factors additively contribute to Sox2 looping with its distal enhancer [Bisulfite-Seq]

first: Elzo

last: de Wit

overall_design: Bisulfite conversion and sequencing was performed on sorted Sox2 SCR 129/CAST F1 hybrid methylation reporter populations (Song et al. 2019) based on which allele the SCR is methylated (DP = unmethylated on both alleles, GFP = unmethylated CAST, RFP = unmethylated 129).

first: Moreno

last: Martinovic

first: Koen

last: Flach


title: Time-course transcriptomes from shoot apex and leaves of Arabidopsis thaliana

city: La Jolla

first: Jose

middle: Luis

last: Pruneda-Paz

state: CA

address: 9500 Gilman Dr Biology #3125 Biology #3125

department: Cell and Developmental Biology

institute: University of California San Diego

summary: The circadian clock optimizes fitness across diverse life forms by synchronizing physiological and behavioral rhythms with daily environmental cycles. In multicellular organisms, clock-controlled rhythms differ across tissues and organs; however, the molecular mechanisms that regulate this spatial specificity are not fully understood. Here, we compare circadian transcriptomes from the shoot apex and leaves of Arabidopsis thaliana and reveal that, despite sharing a common core clock composition, these two organs exhibit striking differences in their rhythmic gene expression landscapes. Notably, rhythmic genes in the shoot apex tend to peak earlier than in leaves, mirroring the phase difference observed in core clock gene expression between the two organs. Our findings suggest that while organ-specific rhythmic gene sets are established independently of core clock transcript levels, their peak expression is governed by the phase of core clock transcript oscillations in each organ.

overall_design: Shoot apex and true leaf samples from Arabidopsis thaliana plants grown under free runing conditions (constant light, ~60 μmol m-2 s-1) after entrainment under 12 hours light (~100 μmol m-2 s-1)/12 hours dark cycles for 14 days. Samples were collected 90, 94, 98, 102, 106, and 110 hours after transfer to the free running condition from two independent experiments.

first: Nicholas

last: Deason

first: Zheng

first: Peiyun

last: Chen

first: Neeraja

last: Vegesna

first: Julie

last: Law

first: Colleen

last: Doherty

first: José


title: Editing of the of the gene model underlying the major protein quantitative trait loci (QTL), cqSeed protein-003, and its paralog in soybean

city: Lincoln

first: Chi

last: Zhang

state: NE

address: 1901 Vine Street

institute: University of Nebraska - Lincoln

summary: A major seed protein quantitative trait locus (QTL) in soybean resides on chromosome 20, cqSeed protein-003, which was recently mapped to gene model Glyma.20G085100 (Gm20P), with its paralog present on chromosome 10, Glyma.10G134400 (Gm10P). To gain insight into how Gm20P and GM10P influence seed reserve content in the crop, genome editing reagents were designed to create null mutations in both Gm20P and Gm10P. Two soybean lines were identified and characterized, possessing INDELs in Gm10P and Gm20P, and lacking editing reagents. One is a gm20p mutant, and the other is a gm10p gm20p double mutant. Seed protein content of the gm10p gm20p double mutant was significantly lower relative to the gm20p mutant and wildtype, with a concomitant increase in oil and starch content. A delayed maturity phenotype was observed in the single and dual edited lines under field settings across multiple environments. The delay in maturity phenotype was influenced by day length, wherein under a short-day environment, the delay mirrored what was observed under field conditions, while under a long-day environment, no delay in maturity was observed, but changes in growth were detected in the double mutant line. Transcriptomic analysis revealed repression of genes involved in light signaling and enhanced expression of JAZs alleles that repress JA signaling, suppression of ABA-responsive genes and senescence-related genes, and elevation of genes that inhibit IAA signaling in the gm10p gm20p double mutant. The status of a wide range of downstream transporter genes for transport of hormones, metabolites, heavy metals, and essential nutrients, nitrogen (N) and phosphorus (P), was significantly reformed as a result of altered interactions of light-phytohormone signaling in the double mutant. Furthermore, the double null mutant displayed higher sensitivity to salt and ABA during germination. These results suggest that both Gm10P and Gm20P alleles modulate light signaling, which in turn impacts soybean development, maturity, and seed reserve content.

overall_design: Differetial analysis of mRNA expression profiles in the transgenic soybeans  and the wildtype soybeans

first: Ming

last: Guo

first: Thomas

last: Clemente


title: Bisphenols exposure induces bone loss and osteoporosis by binding to and activating the endocannabin

city: Jackson

first: Bioinformatics

last: Core

state: MISSISSIPPI

address: 2500 N state street

institute: Molecular and Genomics Core Facility

summary: Osteoporosis (OP) affects over 200 million people worldwide. It is anticipated that 33% of women and 20% of men will be diagnosed in their lifetime, and those numbers are expected to rise. There is no efficient cure for osteoporosis, and all the direct causes have not yet been determined. However, a common class of xenoestrogens called bisphenols may be linked to this disease. Bisphenols are a group of endocrine disrupters commonly used in plastic food containers, baby bottles, children’s toys, and electronics. Bisphenol A (BPA) has been found to inhibit bone growth in vivo. However, the exact mechanism of action, and the pathways involved with inhibiting bone growth, have not been identified. Bone growth has been found to be connected to the endocannabinoid system through cannabinoid receptor 1 (CB1) and 2 (CB2). Our findings demonstrate that there is an additive effect between bisphenols A (BPA), S (BPS), or tetrabromobisphenol A (TBBA) and the cannabinoid pathway that reduces osteoblast number and bone calcification. Since the endocannabinoid pathway is known to regulate tissues, organs and systems throughout the body, this interaction demonstrates a greater need to study the effects of these safer alternatives on embryonic development in relation to the endocannabinoid system. Additionally, we found that activation of trpv1 occurred, but the negative impact on bone formation is linked to downregulation of apoa1b, apoa2, and ucp-1 as well as, dysregulated collagen synthesis, and ribosomal protein changes. Downregulation of apoa1 causes decreased expression of ucp-1 and subsequent inflammation in bone tissues, and dysregulated collagen synthesis Furthermore, RNA-seq demonstrated increased expression of over 30 genes linked to increased osteoclastogenesis, and bone resorption.

overall_design: Animal husbandry guidelines for all zebrafish studies were designed, reviewed and approved by the Institutional Animal Care and Use Committee (IACUC) of the University of Mississippi Medical Center (IACUC #: 2024-1362). In accordance with IUCUC standardized protocols, embryos generated from the AB wildtype, CB1 receptor knockout (CB1-KO), CB2 receptor knockout (CB12-KO) (Liu et al., 2016) and sp7-eGFP transgenic zebrafish (DeLaurier et al., 2010) strains were raised in E3 medium under at 28.5°C. WIN 55,212-2 (WIN), bisphenol A (BPA), bisphenol S (BPS), and 3,3’,5,5’-tetrabromobisphenol A (TBBPA) were dissolved in dimethyl sulfoxide (DMSO) in a stock solution of 10 mM. BPA, BPS and TBBPA were further diluted to 10 μM as an intermediate stock solution. Both the 10 mM and 10 μM solutions were stored at -20°C. Embryos were placed into 25 mL of E3 media in 50 mL tubes. Appropriate chemical volumes were added directly into the medium to get exposure concentrations of 120 or 200 nM for each bisphenol, and 108 or 180 nM for WIN. Additionally, suboptimal co-treatments of each bisphenol (120 nM) and WIN (108 nM) were used as well. Next, the embryos were placed back into the 28.5 °C incubator until time of fixation.

first: Matthew

last: Dubuisson

first: Carol

middle: K

last: Cox

first: Jasleen

last: Kaur

first: Mclean

middle: H

last: Williamson

first: Wilson

last: Clements

first: Madelyn

last: Logan

first: Jerry

last: Monroe

first: Yann

last: Gibert


title: DCPS modulates TDP-43 mediated neurodegeneration through P-body regulation [RNA-seq]

city: Baltimore

first: Shuying

last: Sun

state: MD

address: Hunterian 205

department: Physiology

institute: jhmi

summary: The proteinopathy of the RNA-binding protein TDP-43, characterized by nuclear clearance and cytoplasmic inclusion, is a hallmark of multiple neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer’s disease (AD). Through CRISPR interference (CRISPRi) screening in human neurons, we identified the decapping enzyme scavenger (DCPS) as a novel genetic modifier of TDP-43 loss-of-function (LOF)-mediated neurotoxicity. Our findings reveal that TDP-43 LOF leads to aberrant mRNA degradation, via disrupting the properties and function of processing bodies (P-bodies). TDP-43 interacts with P-body component proteins, potentially influencing their dynamic equilibrium and assembly into ribonucleoprotein (RNP) granules. Reducing DCPS restores P-body integrity and RNA turnover, ultimately improving neuronal survival. Overall, this study highlights a novel role of TDP-43 in RNA processing through P-body regulation and identifies DCPS as a potential therapeutic target for TDP-43 proteinopathy-related neurodegenerative diseases.

