title: Role of Liver Fatty Acid-Binding Protein (LFABP) in Adipose Tissue Metabolism

city: Newark

first: Adriana

last: Messyasz

address: 185 South Orange Avenue

institute: Rutgers-New Jersey Medical School

summary: Obesity and adipose tissues quality are important risk factors for the development of type 2 diabetes and metabolic syndrome; this risk is related to intrinsic differences in the behavior of adipocytes in different fat depots. We have shown that the liver fatty acid-binding protein null (LFABP-/-) mouse is a model of the ‘metabolically healthy obese’ (MHO) state. Here, we demonstrate that the LFABP-/- mouse is a novel model of hyperplastic subcutaneous adipose tissue (SAT). LFABP-/-mice fed a high-fat diet (HFD) for 12 weeks gained 27% more weight (BW, g: 43.6 LFABP-/- vs 34.4 WT, P<0.001, n=10) and their fat mass was almost double (Fat, g: 15.4 LFABP-/-vs8.3 WT, P<0.001, n=10) that of WT. Intriguingly, despite the substantial increase in mass, inguinal white adipose tissue (iWAT) adipocyte size was >4-fold smaller (46pL LFABP-/-vs222pL WT per cell, P<0.001, n=5) and adipocyte number was 5-fold higher (23.6 LFABP-/-vs4.7 WT x 106, P=0.001, n=5) in the iWAT of LFABP-/-compared to WT mice. Upon obesity development, Lfabp deletion results in transcriptomic differences that include large effects on cholesterol biosynthesis and extracellular matrix (ECM) remodeling, likely leading to tissue growth and a state of ‘adaptive fibrosis’ and ‘homeostatic adipogenesis’ for safe excess energy storage. Since LFABP is not expressed in adipose tissues, these results suggest that its ablation promotes interorgan signaling that may limit hypertrophy and drive hyperplasia in expansion of potentially metabolically beneficial SAT, contributing to the MHO phenotype of the LFABP-/-mouse.

overall_design: Male mice on a C57Bl/6J background were used for this study separated in two groups: (a) LFABP-/- males (n=5), and (b) (WT) males (n=5). The WT mice served as controls. Mice were maintained on a 12-h light/dark cycle and had unrestricted access to standard rodent chow. At 2 months of age, male LFABP-/-, and WT mice were housed 2-3 per cage and fed a 45 kcal % fat diet high in saturated fat (D10080402, Research Diets, Inc., New Brunswick, NJ) for 12 weeks. At the end of the HF feeding, mice were food deprived for 4 hours and anesthetized with ketamine/xylazine/acepromazine (80:100:150 mg/kg, intraperitoneally, respectively), prior to collection of blood and tissues. Adipose tissue depots (iWAT and iBAT) and the liver were dissected rapidly, snap-frozen in liquid nitrogen and then stored at -80oC for future analysis. Total RNA was extracted from the iWAT, iBAT, and the liver of HF-fed LFABP-/- (n=5) and WT (n=5) males, and 15uL of RNA extract were submitted for bulk RNA-seq analysis to the Molecular and Genomics Informatics Core Facility of Rutgers University.

first: Anastasia

last: Diolintzi

first: Yinxiu

last: Zhou

first: Angelina

last: Fomina

first: Seema

last: Husain

first: Susan

last: Fried

first: Labros

last: Sidossis

first: Judith

last: Storch


title: RNA-seq for the soybean leaves

status: Public on Jun 18 2025

city: guangzhou

first: qi

last: guo

address: Wushan Street five road No. 483

country: China

institute: South China Agricultural University

type: Expression profiling by high throughput sequencing

summary: To investigate the molecular mechanism underlying the involvement of GmPAP23 in intracellular phosphorus recycling, an  transcriptomic analysis was performed using the mature leaves of WT and OX5 lines grown under P sufficient conditions at R6 stage,the comparison between WT and OX5 lines revealed that a total of 1658 DEGs were identified between WT and OX5 lines, of which 828 genes were upregulated and 830 genes were downregulated

first: Jiang

last: Tian

first: Cuiyue

last: Liang

first: Qi

last: Guo


title: Profiling of Circulating extracellular vesicles microRNAs Reveals Diagnostic Potential and Pathways in Non-Obstructive and Obstructive Azoospermia

city: Xuzhou

first: Dianshuang

state: Jiangsu

address: 209 Tongshan Road

institute: Xuzhou Medical University

type: Non-coding RNA profiling by high throughput sequencing

summary: The accurate diagnosis of non-obstructive azoospermia (NOA) and obstructive azoospermia (OA) is crucial for selecting appropriate clinical treatments. This study aimed to investigate the pivotal role of miRNAs in circulating plasma exosomes in distinguishing between NOA and OA, as well as uncovering the signaling pathways involved in azoospermia pathogenesis. In this study, differential expression of extracellular vesicles (EVs) miR-513c-5p and miR-202-5p was observed between NOA and OA patients, while the selenocompound metabolism pathway was identified as relevant to azoospermia pathogenesis through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis. The predictive power of these microRNAs was evaluated using ROC-AUC analysis, demonstrating promising sensitivity, specificity, and area under the curve values. A binomial regression equation incorporating circulating plasma levels of EVs miR-202-5p and miR-513c-5p along with follicle-stimulating hormone was calculated to provide a clinically applicable method for diagnosing NOA and OA. This study presents a non-invasive testing approach for distinguishing between NOA and OA, offering a valuable tool for clinical practice.

overall_design: The study included patients with NOA, OA, and normozoospermic controls. Circulating plasma exosomal microRNAs were profiled using the NextSeq System.

first: Yujuan

last: Qi

first: Yalun

last: Wu

first: Kun

last: Pang

first: Yu

last: Qiao

first: Honglin

last: Li

first: Zhenbei

first: Fangfang

last: Hu

first: Yijuan

last: Cao

first: Wen

last: Yang

first: Conghui

last: Han

first: Zuobin

last: Zhu


title: Tumor and microenvironment reprogramming during radiochemotherapy in glioma using a combined diagnostic imaging and single-cell RNA sequencing approach

city: Milano

first: Stefano

last: de Pretis

address: Via Olgettina, 58

department: Center for Omics Sciences

country: Italy

institute: IRCCS San Raffaele Institute

summary: Glioblastoma (GBM) is the most common primary brain tumor in adults with a median survival of 11-12 months. Standard therapy consists of radiotherapy (RT) plus chemotherapy with Temozolomide (TMZ), and no alternative treatment is available. We assessed changes in tumor microenvironment (TME) after RT associated with TMZ and metformin (MET) in a syngenic murine GBM model using single-cell RNA-sequencing (scRNA-seq). RT induced an enrichment of GO annotation related with cell cycle, translation and ribosome biogenesis in all tumor clusters, except the radio resistant one where an increase in the inflammatory phenotype was observed. Resident GAM were reduced after RT alone and differentially modulated by RT-drug combinations. After RT alone, we detected an increase in GAM markers and a downregulation of glycolytic metabolism in both microglial and peripheral macrophage subclusters. Association of TMZ increased the pro-inflammatory phenotype of some GAM clusters in comparison to RT. A different signature was observed for the TMZ-MET association but limited to peripheral infiltrating GAM.

overall_design: Assessment of tumor microenvironment (TME) changes after RT associated with TMZ and metformin (MET) in a syngenic murine GBM model using single-cell RNA-sequencing (scRNA-seq). Assessment of tumor microenvironment (TME) changes after RT associated with TMZ and metformin (MET) in a syngenic murine GBM model using single-cell RNA-sequencing (scRNA-seq).

first: Silvia

last: Valtorta

first: Rosa

middle: M

last: Moresco


title: The Impact of TLR5 on Liver Function in Age-Related Metabolic Disorders

city: Hwasun-gun, Jeollanam-do

first: Dong-Hyun

last: Kim

state: Not Applicable

address: 264, Seoyang-ro, Hwasun-eup,

country: South Korea

institute: Medispan

summary: Toll-like receptor 5 (TLR5) plays a critical role beyond its traditional function in innate immunity, significantly impacting metabolic regulation and liver health. Previously, we reported that TLR5 activation extends healthspan and lifespan in aging mice. This study demonstrates that TLR5 deficiency leads to pronounced metabolic abnormalities with age, primarily affecting liver metabolic functions rather than intestinal inflammation. Comprehensive RNA sequencing analysis revealed that TLR5 deficiency induces gene expression changes in liver tissue similar to those caused by the methionine-choline deficient (MCD) diet, particularly affecting lipid metabolism and circadian rhythm-related genes. TLR5 KO mice displayed an increased propensity for liver fibrosis and lipid accumulation under the MCD diet, exacerbating liver pathology. Both hepatocytes and hepatic stellate cells in TLR5 KO mice were functionally impacted, leading to metabolic dysfunction and fibrosis. These findings suggest that TLR5 could be a significant target for addressing metabolic diseases that arise and worsen with aging. Furthermore, understanding the mechanisms by which TLR5 activation extends healthspan could provide valuable insights into therapeutic strategies for enhancing longevity and managing age-related metabolic disorders.

overall_design: mRNA profiles of the liver were established via deep sequencing. The profiles were generated in the livers of two groups of 32-week-old mice: a wild-type (WT) group and an Toll-like receptor 5 knockout group (TLR5 KO). Both groups were fed a standard diet or a methionine-choline deficient (MCD) diet for 2 weeks.

first: Kyung

middle: A

last: Cho


title: Single cell gene expression profiles of mouse tricuspid valves

city: Philadelphia

first: Mark

last: Kahn

state: PA

address: 3400 Civic Center Blvd

department: Cardiovascular Institute

country: USA

institute: University of Pennsylvania

summary: Tricupsid valves from mice with valve endothelial cell specific deletion of KLF2/4 were profiled using scRNAseq.

overall_design: Tricuspid valves were harvested from Prox1CreERT2;KLF2fl/fl;KLF4fl/fl mice and controls at 4, 7 and 14 days post tamoxifen. Tricuspid valves from 5 mice were pooled together for each group and timepoint. Each group and timepoint were performed in duplicate.

first: Jesse

last: Pace

first: Lauren

last: Goddard


title: Influence of 5'-(N-ethylcarboxamido)adenosine on gene expression in mouse myocardial infarction model

city: Gwangju

first: Yunju

last: Jo

address: 123, Cheomdangwagi-ro

institute: Gwangju Institute of Science and Technology

summary: To investigate the potential mechanism of NECA against MI-induced myocardial damage

overall_design: Total RNAs of mouse infarcted myocardium were used to identify differential gene expression following NECA treatment

first: Dongryeol

last: Ryu

first: Jee-Heon

last: Jeong

first: Shibo

last: Wei

first: Tiep-Tien

last: Nguyen

first: Yan

last: Zhang

first: Wonyoung

last: Park

first: Nhu-Nam

first: Jiwoo

first: Chang-Myung

last: Oh

first: Doyoun

first: Jin

first: Ki-Tae

last: Ha


title: Single cell analysis of antigen-presenting cells in the large intestine

city: New York

first: Jordan

last: Zhou

state: NY

address: 413 E 69th St

institute: Weill Cornell Medical College

summary: Antigen-presenting cells are responsible for the initiation of T cell responses and critically shape tolerogenic or inflammatory immune responses to the gut microbiota. Here, we employed the pathobiont Helicobacter hepaticus, and performed single-cell RNA sequencing for all antigen-presenting cells in the large intestine in various contexts.

overall_design: MHCII+ cells were sorted from the large intestine of naïve C57BL/6J mice, C57BL/6J mice colonized with Helicobacter hepaticus, and Il10-/- mice colonized with Helicobacter hepaticus. We mixed a 9:1 ratio of CD19- cells to CD19+ cells, to enrich for non-B cell populations. Cells were pooled from two mice for each sample.

