title: FHL5 cofactor mediates vascular disease risk by regulating smooth muscle cell transcriptional networks [RNA-seq]

status: Public on Oct 31 2022

city: Charlottesville

first: Clint

middle: L

last: Miller

state: VA

department: Center for Public Health Genomics

country: USA

institute: University of Virginia

type: Expression profiling by high throughput sequencing

summary: Genome-wide association studies (GWAS) have identified hundreds of loci associated with vascular diseases such as coronary artery disease (CAD) and myocardial infarction (MI), and hypertension. However, the biological roles for many of these loci enriched in the vessel wall remains unknown. Among these, UFL1-FHL5 (chr6q16.1) emerged as a genome-wide significant locus in a recent CAD/MI meta-analysis. Here, we use an integrative approach leveraging human genetics, epigenomic profiling, and in vitro functional and ex vivo imaging analyses to prioritize FHL5 as the top candidate causal gene and reveal the molecular mechanisms of its pleiotropic genetic associations. Notably, FHL5 overexpression in coronary artery smooth muscle cells (SMC) increased vascular calcification and dysregulated processes related to extracellular matrix organization and calcium handling. Lastly, by mapping FHL5 binding sites genome-wide using CUT&RUN, we identified regulatory interactions with downstream disease loci having putative roles in SMC phenotypic modulation. Together, these trans-acting mechanisms may account for a portion of the heritable risk for CAD/MI and other complex vascular diseases.

overall_design: Bulk RNA-seq of 500,000 HA, FHL5, FHL5-NLS overexpressing HCASMC-hTERT was performed under basal conditions. Paired-end sequencing (42bp x 2) was performed on the Illumina NextSeq 500 instrument.

first: Doris

last: Wong


title: mouse M-BMDM of WT and STAT2 T403A

city: qingdao

first: qiaoling

last: song

address: Xiang Gang East Road NO.23

country: China

institute: Ocean University of China

summary: Bone marrow cells were isolated from wild type mouse (WT) or STAT T403A mutant mouse (T403A) and primed with M-CSF (M BMDM) separately. The difference between these two M-BMDMs were distinguished by RNA-seq analysis.

overall_design: WT-M-BMDM, T403A-M-BMDM

first: Zhan

last: Zhao

first: Chenyang

first: Jinbo

last: Yang

first: Qiaoling

last: Song


title: Whole-transcriptome sequencing and ceRNA interaction network construction for temporomandibular joint osteoarthritis

city: Jiamusi

first: Fan

last: Wu

address: Southwest Gang Street

institute: Jiamusi University

type: Non-coding RNA profiling by high throughput sequencing

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

overall_design: Refer to individual Series


title: Development of a Mouse Model of Sturge-Weber Syndrome and Therapeutic Response to Imatinib

city: Atlanta

first: Yoonhee

last: Jung

state: Georgia

address: 615 Michael Street

department: Human Genetics

institute: Emory university

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Sturge-Weber Syndrome (SWS) is a common vascular malformation caused by mutation of GNAQ in endothelial cells. No effective medical therapy exists for SWS, and therapy is mainly surgical. Progress in the medical treatment of SWS has been hindered by the lack of an animal model. We introduced mutant GNAQ into an immortalized murine endothelial cell line, MS1. The resultant cells form slow growing vascular malformations that morphologically and biochemically resemble human SWS. One of the genes upregulated as a result of mutant GNAQ is c-kit, which is a targetable event. Given that the FDA approved drug imatinib targets c-kit as well as its original target, bcr-abl, we evaluated the ability of imatinib to prevent the growth of vascular malformations in mice. We saw that imatinib significantly inhibits the growth of vascular malformations in vivo. Repurposing of imatinib for the treatment of SWS should be evaluated in a clinical trial.

overall_design: ATAC-seq analysis.

first: Maiko

last: Sasaki

first: Paula

last: North

first: Justin

last: Elsey

first: Keith

last: Choate

first: M

middle: A

last: Toussaint

first: Rakan

middle: R

last: Radi

first: Adam

middle: J

last: Perricone

first: Victor

last: Corces

first: Jack

last: Arbiser


title: Transcriptome analysis between hepatocellular carcinoma and adjacent tissues

city: Jiaxing

first: Huadong

last: Ni

address: zhonghuan nan road 1882

institute: Department of Anesthesiology and Pain Research Center, The Affiliated Hospital of Jiaxing University

summary: mRNA/ lncRNA/ circRNA profiles of hepatocellular carcinoma and the adjacent tissues were generated by deep sequencing using Illumina NovaSeq 6000.