overall_design: RNA-seq profile and RNA half-life profiles of control (shCTR shCTR) i3Neurons and knockdown (shTDP-43 shCTR, shTDP-43 shDCPS) i3Neurons on differentiation day 14.

first: Yingzhi

last: Ye

first: Yu

last: Xiao


title: PGC-1alpha pathway dysregulation disrupts myofiber specification in a mouse model of SBMA [snRNA-Seq]

first: Andrew

last: Lieberman

overall_design: Nuclei were extracted from tibialis anterior (skeletal muscle) of 52-week WT or AR113Q male mice using the 10X Chromium Nuclei Isolation kit, for comparison of gene expression at the single nucleus level using the 10X Genomics platform.

first: Curtis

last: Kuo

first: Laura

last: Chopp

first: Zhigang

last: Yu

first: Luhan

last: Ni

first: Hien

last: Zhao

first: Janghoo

last: Lim


title: A lipid metabolism defect is an underlying contributor to Diamond Blackfan anemia syndrome

first: Kaiwen

last: Deng

state: Michigan

address: 3305 NCRC Building 520

summary: Analysis of neither Diamond Blackfan anemia syndrome (DBAS) cohorts nor animal models has revealed a potential mechanism for the variable anemia phenotype, a key feature of this disease. Here, we utilized an established Rpl5Skax23-Jus/+ murine DBAS model in order to study this dynamic erythropoiesis deficiency. These haploinsufficient mice exhibit variably penetrant craniofacial and cardiac defects mimicking the phenotypes of DBAS patients bearing RPL5 mutations. We additionally discovered that this specific heterozygous splicing mutation is pathogenic and leads to intron retention. By examining the transcriptome of fetal liver erythroid progenitors at E12.5, we demonstrate that the downregulation of erythroid differentiation pathways is consistent with the DBAS phenotype. We also identified dysregulation of lipid metabolism genes with significant reduction in the abundance of Scd1 in a subset of E12.5 mutant embryos at risk for erythroid failure. SCD1, a key enzyme that converts saturated to monounsaturated fatty acids, has not been previously linked to erythropoiesis or DBAS. When anemia was induced in adult mice, pretreatment with an SCD1 inhibitor resulted in improved erythropoiesis. This analysis suggests a key role of lipid metabolism in the variable anemia penetrance in DBAS and highlights a previously unappreciated pathway that may serve as a potential target for drug development.

overall_design: RNA-seq profiling of wildtype and Rpl5 mutant E12.5 fetal liver erythroid progenitors.

last: Wang

first: Joseph

last: Min

first: Xiaofang

last: Liu

first: Greggory

last: Myers

first: Lei

first: Susan

last: Hammoud

first: Adham

last: Adam

first: Rilie

last: Saba

first: Vaneesha

last: Natogi

first: Claire

last: Drysdale

first: Brandon

last: Chen

first: Hiroki

last: Ueharu

first: Jennifer

last: Yee

first: Jacob

last: Kitzman

first: Costas

last: Lyssiotis

first: Yuji

last: Mishina

first: Morgan

last: Jones

first: Vesa

last: Kaartinen

first: Yuanfang

last: Guan

first: Rami

last: Khoriaty

first: James

last: Engel

first: Sharon

last: Singh


title: Inhibition of H3K79me2 by DOT1L inhibitor EPZ5676 promotes mouse embryonic lung branching morphogenesis via increasing epithelium proliferation

city: guangzhou

first: chen

last: huan

address: guangzhou

institute: guangzhou laboratory

summary: Histone modifications play a crucial role in regulating pulmonary branching morphogenesis, yet their specific contributions remain incompletely understood. Here, we demonstrate that H3K79me2 is broadly distributed throughout the airway epithelium in the early developmental stages of mouse embryonic lungs. Inhibition of H3K79me2 through EPZ5676, a DOT1L inhibitor, significantly enhanced branching morphogenesis in lung explant cultures. RNA-seq analysis revealed that EPZ5676 promotes epithelial cell differentiation and proliferation. Notably, in mesenchyme-free cultures, EPZ5676 alone did not influence epithelial morphogenesis but synergistically stimulated epithelial branching in the presence of FGF7. These findings identify H3K79me2 as a potential negative regulator of pulmonary branching morphogenesis and highlight the DOT1L inhibitor EPZ5676 as a promising epigenetic therapeutic target for promoting lung development and addressing pulmonary developmental disorders.

overall_design: RNA-seq profiling of explants from wild-type E11.5 lungs and corresponding periods after 72h of in vitro culture in control and EPZ5676-treated groups.

first: Huan

first: Yunjing

last: Du


title: Single-cell RNA sequencing data of anti-PD-1 antibody tolerant LLC cells

city: Hiroshima

first: Masahiko

last: Sumii

address: 1-2-3 Kasumi, Minami-ku,

country: Japan

institute: Hiroshima University Hospital

summary: Even after anti-PD-1 antibody is administrated to subcutaneous model mouse using LLC cells, there are a few cells which survive, and these tolerant cells are considered to be the source of later recurrence. We performed single-cell analysis to explore the mechanism behind the tolerance to anti-PD-1 antibody in LLC cells

overall_design: LLC cells surviving 7 days after treatment with anti-PD-1 antibody (PD-1 treatment) and control LLC cells without treatment (Control) were collected and  analyzed using scRNA-seq.

first: M

first: T

last: Masuda


title: Expression data of control or anti-PD-1 antibody tolerant LLC cells

summary:
Even after anti-PD-1 antibody is administrated to subcutaneous model mouse using LLC cells, there are a few cells which survive, and these tolerant cells are considered to be the source of later recurrence.
We used microarray analysis to explore the mechanism behind the tolerance to anti-PD-1 antibody in LLC cells

overall_design: LLC cells surviving 7 days after treatment with anti-PD-1 antibody (P) and control LLC cells without treatment (C) were collected and RNA was extracted and hybridized on Affymetrix microarrays


title: Folate Receptor Beta Regulates Macrophage NLRP3 Inflammasome Activation and Pyroptosis in a Folate-Independent Manner [methylation array]

first: David

last: Aronoff

type: Methylation profiling by genome tiling array

overall_design: Following treatment with phorbol 12 myristate 13 acetate (PMA) THP-1 WT or FOLR2 KO cells were rested in T-75 tissue culture flasks at 37C for 24 hours. Cells were then harvested from tissue culture flasks, plated in 6-well tissue culture plates at 5e6 cells/well with 2 mL of media and rested at 37C for 24 hours. Cells were harvested and DNA extracted with Qiagen QIAamp DNA Mini kit. DNA amounts were quantified via Nanodrop and stored at -20C until being run on Illumina Infinium MethylationEPIC v2.0 BeadChip microarray.

first: Lisa

last: Rogers

first: Kyle

last: Firestone

first: Riya

last: Chinni

first: Anna

last: Branco

first: Kayla

last: Wrobleski

first: Teresa

last: Chou

first: Jeffery

last: Goldstein

first: Xiaoping

last: Gu

first: Emily

last: Mason

first: Shaoyou

last: Chu

first: Michael

last: Rubart-von der Lohe

first: Philip

last: Low


title: Expression data of anti-PD-1 antibody tolerant KLN205 cells

summary:
Even after anti-PD-1 antibody is administrated to subcutaneous model mouse using KLN205 cells, there are a few cells which survive, and these tolerant cells are considered to be the source of later recurrence.
We used microarray analysis to explore the mechanism behind the tolerance to anti-PD-1 antibody in KLN205 cells

overall_design: KLN205 cells surviving 7 days after treatment with anti-PD-1 antibody (D) and control KLN205 cells without treatment (C) were collected and RNA was extracted and hybridized on Affymetrix microarrays


title: LncRNA NEAT1 promotes immunosuppression in gastric cancer by maintaining the m6A methylation of SEMA3A in CAFs via exosomes under endoplasmic reticulum stress [SGC7901]

first: xi

last: dongxin

address: No. 1, Xinzao Road, Xinzao Town, Panyu District, Guangzhou

institute: guangzhou medical university

summary: In order to find out the impact of endoplasmic reticulum stress (ERS) to the tumor microenvironment (TME) of gastric cancer. Transcriptome sequence of exosomes between ERS-GC group and normal GC group. 192 lncRNAs were found to be highly expressed in the exosomes of gastric cancer cells under ERS state.

overall_design: Human gastric cancer cell line SGC7901 was cultured in RPMI 1640 medium (Solarbio) supplemented with 10% fetal bovine serum (FBS, Biological Industries).All the cells were digested with trypsin (containing EDTA, Solarbio) at a density of 80–90% for passaging at a 1:2 or 1:3 ratio and all the cells were cultured in a cell culture incubator (ESCO, Singapore) containing 5% CO2 at 37 °C. ERS state was induced by treating SGC7901 with 5μg/ml TM for 24h. Exosomes were collected from normal gastric cancer cells and gastric cancer cells in ERS state culture supernatant, and exosomal trace RNA was purified and other pretreatments, and the library was synthesized by reverse transcription, end repair and adapter, PCR amplification, etc., and then sequenced on the machine after library quality inspection.