first: Wenqing

first: Gregory

last: Sonnenberg


title: Bulk RNA-seq of CCR6+ ILC3s

summary: To determine the function of STING in ILC3s, we performed bulk RNA sequencing on CCR6+ ILC3s sorted from the large intestine of naïve Sting1 f/f and ROR t-cre x Sting1 f/f mice.

overall_design: CCR6+ ILC3s (sorted as CD45-dim CD90-hi CD3- CD5- NK1.1- TCR  - CD11b- CD11c- B220- CD127+ CCR6+) were sorted from the large intestine of naïve Sting1 f/f and ROR t-cre x Sting1 f/f mice. Cells were sorted from 4 individual mice as biologic replicates for each group.


title: The TFIID subunit Taf13 is dispensable for RNA polymerase II transcription, but essential for early embryogenesis (ChIP-Seq)

city: Illkirch

first: Igor

last: Martianov

address: 1 rue Laurent Fries

country: France

institute: IGBMC

type: Genome binding/occupancy profiling by high throughput sequencing

summary: RNA polymerase II transcription initiation requires assembly of a preinitiation complex (PIC). According to the stepwise model of PIC assembly, TFIID is the first GTF to be recruited. TFIID comprises TBP and 13 TBP-associated factors (TAFs). We focused on TAF13, the smallest subunit of TFIID. Taf13 has a histone-like domain that heterodimerizes with its partner Taf11. Recently published structures of TFIID place the Taf13-Taf11 heterodimer in lobe A where it forms a “bridge” between TBP and TFIID. According to this structure, the Taf11-Taf13 heterodimer has been suggested to be critical for TBP deposition at promoters. To better address this question, we generated mouse Embryonic Stem Cells (ESCs) cell lines and genetically modified mice where the gene coding for Taf13 was inactivated. Taf13-null mice died at E6.5-E7.5, whereas ESCs survived up to 15 days after inactivation of Taf13, but showed slower growth as compared to controls. To understand how Taf13 inactivation impacts TFIID and RNA polymerase II (Pol II) recruitment, we performed ChIP seq for the TBP and Taf1 subunits of TFIID along with PolII on ESC lines expressing or not Taf13. ChIP seq for histone marks H3K4Me3 and H3K27ac were also performed. Taf13 inactivation does not impair TBP recruitment at promoters, while that of Pol II was reduced both at the promoter and gene body. Surprisingly, recruitment of Taf1 was increased and while the H3K4Me3 mark was not affected, H3K27ac was notably increased in the absence of Taf13. Taken together, these data showed that loss of the Taf11-Taf13 heterodimer did not strongly impact TBP recruitment to promoters, but led to increased Taf1 and H3K27ac levels, but reduced paused and elongating Pol II.

overall_design: ChIP was performed on MNase digested ESC chromatin for TBP, Taf1 and Taf13 (ChIP against HA) and sonicated chromatin for PolII, H3K4Me3 and H3K27ac. Each ChIP was done on chromatin from Taf13-/- ESCs ectopically expressing or not ectopic 3XHATaf13.

last: Martiyanov

first: Stephanie

last: Le Gras

first: Irwin

last: Davidson


title: The TFIID subunit Taf13 is dispensable for RNA polymerase II transcription, but essential for early embryogenesis (RNA-Seq)

summary: RNA polymerase II transcription initiation requires assembly of a preinitiation complex (PIC). According to the stepwise model of PIC assembly, TFIID is the first GTF to be recruited. TFIID comprises TBP and 13 TBP-associated factors (TAFs). We focused on TAF13, the smallest subunit of TFIID. Taf13 has a histone-like domain that heterodimerizes with its partner Taf11. Recently published structures of TFIID place the Taf13-Taf11 heterodimer in lobe A where it forms a “bridge” between TBP and TFIID. According to this structure, the Taf11-Taf13 heterodimer has been suggested to be critical for TBP deposition at promoters. To better address this question, we generated mouse Embryonic Stem Cells (ESCs) cell lines and genetically modified mice where the gene coding for Taf13 was inactivated. Taf13-null mice died at E6.5-E7.5, whereas ESCs survived up to 15 days after inactivation of Taf13, but showed slower growth as compared to controls. In order to understand how inactivation of Taf13 impact the genes expressions we performed bulk mRNA-seq from the Taf13 expressing and null lines. This analysis showed that loss of TAF13 resulted in a greater than two-fold upregulation of 562 genes but only 41 of them were up-regulated more than four-fold. On the other hand, 382 genes were down-regulated, 34 of which showed more than a four-fold repression. Ontology analyses showed that the affected genes did not belong to any specific pathway, but we noticed that many primitive endoderm markers were up-regulated by TAF13 deficiency (Sox7, Sox17, Gata4, Gata6) and some ESC markers were downregulated (Nanog, Klf4, Zfp42) while the pluripotency markers Sox2 and Oct3/4 were unchanged.

overall_design: Cells were grown in the absence and in the presence of doxycycline for 7 days prior to the RNA extraction. For each condition cells were grown in triplicate (three different Petri dishes). mRNAs then were sequenced.

first: Celine

last: Keime


title: Effect of MacroD1 knockout on gene expression of heart on mouse septic model

city: Shang hai

first: chen

middle: xiao

last: qiang

state: China

address: 650 New Songjiang Road

department: Department of Cardiology

institute: Shanghai General Hospital, Shanghai Jiaotong University School of Medicine

summary: Metabolic plasticity of tissues determines the degree and reversibility of organ damage under inflammatory challenges. While treating septic cardiomyopathy (SCM) with high mortality, metabolic management should be considered. Still, similar pan-organ metabolic anomalies usually yield contrasting results in each one, highlighting the necessity to identify cardiac-specific metabolic regulators. Nicotinamide adenine dinucleotide (NAD+) signaling is fundamental to cellular metabolic homeostasis and inflammatory response, and cardiomyocyte-enriched NAD+-consuming enzymes programming metabolism against sepsis and their roles in SCM remain undefined. In this study, we explored the expression patterns of NAD+-consuming enzymes of heart and found Mono-ADP-ribosyl hydrolase MacroD1 protein was distinctly enriched in rodent and AC16 human cardiomyocytes and upregulated during severe endotoxemia. Genetic and pharmacological inactivation of MacroD1 counteracted myocardial metabolic impairment, lipid accumulation, inflammatory infiltrate, cardiac dysfunction, and mortality risk induced by septic challenges in mice. Mechanistically, MacroD1 selectively modulated the activity of mitochondrial complex I (MCI), a proximal respiratory unit most vulnerable to early endotoxemia. Its inhibition enhanced MARylation of NDUFB9, an accessory assembly factor of MCI proton-pumping module ND5, and therefore binding to ND5 for preserving MCI activity in sepsis, restraining bioenergetic deficiency, oxidative stress-coupled NLRP3 inflammasome activation, and pyroptosis of cardiomyocytes. Our research reveals that MacroD1 dictates cardiac tolerance to sepsis by configuring MCI-coupled bioenergetic reserve and pyroptosis of cardiomyocytes. Blockade of MacroD1 promises specific prevention of SCM.

overall_design: A total of 8 samples were divided into 4 groups for analysis. After the 8-week-old cardiac-specific conditional MacroD1 knockout mice (Mac_ko) and control mice (WT) were treated with LPS (10mg/kg) or saline for 18 hours, the hearts were extracted for high-throughput sequencing analysis. The specific groups were as follows: WT, Mac_ko, WT+LPS, Mac_ko+LPS. (n=2 for each group).

first: Xiaoqiang

last: Chen

first: Tianyou

last: Yuan

first: Danchuan

last: Zheng

first: Fangfang

last: Li

first: Hao

last: Xu

first: Maoqing

last: Ye

first: Shaowen

last: Liu

first: Jun


title: RNA-seq of Caco-2 cells treated with hypoxia/reoxygenation

city: Dalian

first: Xiaofeng

last: Tian

address: Zhongshan Road NO.467

department: General Surgery

institute: The Second Hospital of Dalian Medical University

summary: We analyzed the expression profiles of 2258 mRNAs on Caco-2 cells treated with hypoxia/reoxygenation or control using RNA-seq analysis. And find that 1052 mRNAs are up-regulated and 1206 are down-regulated.

overall_design: In the study, we profiled mRNA expression in Caco-2 cells of 3 control group and 3 hypoxia/reoxygenation group.

first: Zhao

last: Xuzi

first: Ding

last: Ze

first: Liu

last: Deshun

first: Wang

last: Zhecheng

last: Yan

first: Yao

last: Jihong

first: Tian

last: Xiaofeng


title: A First-In-Class Inhibitor of Skp1-Skp2 Interaction Has Potent Preclinical Efficacy Against Castration-Resistant Prostate Cancer

city: Seattle

first: Ilsa

last: Coleman

state: WA

address: 1100 Fairview Ave N, E2-112

department: Human Biology

institute: Fred Hutchinson Cancer Center

summary: Metastatic, castration-resistant prostate cancer (mCRPC) directly contributes to the mortality and morbidity of prostate cancer. It is imperative to identify new molecular targets and discover effective therapeutic agents against lethal mCRPC. We have developed a new class of small-molecule compounds and evaluated their anticancer activities in preclinical models using molecular, cellular, and animal approaches. GH501 demonstrates nanomolar potency in the NCI-60 human cancer cell panel and multiple mCRPC cell lines with diverse genetic backgrounds, including those resistant to androgen deprivation therapy drugs. Mechanistically, GH501 may bind S-phase kinase-associated protein 1 (Skp1) and disrupt the physical interaction between Skp1 and S-phase kinase-associated protein 2 (Skp2) within the Skp1-Cullin1-F-box protein ubiquitin ligase complexes (SCF), thereby affecting multiple oncogenic signals implicated in mCRPC progression, including p21, p27, β-catenin, cyclin D1, E2F1, enhancer of zeste homolog 2, c-Myc, and survivin. GH501 exhibits excellent in vitro and in vivo safety pharmacology, and GH501 monotherapy effectively inhibits the in vivo growth of cell- and patient-derived xenografts in intraosseous and subcutaneous models. These results indicate that GH501 is a promising therapeutic candidate for the treatment of mCRPC and warrants further preclinical development.

overall_design: RNA sequencing of C4-2 prostate tumor cells treated with GH501 using Illumina TruSeq Library prep and sequenced on Illumina HiSeq 2500.

first: Xin

first: Kenza

last: Mamouni

first: Rui

last: Zhao

first: Lijuan

last: Bai

first: Yanhua

first: Yifei

last: Wu

first: Zhong-Ru

last: Xie

first: Giuseppe

last: Sautto

first: Degang

first: Nathan

middle: J

last: Bowen

first: Alira

last: Danaher

first: Dehong

first: Nicholas

last: Cook

first: Skylar

last: Grayson

first: Peter

middle: S

last: Nelson

first: Qichao

last: Bao

first: Jia

last: Zhou

first: Adeboye

middle: O

last: Osunkoya

first: Omer

last: Kucuk

first: Lajos

last: Gera

first: Daqing


title: RNA-seq of depletion of TMEM2 during Caco-2 cells treated with hypoxia/reoxygenation

first: Xiaofeng

last: Tian

summary: We analyzed the expression profile of 183891 mRNAs in Caco-2 cells with or without TMEM2 knockdown using RNA-seq analysis under hypoxia/reoxygenation condition.

overall_design: In the study, we profiled mRNA expression in Caco-2 cells of 3 hypoxia/reoxygenation group and 3 hypoxia/reoxygenation with TMEM2 knockdown group.