overall_design: RNA profiles of  test and control samples

first: Junli

last: Ma

first: Jing

last: Shi

first: Cao

last: Guo

first: Yang

last: Li


title: HDAC2 in primary sensory neurons constitutively restrains chronic pain   by repressing α2δ-1 expression and associated NMDA receptor activity

city: Houston

first: Hui-Lin

last: Pan

state: Tx

address: 1515 Holcomb Blvd

institute: MD Anderson Cancer Center

summary:
Purpose: To investigate genome-wide gene regulation by HDAC2 in dorsal root ganglion neurons in mice.
Methods: The mRNA was extracted from the mouse dosal root ganglion of 8-week-old HDAC2 condition knockout (Advillin-Cre+/HDAC2loxP++, hdac2-cko) and littermates controls (WT, without Cre).  After quality control, library was constructed and sequenced on the Illumina Platform with pared end 150 bp (Novogene Corporation Inc. Sacramento CA).  Three replicates for each sample were done.
Results: Hdac2-cKO DRGs shows a significant increase in 210 genes and a decrease in 455 genes (P<0.05).

overall_design: RNAs were isolated from DRGs in HDAC2 condition knockout (Advillin-Cre+/HDAC2loxP++, hdac2-cko) and littermates controls (WT, without Cre). RNA of there two groups were sequenced on illumina platform. Each group has three repeats. Different expression was anlysis using Hisat2-FeatureCounts-Deseq2 pipline.

first: Jixiang

last: Zhang


title: A lncRNA, SPRIGHTLY, interacts with Polypyrimidine Tract Binding Protein 1 (PTBP1) and modulates SET And MYND Domain Containing 3 (SMYD3) exon skipping.

city: St. Petersburg

first: Rudrmani

last: Pokhrel

state: United States

address: 600 Fifth Street S.

department: Oncology

institute: Johns Hopkins All Children’s Hospital

summary: During the course of surveying Medulloblastoma (MB) group specific lncRNAs, we found that SPRIGHTLY was highly upregulated in group 4 cell lines and patient derived xenografts (PDX). Its knock down reduced cell proliferation, invasion, and colony formation. It binds to the intron region of SMYD3 pre-mRNA and regulates SMYD3 exon 5 skipping together with PTBP1 protein. In group 4 cell line, the increase of SMYD3 affects EGFR pathway and regulates its downstream gene transcription. Inquiring SMYD3 and SMYD3 E5D transcripts expression in the patient RNA-seq data suggests that balancing two transcripts level seems to be associated with tumor development or maintenance.

overall_design: Group 4 MB cell line, CHLA01-MED cells were transfected with plasmid harvoring SMYD3-Myc or SMYD3 E5 deletion-Myc gene and stable clones were selected. To knock down the SPRIGHTLY, cells were transduced with lentivirus having two gRNAs, which are targetting before and after SPRIGHTLY gene and Cas9 gene. Single clones showing reduced SPRIGHTLY expression was selected.

first: Bongyong

last: Lee

first: Menglang

last: Yuan

first: Rudramani


title: GDF15 Secretion is Increased in Resposne to Skeletal Muscle Contraction and Potentiates Glucose-Stimulated Insulin Release in Pancreatic β-cells

city: Baton Rouge

first: John

middle: P

last: Kirwan

state: LA

address: 6400 Perkins Road

institute: Pennington Biomedical Research Center

summary: Lifestyle intervention including exercise restores glucose homeostasis and pancreatic β-cell function in type 2 diabetes (T2D). However, exercise compliance is a challenge. Novel alternative or adjuvant approaches are necessary. During exercise, the contracting skeletal muscle acts as endocrine organ via the secretion and endocrine signaling of functional proteins. We postulated that contracting skeletal muscle secretes proteins that target pancreatic β-cells and regulate insulin secretion and glucose metabolism. To test this hypothesis, we used an in vitro cell-based skeletal muscle contraction system to uncover proteins released in the muscle secretome. Using an RNAseq screen, we identified growth differentiation factor 15 (GDF15) as a lead candidate. β-cells, human pancreatic islets, and C57BL/6J mice exposed to acute GDF15 treatment exhibited increased glucose-stimulated insulin secretion, and the mechanism involved activation of the insulin release pathway. Chronic GDF15 treatment in db/db mice reduced insulin resistance and preserved pancreatic PDX-1 expression. Consistently, plasma GDF15 increased concurrently with C-peptide prior to the onset of chronic hyperglycemia in humans with pre-diabetes. In addition, in humans with T2D, exercise-induced GDF15 was associated with enhanced β-cell function. These findings support GDF15 as a potential therapeutic target for type 2 diabetes and associated co-morbidities.