first: Youqin

last: Xu

first: Rui

first: Zixin

last: Chen

first: Hangyu

last: Zhou

first: Jiaqi

last: Liao

first: Kaiyuan

last: Ji

first: Shengnan

last: Yang

first: Xuxian

last: Zhong

first: Yuanyuan

last: Li

first: Qianbing

last: Zhang

first: Linping

last: Zhao

first: Qiang

last: Zuo


title: Fentanyl-Induced Rapid Cortical Damage and Cardiopulmonary Arrest Linked to Atypical Dynamics of Apoptosis and Immune Response in a Mouse Model

city: Silver Spring

first: Aarti

last: Gautam

address: 503 Robert Grant Avenue

department: Medical Readiness Systems Biology

institute: WRAIR

summary: The rapid onset of fentanyl outpaces the FDA-approved drugs to impair cardiopulmonary system and brain functions. Rising number of fentanyl related mortalities and overdoses, and near absence of any viable therapy calls for a comprehensive interrogation. In this study, adult SKH-1 mice were exposed to different doses of fentanyl citrate and organs (cortex, heart, lung) were collected at 0h (40min), 6h, 24h, and 7d post-administration. Total RNA was extracted and gene expression was profiled using Agilent SurePrint G3 Mouse GE 8x60K microarrays. This study aims to investigate the molecular perturbations associated with fentanyl overdose and identify early molecular markers of tissue-specific injury.

overall_design: Three doses of fentanyl (HNLD: 62 mg/kg, LD10: 110 mg/kg, LD50: 135 mg/kg) were administered subcutaneously. Samples were collected at 0h (40min), 6h, 24h, and 7 days post-exposure. Sham controls were collected at matching timepoints. Microarrays were performed using dual-color (Cy5-labeled sample, Cy3-labeled Agilent Mouse Universal Reference RNA) hybridizations.

first: Nabarun

last: Chakraborty

first: Mital

last: Patel

first: Swapna

last: Kannan

first: George

last: Dimitrov

first: Jonathan

last: Boyd

first: Rasha

last: Hammamieh


title: Evaluation of transcriptomic responses in mouse larynx after cigarette smoke (CS) and electronic cigarette (E-Cigarette) exposures

city: Stanford

first: Meena

last: Easwaran

state: California

address: 240 Pasteur Dr, BMI 1400

institute: Stanford University

summary: Cigarette smoking is strongly associated with various laryngeal conditions, such as laryngitis, Reinke’s edema, laryngeal leukoplakia, and laryngeal cancer. Although E-Cigarettes have emerged as a prevalent alternative to traditional cigarettes, their effects on the larynx are not thoroughly characterized, and there is limited understanding of the molecular alterations induced by their aerosols. The objective of this study is to conduct a direct comparison of the laryngeal transcriptomic responses resulting from exposure to conventional CS and E-Cigarette aerosol. Utilizing high-throughput mRNA sequencing analysis, this research intends to identify both unique and overlapping molecular signatures associated with each form of exposure. The findings of this investigation will contribute to a deeper understanding of the implications of these tobacco products on laryngeal health and will serve as a valuable foundation for future studies in this domain.

overall_design: mRNA-seq profiling of mouse larynges was conducted in air-exposed control, CS-exposed, and E-Cigarette-exposed groups after a 4-week exposure period.

first: Elizabeth

last: Erickson-DiRenzo


title: A cellular anatomy of normal adult human female urethra [Xenium]

city: Dallas

first: Douglas

last: Strand

address: 5323 Harry Hines Blvd JA5.150 JA5.150

department: Urology

institute: UT Southwestern Medical Center

summary: A cellular atlas of healthy human female urethra could provide a better mechanistic understanding of voiding dysfunction and infection. Single cell RNA sequencing was performed on young adult human female urethra with in situ validation of putative cell types. The proximal urethra and dorsal ducts were shown to contain a transitional epithelium with basal, intermediate and luminal layers as well as rare neuroendocrine epithelia. Squamous epithelium was predominantly found in the distal urethra. Novel fibroblast subtypes were validated in situ as displaying regional localization with insight into putative functions. Finally, a comparison of male prostatic urethra and female urethra was performed using both single cell and spatial transcriptomics. These data provide a cellular and molecular landscape of male and female urethra to be used as a reference for understanding disease.

overall_design: Two 5 µm sections each of human prostatic and female urethra in transverse and sagittal orientation (4 sections total) were prepared from FFPE tissue and mounted on Xenium slides (10x Genomics). Manufacturer recommendations for sample processing and operation of the Xenium analyzer were followed for downstream sample preparation and data collection.

middle: W

first: John

last: Lafin


title: Fentanyl-Induced Rapid Cortical Damage and Cardiopulmonary Arrest Linked to Atypical Dynamics of Apoptosis and Immune Response in a Mouse Model  [miRNA]

summary: The rapid onset of fentanyl impairs cardiopulmonary and neurological function, often outpacing clinical intervention. To understand its tissue-specific molecular effects, we administered three escalating doses of fentanyl (HNLD, LD10, and LD50) to SKH-1 mice and collected cortex, heart, and lung samples at 0h, 6h, 24h, and 7d post-injection. This study employed miRNA-seq to uncover conserved regulatory signatures underlying apoptosis and immune response networks. Using a machine-learning pipeline, we identified phylogenetically conserved miRNA-mRNA axes with translational potential, such as miR-877-3p in cortex and miR-146b-5p in lungs, providing early leads for therapeutic intervention in fentanyl overdose.

overall_design: Adult SKH-1 Elite mice were administered subcutaneous fentanyl at 62, 110, or 135 mg/kg (HNLD, LD10, LD50) or vehicle control, and euthanized at 0h (40 min), 6h, 24h, or 7d post-injection. Cortex, heart, and lung tissues were collected for miRNA profiling using Illumina TruSeq Small RNA Sample Prep and sequenced on the Illumina NextSeq 500 platform. Single-end 50 bp reads were mapped to the mm9 genome and miRBase v21. miRNAs conserved between mouse and human were prioritized, and those with functional homology across species were used to identify miRNA-mRNA pairs with regulatory significance across tissues and timepoints.


title: Impaired taurine transport contributes to the development of bronchopulmonary dysplasia

city: Milwaukee

first: Masaki

last: Lin

state: Wisconsin

address: 8701 W Watertown Plank Rd

institute: Medical College of Wisconsin

summary: Sprague-Dawley rat pups were used to study the effect of taurine supplementation on hyperoxia-exposed lungs. The study, which was conducted with meticulous attention to detail, found significant effects of taurine supplementation. Rat pups were randomly assigned to room air (NOX) and >90% oxygen (HOX) from postnatal day 1 (P1) to P10. Half of the pups of each group received a daily taurine (100 mg/kg) intraperitoneal injection or an equal volume of PBS (two by two design). The four groups were NOX-PBS, NOX-taurine, HOX-PBS, and HOX-taurine. At P10, a comprehensive range of methodologies was employed, including morphometrics, histology, metabolomics, and immunoblots. Two pups, one male and one female, were randomly selected for single-cell RNA sequencing at P10

overall_design: Lung cells from each pup, a total of eight pups, were barcoded before combing for sc-RNAseq run through the Chromium platform at 25 billion reads.

first: Xigang

last: Jing

first: Yekai

last: Wang

first: Mark

last: Roethle

first: Shuang

last: Jia

first: Michelle

last: Teng

first: Ganesh

last: Konduri

first: Martin

last: J. Hessner

first: Kirkwood

last: A. Pritchard

first: Billy

last: Day

first: Yan

last: Jin

first: Stephen

last: Naylor

first: Chien-Wei

first: Haiwei

last: Gu

first: Jianhai

last: Du

first: Ru-Jeng


title: DCPS modulates TDP-43 mediated neurodegeneration through P-body regulation [ARTR-seq]

first: Shuying

last: Sun

overall_design: ARTR-seq profile of control (shCTR shCTR) i3Neurons and knockdown (shTDP-43 shCTR, shTDP-43 shDCPS) i3Neurons on differentiation day 14.

first: Yingzhi

last: Ye

first: Yu

last: Xiao


title: Spatially organizing million callus cells identify the core-network enable tomato shoot regeneration [spatial]

city: weifang

first: yongqi

last: liu

state: shandong

address: 699 Binhu Road, Xiashan District

institute: Peking University Institute of Advanced Agricultural Sciences

summary: Plants can regenerate entire organs from somatic cells, offering a powerful system to uncover fundamental principles of cellular reprogramming and self-organization. Unlike animals, depending on pre-existing stem cell niches, plants re-establish pluripotency de novo. Although current understanding emphasizes hormonal control and external environmental cues, a unifying framework that explains how millions of cells coordinate fate decisions across space and time remains elusive. Here, we construct a million-cell spatial transcriptomic atlas of plant regeneration, achieving mesoscale resolution observation for all stages of tomato callus development. This atlas reveals a tripartite stem cell niche architecture: an outer signaling layer, intermediate plastic zone, and a quiescent core, features reminiscent of animal regenerative niches. We uncover a fundamental Inducer-Maintainer-Trigger (IMT) triad model, wherein PI-2 (Inducer) establishes a stem cell activating microenvironment, DCL2/22-nt siRNAs (Maintainer) safeguard pluripotency through post-transcriptional regulation, and EPFL8 (Trigger) initiates stem cell niche establishment. This triad model unifies niche signaling, small RNA-mediated plasticity, and metabolic-state-dependent activation, drawing parallels between plant and animal regeneration. Beyond resolving key questions in plant biology, our findings highlight deep evolutionary convergence in regenerative logic across multicellular life, offering new blueprints for engineering regeneration in synthetic biology, crop science, and tissue engineering.