first: Zhao

last: Xuzi

first: Ding

last: Ze

first: Liu

last: Deshun

first: Wang

last: Zhecheng

last: Yan

first: Yao

last: Jihong

first: Tian

last: Xiaofeng


title: The TFIID subunit Taf13 is dispensable for RNA polymerase II transcription, but essential for early embryogenesis

first: Igor

last: Martianov

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

overall_design: Refer to individual Series


title: RNA-seq for 6 mouse intestinal tissue samples

summary: We analyzed the expression profiles of 19763 mRNAs on intestine tissues from mice suffering from sham and intestinal I/R using RNA-seq analysis. And find that 559 mRNAs are up-regulated and 354 are down-regulated significantly.

overall_design: In the study, we profiled mRNA expression in the intestine from mice of 3 sham group and 3 intestinal ischemia/reperfusion group.


title: A developing HPA axis permits neonatal immune sensitivity to common allergens.

status: Public on Jun 17 2025

first: Dr. Shruti

last: Naik

address: 1425 Madison Ave

department: Immunology and Immunotherapy

institute: Icahn School of Medicine at Mount Sinai

summary: Atopic and allergic diseases predominantly manifest in early life, a period of profound growth and maturation. Yet, there is a dearth of information on the impact of developmental parameters on the neonatal immune reaction to allergens. Here we demonstrate that common allergens including house dust mite (HDM) elicited potent type 17 inflammatory responses from neonatal but not adult mice. HDM-induced inflammation was abolished in Rorgt-, gd T cell-, or epithelial IL-17RC- deficient animals and surprisingly did not require nociceptors or lymph node engagement. Instead, neonatal CD301b+ type 2 conventional dendritic cells (cDC2s) abundantly engulfed allergen and locally activated gd T cells in the skin. Despite uptaking equivalent antigen to neonates, adult cDC2s did not promiscuously activate in the skin. Mechanistically, this discrepancy was not attributable to cell-intrinsic differences arising from the distinct developmental origins of neonatal and adult cDC2s. Instead, neonatal cDC2 hyperactivation could be traced to a lower systemic glucocorticoid level, a consequence of an immature hypothalamic-pituitary-adrenal (HPA) axis in early life, and could be reversed by cortisol administration at the time of allergen challenge. These findings bring to fore the influence of organismal developmental factors in shaping immune sensitivity to allergens in early life.

overall_design: To unbiasedly investigate the inflammation phenotype in allergens inoculated neonate skin, we performed bulk RNA sequencing with full thickness skin biopsy isolated from PBS control or allergens challenged neonate and adult mice. To study the mechanism how Corticosterone regulate neonate dendrtiic cell allergic response, we sorted dendritic cells from corticosterone or DMSO and HDM or PBS treated neoante skin and applied to bulk RNA sequencing.

first: Yue

last: Xing

first: Jill

last: Wisnewsky

first: Kody

last: Mansfield

first: Aleksandr

last: Prystupa

first: Ikjot

last: Sidhu

first: Shruti


title: Single-cell and in situ spatial analyses reveal the diversity of newly born hematopoietic stem cells and of their niches [scRNA-Seq]

city: Paris

first: Lea

last: Torcq

address: 25 Rue du docteur Roux

institute: Institut Pasteur

summary: Hematopoietic stem cells (HSCs) and more committed progenitors (collectively referred to as HSPCs) emerge from vessels during development, via Endothelial-to-Hematopoietic Transition (EHT). Recently, using the zebrafish embryo, we showed that two EHT cell types emerge from the dorsal aorta, raising the question of their subsequent fate. To address this issue, we established a complex pipeline based on single-cell photoconversion and transgenic lines to characterize the abilities of EHT cell progenies to conquer hematopoietic organs and to obtain their transcriptomic profiles. We show that the two EHT cell types lead to partly differentially fated cells, with significant differences in thymus colonization and T-lymphoid lineage commitment. In addition, we investigated implantation of HSPCs in niches, with the support of HSPC signatures (gata2b and cd34/podocalyxin), retrieved from our single-cell datasets. This revealed, at unprecedented resolution, the homing of HSPCs in niches of entire early larvae, including the pronephros, the sub-aortic and caudal regions, as well as the area contacting the supra-intestinal artery. Our work provides new insights on fundamental aspects of HSPC fate acquisition, from their emergence to their homing in specific niches.

overall_design: Single-cell transcriptomics analysis of newly born hematopoietic stem and progenitor cells. This dataset comprises progenies of cells photoconverted at 2dpf and sorted by FACS at 5dpf, using the Tg(kdrl:nls-kikume) transgenic line, as well as sorted (FACS) hematopoietic cells from transgenic reporter lines, namely from the Tg(runx1+23:eGFP) and the outcross of the Tg(cd41:eGFP) and Tg(gata2b:RFP) lines. Larvae were collected after dissection (separating the rostral, anterior and posterior region along a transversal section at the posterior limit of the elongated yolk and at the posterior limit of the swim bladder), dissociation and sorting using a BD FACS AriaIII cell sorter. Progenies of photoconverted cells comprise progenies of single-EHT photoconversion (either EHT pol+ or EHT pol-) or whole hemogenic endothelium photoconversion. Cells were sorted in 384 wells plates (28 plates, in 2 independent sessions of 14 plates each) and the transcriptomic library was prepared according to the MARS-seq protocol 2.0 (Keren-Shaul et al. 2019). Libraries were then sequenced using the NextSeq 500/550 High Output Kit v2 (75 cycles) (Illumina). Raw reads were converted to fastq files using bcl2fastq package (2.20.0). Reads were demultiplexed and mapped to the Lawson Lab curated genome [(Lawson et al., 2020), v4.3.2] using the MARS-seq pipeline scripts (Keren-Shaul et al., 2019).

first: Catherine

last: Vivier

first: Sandrine

last: Schmutz

first: Yann

last: Loe-Mie

first: Anne

last: Schmidt


title: High cellulose diet aggravates food allergy through gut homeostasis disruption

city: Nanjing

first: Jialu

last: Shi

address: No.87 DingJiaQiao

institute: southeast university

summary: This study investigated the impact of a high cellulose diet (HCD) on intestinal homeostasis and food allergy development in BALB/c mice. While soluble fibers are known to mitigate FA via short-chain fatty acid (SCFA) production, the role of insoluble fibers like cellulose remains unclear. Mice fed HCD exhibited gut dysbiosis, characterized by increased Proteobacteria, decreased tight junction protein expression, and intestinal barrier impairment, despite unchanged SCFA levels. RNA sequencing revealed HCD-induced upregulation of immune pathways, including the positive regulation of B and T cells differentiation and antigen receptor-mediated signaling pathway. Following ovalbumin (OVA) sensitization, HCD-fed mice displayed exacerbated allergic symptoms, including elevated OVA-specific IgE, IgG, histamine, and mMCP-1 levels. Gut microbiota analysis highlighted enrichment of potentially pathogenic taxa in HCD+OVA groups. Fecal microbiota transplantation (FMT) from HCD donors to antibiotic-treated recipients showed severe food allergy responses, confirming microbiota-mediated effects. These findings demonstrate that HCD exacerbates food allergy through gut microbial dysbiosis, intestinal barrier disruption, and intestinal immune disorder.

overall_design: After feeding with NCD or HCD diets for 60 days, mice were divided into four groups: NCD group, NCD+OVA group, HCD group, and HCD+OVA group. As shown in Fig. 2A, mice were sensitized twice by intraperitoneal injection of 50 μg OVA (Sigma-Aldrich, USA) and 1 mg aluminum potassium sulfate adjuvant (Sigma-Aldrich, USA) on days 0 and 14. After two weeks, mice were challenged with oral administration of 50 mg OVA every other day, totaling five administrations. The NCD and HCD groups were treated with an equal volume of saline. After the final challenge, blood, spleen and IECs from each mouse were collected.


title: The transcriptional effects of osteocyte-derived mitochondria on endothelial cells

city: Shanghai

first: Junjie

last: Gao

address: 600 Yishan Road

institute: Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine

summary: In this study, osteocytes were proved to be capable of delivering mitochondria to endothelial cells in cortical bone and promotes its angiogenesis. By utilizing RNA seq, we investigated the effect of osteocytes-derived mitochondria on endothelial cells.

overall_design: bEnd.3 cells were co-cultured with or without mitochondria isolated from MLO-Y4 cells in vitro. After 24 hours, bEnd.3 cells were collected for further RNA-Seq analysis.

first: Peng

last: Liao


title: Foxi1 regulates multipotent mucociliary progenitors and ionocyte specification through transcriptional and epigenetic mechanisms

city: Freiburg

first: Peter

last: Walentek

state: BW

address: Breisacherstr. 113

department: Internal Medicine IV & IMITATE

country: Germany

institute: University Freiburg Medical Center

summary: Foxi1 is a master regulator of ionocytes (ISCs / INCs) across species and organs. Two subtypes of ISCs exist, and both - and -ISCs regulate pH- and ion-homeostasis in epithelia. Gain and loss of FOXI1 function are associated with human diseases, including Pendred syndrome, male infertility, renal acidosis and cancers. Foxi1 was predominantly studied in the context of ISC specification, however, reports indicate additional functions in early and ectodermal development. Here, we re-investigated the functions of Foxi1 in Xenopus laevis embryonic mucociliary epidermis development and found a novel function for Foxi1 in the generation of Notch-ligand expressing mucociliary multipotent progenitors (MPPs). We demonstrate that Foxi1 has multiple concentration-dependent functions: At low levels, Foxi1 maintains ectodermal competence in MPPs through transcriptional and epigenetic mechanisms, while at high levels, Foxi1 induces a multi-step process of ISC specification and differentiation in cooperation with Ubp1 and Dmrt2. We further describe how foxi1 expression is affected through auto- and Notch-regulation, and how this developmental program affects mucociliary patterning. Together, we reveal novel functions for Foxi1 in Xenopus mucociliary epidermis formation, relevant to our understanding of vertebrate development and human disease.

overall_design: bulk mRNA-seq of stage 20 and stage 32 Xenopus laevis mucociliary organoids from uninjected or foxi1 (1.5 pmol), ubp1 (3 pmol) or dmrt2 (1 pmol) morpholino-injected embryos

first: Hansen

last: Mona

first: Weber

last: Damian

first: Haegele

last: Sandra

first: Walentek

last: Peter


title: Splenic CD169+Tim4+ Marginal Zone Metallophilic Macrophages Are Essential for Wound Healing and Resolution of Inflammation After Myocardial Infarction

city: Birmingham

first: Min

state: AL

address: 1900 University Blvd, THT Building Suite #130G

institute: University of Alabama at Birmingham

summary: Fidelity of wound healing after myocardial infarction (MI) is an important determinant of subsequent adverse cardiac remodeling and failure. Macrophages derived from infiltrating Ly6Chi blood monocytes are a key component of this healing response; however, the importance of other macrophage populations is unclear. Here, we establish in mice an essential role for splenic CD169+Tim4+ marginal metallophilic macrophages (MMMs) in post-MI wound healing. Splenic CD169+Tim4+ MMMs circulate in blood as Ly6Clow cells expressing express core macrophage markers and help populate CD169+Tim4+LYVE1low macrophages in the naïve heart. After acute MI, splenic MMMs augment phagocytosis and robustly mobilize to the heart, resulting in marked expansion of cardiac CD169+Tim4+LyVE1low macrophages with an immunomodulatory and pro-resolving gene signature. These macrophages are obligatory for apoptotic neutrophil clearance, suppression of inflammation, and induction of a reparative macrophage phenotype in the infarcted heart. Splenic MMMs are both necessary and sufficient for post-MI wound healing, and limit late pathological remodeling. Pharmacological expansion of the splenic marginal zone and MMMs during acute MI alleviates inflammation and cardiac remodeling. Finally, humans with acute ST-elevation MI also exhibit expansion of circulating CD169+Tim4+ macrophages. We conclude that splenic CD169+Tim4+ MMMs are required for pro-resolving and reparative responses after MI and can be manipulated for therapeutic benefit to limit long-term heart failure.