overall_design: Control and EPS stimulated muscle cell lysate were analyzed, with 4 replicates in each group

first: Hui

first: Anny

last: Mulya

first: Stephan

last: Nieuwoudt

first: Ricky

last: Chan


title: miRNA Expression in PDGFRA Mutant GISTs

city: Bologna

first: Gloria

last: Ravegnini

state: BO

address: via irnerio 48

department: PHARMACY AND BIOTECHNOLOGY

country: Italy

institute: UNIVERSITY OF BOLOGNA

summary: Context: Gastrointestinal stromal tumors (GISTs) harboring mutations in the PDGFRA gene occur in only about 5–7% of patients. The most common PDGFRA mutation is exon 18 D842V, which is corre-lated with specific clinico-pathological features compared to the other PDGFRA mutated GISTs. Herein, we present a miRNA expression profile comparison of PDGFRA D842V mutant GISTs and PDGFRA with mutations other than D842V (non-D842V). miRNA expression profiling was carried out on 10 patients using a TLDA miRNA array. Then, miRNA expression was followed by bioinformatic analysis aimed at evaluating differential expression, pathway enrichment, and miRNA-mRNA networks. We highlighted 24 differentially expressed miRNAs between D842V and non-D842V GIST patients. Pathway enrichment analysis showed that deregulated miRNAs targeted genes that are mainly involved in the immune response pathways. The miRNA-mRNA networks highlighted a signature of miRNAs/mRNA that could explain the indolent behavior of the D842V mutated GIST. The results highlighted a different miRNA fingerprint in PDGFRA D842V GISTs compared to non-D842Vmutated patients, which could explain the different bio-logical behavior of this GIST subset.

overall_design: qPCR miRNA expression profiling. Total RNA from serum of 10 GIST patients was extracted and PDGFRA Exon 18 D842V GISTs versus PDGFRA Exon 18 non D842V GISTs

first: Sabrina

last: Angelini

first: Francesca

last: Gorini

first: Patrizia

last: Hrelia


title: Preliminary investigation of the effect of transfected HBx on the expression pattern of circRNAs in hepatocellular carcinoma

city: Haikou

first: Liu

last: Luzheng

address: Hainan General Hospital

department: Department of Hepatobiliary and Pancreatic Surgery

institute: The Affiliated Hainan Hospital of Hainan Medical University （Hainan General Hospital）

overall_design: HCC cell lines with HBx overexpression (HepG2 H6679) and empty vector control (HepG2 H5298) were successfully constructed. The two cell lines were sequenced using high-throughput second-generation transcriptome sequencing technology (RNA-seq), and the identified circRNAs were validated using qPCR (quantitative real-time PCR). The differentially expressed circRNAs were analyzed. Bioinformatics analyses, including clustering, differential expression, GO analysis, and KEGG pathway, were performed. Target Scan and Miranda software were employed to predict micro-RNAs corresponding with circRNAs.

first: Luzheng

last: Liu

first: Jiacheng

last: Chen

first: Liang

first: Cheng

first: Dafeng

last: Xu

first: Shixun

last: Lin

first: Xiangxiang

last: Luo

first: Jincai

last: Wu


title: RNA-seq study of SRSF2 over-expressing lung cancer cell lines

city: Fuzhou City

first: hongguang

state: Fujian Province

address: NO.29 of Xinquan Road, Gulou District

institute: Fujian Medical University Union Hospital

summary: Immune checkpoints blockade therapy may have clinical symptoms of hyper-progressiveness (HP). The molecular mechanism of HP is still to be revealed. This study inspected transcriptome difference between clinical hyper-progressive samples to immunotherapy-response samples based public datasets. Spliceosome factors SRSF2 were found most enriched in neoantigen-related splicing events. Similar splicing pattern and increased cell invasion were found in two lung cancer cell lines after SRSF2 over-expressed.This study shows that dysregulation of SRSF2 -related splicing might be an important feature of immune hyper-progress occurrence.