overall_design: Spatial transcriptomic profiling of tomato callus tissues across all developmental stages of shoot regeneration was performed using multiple high-resolution platforms. This included BMKMANU S1000/S3000 RNA-Seq (Illumina NovaSeq), BGI Single-Cell Stereo-Seq (DNBSEQ-T10), and ISSeq-based spatial transcriptomics. The study generated a million-cell spatial atlas to resolve tripartite stem cell niche dynamics (outer signaling layer, intermediate plastic zone, quiescent core). Biological replicates (n=3) were analyzed for each stage (0h, 6h, 72h post-wounding/systemin treatment).

first: Shaoman

last: Zhang

first: Xiehai

last: Song

first: Zhiliang

last: Yue

first: Yongqi

last: Liu

first: Bosheng

last: Li


title: A post-translational regulatory map of chronic antigen-driven human T cell dysfunction

city: New York

first: Jahan

last: Rahman

state: New York

address: 417 E 68th St

department: Center for Hematologic Malignancies

institute: Memorial Sloan Kettering

summary: T cells exposed to persistent antigen, either in the context of chronic viral infections or tumors, iteratively lose both self-renewal and cytotoxic capacity. Several transcriptional, epigenetic, and metabolic drivers of this process have been identified. However, the post-transcriptional regulatory mechanisms influencing the proteome of dysfunctional T cells are not well understood. Here we present a time-resolved cysteine reactivity landscape of human T cells during the development of chronic antigen-driven dysfunction. Persistent T cell receptor stimulation of human T cells following activation significantly remodeled the T cell proteome compared with cytokine-mediated expansion, including changes in canonical T cell exhaustion-associated proteins as well as proteins related to mitochondrial function, redox homeostasis, nucleotide metabolism, and cell cycle progression. Exhausted T cells displayed frequent reactivity changes in nucleotide-binding domains across several protein classes that were associated with progressive loss of mitochondrial ATP production and activation of nucleotide salvage. Our comprehensive proteomic resource thus reveals a unique set of post-transcriptional changes as part of an exhausted T cell program and lays the groundwork for novel cysteine-directed therapeutics to enhance cancer immunotherapy.

overall_design: RNA-seq of primary human T-cells following activation with plate-bound anti-human CD3 and anti-human CD28, expanded in the presence of human IL-7 and IL-15, with (chronic) or without (acute) additional plate-bound anti-CD3 for the indicated number of days.

first: Hiroyuki

last: Kojima

first: Charlotte

last: Wayne

first: Tzu-Jou

last: Chen

first: Henry

last: Sanford

first: Nicole

last: Lin

first: Joshua

last: Schoenfeld

first: Beatrice

first: Tiffany

first: Cameron

last: Roberts

first: Kartik

last: Menon

first: Jiankun

last: Lyu

first: Omar

last: Abdel-Wahab

first: Santosha

last: Vardhana

first: Ekaterina

last: Vinogradova


title: Transcriptomic profiling of a human iPSC-derived blood-brain barrier-on-chip model of ischemic stroke

city: Hefei

first: Jianhua

last: Qin

state: Anhui

address: No.96 JinZhai Road Baohe District

department: School of Biomedical engineering

institute: University of Science and Technology of China

summary: Ischemic stroke is a leading cause of death and disability worldwide, characterized by reduced cerebral perfusion and blood-brain barrier (BBB) disruption. To model the human-specific pathophysiology of ischemic stroke, we developed a fully iPSC-derived blood-brain barrier-on-chip (iBBB-on-chip) comprising brain microvascular endothelial cells (iBMECs), pericytes (iPericytes), and astrocytes (iAstrocytes). After establishing a functional BBB structure, we induced ischemic injury by exposing the chip to oxygen-glucose deprivation (OGD) under static conditions. Transcriptome profiling of brain side ande endothelial side was performed to investigate molecular responses to ischemic stress.

overall_design: Cells were seeded into designated channels within the chip and co-cultured for four days to allow barrier formation. The ischemic condition was mimicked by subjecting the chips to oxygen-glucose deprivation (1% O₂, glucose-free, serum-free medium) for 24 hours. Control chips were maintained under normoxic conditions (20% O₂, complete medium). 24h after OGD treatment, iBMECs and brain cells (iPericytes, and iAstrocytes) were collected from the lower vascular channel and upper brain channel, respectively.


title: Spatially organizing million callus cells identify the core-network enable tomato shoot regeneration [scRNA-Seq]

first: yongqi

last: liu

overall_design: To investigate the shoot regeneration process in tomato callus cells, we conducted single-cell RNA sequencing on callus tissues at different stages of development.  Tissues were collected at 12, 14, and 16 days post-induction for sequencing.

first: Shaoman

last: Zhang

first: Xiehai

last: Song

first: Zhiliang

last: Yue

first: Yongqi

first: Bosheng


title: Research on the dynamic changes of signaling pathways during SARS-CoV-2 infection of host cells

city: Chengdu

first: chen

last: li

address: Renmin South Road

institute: Sichuan Univercity

summary: SARS-CoV-2 continues to pose a substantial public health challenge owing to its high transmissibility and rapid mutation capacity. The immune regulation of SARS-CoV-2 is a complex process involving both viral immune evasion mechanisms and the dynamic balance of host immune responses. We performed RNA-seq sequencing on host cells at different time points post-infection, followed by pairwise comparative enrichment analysis and clustering analysis, ultimately identifying the regulatory changes in signaling pathways during the infection process.

overall_design: To investigate the temporal dynamics of host immune responses, we conducted an RNA-sequencing analysis on SARS-CoV-2-infected (BetaCoV/Wuhan/IVDC-HB-01/2019 strain) Calu-3 cells (MOI 2) at 6-, 24-, 48- and 72-hours post-infection (hpi). We then collected samples for RNA extraction and RNA-seq sequencing and performed gene expression profiling analysis. Pairwise comparative gene expression profiling analysis of RNA-seq data between different infection time points.

first: Jing-wen

first: Han-cheng

last: Wei

first: Qingxin

last: Yang

first: Yu-hang

last: Wang


title: A cellular anatomy of normal adult human female urethra

first: Douglas

last: Strand

state: TX

overall_design: Entire lower urinary tracts were collected fresh in partnership with a local transplant alliance. These systems were dissected into individual organs, and prostatic and female urethra were collected and digested into a single cell suspension for sequencing with the 10x Genomics Chromium platform.

first: John

last: Lafin


title: Spatially organizing million callus cells identify the core-network enable tomato shoot regeneration [RNA-Seq 2]

overall_design: The experimental design involves mRNA-seq profiling of tomato (Solanum lycopersicum cv. Micro-Tom) callus tissues at different developmental stages (0–16 days post induction) and under various genetic or chemical treatments. Samples include: Time-series callus: 0, 1, 2, 4, 6, 8, 10, 11, 12, 13, 14, 15, and 16 days post explant culture on shoot induction medium (SIM). Genetic mutants: EPFL8 knockout (epfl8-mutant), DCL2 mutants (dcl2), and PI-2 mutants (pi-2). Chemical treatments: Mock controls, Torin2 (an autophagy inhibitor), and systemin peptide treatments. Biological replicates: Three independent replicates per condition. Samples were collected at specified time points, and total RNA was extracted for mRNA-seq library construction. Libraries were sequenced on DNBSEQ-T7 or MGISEQ-2000RS platforms. Differential gene expression analysis was performed to identify key regulators of shoot regeneration.

last: Liu


title: In vitro investigation of epigenetic regulators related to chemo-resistance and stemness of CD133+VE cells sorted from U87MG cell line

city: Amman

first: Heba

last: Saadeh

state: Not Applicable

address: Queen Rania Street

country: Jordan

institute: The University of Jordan

summary:
Glioblastoma (GBM) is the most common and malignant adult primary brain tumor with frequent relapse and resistance to therapies. Glioma stem cells, a rare population, is thought to be the reason behind the treatment’s failure. It is imperative to investigate the disease mechanisms and identify the biomarkers by which glioma stem cells would contribute to treatment relapse and resistance to already available chemotherapeutic agents.
The CD133+VE cells were isolated from U87MG cell line and characterized by morphological features, cell viability, self-renewal efficiency, migration potential and karyotyping. Doxorubicin Cisplatin, Irinotecan, Etoposide and Temozolomide were used to determine the anti-proliferative effect on CD133+VE cells. Confocal microcopy was used to localize the chemotherapeutic agents in the CD133+VE cells. In quest of epigenetic biomarkers, RNA sequencing was performed to find the role of lncRNAs in stemness and resistance to therapies. U87cell line and CD133-VE cells were kept as controls for all the experiments.
It was found that CD133+VEcells were highly proliferative with increased migration potential, elevated IC50 values against chemotherapeutic agents and showed distinct karyotyping related to pluripotency. Chemotherapeutic agent such as Doxorubicin was localized outside the nucleus revealing the drug resistance as evident by confocal microscopy. RNA sequencing revealed 126 differentially expressed lncRNAs (DELs) in CD133+VEcells among which lncRNA LOXL1-AS1 was highly upregulated and lncRNA PAX8-AS1 was significantly downregulated. These lncRNAs has been reported to be related to drug resistance, migration and epithelial- to- mesenchymal transmission (EMT), self-renewal and stemness properties contributing to poor prognosis and disease relapse.