overall_design: Compare the gene expresion profiling analysis of RNA seq data in naïve and 1 day post MI blood, spleen and heart. (Comparitive gene expression profiling analysis of CD169+ CD169- in blood, LYVE1 high and low in spleen and heart)

first: Mohamed

last: Ismahil

first: Gregg

last: Rokosh

first: Sumanth

middle: D

last: Prabhu


title: CRISPR Screen Reveals SOX2 as a Critical Regulator of CD133 and Cellular Stress Response in Glioblastoma II

city: Hamilton

first: Sheila

last: Singh

state: ON

address: 1280 Main Street West

department: Biochemistry and Biomedical Sciences

country: Canada

institute: McMaster University

summary: Glioblastoma (GBM) remains a formidable challenge in clinical settings due limited treatments available. The surface protein CD133 marks glioblastoma stem cells (GSCs), cells capable of overcoming therapeutic pressures and correlate with more aggressiveness tumor phenotypes. In this study, we employed a CRISPR-Cas9 functional screen to deconvolute CD133 dynamics in tumors. This led us to establish that SOX2 is a key player in controlling the PROM1 gene, which in turn influences how cells react to stress factors, including those induced by chemoradiation treatment. The discoveries in this study shed light on the complex web of mechanisms that control the survival and resistance of GSCs, offering promising new avenues for targeting and potentially overcoming therapy resistance.

overall_design: The CRISPR screen was established, where 1E8 cells were transduced with the TKOv3 lentivirus library at an MOI of 0.3, representing more than 400-fold coverage per sgRNA after selection with puromycin. Media was changed 24 hours after infection to puromycin-containing medium (1.2µg/mL). 72 hours after transduction, 3E7 puromycin-selected cells were collected for genomic DNA extraction at starting timepoint, and 9E7 cells were evenly divided into triplicates (3E7 cells each, 2.5E6 cells per 15cm dish). Passaging subsequently occurred every 7 days (approximately 3 cell doublings), where 3E7 cells in each replicate were reseeded until the 12th doubling (T12) when sorting was performed. A representative portion of the final population of cells (bulk/unsorted) was collected for sequencing prior to staining for flow cytometry followed by the top and bottom 5th-percentiles of CD133 surface expression being collected in cooled flow tubes. Collected cells were centrifuged and stored at -80 °C until genomic extraction as described below.

first: Neil

last: Savage

middle: K

first: Chirayu

middle: R

last: Chokshi

first: Chitra

last: Venugopal

first: Kevin

last: Brown

first: Jason

last: Moffat


title: Genetic and pharmacological targeting of nicotinic acetylcholine receptor action blocks tumor progression in mouse models of breast cancer

city: San Diego

first: Matthew

middle: Allan

last: Heard

state: California

address: 2534 Pheasant Drive

department: Surgery

institute: UC San Diego

summary: The alpha 7 nicotinic acetylcholine receptor has a functional role in myeloid immune cells in models of injury and infection, but a role in tumor associated immune cells has not been established. Here we focus on the role of CHRNA7 in myeloid immune cells  in immune competent triple negative breast cancer mouse models. The purpose of our scRNAseq studies was to evaluate the role of CHRNA7 deletion on the in vivo immune cell transcriptional profile. We established primary cultures of bone marrow-derived myeloid cells following differentiation with M-CSF and IL-4, which yields a mix of macrophages and dendritic cells (BMDMs/BMDCs). Single-cell RNA sequencing of bone marrow–derived macrophages and dendritic cells (BMDMs/BMDCs) revealed that CHRNA7 knockout (KO) cells exhibit distinct transcriptional profiles compared to wild-type (WT), including reduced expression of inflammatory and leukocyte migration pathways and increased expression of stress and apoptotic signaling genes. CHRNA7KO cells upregulated hypoxia- and ubiquitination-related genes, while CHRNA7WT cells expressed higher levels of TNFα signaling and immune function markers. These results support a cell-intrinsic role for CHRNA7 in regulating immune gene expression. These results led us to perform further in vivo studies to assess the effect of a specific CHRNA7 agonist, AR-R17779 on immune cell activation, tumor burden, and metastasis.

overall_design: To investigate the expression of different cell type markers with sequencing between wildtype and CHRNA7 KO bone marrow derived myeloid immune cells.

first: Sakeef

last: Sayeed

first: Brian

last: Eliceiri


title: WNT signaling in human pluripotent stem cells promotes HDAC2-dependent epigenetic programs and development of retinoic acid-responsive mesoderm

city: Tucson

first: Bao

last: Thai

state: AZ

address: 1656 E Mabel St

institute: University of Arizona

summary: Human pluripotent stem cells (hPSCs) can be used as a scalable source of lymphocytes for adoptive cell therapies, contingent on the robust generation of definitive hematopoietic intermediates. Early WNT activation with CHIR99021 during mesoderm induction promoted the formation of KDR+ ALDH1A2+ mesodermal progenitors and subsequent generation of T cells in a retinoic acid (RA)-dependent manner. Integrated scRNA-seq and ATAC-seq defined a WNT-dependent developmental trajectory from hPSCs to KDR+ ALDH1A2+ mesoderm. Gene regulatory network modeling predicted HDAC2 and E-box transcription factors as regulators of RA-responsive mesodermal differentiation downstream of WNT. HDAC2 knockout impaired, while HDAC2 overexpression enhanced, KDR+ ALDH1A2+ progenitor formation. E-box factor manipulation had no discernible effect. An orthogonal chemical screen confirmed that HDAC2 inhibition suppressed KDR+ ALDH1A2+ mesodermal progenitors, whereas modulating histone methylation enhanced their formation. These findings reveal mechanisms by which WNT signaling promotes RA-responsive mesoderm and suggest methods to improve the generation of lymphocytes from hPSCs.

overall_design: scMulti-omics seq: 5 samples - day 0 undifferenitated H1 hESCs, day 1.5 H1-derived embryoid bodies treated with early and late CHIR99021, and day 3 H1-derived embryoid bodies treated with early and late CHIR99021. Late treatment of CHIR99021 was on day 2, while early day 0 of embryoid body differentiation. Libraries were prepared using the 10x Genomics platform

first: Deepta

last: Bhattacharya


title: Med14 phosphorylation shapes genomic response to GLP-1 agonist [snRNA-seq]

city: La Jolla

first: Sam

last: Van de Velde

state: CA

address: 10010 North Torrey Pines Road

department: PBL

institute: Salk Institute

summary: Under feeding conditions, increases in circulating glucose concentrations trigger the release of glucagon-like peptide (GLP-1) from intestinal L cells. GLP-1 promotes insulin secretion and pancreatic beta cell viability in part via triggering of the beta cell GLP-1 receptor and subsequent induction of the cAMP signaling pathway, leading to the protein kinase A (PKA) mediated phosphorylation of CREB and induction of CREB target genes. By contrast with the acute effects of this pathway on immediate early CREB target genes, which attenuate the cAMP-CREB response, sustained exposure of beta cells to GLP-1 agonist (exenatide-4; Ex-4) or adenyl cyclase activator (Forskolin; FSK) stimulates the expression of beta cell specific CREB target genes with delayed kinetics. In a proteomic screen for transcriptional co-regulators that mediate the long-term effects of GLP-1, we identified Med14, a backbone subunit of the Mediator complex. Exposure to either Ex-4 or FSK stimulates Med14 phosphorylation at Ser983, corresponding to a conserved PKA recognition site (RRXS) that is located within an intrinsically disordered region of Med14. Phosphorylation of Med14 is essential for maintenance of enhancers that drive induction of beta cell-specific and diabetes-linked genes.  Mutation of Med14 at Ser983 to alanine decreased beta cell numbers and repressed growth factor signaling in primary mouse islets. Our work reveals how phosphorylation of a general transcription factor in response to GLP-1 analogs triggers a broad genomic response with salutary effects on beta cell function.

overall_design: Single nucleus RNA-seq profiling of cultured mouse primary islet tissue (WT and Med14_S983A mutant). Control and 16h exposure to Glp-1 analog Exendin-4 (16h)

first: April

last: Williams

first: Garrett

last: Evensen


title: RNA-seq analysis of intestinal organoids to investigate the roles of Rnaseh2b and Atg16l1 in gene regulation

city: Kiel

first: Konrad

last: Aden

address: Rosalind-Franklin-Straße 12

institute: Institute of Clinical Molecular Biology, CAU

summary: This dataset contains RNA-seq profiles of intestinal organoids derived from wild-type, Rnaseh2b knockout, Atg16l1 knockout, and Rnaseh2b/Atg16l1 double knockout mice. Rnaseh2b deficiency is associated with DNA damage and tumorigenesis, while Atg16l1 loss impairs autophagy and has been implicated in inflammatory bowel disease (IBD). Interestingly, the double knockout mice did not develop tumors, suggesting a complex interaction between DNA damage and autophagy pathways. This transcriptomic dataset offering insights into the molecular crosstalk underlying intestinal homeostasis, inflammation, and tumor suppression.

overall_design: RNA-seq profiling of intestinal organoids derived from wild-type, Rnaseh2b knockout, Atg16l1 knockout, and Rnaseh2b/Atg16l1 double knockout mice.

first: Joanna

middle: P

last: Bernardes

first: Nassim

last: Kakavand

first: Hang

last: Xiang


title: Med14 phosphorylation shapes genomic response to GLP-1 agonist [ATAC-seq]

overall_design: ATAC-seq of WT and Med14S983A mutant INS-1 cells treated with Exendin-4 (10nM) or forskolin (FSK; 10 uM) for 1 hour


title: Efficacy and Safety of Butyrate Supplementation in Rheumatoid Arthritis

city: Beijing

first: Xin

last: Zhang

state: Beijing

address: 38 Xueyuan Road

department: Institute of Systems Biomedicine

institute: Peking University

summary: To explore the effect of butyrate on intestinal epithelial cells  in collagen-induced arthritis (CIA) mouse model, we conducted Single-Cell RNA Sequencing profiling of intestinal tissue in response to butyrate treatment.

overall_design: The whole intestinal from two mice (one mice from each group: CIA, and Butyrate) were disassociated to isolate the cells for single cell RNA-Sequencing (scRNA-Seq).

first: Ruoyi

last: Wang

first: Naidi

first: Jing

last: He

first: Dan

last: Lu


title: Med14 phosphorylation shapes genomic response to GLP-1 agonist [RNA-seq]

overall_design: RNA-seq profiling of INS-1 cells (WT and Med14_S983A mutant) after exposure to Glp-1 analog Exendin-4 or forskolin. Control (no treatment), acute (1h) and sustained (16h) exposure. ERCC spike-in mix was added to each sample for normalization. All samples are in duplicates.

first: Jingting

last: Yu


title: Exon Skipping of Ste20-Like Kinase Enhances Glycolysis and Tumor Progression by Activating Enolase 1 mediated Phosphoenolpyruvate Production

city: Wuhan

first: Chen

last: Zeyu

state: Huibei

address: No. 1095, Jiefang Avenue

institute: Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology

summary: Dysregulated RNA splicing is activated in tumors; however, the metabolic landscape and consequent implications of this process remain largely unexplored. In this study, we identified exon skipping in Ste20-like kinase (SLK), resulting in a variant isoform of SLK (SLKv), which promotes glycolysis in tumor cells. Mechanistically, SLKv enhances the activity of enolase 1 (ENO1) by binding and phosphorylating the ENO1 serine 2 residue. This modification increases the efficiency of ENO1 in catalyzing the production of phosphoenolpyruvate (PEP). Notably, the accumulation of PEP further accelerates glycolysis by binding to and activating the glycolytic enzyme hexokinase 2 (HK2), phosphofructokinase muscle (PFKM), and phosphoglycerate mutase 1 (PGAM1). Meanwhile, transforming growth factor β (TGFβ) promotes exon skipping of SLK by upregulating the splicing factor KH RNA binding domain containing, signal transduction associated 1 (KHDRBS1). The application of antisense oligonucleotides (ASO) that target SLKv hinders glycolysis and tumorigenesis. These findings establish SLKv as a critical promoter of glycolysis and present a novel metabolic target for cancer therapy.