overall_design: SRSF2 over-expressing lung cancer cell lines compared to normal cell lines.Total RNA transcriptome from these samples was profiled by RNA-seq.

first: Dan

last: Xue

first: Teng-Teng

last: Zhu

first: Hong-Guang

first: Pei-Lin

last: Guo

first: Meng-Ling

last: Li

first: Mei-E

last: Yu

first: Fan

last: Yang

first: Sheng

first: Xiang-Qi


title: Antigen-expanded CD8+ gd T cells with NK-like phenotype and function respond in persistent infection [Bulk RNA-seq]

city: Chicago

first: Roshni

last: Roy Chowdhury

address: 924 E 57th Street

institute: University of Chicago

summary: Gamma Delta (gd) T cells play unique protective roles in different settings of acute and chronic infections. However, what they respond to and how they function in the acute versus chronic phases of the same infection remains unclear. It is well documented that cytolytic gd T cells that express Vg9Vd2 TCRs and respond to phosphoantigens (pAgs) expand in acute Mycobacterium tuberculosis (Mtb) infection in humans. However, most infections with Mtb manifest as a chronic, clinically asymptomatic state. While past work indicates that gd T cells contribute to Mtb infection control, their response during this phase of Mtb infection is not well understood. Here, we analyze peripheral blood gd T cells from a South African adolescent cohort and show that a unique CD8+ gd T cell subset with features of “memory inflation” expand in chronic Mtb infection.

overall_design: We performed bulk RNA sequencing (bulk-RNA-seq) on FACS sorted CD8+ and CD8- gd T cells from peripheral blood samples of five donors with persistent Mtb infection.

last: Chowdhury

first: Oliver

last: Kask

first: Megha

last: Dubey

first: Yueh-hsiu

last: Chien


title: RNA profiling of genistein and Tanshinone I treated cervical cancer cells

city: YangZhou

first: Shuna

last: Cui

state: JiangSu

address: Jiang Yang Middle Road 136,

department: Medical College of Yangzhou University

institute: YangZhou university

summary:
Phenotypically, we observed that both genistein and Tanshinone I exert the inhibitory effects on the proliferation and metastasis of cervical cancer.
The aim of this study was to comprehensively decipher the anti-metastasis effect and molecular mechanism of genistein and Tanshinone I on the cervical cancer.
The results showed that genistein and Tanshinone I strongly change the RNA profiling of the cervical cancer cells in different manners: genistein mainly targets on regulation of RNA transcription, central carbon metabolism in cancer, microRNAs in cancer and focal adhesion etc; Tanshinone I mainly effects on central carbon metabolism in cancer, mitophagy process.

overall_design: In this study, we aim to elucidate the changes of mRNA profiles of human cervical cancer due to genistein and Tanshinone I treatments. We designed our experiments in three groups: Hela cells from human cervical cancer were treated with I) 50 μM genistein, labeled as Geni; ii) 50 μM Tanshinone I, labeled as TanI; and iii) 50 μM solvent control, labeled as Ctrl for 5h. Three replicates were set for each individual group.

first: Tingting


title: Simultaneous identification of m6A and m5C reveals coordinated RNA modification at single-molecule resolution [mouse frontal cortex]

city: Canberra

first: Pablo

last: Acera Mateos

state: ACT

address: 131 Garran Rd

department: The Shine-Dalgarno Centre for RNA Innovation

country: Australia

institute: ANU

summary: The expanding field of epitranscriptomics might rival the epigenome in the diversity of biological processes impacted. However, the identification of multiple modification types in individual RNA molecules remains challenging. We present CHEUI, a new method that detects N6-methyladenosine (m6A) and 5-methylcytidine (m5C) in individual transcript molecules in a single condition as well as differential methylation between two conditions, using nanopore signals. CHEUI processes observed and expected signals with convolutional neural networks to achieve high single-molecule accuracy and outperform other methods in detecting m6A and m5C sites and quantifying their stoichiometry. Moreover, CHEUI’s unique capability to identify different modifications in the same signal data reveals a non-random co-occurrence of m6A and m5C in transcripts in human cell lines and during mouse embryonic brain development. CHEUI unlocks the capability of studying links between multiple RNA modifications and phenotypes, enabling the discovery of new epitranscriptome functions. Furthermore, CHEUI's training and testing protocols are adaptable to other modifications, making it a versatile RNA technology.