overall_design: RNA-Seq profiling of control U87 glioma cell line (2 sample) and their sorted cancer stem cells CD133 positive CSC (3 samples)

first: Elham

last: Abusharieh

first: Nazneen

last: Aslam

first: Malek

last: Zihlif

first: Yasser

last: Bustanji

first: Suha

last: Wehaibi

first: Duaa

last: Abuarqoub

first: Diana

last: Shaheen

first: Raghda

last: Barham

first: Abdalla

middle: S

last: Awidi


title: Shared anti-biofilm targets of biofilm regulators Wor3 and Bcr1 in Candida albicans

city: Athens

first: Katharina

last: Goerlich

state: GA

address: 120E Green St

department: Microbiology

institute: University of Georgia

summary:
Candida albicans is an opportunistic fungal pathogen and a natural component of the
human microbial flora. One central C. albicans virulence trait is the ability to produce a
biofilm, which is regulated by several transcription factors. Mutations of some biofilm
transcriptional regulators cause the same severe biofilm-defective phenotype in multiple
clinical isolates. Mutations of others, such as Wor3, Bcr1, Ndt80, and Ume6, have mild
or variable phenotypes among clinical isolates. We hypothesized that Wor3 may have a
shared function with one of the other variable-phenotype biofilm regulators. This
hypothesis predicts that a double mutant lacking Wor3 and the shared-function
regulator will have a severe biofilm defect in all clinical isolates. We observed that a
wor3Δ/Δ bcr1Δ/Δ has a severe biofilm defect in vitro in 5 strain backgrounds tested. It
also has a severe oral biofilm defect in a mouse oropharyngeal candidiasis model in the
SC5314 reference strain background. RNA-seq data indicate that 5 genes encoding
cell surface/secreted proteins are upregulated in wor3Δ/Δ, bcr1Δ/Δ, and wor3Δ/Δ
bcr1Δ/Δ strains: CWH8, DAG7, JEN2, PGA6, and YWP1. Deletion mutations of CWH8,
DAG7, PGA6, or YWP1 enables biofilm formation in vitro in an SC5314-derived
wor3Δ/Δ bcr1Δ/Δ strain, and deletion of YWP1 enables biofilm formation in vitro in
wor3Δ/Δ bcr1Δ/Δ strains from 4 other genetic backgrounds. YWP1 has been shown to
have anti-biofilm activity previously, but CWH8, DAG7, and PGA6 are newly described
anti-biofilm genes. Our study illustrates the value of strain variation considerations for
gene function analysis and the importance of repression targets of biofilm regulators. In
addition, our results expand the number of anti-biofilm genes.

overall_design: RNA-seq profiling of WT C. albicans cells and their mutant derivatives (wor3△/△, bcr1△/△, and wor3△/△bcr1△/△). Cells were grown for 4h at 37C in RPMI+10%FBS.

first: Aaron

last: Mitchell


title: Global transcriptome of Arabidopsis mutants nac42-L1 and nac42-L2 inoculated by the fungal pathogen Sclerotinia sclerotiorum following temperate and mediterranean acclimation

city: Castanet tolosan

first: Sylvain

last: Raffaele

address: 28 chemin de borde rouge

country: France

institute: INRAE

summary: The short-term, reversible process that allows plants to cope with immediate environmental fluctuations is often referred to as acclimation. Plant acclimation help maintain the balance of natural systems, supporting biodiversity and the services that ecosystems provide, such as carbon sequestration and water regulation. With climate change modifying the distribution area of plants and causing more frequent and severe weather events, knowledge of how plants acclimate can inform strategies to manage ecosystems and agriculture. Analyses of plant immune responses under abiotic constraints generally focus on pathogen inoculation under prolonged and stable abiotic conditions. Daily fluctuations of the environment may alter plant metabolism, growth and flowering as well as gene regulation and invasive growth of fungal pathogens. Yet, how plant immunity acclimates to daily temperature fluctuations remains largely unexplored. To study the molecular bases of quantitative disease resistance acclimation, we performed a global transcriptome analysis of Arabidopsis thaliana accessions Col-0, Rld-2 and Sha grown in temperate, continental and Mediterranean climates, followed or not by Sclerotinia sclerotiorum inoculation.

overall_design: Periphery of S. sclerotiorum disease lesions collected 24 hours post-inoculation on detached leaves of A. thaliana mutants. Plants were previously acclimated under two different day/night temperature regimes. Samples were collected in three independent replicates of the experiment.

first: Marie

last: Didelon

first: Florent

last: Delplace


title: Knee osteoarthritis (OA)-related phenotypes of myeloid-derived suppressor cells (MDSCs) is mediated by infrapatellar fat pad (IPFP)-derived factors in a body mass (BMI)-dependent manner and positively correlates with IPFP-derived adiponectin levels

city: Bangkok

first: Rangsima

last: Reantragoon

address: 1873 Rama 4 Road

country: Thailand

institute: Faculty of Medicine, Chulalongkorn University

summary: In osteoarthritis (OA), immune cells including myeloid-derived suppressor cells (MDSCs) infiltrate infrapatellar fat pad. MDSCs play a crucial role in immune suppression in cancer and autoimmunity, but their function change upon increasing of body mass index (BMI). However, role of MDSC in OA is less studied. Therefore, this study aimed to investigate the the effect of BMI on gene expression profile in MDSC from knee OA patients.

overall_design: Infrapatellar fat pads from 12 OA patients with various body mass index (BMI) were used to investigate gene expression profile of Myeloid-derived suppressor cells (MDSCs). The individual sample was catagorized into 3 groups; low, moderat and high BMI. Each group contained 4 individual sample.

first: Varote

last: Shotelersuk


title: N6-Methyladenosine-Modified circPICALM Encodes a Protein That Promotes Intrahepatic Cholangiocarcinoma Metastasis

city: Chongqing

first: hui

last: li

state: Chongqing

address: No. 181 of Hanyu Road

department: Hepatobiliary Pancreatic Tumor Center

institute: Chongqing University Cancer Hospital

summary: Intrahepatic cholangiocarcinoma (ICC) is a highly aggressive primary liver cancer characterized by rapid progression and strong metastatic potential. Circular RNAs (circRNAs) are emerging as crucial regulators in the complex biology of cancer, yet their specific roles in ICC metastasis remain poorly defined. In this study, circRNA sequencing of paired primary and recurrent ICC tissues revealed that elevated expression of circRNA PICALM (circPICALM) is strongly linked to ICC metastasis and patient prognosis.

overall_design: Tumor samples were obtained from surgical specimen archives of ICC patients who had not undergone any preoperative treatments at Chongqing University Cancer Hospital between 2015 and 2023. Recurrent ICC tissues were defined as those obtained from patients who experienced recurrence within two years of their primary surgical resection, a timeframe commonly associated with metastatic progression.  3 pairs  of primary and recurrent ICC tissues were subject to circRNA sequencing.


title: LncRNA NEAT1 promotes immunosuppression in gastric cancer by maintaining the m6A methylation of SEMA3A in CAFs via exosomes under endoplasmic reticulum stress

first: xi

last: dongxin

summary: Endoplasmic reticulum stress (ERS) regulates the function of immune cells in the tumor microenvironment and suppresses the antitumor immune response. In order to formulate the TME of ERS-GC, we cocultured the human CAFs with the supernatant of human gastric cancer cells stimulated by TM. Mass spectrometry sequencing revealed that ERS state regulated the overexpression of 58 proteins and downregulation of the expression of 56 proteins in CAFs, including m6A-modified proteins and SEMA3A, an immunosuppression-related protein.

overall_design: Endoplasmic reticulum stress (ERS) regulates the function of immune cells in the tumor microenvironment and suppresses the antitumor immune response. In this study, the ERS effects in the microenvironment of gastric cancer (GC) were studied by the establishment of an ERS cell model of gastric cancer. To investigate the differential expressed genes in human gastric cancer fibroblasts (h-CAFs) under ERS state compared to normal h-CAFs, transcriptome sequencing analysis was conducted to identified 2810 upregulated genes and 2260 downregulated genes in ERS h-CAFs.