overall_design: RNA-seq profiling of wildtype MHCC-97H, MDA-MB-231 and HCT-116 treatment with DMSO/ H3B-8800 in 24hrs

first: Zeyu

last: Chen


title: Chromosome 8 gain drives cancer progression by hijacking the translation factor 4E-BP1 sensitizing for targeted CDK4/6 inhibition [II]

city: Heidelberg

first: Thomas

middle: Georg Philipp

last: Grunewald

address: Im Neuenheimer Feld 280

department: Division of Translational Pediatric Sarcoma Research

institute: German Cancer Research Center (DKFZ)

summary:
We report that chr8 gain-driven gene expression patterns correlate with poor overall survival of EwS patients. This effect is predominantly mediated by increased expression of the translation initiation factor binding protein 4E-BP1 encoded by EIF4EBP1 on chr8.
Integrated multi-omics profiling uncovered that 4E-BP1 orchestrates a pro-proliferative proteomic network. Consistently, silencing of 4E-BP1 in the EwS model reduced cell proliferation, clonogenicity, spheroidal growth in vitro, and tumorigenesis in vivo. Drug screens and functional assays revealed that high 4E-BP1 expression sensitizes for pharmacological CDK4/6-inhibition in preclinical models

overall_design: We transduced EwS cell lines with a lentivirus containing a vector-system (pLKO Tet-on) with doxycycline (Dox)-inducible shRNAs, specifically directed against EIF4EBP1 or a non-targeting control shRNA (shCtr)

first: Cornelius

last: Funk

first: Anna

middle: C

last: Ehlers

first: Felina

last: Zahnow

first: Julian

last: Musa

middle: G

last: Grünewald


title: Chromosome 8 gain drives cancer progression by hijacking the translation factor 4E-BP1 sensitizing for targeted CDK4/6 inhibition


title: RIP-seq of DDX49 related RNAs in HHL5 cells transfected Flag-DDX49 following OA/PA treatment for 24 hours

first: Jin

last: Hou

address: 800 Xiangyin Road

institute: Second Military Medical University

summary: DDX49 is a RNA-binding protein, to explore DDX40 related RNAs in MASLD and MASH, we used RIP-seq to analysis to identify the mRNAs bound by DDX49 in HHL5 cells transfected with Flag tagged DDX49 following OA/PA treatment for 24 hours

overall_design: We transfected Flag-DDX49 into HHL5 cells following OA/PA treatment for 24 hours,  then lysed the cells and used magnetic beads coated with Flag antibodies to pull down the RNA bound to DDX49. Subsequently, we extracted total RNA using Trizol method and conducted sequencing analysis.


title: CircESR1 and HNRNPAB function in estrogen receptor positive (ER+) breast cancer [RNA-Seq]

city: Hefei

first: Xu

last: Junchao

state: Anhui

address: No. 443, Mount Huangshan Road, Daoxiangcun Street

institute: University of Science and Technology of China

summary: Breast cancer (BC) is the most prevailing type of cancer among women in the world. ERα protein, which is transcribed and translated by estrogen receptor gene ESR1, is one of the marker molecules for clinical classification of BC. However, whether circRNAs specifically expressed in hormone receptor-positive BC play a role which is independent of ERα (estrogen receptor alpha) protein activity and signaling pathways is unknown. Whether these circRNAs could impinge on the sensitivity of ER+ BC cells to the endocrine therapy and targeted drug therapy is also unexplored.By screening circRNAs involved in estrogen receptor (ER) signaling, circESR1 was identified as a circRNA exhibiting high specificity of expression in ER+ breast cancer. Our studies elucidate a novel signaling complex centering around circESR1 and HNRNPAB in ER+ breast cancer and suggest that circESR1 might represent a potential therapeutic target for this disease.

overall_design: Unbiased transcriptome sequencing (bulk RNA-seq) was performed to have identified differentially expressed genes (DEGs) due to circESR1 or HNRNPAB depletion in MCF-7 cells. In details, MCF-7 cells were infected circESR1 or HNRNPAB shRNAs with lentivirus. Then the RNA was isolated. Total RNA sample was extracted and quantified with OD 260/280 ratio > 1.8 and OD 230/260 ratio > 2 were sent to BGI Genomics (Shenzhen, China) for sequencing.

first: Junchao

last: Xu

first: Tao

last: Zhu


title: HNRNPAB interacted with mRNAs in estrogen receptor positive (ER+) breast cancer [RIP-Seq]

summary: Breast cancer (BC) is the most prevailing type of cancer among women in the world. HNRNPAB belongs to heterogeneous nuclear ribonucleoproteins (hnRNPs) subfamily.In recent years, studies have found that HNRNPAB can be involved in the progression of various human cancers. It not only combines with DNA and RNA, but also mediates mRNA nuclear transport, regulates gene transcription and translation, and regulates the proliferation, migration, invasion, aging, and other phenotypes of tumor cells. HNRNPAB is closely related to the poor prognosis of cancer patients. In addition, HNRNPAB is also involved in regulating the infection process of influenza virus. It has been simply reported that the relevance of HNRNPAB as a prognostic value in BC.

overall_design: RIP assay was performed by using anti-HNRNPAB antibody (ab199724, Abcam, Cambridge, UK) and according to the manufacturer’s protocol of the EZ-Magna RIP™ Kit (17-701, Millipore, Darmstadt, Germany). Finally, RNA was purified after proteinase K digestion and extracted using TRIzol reagent (GK20008, GlpBio, California, USA). Then we sent the RIP experiment's input group and the anti-HNRNPAB antibody enrichment group to Aksomics (KangChen Bio-tech, Shanghai, China) for RIP-seq.


title: High throughput expression profiling of induction of microspore reprogramming to embryogenesis in Brassica napus L. [dataset 1]

city: Madrid

first: Pilar

last: Sánchez Testillano

state: Madrid

address: C/ Ramiro de Maeztu, 9

department: Biotechnology

country: Spain

institute: Margarita Salas Center of Biological Research (CIB)

summary: Microspore embryogenesis is an in vitro system in which haploid microspores (precursor celsl of pollen grains) are reprogrammed towards embryogenesis by the application of a heat stress (HS) treatment. This process is of great interest in plant breeding as it enables accelerated production of double-haploid plants. The induction of in vitro microspore reprogramming comprises a complex chain of events that still remain unknown. The process can be induced at the responsive developmental stage of vacuolated microspore.  In order to evaluate the transcriptional changes acompaying microspore embryogenesis induction  in Brassica napus, an expression profiling through high throughput RNA sequencing, and a pipeline for bioinformatic analysis was performed. The analyses have been implemented for two samples: (1) vacuolated microspores (VM), before stress treatment, initial stage of the microspore culture, and (2) stress-treated microspores, 4 days after the application of the HS, when proembryos (PE) are formed; PE correspond to the first morphological sign of embryogenesis induction. The results obtained would provide valuable information about this complex process.

overall_design: 6 samples were analyzed (1 genotype, 1 treatment). Two to three biological replicates were analyzed for each condition.

first: Cristina

last: Rueda-Varela

first: Elena

last: Carneros

last: Caro

first: Yolanda

last: Pérez-Pérez

first: Alfonso

last: García-Rubia

first: Ana

last: Martínez

first: Carmen

last: Gil

last: Testillano


title: Transcriptomic analysis of B. subtilis RNC-6 under varying pH conditions

city: Noida

first: Rajnish

middle: Prakash

last: Singh

address: A 10, A Block, Block A, Industrial Area, Sector 62, Noida

country: India

institute: Jaypee Institute of Information Technology

summary: RNA-sequencing was performed to analyzed the genes suporing the growth of bacterium B. subtilis.

overall_design: the bacterial cells were grown in varying pH conditions like pH 4.0 and pH 5.0 for overnight folowed by RNA extraction and library preparations.

first: Singh

last: Rajnish


title: RNAseq profiling of female and male wildtype or Malat1-/- naïve CD4+ T cells and in vitro differentiated Th2 cells

city: Sydney

first: Kylie

last: James

state: NSW

address: 384 Victoria Street, Darlinghurst

department: Translational Genomics

country: Australia

institute: Garvan Institute of Medical Research

summary: Transcriptomic profiling of Malat1-deficient and WT Th2 and naïve CD4+ T cells isolated from spleens and lymphnodes of female and male mice to determine sex-specific effects of Malat1 on CD4+ T cell differentiation in vitro.

overall_design: Examination of expression profiles of splenic and lymph node CD4+ T cells from naive female (samples 1-4) and male (samples 9-12) WT and Malat1-/- female (samples 5-8) and male (samples 13-16) mice and Th2 stimulated female (samples 17-20) and male (samples 25-28) WT and Malat1-/- female (samples 21-24) and male (samples 29-32) mice using RNASeq.

first: Dimitris

last: Lagos

first: Katie

last: West


title: CD4+ T cells reactive to a hybrid peptide from insulin-chromogranin A adopt a distinct effector fate and are pathogenic in autoimmune diabetes

city: Minneapolis

first: Todd

last: Knutson

state: MN

address: 117 Pleasant St SE

department: Minnesota Supercomputing Institute

institute: University of Minnesota

summary: T cell-mediated islet destruction is a hallmark of autoimmune diabetes. Here, we examined the dynamics and pathogenicity of CD4+ T cell responses to four different insulin-derived epitopes during diabetes initiation in non-obese diabetic (NOD) mice. Single-cell RNA sequencing of tetramer-sorted CD4+ T cells from the pancreas revealed that islet-antigen-specific T cells adopted a wide variety of fates and required XCR1+ dendritic cells for their activation. Hybrid-insulin C-chromogranin A (InsC-ChgA)-specific CD4+ T cells skewed toward a distinct Th1 (T helper type 1) effector phenotype, whereas the majority of insulin B chain and hybrid-insulin C-islet amyloid polypeptide-specific CD4+ T exhibited a regulatory T cell phenotype and early or weak Th1 phenotype, respectively. InsC-ChgA-specific CD4+ T cells were uniquely pathogenic upon transfer, and an anti-InsC-ChgA:IAg7 antibody prevented spontaneous diabetes. Our findings highlight the heterogeneity of T cell responses to insulin-derived epitopes in diabetes and argue for the feasibility of antigen-specific therapies that blunts the response of pathogenic CD4+ T cells causing autoimmunity.

overall_design: Pancreas-infiltrating CD4+ T cells from 10-week-old mice were sorted using islet-peptide-specific MHCII tetramers for InsC-ChgA, InsC-IAPP, InsBp8E, or InsB p8G. The RNA from tetramer-bound single-cells was then sequenced and cells from individual mice were identified using hashtag oligonucleotides, and antigen-specific cells were identified using unique oligonucleotide tags specific for each tetramer. The data were were analysed for gene expression levels and tetramer positivity. The dataset contains 13 HTO (mouse specific) tags and 4 TET (tetramer specific) tags.