overall_design: Mouse frontal cortex tissues were extracted and sequenced using Nanopore d-RNA from embryonic day (E) 12, E15 and E18.

first: P

first: A

last: Sethi

last: Ravindran

first: M

last: Guarnacci

last: Srivastava

first: J

first: K

last: Woodward

first: Z

middle: W

last: Yuen

last: Gao

first: L

middle: M

last: Starrs

first: W

last: Hamilton

first: R

last: Hayashi

first: V

last: Wickramasinghe

first: T

last: Preiss

first: G

last: Burgio

first: N

last: Dehorter

last: Shirokikh

first: E

last: Eyras


title: Whole genome miRNA analysis of in-vitro differentiated myotubes from Emery-Dreifuss Muscular Dystrophy patients.

city: Edinburgh

first: Jose

middle: Ignacio

last: de las Heras

address: Max Born Crescent

department: Wellcome Trust Centre

country: United Kingdom

institute: University of Edinburgh

summary: Emery-Dreifuss muscular dystrophy (EDMD) is a genetically and clinically variable disorder. Here we performed transcriptome analysis on 10 EDMD patients covering mutations in 7 EDMD-linked genes, compared to 2 healthy controls. Myoblasts were isolated from muscle biopsies and differentiated in-vitro for 6 days. Differentiated myotubes were isolated, total RNA extracted and the small <200 nt fraction sequenced. The genes and mutations included were: patient 1 (TMEM214, p.R179H), patient 2 (PLPP7/NET39, p.M92K), patient 3 (SUN1, p.G68D, p.G388S), patient 4 (SYNE1, p.6869*, p.6869*), patient 5 (EMD, p.S58Sfs*1), patient 6 (FHL1, c.688+1G>A), patient 7 (FHL1, p.C224W), patient 8 (FHL1, p.V280M), patient 9 (LMNA, p.T528K), patient 10 (LMNA, p.R571S).

overall_design: miRNA analysis was performed comparing in-vitro differentiated EDMD patients against healthy controls. All samples were analysed in triplicate (separate in-vitro differentiation experiments).

middle: I

first: Eric

middle: C

last: Schirmer


title: Effect of depletion of Piezo1 on gene expression during apoptosis of anulus fibrosus cells induced by mechanical stretch

city: Xining

first: Liu

last: Chenhao

state: Qinghai

address: Xinqiao Street

department: Orthopedic

institute: Qinghai Provincial People's Hospital

summary: To investigate the effect of Piezo1 in the apoptosis of anulus fibrous cells (AFCs) induced by mechanical stretch. We established AFCs in which Piezo1 channel has been knocked down by shRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of AFCs treated withpLVX-shRNA-Puro(Lv-Ctrl group) and AFCs treated with pLVX-shRNA-Puro-Piezo1(Lv-Piezo1 group).

overall_design: Comparative gene expression profiling analysis of RNA-seq data for AFCs AFCs in Lv-Ctrl group and Lv-Piezo1 group.

first: Chenhao

last: Liu

first: Yu

last: Zhai


title: Host transcriptome profiling analysis induced by Md5BAC △meq△pp38, Md5BAC △LORF9, Md5BAC △UL23 recombinant viruses

city: Zhengzhou

first: ZHU Xiaojing

middle: Xiaojing

last: ZHU

state: Henan

address: 15 Longzihu University Park, Zhengdong New District

institute: Henan Agricultural University

summary: Marek’s disease virus (MDV) induces immunosuppression and neoplastic disease in chickens. The virus is controllable via an attenuated meq deletion mutant virus which has the disadvantage of retaining the ability to induce lymphoid organ atrophy. To overcome this deficiency and produce more vaccine candidates, a recombinant MDV was generated from the highly virulent Md5BAC strain, in which both meq and a cytolytic replication related gene, pp38, were deleted. In addition, LORF9 and UL23 genes were separately deleted. Gene expression profiling analysis were compared between these recombinant viruses and the CVI988/Rispens vaccine strain and the Md5BAC wild strain using data obtained from RNA-seq.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for CVI988/Rispens vaccine strain, Md5BAC and 3 recombinant viruses (Md5BAC △meq△pp38, Md5BAC △LORF9, Md5BAC △ UL23).