first: Youqin

last: Xu

first: Rui

first: Zixin

last: Chen

first: Hangyu

last: Zhou

first: Jiaqi

last: Liao

first: Kaiyuan

last: Ji

first: Shengnan

last: Yang

first: Xuxian

last: Zhong

first: Yuanyuan

last: Li

first: Qianbing

last: Zhang

first: Linping

last: Zhao

first: Qiang

last: Zuo


title: Fibroblasts Are the Primary Contributors to a Disrupted Micro-Environment in End-Stage Pediatric Hypertrophic Cardiomyopathy

city: Houston

first: Yi

state: Texas

address: 6770 Bertner Avenue

institute: The Texas Heart Institute at Baylor College of Medicine

summary: Hypertrophic cardiomyopathy (HCM) is a relatively rare but debilitating diagnosis in the pediatric population, and patients with end-stage HCM require heart transplantation. Here, we have examined the transcriptome in ventricular tissue from this patient group to identify cell states and underlying cellular processes unique to pediatric HCM.

overall_design: Three pediatric patients (ages 11.3, 14.2, and 16.8) with end-stage HCM were profiled by snRNA-seq and integratively compared with publically available donor control data.

first: Xiao

first: Hanna

last: Tadros

first: Diwakar

last: Turaga

first: James

last: Martin


title: Angiopoietin-2 aggravates Alzheimer’s disease by promoting BBB breakdown and neuroinflammation.

city: Seongbuk-gu, Seoul

first: Seoyeon

last: Kim

address: 145, Anam-ro

country: South Korea

institute: Korea University

summary: Disruption of the blood-brain barrier (BBB) and increased vascular leakage contribute to neuroinflammation in Alzheimer’s disease (AD), driving disease pathogenesis and progression. However, the mechanisms underlying BBB dysfunction and neuroinflammation in AD remain unclear. Angiopoietin-2 (ANGPT2), a ligand for the TIE2 receptor, is known to destabilize blood vessels and compromise vascular integrity under inflammatory conditions. To investigate the role of ANGPT2 in AD pathology, we overexpressed ANGPT2 specifically in brain endothelial cells using an adeno-associated virus (AAV) system in 5xFAD transgenic mice. Single-nucleus RNA sequencing (snRNA-seq) revealed distinct transcriptional changes associated with ANGPT2 overexpression, pointing to multiple pathways through which ANGPT2 may exacerbate AD progression. These findings identify ANGPT2 as a key driver of BBB dysfunction and neuroinflammation in AD, highlighting it as a potential therapeutic target for mitigating disease progression.

overall_design: The brains of 6-month-old 5xFAD mice were collected as fresh-frozen samples two months after a retro-orbital injection of either a control AAV or ANGPT2 AAV at 4 months of age. ANGPT2 AAV samples (n=4) were compared to the control AAV samples (n=3).

first: Eunhyeong

last: Lee

first: Minah

first: Joon-Yong

last: An


title: Liver sinusoidal scores: a new tool for the diagnosis and prognosis of chronic liver disease

city: Barcelona

first: Juanjo

last: Lozano

address: C/ Rosselló 153

department: Plataforma de Bioinformatica

institute: CIBEREHD

summary: Background and Aims: Sinusoidal cells drive the progression of chronic liver disease (CLD). Therefore, novel biomarkers for CLD should reflect the state of sinusoidal cells. However, the liver is mainly constituted from hepatocytes (80-90% of cells), while sinusoidal cells only represent the 10% of the cellular populations. Therefore, determination of biomarkers from plasma or bulk transcriptomics underrepresents smaller sinusoidal cell subpopulations, such as liver sinusoidal endothelial cells (LSECs), hepatic stellate cells (HSCs), and macrophages (MPs). On the other hand, recent studies performing single-cell sequencing allow for finer phenotype determination, but these analyses are too expensive for routine implementation in patient care. The aim of this study is to propose biologically-relevant markers of liver sinusoidal phenotype for the diagnosis and prognosis of CLDs. Methods: We estimated the relevant sinusoidal cell subpopulations in an internal cohort of 11 controls and 12 cirrhotic livers by gene deconvolution. Then, we reanalyzed published single-cell sequencing data in order to find a gene signature specific to these subpopulations. We combined the expression of these sinusoidal genes into 3 sinusoidal scores (endothelial, mesenchymal and macrophage) correlating with patient phenotypes. The ability of these scores to classify patients and predict fibrosis progression, regression and clinical decompensation was assessed in an internal cohort of 113 patients and further validated in 3 external cohorts for a total of 1008 patients with F3-F4 CLD (Simtuzumab, ATLAS & STELLAR trials). Results: We obtained a sinusoidal gene signature which was more specific for than traditional markers of LSEC capillarization, HSC activation and macrophage polarization. The three sinusoidal scores generated with these gene signatures were significantly higher in those patients with worse clinical parameters in our internal cohort and in the external validation cohort. The sinusoidal scores at baseline were significantly higher in patients that progressed from F3 to F4 fibrosis stage after 96 weeks of follow-up compared to those that stayed at F3. Similarly, the baseline sinusoidal scores were significantly lower in those patients that regressed from F4 to F3 compared to those that stayed at F4. Finally, the scores were able to predict decompensation in the following 96 weeks of follow-up (AUROC = 0.98) in the validation cohort and correlated with conventional parameters for evaluation of clinical decompensation (HVPG, Child-Pugh and MELD). Conclusions: This sinusoidal gene panel could aid in the diagnosis and prognosis of patients with CLD and predict future complications of cirrhosis. This technique can be easily assessed by RT-PCR and could be a useful tool for clinical decision making in the future, possibly aiding in assessment of drug response or in choosing the most relevant cell target for therapy.

overall_design: RNA expression was determinedby RNAseq in human liver tissue from healthy (n=11) or cirrhotic (n=12) patients . We performed sequencing using Illumina HiSeq2500 system,  single-end reads and 101 length.

first: Sergi

last: Guixé-Muntet

first: Anabel

last: Fernández-Iglesias

first: David

last: Lopez

first: Emilio

last: Tonina

first: Yiliam

last: Fundora

first: Anna

last: Zagorska

first: Jordi

last: Gracia-Sancho


title: Rhinolophus sinicus limb embryonic development single cell transcriptome

city: KunMing

first: Xue

last: Lv

state: Yunnan

address: No.17 Longxin Road

institute: Kunming Institute of Zoology, CAS

summary: Bats are the only mammals capable of true flight, possessing unique wings primarily composed of elongated digits and interdigital membranes.  However, the developmental coordination between digit elongation and interdigital membrane expansion remains poorly understood.  Here, we conduct a single-cell analysis of developing bat limbs of Chinese horseshoe bat and for key development stages of limb. Within the sequenced 30 thousand cells, we identify a specific population of mesenchymal progenitors in the bat forelimb that express high levels of PDGFD.  This cell population has the potential to differentiate into the interdigital membrane and release growth factors that promote the proliferation of bone-related cells.  Compared to hindlimbs, the developing bat forelimbs undergo prolonged chondrogenesis and delayed osteogenesis, resulting in more chondrocytes and fewer osteoblasts.  The bone-related cells also can release growth factors that facilitate the proliferation of skin-related cells.  Our findings suggest that interactions mediated by growth factors among different cell populations play a vital role in coordinating the development of digit elongation and interdigital membrane expansion in bat forelimbs.

sample_organism:
Mus musculus
Rhinolophus sinicus

platform_organism:
Mus musculus
Rhinolophus sinicus

overall_design: Following the pipeline described by (Rosenberg et al. 2018), we generated single-nucleus RNA-seq libraries of bat forelimbs and hindlimbs from R. sinicus embryos at CS16, CS18, and CS20, as well as the forelimbs of mouse embryos at the matched developmental stages: E13.5, E14.5 and E16.5.

first: Zhen

last: Liu

last: Lyu

first: Jing

last: Bai


title: Identified gene changes through RNA-sequencing following the knockdown of the COP1 gene in liver cancer

city: Daegu, Republic of Korea

first: EUN-HYE

last: JEON

address: 1095 Dalgubeol, Dalseo-gu

department: Molecular Medicine

institute: Keimyung University School of Medicine

summary: COP1 is a ubiquitin E3 ligase that degrades the cancer suppressor gene p53. COP1 is overexpressed in human hepatocellular carcinoma, and there is evidence that knocking down COP1 can inhibit the growth of liver cancer. We hypothesized that COP1 may also be involved in the metabolism of liver cancer. To explore this, we treated human liver cancer cell lines Huh7 and HepG2 with COP1-siRNA and conducted RNA sequencing.