first: Jason

last: Mitchell

first: Justin

last: Spanier

first: Alexander

last: Dwyer

first: Mohannad

middle: H

last: Alkhatib

first: Gina

last: Qian

first: Matthew

middle: E

last: Weno

first: Yixin

last: Chen

first: Zachary

last: Shaheen

first: Christopher

last: Tucker

first: Takashi

last: Kangas

first: Milagros

last: Silva Morales

first: Nubia

last: Silva

first: Tsuneyasu

last: Kaisho

first: Michael

last: Farrar

first: Brian

middle: T

last: Fife


title: Single-nucleus RNA seq profiling of term human placenta from maternal obese and lean conditions

city: Cambridge

first: Fatima

last: Gunter-Rahman

state: MA

address: 77 Massachusetts Ave

institute: MIT

summary: We used sn-RNA-seq to profile the transcriptome of term placenta from two different maternal BMI conditions (maternal obesity: BMI >= 35; lean: 18.5-25).

overall_design: Frozen human term placental samples were defrosted and nuclei were isolated. 20 samples (10 from the maternal facing side, 10 from the fetal facing side) were profiled using sn-RNA-seq (10X, v 3.1). Maternal facing side: 3 lean and 7 MO samples Fetal facing side: 4 lean and 6 MO samples


title: scRNA-seq analysis of the open and closed sides of the mouse olfactory epithelium following unilateral naris occlusion

city: Aurora

first: Stephen

middle: William

last: Santoro

state: Colorado

department: Department of Pediatrics, Section of Developmental Biology

institute: University of Colorado Denver - Anschutz Medical Campus

summary: The objectives of this study were to characterize the effects of olfactory deprivation via unilateral naris occlusion (UNO) on the relative abundance of distinct cell types and subtypes.

overall_design: Profiling the transcriptomes of single cells dissociated from the open and closed sides of the olfactory epithelia of PD28 mice following unilateral naris occlusion at PD14

middle: W

first: Karlin

last: Rufenacht

first: Rebecca

last: O'Rourke

first: Kawsar

last: Hossain


title: Foxd1 expression identifies a distinct subset of hepatic stellate cells involved in liver fibrosis

city: Akita

first: Megumi

last: Tatematsu

department: Department of Medical Biology

country: Japan

institute: Akita University Graduate School of Medicine

summary: Hepatic stellate cells (HSCs) are pericytes of the liver and are responsible for liver fibrosis and cirrhosis, which are end stages of chronic liver diseases. TFG-β activates HSCs leading to differentiation of myofibroblasts in the process of liver fibrosis. While heterogeneity of HSCs is appreciated in the fibrotic liver, it remains elusive which HSC subsets mainly contribute to fibrosis. We here show that expression of pericyte marker, Foxd1, specifically marked a subset of HSCs in the Foxd1-fate tracer mice. HSCs fate-mapped by Foxd1 were preferentially localized in portal area and peripheral zone of normal liver and fibrotic liver induced by carbon tetrachloride. Furthermore, the deletion of Cbfβ, which is necessary for TGF-β signaling, in Foxd1-expressing cells ameliorated liver fibrosis. Thus, we identified an HSC subset which preferentially responds to liver injuries.

overall_design: To examine the differences between tdTomato-positive and -negative hepatic stellate cells from Foxd1fm mice, RNA-seq was performed using untreated or carbon tetrachloride-treated mice (biological triplicates).


title: Gene expression profile at single cell level from migrasomes injected and uninjected skin

first: Zhou

last: Haoyu

address: LuoYu road

institute: Wuhan University

summary: We report the application of migrasomes in wound healing process. ScRNA-seq was used to compare the differences in ctrl and mig group.

overall_design: Purified migrasomes were injected in mig group in the wound healing rat model. Nothing was injected in ctrl group.

first: Haoyu

last: Zhou

first: Zhan

last: Liu

first: Guoliang

last: Sa

first: Xuewen

last: Yang


title: The hydrolase receptor DWARF14 is required for zaxinone perception in plants

city: Thuwal

first: Juan Camilo

last: Moreno Beltran

address: King Abdullah University of Science and Technology

country: Saudi Arabia

institute: KAUST

summary: Strigolactones (SLs) are plant hormones involved in plant growth, stress response and plant-organism interactions. DWARF14 (D14) is a α/β hydrolase involved in the perception of SLs in plants. Zaxinone has been reported as a plant endogenous apocarotenoid that modulates growth and biotic interactions, however, the molecular basis of its perception remains elusive. Here we identified a new D14 ligand, the apocarotenoid zaxinone. We showed that hundreds of genes, and specifically CAROTENOID CLEAVAGE DEOXYGENASE7 (CCD7) and CCD8, require At/OsD14, and at lower extent MORE AXILLARY BRANCHING2 (MAX2)/D3, for their transcriptional induction. We find that zaxinone and D14 physically interact in vitro with lower affinity than GR24; the resolution of the AtD14-zaxinone complex, by X-ray crystallography, provided additional evidence that zaxinone antagonizes SL by binding D14. Zaxinone treatments in d14 mutants revealed that At/OsD14 are essential to trigger the induction of CCD7 and CCD8 genes, SL content (roots and exudates) and Striga seed germination validating their interaction in planta. Moreover, OsD14 is required to trigger the zaxinone growth-promoting effect in roots. These findings reveal a perception mechanism for the hormone candidate zaxinone through the SL receptor D14 to regulate transcription of SL genes, SL content and growth in higher plants.

overall_design: To investigate the function of zaxinone on gene expression, we treated 5-weeks old Arabidopsis plants, including wt col-0, d14, kai2 and max2 mutants, by applying this compound in the hydroponic media. Root samples were harvested after 6 hours of treatment.

first: Juan

last: Moreno

first: Umar

last: Hameed

first: Aparna

last: Balakrishna

first: Abdugaffor

last: Ablazov

first: Muhamad

last: Jamil

first: Jianing

last: Mi

first: Kit

middle: X

last: Liew

first: Alexandre

last: de Saint Germain

first: Stefan

last: Arold

first: Salim

last: Al-Babili


title: A developing HPA axis permits neonatal immune sensitivity to common allergens

city: New York

first: Dr. Shruti

last: Naik

state: NY

address: 1425 Madison Ave

institute: Icahn School of Medicine at Mount Sinai

summary: Atopic and allergic diseases predominantly manifest in early life, a period of profound growth and maturation. Yet, there is a dearth of information on the impact of developmental parameters on the neonatal immune reaction to allergens. Here we demonstrate that common allergens including house dust mite (HDM) elicited potent type 17 inflammatory responses from neonatal but not adult mice. HDM-induced inflammation was abolished in Rorgt-, gd T cell-, or epithelial IL-17RC- deficient animals and surprisingly did not require nociceptors or lymph node engagement. Instead, neonatal CD301b+ type 2 conventional dendritic cells (cDC2s) abundantly engulfed allergen and locally activated gd T cells in the skin. Despite uptaking equivalent antigen to neonates, adult cDC2s did not promiscuously activate in the skin. Mechanistically, this discrepancy was not attributable to cell-intrinsic differences arising from the distinct developmental origins of neonatal and adult cDC2s. Instead, neonatal cDC2 hyperactivation could be traced to a lower systemic glucocorticoid level, a consequence of an immature hypothalamic-pituitary-adrenal (HPA) axis in early life, and could be reversed by cortisol administration at the time of allergen challenge. These findings bring to fore the influence of organismal developmental factors in shaping immune sensitivity to allergens in early life.

overall_design: To unbiasedly investigate the inflammation phenotype in allergens inoculated neonate skin, we performed bulk RNA sequencing with full thickness skin biopsy isolated from PBS control or allergens challenged neonate and adult mice. To study the mechanism how Corticosterone regulate neonate dendrtiic cell allergic response, we sorted dendritic cells from corticosterone or DMSO and HDM or PBS treated neoante skin and applied to bulk RNA sequencing.

first: Yue

last: Xing

first: Jill

last: Wisnewsky

first: Kody

last: Mansfield

first: Ikjot

last: Sidhu

first: Aleksandr

last: Prystupa

first: Shruti


title: XBP1-mediated activation of STING signaling in macrophages contributes to the progression of liver fibrosis

city: nanjing

first: Qi

last: Wang

state: Jiangsu

address: The First Affiliated Hospital of Nanjing Medical University, 300 Guang Zhou Road

institute: The first affliated hospital of nanjing medical university

summary: Our findings demonstrate that XBP1 controls macrophage cGAS/STING/NLRP3 activation by regulating macrophage self-mtDNA cytosolic leakage via BNIP3-mediated mitophagy modulation, providing a novel target against liver fibrosis.

overall_design: BMDMs were isolated from Xbp1FL/FL and Xbp1M-KO mice and lysed in TRIzol reagent (Invitrogen, Carlsbad, CA) after LPS stimulation for 6 h, and then Xbp1FL/FL and Xbp1M-KO BMDMs were subjected to RNA sequencing analysis (n = 3/group).

first: Qingfa

last: Bu

first: Zhexiong

last: Lian

first: Ling

last: Lu

first: Haoming

last: Zhou


title: Brain transcriptome analysis of Myt1l heterozygote mutation mice in different brain regions (RNA-Seq II)

city: Daejeon

first: Eunjoon

last: Kim

address: Kuseong-dong

department: Center for Synaptic Brain Dysfunctions/Department of Biological Sciences

institute: IBS/KAIST

summary: Myt1l, a zinc-finger transcription factor, promotes neuronal differentiation and is implicated in autism spectrum disorders (ASD) and intellectual disability. However, it was previously unclear whether Myt1l promotes neuronal differentiation in vivo, how its deficiency leads to disease-related mouse phenotypes, and whether and how ASD-risk genes with strong embryonic and perinatal gene expression can yield strong adult-stage ASD-related phenotypes. Here, we report that Myt1l-heterozygous knockout (Myt1l-HT) mice display postnatal age-differential ASD-like phenotypes: Newborn Myt1l-HT mice show ASD-like transcriptomic changes involving suppressed neuronal and synaptic gene expression and suppressed right reflex. Juvenile Myt1l-HT mice display mixed ASD-like and reverse-ASD transcriptomic patterns and large normal behaviors, accompanying increased prefrontal excitatory synaptic transmission. However, adult Myt1l-HT mice show additional ASD-like transcriptomic changes involving astrocytic and microglial genes, along with behavioral deficits and excessive prefrontal inhibitory synaptic transmission. Therefore, Myt1l HT leads to newborn-stage ASD-like neuronal suppression, temporary juvenile normalization, and subsequent adult-stage ASD-like deficits.

overall_design: Sub-brain transcriptome of Myt1l heterozygote mutation mice in prefrontal cortex, hippocampus, and striatum

first: Seongbin

first: Hyojin

last: Kang


title: Brain transcriptome analysis of Myt1l heterozygote mutation mice

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

overall_design: Refer to individual Series


title: In vitro and in vivo efficacy of the antimycobacterial molecule SQ109 against the human pathogenic fungus, Cryptococcus neoformans

status: Public on Jun 16 2025

city: Blacksburg

first: Ramu

last: Anandakrishnan

state: VA

address: 1410 Prices Fork Rd., Lab 101

department: Biomedical Sciences

institute: Edward Via College of Osteopathic Medici

summary: Cryptococcosis is an opportunistic fungal infection affecting individuals with compromised immunity, particularly those with HIV. The limited accessibility to effective treatments, emerging resistance to current antifungals, and treatment-related toxicities underline the pressing need for more effective therapeutic options. In this study, we conducted a whole-cell screening of ~ 3,700 FDA-approved drugs and clinical molecules against the Cryptococcus neoformans H99 strain to identify potential antifungal candidates. The anti-mycobacterial agent SQ109 was identified as one of the most potent hits, with broad antifungal activity. SQ109 exhibited potent activity against Cryptococcus spp., with an MIC90 of 4 μg/mL. In the time-kill assay, SQ109 demonstrated fungicidal activity against proliferating cryptococcal cells in a concentration-dependent manner. Unlike fluconazole (FLC) and flucytosine (5-FC), C. neoformans showed minimal tendency to develop resistance to SQ109 during frequent passaging. Furthermore, SQ109 exhibited a potent efficiency in the murine model of cryptococcal infection, resulting in a 50% survival rate among the group treated with 25 mg/kg for 10 consecutive days. The transcriptomic analysis revealed that SQ109 disrupts ergosterol biosynthesis, affecting membrane integrity and oxidative stress homeostasis, which aligns with its interaction with other ergosterol pathway inhibitors, including FLC.  Additionally, molecular docking and structural analysis indicated that squalene synthase protein ERG9 is the most likely target of SQ109 within the ergosterol biosynthesis machinery of cryptococcal cells.  These findings highlight the therapeutic potential of SQ109 in combating cryptococcal infections, both as a standalone therapy and as an adjuvant to FLC monotherapy.