first: Guoqing

last: Zhuang

first: Aijun

last: Sun


title: Wide phenotypic spectrum of human stem cell-derived excitatory neurons with Rett syndrome-associated MECP2 mutations

city: Toronto

first: James

last: Ellis

state: ON

address: 686 Bay Street

country: Canada

institute: Hospital for Sick Children

overall_design: RNAseq of CLT WT and RTT missense iPSCs for submission to Pluritest to analyze pluripotency status

middle: S

last: Mok

first: J


title: Simultaneous identification of m6A and m5C reveals coordinated RNA modification at single-molecule resolution

first: Pablo

last: Acera Mateos

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus


title: Mammalian CDC14 phosphatases control bivalent promoters and exit from stemness in pluripotent cells [snGEX]

city: Madrid

first: Osvaldo

last: Graña

state: Comunidad de Madrid

address: C/ Melchor Fernández Almagro, 3

department: Structural Biology

country: Spain

institute: CNIO

summary: CDC14 phosphatases are critical components of the cell cycle machinery that drives exit from mitosis in yeast. However, the two mammalian paralogs, CDC14A and CDC14B, are dispensable for cell cycle progression or exit, and their function remains unclear. By generating a double Cdc14a; Cdc14b -null mouse model, we report here that CDC14 phosphatases control cell differentiation in pluripotent cells, and their absence results in deficient development of the neural system. Lack of CDC14 impairs neural differentiation from embryonic stem cells (ESCs) accompanied by deficient induction of genes controlled by bivalent promoters. CDC14 directly dephosphorylates and destabilizes Undifferentiated embryonic Transcription Factor 1 (UTF1) during the exit from stemness. Multiomic single-cell analysis of differentiating ESCs suggest that increased UTF1 levels in the absence of CDC14 prevent the firing of bivalent promoters required for differentiation. These results, along recent data suggesting a critical role for cell cycle kinases in pluripotency, suggest that cell cycle kinase-phosphatase modules such as CDK-CDC14 are critical for linking cell cycle regulation and self-renewal, with a specific function for CDC14 phosphatases modulating key epigenetic regulators during the terminal exit from pluripotency.

overall_design: Wild-type and Cdc14ab KO mESC at day 0 (LIF-containing medium) and day 5 of the neural differentiation protocol were subjected to single-cell ATACseq coupled to single-cell RNAseq in the same cell

first: Carolina

last: Villarroya

last: Graña-Castro

first: Marcos

last: Malumbres


title: Mammalian CDC14 control differentiation from pluripotent cells by modulating UTF1 activity on bivalent promoters

summary: CDC14 phosphatases are critical components of the cell cycle machinery that drives exit from mitosis in yeast. However, the two mammalian paralogs, CDC14A and CDC14B, are dispensable for cell cycle progression or exit, and their function remains unclear. By generating a double Cdc14a; Cdc14b-null mouse model, we report here that CDC14 phosphatases control cell differentiation in pluripotent cells and their absence results in deficient development of the neural system. Lack of CDC14 impairs neural differentiation from embryonic stem cells (ESCs) accompanied by deficient induction of genes controlled by bivalent promoters. During ESC differentiation, CDC14 directly dephosphorylates and destabilizes Undifferentiated embryonic Transcription Factor 1 (UTF1), a critical regulator of stemness. In the absence of CDC14, increased UTF1 levels prevent the firing of bivalent promoters, resulting in defective induction of the transcriptional programs required for differentiation. These results suggest that mammalian CDC14 phosphatases function during the terminal exit from the cell cycle by modulating the transition from the pluripotent to the differentiated chromatin state, at least partially by controlling chromatin dynamics and transcription in a UTF1-dependent manner.

overall_design: Wild-type, single and double Cdc14 a and b KO ESCs obtained from mice were subjected to neural differentiation protocol. Samples were collected at days 0, 2 and 7 of the differentiation protocol and subjected to RNAseq


title: Effect of PT2385 treatment during cytotrophoblast differentiation under hypoxia

city: Woluwé-Saint-Lambert

first: Arthur

middle: Henri

last: Colson

address: Avenue Hippocrate, 54

department: Institut de recherche expérimentale et clinique

country: Belgium

institute: Université catholique de Louvain

summary:
To investigate the therapeutic effect of HIF-2 inhibitor in placental dysfunction, we used primary cytotrophoblasts isolated from human placentas at term and cultured them under 2.5% O2 for 4 days.
We either treated the cells with PT2385 at 10 µmol/L or vehicle and then performed gene expression profiling analysis using data obtained from RNA-seq of 3 different placentas.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for treated and untreated cytotrophoblasts.