overall_design: Human hepatocellular carcinoma cell lines (Huh7, HepG2) were treated with either NC-siRNA or COP1-siRNA. Cells were harvested 48 hours post-treatment. RNA was extracted from these cells and subjected to RNA-sequencing

first: Eun-Hye

last: Jeon

first: Yun-Han


title: Roots in Action for the Fe Response: Early Response-Omics in Tomato Dependent on the N-Form Applied

city: Udine

first: Fabio

last: Marroni

address: Via delle Scienze 208

institute: Università di Udine

summary: In soils, the bioavailability of nitrogen (N) and iron (Fe) is often not adequate to sustain plant demand, with these nutrients being two of the main constraints for crop production. Among macro- and micro-nutrients, N and Fe are the two nutrients mainly applied as fertilizers. There is a gap of knowledge about the interplay between N forms (nitrate, ammonium and urea) and the Fe response activated in plants under shortage condition of the nutrients. Depending on the N form available to roots, plants activate different transcriptional and metabolic pathways and adjust the release of root exudates. The release of protons and other exudates by roots can promote the bioavailability of Fe in the rhizosphere. In the present work the reciprocal relationship between availability of Fe and different N forms (nitrate, ammonium, or urea) has been investigated for the molecular mechanisms activated by plants to promote their acquisition by omic data integration (“exudomic” x transcriptomic analyses). Transcriptomic profiles of tomato roots exposed for 4 hours to urea or ammonium clustered together, as well as their relative metabolomic profiles of root exudates after 24 hours of treatment. Interesting modulation of transcription factors (bHLH, MYB, ZAT12), of transporters (UmamiTs) and a proteolytic regulator of a phenylpropanoid enzyme (KFB-PAL) seems to play a key role to define the tomato exudome and corroborate the occurrence of a strong interplay between Fe N nutritional pathways.

overall_design: RNA-seq to Solanum lycopersicum roots in the following conditions: control (-Fe-N), Iron resupply (+Fe-N), Iron and Nitrate resupply (+Fe+Ni),Iron and ammonium resupply (+Fe+A), Iron and urea resupply (+Fe+U)


title: Gene expression profile of nociceptors innervating the skin at a single cell level at steady state and in a Contact hypersensitivity model

city: Toulouse

first: Lilian

last: Basso

address: INSERM UMR1291 – CNRS UMR5051 - University Toulouse III CHU Purpan – BP 3028

institute: INFINITY INSERM U1291

summary: Changes in Gene expression in skin-innervating nociceptor during contact hypersenisitivity are unknown. We sorted skin-innervating nociceptors at steady state, after sensibilization and at D1 and D4 after allergen skin challange.

overall_design: Back -skin innervating nociceptors were retrograddly stained with DiI and sorted by FACS and subsequently sequenced.

first: Basso

last: Lilian

first: Gheziel

last: Nadine

first: Voisin

last: Tiphaine

first: Gaudenzio

last: Nicolas


title: Effects of brown adipose tissue transplantation on post-myocardial infarction pathological remodeling

city: Shanghai

first: YANG

last: Xingbo

address: Shanghai siping road 1239

institute: Tongji

summary: Brown adipose tissue (BAT) is known to reduce the risk of metabolic and cardiovascular diseases. Here we demonstrate that BAT transplantation alleviates pathological cardiac remodeling and reduces the incidence of heart failure post-myocardial infarction (MI). RNA-seq profile of left ventricular tissue from BAT-transplanted mice at Day3 post-MI revealed downregulation of genes associated with pro-inflammatory innate immune cells and chemokines, suggesting reduced infiltration of innate immune cells (e.g., neutrophils) into the myocardium. Concurrently, genes involved in muscle cell differentiation and cardiac repair were upregulated. These results indicate that BAT promotes post-MI cardiac repair by suppressing innate immune cell recruitment, thereby improving cardiac outcomes.

overall_design: RNA-seq profiling of the left ventricles of wildtype MI mouse models with or without BAT transplantation at Day3 post-MI.

first: Tingting

last: Shi

first: Yue

last: Xu

first: Xingbo

last: Yang

first: Yaozu

last: Xiang


title: Multi-omic profiling reveals epithelial remodeling in necrotizing enterocolitis

city: Beijing

first: Yi

last: Xiong

address: 2 Yabao Rd

institute: Children's Hospital of Capital Institute of Pediatrics

summary: Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease predominantly affecting premature infants, characterized by severe intestinal inflammation and tissue necrosis. Despite advances in neonatal care, NEC remains a significant clinical challenge with high mortality and morbidity rates. Understanding the molecular and cellular mechanisms underlying NEC pathogenesis is crucial for developing targeted therapies and improving clinical outcomes. In this study, we utilized a mouse model of NEC induced by hypoxia, formula feeding, and lipopolysaccharide administration to investigate the molecular changes at single-cell resolution. We performed bulk RNA sequencing, single-nucleus RNA sequencing (snRNA-seq), single-nucleus assay for transposase-accessible chromatin sequencing (snATAC-seq) and multiplexed error-robust fluorescence in situ hybridization (MERFISH) spatial transcriptomics on intestinal tissues collected from control and NEC groups at postnatal day 9. Data were analyzed to identify cell populations, epigenetic profiles, and regulatory pathways associated with NEC progression.

overall_design: We utilized a mouse model of NEC induced by hypoxia, formula feeding, and lipopolysaccharide administration to investigate the molecular changes at single-cell resolution. Intestinal tissues were collected from control and NEC groups at postnatal day 9.

first: Andrea

last: Zito

first: Haoyan

last: Liang

first: Haitao

last: Zhu

first: Bo

last: Li

first: Agostino

last: Pierro


title: Identification of Cryosensitive Niches and a Targetable FOS/AP‑1 Program in the Human Ovarian Cortex by Single‑Cell and Spatial Transcriptomics

first: Wen

state: Shanghai

address: No.910 Hengshan Road

institute: International Peace Maternity and Child Health Hospital

summary: Ovary is a vital and dynamic reproductive organ. Ovarian tissue cryopreservation (OTC) plays vital role in female fertility preservation, especially for adolescent female cancer patients. Yet, the sensitive cell populations and cryoinjury molecular mechanisms underlying cryopreservation remain elusive. This study employs single-cell RNA sequencing and spatial transcriptomics to dissect the impacts of temperature stress and cryoprotectant toxicity on the human ovarian cortex. The spatiotemporal molecular characteristics of eight ovarian cell types following vitrification-thawing had been comprehensively characterized. Granulosa, perivascular and stromal cells are identified as most sensitive cell types to OTC procedure. Further analysis using Smart-seq2 on oocytes highlights alterations in “cell cycle” and “DNA methylation” pathways. Notably, the FOS/AP-1 pathway emerges as a crucial response factor to stress and toxicity during cryopreservation. Inhibition of this pathway with T-5224 mitigates vascular damage and reduces apoptosis in vitrification-thawed ovaries. These findings provide insight into the spatiotemporal dynamics during ovarian vitrification and thawing, aiding in prioritizing therapeutic strategies for pre- and post-cryopreservation interventions.

overall_design: Each of the three ovarian cortexes from gender reassignment surgery patients (GRPs) was divided into both fresh and cryopreserved groups (cryo). The age information for the three groups is as follows: 29 years for Fresh & Cyro-1; 34 years for Fresh & Cyro-2; 35 years for Fresh & Cyro-3. Following by collagenase IV digestion, single-cell RNA sequencing (scRNA-seq) was applied to 27,185 fresh ovarian cells. Post standard ovary vitrification-thawing procedure, the cryopreserved group had been digested and conducted with scRNA-seq on 25,480 cells. Since large cells cannot be wrapped in microdroplets (dimeter >40um), Smart-seq2 strategy had been applied to oocyte in the ovarian cortex.

first: Fanghao

last: Guo

first: Di

last: Sun


title: SBNO1 knockdown in the liver cancer cell lines HLF

city: Mannheim

first: Carolina

last: Delatorre

address: Theodor-Kutzer-Ufer 1-3

institute: University Heidelberg

summary: Aberrant Notch signaling has been identified as a possible catalyst for hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA) development. Genetic studies in Drosophila observed that the knockout of strawberry notch (sno) mimics loss of notch. Here, we elucidated the role of the mammalian Strawberry Notch 1 (SBNO1) in HCC and CCA development.

overall_design: HLF cells were transfected with NTC, siSBNO1#1 or siSBNO1#2 using Lipofectamine RNAiMAX Transfection Reagent. Total RNA was extracted using the Macherey-Nagel RNA Extraction Kit (Macherey-Nagel, Düren, Germany).

first: Stephanie

last: Roessler

last: De La Torre


title: SBNO1 knockdown in the iCCA cell lines SNU1079

first: Carsten

last: Sticht

address: Theodor-Kutzer-Ufer

department: ZMF

overall_design: SNU1079 cells were transfected with NTC, siSBNO1#1 or siSBNO1#2 using Lipofectamine RNAiMAX Transfection Reagent. Total RNA was extracted using the Macherey-Nagel RNA Extraction Kit (Macherey-Nagel, Düren, Germany).