overall_design: A total of 18 clinical isolates representing C. neoformans/gattii complex were included in this study. Additional 6 clinical isolates of clinically relevant fungi, including Candida parapsilosis, C. auris, and Aspergillus fumigatus were involved in susceptibility testing. Determination of the MIC for SQ109 and standard antifungals, AmB and FLC, was conducted as described in the Clinical and Laboratory Standards Institute (CLSI) guidelines M27-A3 for yeast and M38-A2 for filamentous fungi.

first: Alkashef

last: Nour

first: Salama

last: Ehab

first: Anandakrishnan

last: Ramu

first: Hazbun

last: Tony

first: Hoernig

last: Micah

first: Brown

last: Anne

first: Lawrence

last: Christopher

first: Saleem

last: Mohamed


title: Responses of primary AML cells to atorvastatin and simvastatin

city: Montreal

first: Guy

last: Sauvageau

state: QC

address: 2950, Chemin de Polytechnique

institute: Institute for Research in Immunology and Cancer

summary: Both, the statin sensitive and resistant AML specimens up-regulate in response to statins expression of genes in mevalonate pathway, but only the resistant cells also respond with activated transcription of MTORC1 pathway genes.

overall_design: Atorvastatin and simvastatin responses of five statin sensitive and five statin resistant specimens were analyzed. For each specimen, 0.1% DMSO (vehicle control) was used as a negative control.

first: Jana

last: Krosl

first: Vincent-Philippe

last: Lavallée

first: Richard

last: Bisaillon

first: Irene

last: Baccelli

first: Bernhard

last: Lehnertz

first: Isabel

last: Boivin

first: Caroline

last: Pabst

first: Sébastien

last: Lemieux

first: Geneviève

last: Boucher

first: Patrick

last: Gendron

first: Frédéric

last: Barabé

first: Anne

last: Marinier

first: Josée

last: Hébert


title: Regulating white blood cell activity through the novel Universal Receptive System

first: Maria

last: Vecherkovskaya

address: 101 Avenue of Americas 3rd floor

institute: Human Microbiology Institute

summary: Regulation of the leucocyte activity is critically important for a properly functioning immune response and the development of novel cell-based therapies. Our previous studies have demonstrated the existence of nucleic-acid-based receptors (Teazeled receptors, TezR), which govern the response of various cell types to a diverse array of environmental, factors.  Here, for the first time, we show that by modulating these TezR receptors, we can upregulate immune cell signaling, migration, endocytosis, and phagocytosis pathways in leukocytes.

overall_design: RNA-Seq profiling of human activated and non-activated human leucocytes

first: Victor

last: Tetz

first: Kristina

last: Kardava

first: Alireza

last: Khodadadi-Jamayran

first: Aristotelis

last: Tsirigos

first: George


title: Effect of depletion of KLF9 on gene expression of small cell lung cancer cells in vitro

city: Guangzhou

first: Wei

last: Zhang

state: 广东Guangdong

address: Zhongshandadao West 55

department: Institute of Brain Science and Rehabilitation Medicine

institute: South China Normal University

summary: To investigate the function of KLF9 in the regulation of small cell lung cancer, we established SCLC cell lines (NCI-H146, NCI-H1688) and knocked down KLF9 with shRNA.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for NCI-H146 and NCI-H1688 cells and its knockdown derivatives (shKLF9).

first: Xiaodong

last: Ma


title: Brain transcriptome analysis of Myt1l heterozygote mutation mice (RNA-Seq I)

first: Eunjoon

last: Kim

summary: Myt1l is a transcription factor for neuronal induction and maintenance during development and Myt1l is highly implicated in autism spectrum disorder (ASD). Myt1l-mutant mice with a heterozygous deletion of exon 9 showed mild autistic-like behaviors (Social deficit and specific repetitive behaviors) and additional behavioral abnormalities including hyperactivity and anxiolytic-like behaviors in adult. To explore the molecular patterns and mechanisms underlying these behavioral abnormalities, we performed RNA-seq analysis of whole brain from wild-type and Myt1l-mutant mice longitudinally from pup stage (~P3) to juvenile (~P21) and adult (~P56) stages. Myt1l-mutant mice showed upregulations of chromosome- and chromatin-related genes and downregulations of synapse- and neurotransmitter-related genes during pup stage. However, from juvenile stage, Myt1l-mutant mice showed upregulations of extracellular matrix- and transporter-related genes and downregulations of mitochondria- and ribosome-related genes. In addition, Myt1l-mutant mice showed pro-ASD transcriptomic patterns on pup stage, but these patterns were reversed toward anti-ASD transcriptomic patterns from juvenile stages to adult stage as compensatory changes likely. These results suggest that the haploinsufficiency of Myt1l acutely alters the transcriptomic pattern into pro-ASD patterns and chronically compensates with the synapse maturation.

overall_design: Whole-brain transcriptome of Myt1l heterozygote mutation mice age of P3, P21 and P56

first: Seongbin

first: Hyojin

last: Kang


title: Single-cell and in situ spatial analyses reveal the diversity of newly born hematopoietic stem cells and of their niches

city: Paris

first: Lea

last: Torcq

address: 25 Rue du docteur Roux

institute: Institut Pasteur

summary: Hematopoietic stem cells (HSCs) and more committed progenitors (collectively referred to as HSPCs) emerge from vessels during development, via Endothelial-to-Hematopoietic Transition (EHT). Recently, using the zebrafish embryo, we showed that two EHT cell types emerge from the dorsal aorta, raising the question of their subsequent fate. To address this issue, we established a complex pipeline based on single-cell photoconversion and transgenic lines to characterize the abilities of EHT cell progenies to conquer hematopoietic organs and to obtain their transcriptomic profiles. We show that the two EHT cell types lead to partly differentially fated cells, with significant differences in thymus colonization and T-lymphoid lineage commitment. In addition, we investigated implantation of HSPCs in niches, with the support of HSPC signatures (gata2b and cd34/podocalyxin), retrieved from our single-cell datasets. This revealed, at unprecedented resolution, the homing of HSPCs in niches of entire early larvae, including the pronephros, the sub-aortic and caudal regions, as well as the area contacting the supra-intestinal artery. Our work provides new insights on fundamental aspects of HSPC fate acquisition, from their emergence to their homing in specific niches.

overall_design: Hematopoietic cells (expressing fluorescent reporters under the control of cd41 and gata2b promoters) from 5dpf Tg(gata2b:Gal4;UAS:RFP; cd41:eGFP) larvae were collected after dissection (separating the anterior and posterior region along a transversal section at the posterior limit of the elongated yolk), dissociation and sorting using a BD FACS AriaIII cell sorter. Transcriptomic libraries were generated using the 10X Genomics Chromium Next GEM Single Cell 3ʹ Kit v3.1  kit, and sequenced on a Novaseq6000 platform to generate 150-bp paired-end reads, and a theoretical count of 40 000 reads per cell. Alignment and demultiplexing was performed using the CellRanger (version v6.1.2) and reads were aligned to the zebrafish genome annotated by the Lawson lab (version 4.3.2).

first: Catherine

last: Vivier

first: Sandrine

last: Schmutz

first: Yann

last: Loe-Mie

middle: A

last: Schmidt


title: mRNA-Engineered CRISPR-Cas Epigenetic Editors Enable Durable and Efficient Gene Silencing in Vivo

city: Shenzhen

first: Jian-Kang

last: Zhu

state: Guangdong

address: 1088 Xueyuan Blvd, Nanshan

institute: Southern University of Science and Technology

type: Methylation profiling by high throughput sequencing


title: The cellular heterogeneity and dynamics of bladder mucosa under homeostasis and injured conditions

city: Haikou

first: Yue

last: Hong

address: 58 Renmin Road

department: School of Life and Health Sciences

institute: Hainan University

summary: To comprehensively explore the cellular heterogeneity and dynamics of bladder mucosa under homeostasis and injured conditions, we performed droplet-based scRNA-seq using the 10x Genomics Single Cell Solution on samples isolated from injured and normal  rabbit bladder. Here the scRNA-seq data demonstrated that urothelial differentiation and regeneration occur in a linear fashion, with a single origin of basal stem/progenitor cell progressively differentiating into intermediate and superficial umbrella cells. And, Basal cell_2 cells expressing TP63 and higher KRT5 as stem/progenitor cell of rabbit bladder urothelium in normal mucosa-injured conditions.

overall_design: Samples isolated from injured (Injury_1, Injury_2) and normal (Normal_1, Normal_2) rabbit bladder droplet-based scRNA-seq to explore the cellular heterogeneity and dynamics of bladder mucosa under homeostasis and injured conditions.

first: Fang

last: Chen

first: Yichen

last: Huang

first: Jiasheng


title: Gene expression profiles of Control and FAK KO Th17 cells

city: Seoul

first: Gap Ryol

last: Lee

address: 35 Baekbeom-ro, Mapo-gu

department: Department of Life Science

institute: Sogang University

summary: T helper type 17 (Th17) cells play critical roles in the pathogenesis of various autoimmune and inflammatory diseases; however, signaling pathways that affect Th17 cell differentiation are not fully understood. Here, we investigated whether focal adhesion kinase (FAK), an integrator of extracellular signals, regulates differentiation of Th17 cells. We measured alteration of gene expression in FAK-deficient Th17 cells compared to WT Th17 cells using RNA-sequencing.

overall_design: We isolated naïve CD4 T cells from Fakfl/fl mice and introduced a Cre recombinase-expressing vector into the cells to induce gene deletion (these cells are referred to Fak KO). These cells were stimulated with plate-bound anti-CD3ε (10 μg/ml) and soluble anti-CD28 (5 μg/ml) antibodies and cultured for 3 days under Th17-polarizing conditions. Then we harvested the cells and conducted RNA-sequencing (RNA-seq) to identify altered genes in Fak KO Th17 cells.

first: Hyeong Su

first: Ji Hyeon


title: Expression data from NE or CORT exposed ADXSCGX mice eye

city: Fukuoka

first: Keisuke

last: Ikegami

address: Nishi-ku Motooka 744

institute: Kyushu University

summary:
Abnormal IOP or IOP rhythm can cause glaucoma development. Intraocular pressure (IOP) has circadian rhythm with nocturnal peak in both nocturnal and diurnal animals.
We used microarrays to detail the mechamisms of circadian rhythm of intraocular pressure because SCG-NE and adrenal CORT transmit time information to the eye.

overall_design: C57BL/6J male mice were used for RNA extraction and hybridization on Affymetrix microarrays. In our previous report, we found that NE or CORT instillation to SCGX and ADX mice eye can induce IOP increase. We instilated NE or CORT to ADX and SCGX mice eye, after 4 hours, we collected eye for RNA extraction.