title: Anueploidy selects for the acquisition of driver genes in breast cancer

city: Toronto

first: Daniel

last: Schramek

state: ON

address: 600 University Avenue

country: Canada

institute: Lunenfeld-Tanenbaum Research Institute

summary: Chromosome instability is highly prevalent in cancer and drives large scale chromosomal imbalances, known as aneuploidies. How aneuploidy contributes to tumorigenesis remains difficult to study due to the vast numbers of genes affected. Here, we established a CRISPR Knock Out and Activation Linked Assay (CRISPR-KOALA), enabling high-throughput bidirectional genetic screens in immune-competent mouse models of cancer. We developed a compendium of the ten most frequent human chromosome arm-level alterations in basal-like breast cancer (BLBC), a disease type driven by large copy number alterations (CNAs).  Using CRISPR-KOALA, we screened the mouse orthologs of all 3,752 genes on these arms and identified 90 cancer driver genes, the vast majority of which have hitherto unknown functions in cancer. These genes drive distinct signalling pathways including MAPK, Hippo and WNT, reflecting the high degree of BLBC heterogeneity. Manipulating the identified cancer driver genes overcomes the need for CNAs in p53-mutant BLBC mouse models. Mechanistically, we uncover PLGRKT as a potent oncogene that lies on chromosome 9p and show that its tumor-promoting activity is associated with highly stress-resistant mitochondria and an increased capacity to detoxify reactive oxygen species. Together, our findings reveal that arm-level CNAs can function to select specific driver genes to promote heterogeneous biological processes.

overall_design: To investigate the transcriptomes of FACS-purified Tigre-, Hipp11-, Fbxw7-, Csnk1a1-, and Mettl14-knockout and HA, Tigre-, Hipp11,  Plgrkt-, including plasminogen-binding deficient mutant, overexpressing mammary tumor cells, generated by lentiviral CRISPR-knockout, CRISPR-activation or open reading frame injections directly in the mammary epithelium of tumor prone Pten;P53;Cas9 compound mutant mice. At least 3 independent tumors were processed and analyzed for each group and directly compared to their respective controls, which were Tigre, Hipp11 for CRISPR-knockout and activation, or HA for open reading frame experiments.

first: Khalid

middle: N

last: Al-Zahrani

first: Ellen

middle: R

last: Langille

first: Jocelyn

last: Nurtanto

first: Andreea

last: Obersterescu

first: Katie

last: Teng

first: Christopher

last: Lowden

first: Julien

last: Dessapt

first: Cynthia

last: Chiu

first: Lauren

middle: V

last: Caldwell

first: David

last: Cook

first: Miguel

last: Pérez-Castro

first: Jacob

last: Berman

first: Ricky

last: Tsai

first: Alexander

last: Bahcheli

first: Geraldine

last: Mbamalu

first: Shifei

last: Wu

first: Masahiro

last: Narimatsu

first: Adele

last: Lopes

first: Iosifina

last: Fotiadou

first: Kin

last: Chan

first: Linkang

last: Zhang

first: K.W. Annie

last: Bang

first: Michael

last: Parsons

first: Larissa

last: Mourao

first: E. Idil

last: Temel

first: Liddy

last: McCulla

first: Sravya

last: Palavalasa

last: Borowsky

first: Colinda

last: Scheele

last: Wahl

first: Hartland

last: Jackson

first: Katherine

last: Stewart

first: Elaine

last: Fuchs

first: Sean

middle: E

last: Egan

first: Miguel Angel

last: Pujana

first: Jüri

last: Reimand

first: Jeffrey

last: Wrana


title: Transcriptional footprints associated with bud fertility in grapevine (Vitis vinifera L.): a developmental study

city: Legnaro

first: Monica

last: Canton

state: Padova

address: Viale dell'Università, 16

department: DAFNAE

institute: University of Padova

summary: Flowering is the most important process in plants and understanding the mechanism controlling its timing and abundance is pivotal especially for crops, which are continuously challenged by biotic and abiotic factors. Data regarding the physiology of flowering in grapevine (Vitis vinifera L.) are fragmentary and distributed over several decades, so it is necessary to provide an updated overview of the different molecular mechanism involved in the transformation of the meristems into flowering structures. In the present study, we adopted transcriptomics (RNA-Seq) to identify the determinants of fertility in the worldwide diffused cultivar Merlot. After assessing the actual fertility over a period of three years, bud samples were collected from different position along the shoot and their transcriptome studied at three phenological stages

overall_design: Bud samples were collected in three replicates from different positions along the shoot (2nd, 5th, and 10th node) and their transcriptome studied at three phenological stages spanning from floral induction (BBCH63; T1) to floral transition (BBCH77; T2) and initiation (BBCH90; T3).

first: Francesco

last: Girardi

first: Giorgia

last: Bettio

first: Angela

last: Rasori

first: Alessandro

last: Botton


title: Location matters: spatial-dependent effects of myofibroblasts determine survival in breast cancer

city: Singapore

first: Kanaga

last: Sabapathy

state: --None--

address: 11 Hospital Crescent

department: Division of Cellular & Molecular Research

country: Singapore

institute: National Cancer Centre Singapore

summary: While cancer-associated fibroblasts (CAFs) have been historically considered pro-tumorigenic, several studies found that myofibroblast-like CAFs (myCAFs) may have tumor-restraining properties. In our previous study (PMID: 37863888), we performed multi-regional bulk transcriptomics profiling of 8 ER+/PR+/HER2- breast tumors and matched peri-tumoral tissues. We identified an adipose-enriched peri-tumoral subtype which was significantly associated with poorer overall survival in breast cancer patients, in contrast to a myofibroblast-enriched subtype. Here, we performed single-nucleus RNA-sequencing of  2 ER+/PR+/HER2- invasive breast carcinomas and their matched peri-tumoral tissues (1-7 cm from tumor margins), as well as 1 reduction mammoplasty (RM) sample. We identified tumor-induced changes in the peri-tumoral adipocytes compared to RM adipocytes, as well as a high abundance of myCAFs in the larger tumor, whereas a distinct myofibroblast-like subpopulation was found in the peri-tumoral tissues of the smaller tumor. Together with deconvolution analyses of TCGA data and 3D co-culture experiments, we show that that myofibroblasts have both tumor-promoting or -restraining roles depending on their location within or surrounding the tumor.

overall_design: Single-nucleus RNA sequencing was performed on 5 samples (2 breast tumor, 2 peri-tumoral stroma, 1 reduction mammoplasty).

first: Hannah

last: Si Hui Lau


title: Susceptibility and Transcriptional Characteristics of C57BL/6 and ICR Mouse Strains in CDAHFD-Induced NASH Models

first: Wang

last: E

address: 280 South Chongqing Road

department: Department of Laboratory Animal Science

institute: Shanghai Jiaotong University School of Medicine

summary: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide. Non-alcoholic steatohepatitis (NASH), a severe form of NAFLD, is not fully elucidated. Therefore, preclinical mouse models are urgently needed as crucial tools to better understand the pathogenesis of NASH. The choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) is a widely used diet-induced model for NASH and subsequent hepatocellular carcinoma (HCC) in lean mice. However, literature on the response of different mouse strains to CDAHFD remains limited. In this study, we explored CDAHFD treatments for both C57BL/6 and ICR mouse strains in an effort to demonstrate the differences in their susceptibility to develop a NASH-like phenotype and further reveal the impact of genetic background on CDAHFD models.

overall_design: Global RNA sequencing of liver tissue from C57BL/6 and ICR mouse strains fed either CDAHFD or  normal chow diet (ND)

first: Li

last: Yao


title: Transcriptomics analysis of white adipose tissue, gastrocnemius muscle and liver tissues from Ogg1Tg mice.

city: New Brunswick

first: Sai Santosh Babu

last: Komakula

state: New Jersey

address: 61 Dudley Rd

department: Department of Nutritional Sciences

institute: Rutgers University

summary: Obesity is associated with increased oxidative stress that damages genomic and mitochondrial DNA. Oxidatively-induced lesions in both DNA pools are repaired via the base-excision repair pathway, initiated by DNA glycosylases such as 8-oxoguanine DNA glycosylase (OGG1). Global deletion of OGG1 and common OGG1 polymorphisms render mice and humans susceptible to metabolic disease. Moreover, mice with transgenic targeting of OGG1 to mitochondria (Ogg1Tg mice) confer significant protection from diet-induced obesity, insulin resistance, and adipose tissue inflammation. Here, we analyzed transcriptomics of gastrocnemius muscle from Ogg1Tg mice and control mice (C57BL/6J mice) by bulk RNA sequencing (RNAseq).

overall_design: Ogg1Tg mice were generated by targeting human OGG1-1a to mitochondria by fusing the protein with the mitochondrial translocation signal and set under the control of CMV/AG promoter.  To understand the role of mitochondrial targeted OGG1, we have euthanized Ogg1Tg mice and  control mice (C57BL/6J mice) at the 20 weeks of age, gastrocnemius muscle tissue was collected, and total RNA was isolated. cDNA library preparation and RNA sequencing were performed at RUCDR infinite biologics, Rutgers University, USA. Prepared cDNA was used for the RNA sequencing using Illumina sequencer.

first: Sai

first: Harini

last: Sampath


title: RNA-seq of three groups mice in hippocampus.

city: Xian yang

first: Hongbo

last: Zhang

state: Shannxi

address: Xi nong road

department: College of Food Science and Engineering

institute: Northwest A&F University

summary: We sought to examine whether  urolithin A  could  alleviate the cognitive impairments of chronic alcoholic mice. RNA-sequencing (RNA-seq) on mice hippocampus were performed in order to identify the key biological processes and pathways regulated by urolithin A.

overall_design: 9 Ctrl mice, 7 EtOH mice, 7 EtOH-UA mice