first: Satoru

last: Masubuchi


title: eIF4e Assembly into Germ Granules is Essential for its Repressive Function

city: Indianapolis

first: Scott

last: Aoki

state: Indiana

address: 635 Barnhill Drive MS-4071

department: Biochemistry and Molecular Biology

institute: Indiana University School of Medicine

summary: In metazoans, germ cells play a fundamental role in ensuring the continuity of animal life. Germ cells contain germ granules, cytoplasmic non-membrane bound organelles also referred to as RNA-protein condensates. These germ granules house a variety of RNAs and proteins essential for germline identity, maintenance, and fertility. In C. elegans, P granules are a specific type of germ granule that localize to the nuclear periphery of developing germ cells and regulate mRNA expression. Proper P granule assembly is dependent on the PGL family of granule-forming proteins. PGL-1, the flagship P granule assembly protein and PGL member, contains two dimerization domains and a C-terminus region. Numerous proteins localize to P granules, most of which are RNA-binding or regulatory proteins. For example, IFE-1 is a eIF4E family member that binds the 5’ cap of mRNAs, directly interacts with PGL-1 in vivo and in vitro, and localizes to P granules. The precise molecular function of PGL and their associated proteins remains unclear; they may act solely as granule assembly proteins, serve as scaffolds to recruit other proteins, or directly regulate RNA. Here, genetics and imaging methods were used to molecularly dissect PGL-1 in vivo to probe how different protein regions are required for granule assembly, P granule binding partner recruitment, and germ cell development. We used CRISPR to (a) tag IFE-1 protein with an mScarlet fluorescent protein, (b) delete protein coding regions of pgl-1 to investigate IFE-1 binding and to understand how IFE-1 assembly into P granules is crucial for its role in germ cell development. Deletion of PGL-1 dimerization domains significantly disrupted P granule formation and IFE-1 recruitment. Removal of the C-terminus region led to abnormal P granule formation, which profoundly affected IFE-1 localization. These findings reveal that the previously uncharacterized C-terminal region plays a critical role in the integrity and functionality of P granules. We are performing immunoprecipitation assays to verify the direct binding of IFE-1 and PGL-1. Our study provides novel insights into the molecular mechanisms governing P granule protein interactions, highlighting their essential biological relevance and potential impact on understanding germ cell development.

overall_design: eCLIP was performed to identify the RNA targets of the C. elegans eIF4e homolog, IFE-1.

first: Carmen

last: Herrera Sandoval

first: Christopher

last: Borchers

first: Boyoon

last: Yang

first: Becky

last: Boyd

first: Heather

last: Hundley


title: Establishing 3D Organoid Models from Patient-Derived Conditionally Reprogrammed Cells to Bridge Preclinical and Clinical Insights in Pancreatic Cancer

first: KIM

last: JINSU

address: 50-1 Yonsei-ro, Seodaemun-gu, Seoul, Korea

department: Internal Medicine

institute: Yonsei University College of Medicine

summary: Pancreatic cancer is a highly aggressive malignancy with limited therapeutic options. To address the limitations of traditional 2D cell culture models, we developed 3D organoid cultures from patient-derived conditionally reprogrammed cell (CRC) lines. These organoids retain the molecular and mutational profiles of the original tumor cells, providing a more accurate model for drug response prediction. Drug sensitivity assays using gemcitabine plus nab-paclitaxel (Abraxane) and FOLFIRINOX revealed that 3D organoids more closely reflect clinical outcomes than 2D cultures, with higher IC50 values consistent with in vivo drug resistance. This platform offers a promising approach for precision medicine in pancreatic cancer.

overall_design: Organoids were established to compare the genetic and molecular characteristics of cells cultured under 2D and 3D conditions, using RNA-seq for transcriptomic profiling.


title: IFIT2-induced transcriptomic changes in Mycobacterium tuberculosis infected macrophages

city: Cape Town

first: Bienyameen

last: Baker

state: Western

address: Francie Van Zijl Drive, Tygerberg

department: Department of Biomedical Sciences

country: South Africa

institute: Stellenbosch University Tygerberg Medical Campus, SAMRC Centre for TB Research

summary: Interferon-induced protein with tetratricopeptide repeat 2 (IFIT2) is known for its antiviral activity and has recently been implicated in the defense against Mycobacterium tuberculosis (M. tb). This study employed global transcriptomics to investigate the downstream effects of IFIT2 induction in THP-1 macrophages infected with R179 M. tb, aiming to elucidate its role and downstream contributing factors that aid it in intracellular M. tb killing. Using a vector-based overexpression approach, IFIT2 expression was induced in THP-1 cells infected with R179 M. tb, followed by RNA extraction 12 hours postinfection and AmpliSeq-based targeted transcriptome sequencing. Bioinformatics analysis identified 282 differentially expressed genes (DEGs), of which 189 were upregulated and 90 were downregulated (FDR <0.05). Filtering for highly significant DEGs (|log2(fold change) | > 1.5) yielded 70 genes, predominantly upregulated, with functional enrichment in pathways such as defense response to viruses and cytokine-mediated signaling. Signaling pathway impact analysis highlighted pathway activation and inhibition of the tuberculosis (TB) pathway. RT-qPCR validation confirmed the upregulation of selected DEGs (ISG15, CMPK2, RSAD2, IFI44L, IFI44), corroborating the AmpliSeq data. This study provides comprehensive insights into the transcriptomic profile induced by IFIT2 in TB, revealing critical downstream contributors and pathways that underpin IFIT2’s ability to combat M. tb infection.

overall_design: RNA-seq profiling of IFIT2-induced THP-1 cells infected with mycobacterium tuberculosis

first: Ewura-Esi

last: Manful

first: Ray-Dean

last: Pietersen


title: Screening of functional genes affecting the quality of translucent eggshell membranes based on RNA-Seq analysis

city: Baoding , China

first: Chun-Hao

last: Han

state: Baoding , China

address: Baoding , China

institute: Hebei Agricultural University

summary: Identification of differentially expressed genes in the isthmus tissues between the chicken translucent group and the opaque group using RNA-seq analysis.

overall_design: By conducting transcriptome analysis on the isthmus tissues of the selected  translucent group and opaque group of hens, differentially expressed genes were identified and screened.


title: Intraindividual rDNA copy number variation and methylation in humans

city: Wuerzburg

first: Jana

last: Durackova

address: Am Hubland

department: Institute of Human Genetics

institute: Julius Maximilians University

summary: The absolute number of rDNA transcription units can vary by about one power of ten among individuals. Apart from extensive rDNA copy number (CN) variation and instability in many cancers, there is little information on the extent of intraindividual CN variation between normal s. Here we used droplet digital PCR and deep bisulfite sequencing to determine both the absolute rDNA CN and the number of presumably active CN with a hypomethylated (0-10%) promoter region in up to six different s of 13 autopsy probands. In general, the absolute rDNA CN as well as the frequency of the minor A variant were highly similar between s (cerebellum, cerebrum, colon, heart, intestine, kidney, and liver  liver and spleen) of the same individual. However, in some probands absolute CN in one or multiple s was much higher than in the other s., consistent with relaxation/breakdown of the CN control system. The amplified copies were inactivated by promoter methylation and, thus, the number of active CN was largely independent from absolute CN. Collectively, our data suggest that with some notable exceptions absolute and even more active rDNA CN are maintained during development and differentiation in different s of the same individual. Despite the low intraindividual variation active CN appeared to systematically vary between s. Cerebellum, which is characterized by the highest density of non-dividing neuronal cells in the body, consistently exhibited lower active CN than other s. We estimate that a minimum number of > 50 active rDNA TU is required for normal /organ function.

overall_design: Deep bisulfite sequencing and droplet digital PCR were used to determine the methylation state of ribosomal DNA core promototer/upstream controls element and 28 rDNA, respectively, in up to 6 different s of 13 autopsy probands

first: Ramya

last: Potabattula

first: Adreas

last: Rosenwald

first: Thomas

last: Haaf


title: Oxalobacter formigenes colonization slows the progression of CKD and reduces cardiac remodeling in CKD

city: New York City

first: Florencia

last: Schlamp

state: New York

address: 435 East 30th Street

institute: NYU Langone Health

summary: Accumulation of oxalate in patients with chronic kidney disease (CKD) is associated with CKD progression and an increased risk of cardiac death. Whether reducing oxalate slows CKD progression and prevents cardiovascular complications remains unexplored. We colonized Oxalobacter formigenes (Oxf), an oxalate-degrading microbiome, in the intestines of control and CKD mice fed with 1% hydroxyproline for 23 weeks. RNA-seq analysis of heart tissues of CKD mice reveals dysregulated expression of metabolic pathways and Oxf colonization reverses these changes. These findings demonstrate that oxalate accumulation plays a role not only in CKD progression but also in cardiovascular complications.

overall_design: Male C57BL/6 adult mice (40) were purchased from Jackson Laboratories (Bar Harbor, ME).  At 6 weeks of age, half underwent two-stage 5/6 nephrectomy (5/6 Nx) surgery, entailing the removal of two-thirds left kidney followed by a right nephrectomy within one week, to induce CKD. The remaining 20 mice underwent sham operations and served as controls. Mice were fed a diet supplemented with 1% hydroxyproline and 0.5% calcium for the duration of the experiment. On day 7, the CKD and sham groups were orally gavaged with either one dose of Oxf (1x109 CFU in 200µl culture medium) or vehicle (V, 200µl culture medium), resulting in four groups of 10 mice each: CKD+Oxf, sham+Oxf, CKD+V and sham+V

first: Xiaozhong

last: Xiong

first: Melody

last: Ho

first: Karim

last: Jaber

first: Rashmi

last: Mishra

first: Amania

last: Charytan

first: Nadim

last: Zaidan

first: Lama

last: Nazzal


title: HMGA2 interacts with KAT6A to regulate MMPs chromatin architecture and promote triple-negative breast cancer metastasis

city: Tianjin

first: Lu

last: Qiao

address: No. 22, Meteorological Observatory Road, Heping District, Tianjin City

institute: Tianjin Medical University

summary: Triple-negative breast cancer (TNBC), the most lethal breast cancer subtype, demonstrates poor prognosis due to its high rates of metastasis, recurrence, and mortality. The metastatic potential in TNBC patients serves as a critical determinant of clinical outcomes. The high mobility group AT-hook 2 (HMGA2) has emerged as a novel chromatin architectural regulator, its specific role in TNBC metastasis requires further investigation.To investigate the mechanism of HMGA2 regulation of TNBC metastasis,we performed RNA-sequencing using shNC or shHMGA2 from MDA-MB-231 cells.

overall_design: Total RNA was extracted from MDA-MB-231 cells expressing a control vector (shNC) or HMGA2 had been knocked down (shHMGA2).


title: Global Transcriptomics Reveals Carbon Footprint of Food Waste in the Bioconversion of Ecofriendly Polymers

city: Binghamton

first: Sha

last: Jin

state: NEW YORK

address: 4400 Vestal Parkway East

institute: Binghamton University

summary: Food waste is a major source of environmental pollution, as its landfills attribute to greenhouse gas emissions. This study developed a robust upcycling bioprocess that converts food waste into lactic acid through autochthonous fermentation and further produces biodegradable polymer polyhydroxybutyrate (PHB). Food can be stored without affecting its bioconversion to lactic acid, making it feasible for industrial application. Mapping autochthonous microbiota in the food waste fermentation before and after storage revealed lactic-acid-producing microorganisms dominate during the indigenous fermentation. Furthermore, through global transcriptomic and gene set enrichment analyses, it was discovered that coupling lactic acid as carbon source with ammonium sulfate as nitrogen source in Cupriavidus necator culture upregulates pathways, including PHB biosynthesis, CO2 fixation, carbon metabolism, pyruvate metabolism, and energy metabolism compared to pairing with ammonium nitrate. There was ∼90 % PHB content in the biomass. Overall, the study provides crucial insights into establishing a bioprocess for food waste repurposing.

overall_design: The RNA seq data was included to investigate the metabolism pathway of the Cupriavidus necator fermentation at different time and to compared the effect using different nitrogen souce.

first: Tianzheng

last: Liu

first: Kaiming

last: Ye