first: Christophe

last: Depoix

first: Isaline

last: Lambert


title: Simultaneous identification of m6A and m5C reveals coordinated RNA modification at single-molecule resolution [HeLa cells]

overall_design: Nanopore direct RNA (d-RNA) sequencing was performed using 3 replicates from HeLa WT cells and 3 replicates from HeLA NSUN2-KO cells.

first: P

first: A

last: Sethi

last: Ravindran

first: M

last: Guarnacci

last: Srivastava

last: Xu

first: K

last: Woodward

first: Z

last: Yuen

last: Gao

first: L

last: Starrs

first: W

last: Hamilton

first: R

last: Hayashi

first: V

last: Wickramasinghe

first: T

last: Preiss

first: G

last: Burgio

first: N

last: Dehorter

last: Shirokikh

first: E

last: Eyras


title: Whole-transcriptome sequencing and ceRNA interaction network construction for temporomandibular joint osteoarthritis [miRNA-Seq]

city: Jiamusi

first: Fan

last: Wu

address: Southwest Gang Street

institute: Jiamusi University

summary: To investigate the functions of ncRNAs in temporomandibular joint osteoarthritis, we established temporomandibular joint osteoarthritis model induced by unilateral anterior crossbite. We then performed gene expression profiling analysis using data obtained from RNA-seq of condylar cartilage at 8 weeks of modeling.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for condylar cartilage of TMJOA and normal groups.


title: Mouse bone marrow derived macrophages

city: qingdao

first: qiaoling

last: song

address: Xiang Gang East Road NO.23

institute: Ocean University of China

summary: Bone marrow cells (BM) were isolated and primed with M-CSF (M BMDM) or GM-CSF (GM BMDM) for 7 days. M-BMDMs were treated with IL6 (20 ng/ml) for 3 h or 24 h while GM-BMDMs were treated for 3 h. The difference between BM, M-BMDM, and GM-BMDM were analyzed to describe the phenotye and function of each population. Moreover, by RNA-seq analysis, the influence of IL6 treatment on GM-BMDMs and M-BMDMs were analyzed.

overall_design: BM, M-BMDM, GM-BMDM, M-BMDM with IL6 for 3 h, M-BMDM with IL6 for 24 h, GM-BMDM with IL6 for 3 h

first: Qiaoling

last: Song

first: Chenyang

last: Zhao

first: Jinbo

last: Yang

first: Lei

last: Zhang


title: SOCS3 deficiency blocked autophagy-dependent myeloid differentiation of early-stage myeloid-derived suppressor cells via the miR-155/C/EBPβ/Wnt axis

city: Tianjin

first: Wenwen

address: huanhuxi road

institute: Tianjin Medical University Cancer Institute and Hospital

summary: To explore which pathways participated in dysfunctional eMDSC differentiation, we performed RNA sequencing on Gr-1 cells, eMDSCsfl/fl and eMDSCsKO to screen for potential candidates that might participate in the SOCS3-deficiency-induced differentiation arrest in eMDSCs.

overall_design: mRNA profiles of Gr_1, WT and SOCS3-/- mice were generated by deep sequencing, in triplicate, using Illumina.

first: Rui

first: Mengmeng

last: Jiang


title: IL-17 Signaling in Steatotic Hepatocytes and Macrophages Promotes Alcoholic Liver Disease-induced Hepatocellular Carcinoma [II]

city: La Jolla

first: Tatiana

last: Kisseleva

state: CA

address: 9500 Gilman Drive

institute: University of California, San Diego

summary: IL-17A is a tumor-promoting cytokine, which critically regulates inflammatory responses in myeloid cells, and cholesterol synthesis in steatotic hepatocytes in experimental model of alcohol-induced HCC. Therefore, IL-17A may be a potential therapeutic target for EtOH-induced HCC patients.

overall_design: IL-17RAdHEPand IL-17RAF/F mice (C57BL/6, 2 weeks old)were injected i.p. with DEN (25mg/kg body weight, Sigma).  DEN-challenged mice were subjected to isocaloric liquid EtOH feeding, or chow-fed for 18 weeks.

first: Hsiao-Yen

last: Ma

first: Sara

middle: B

last: Rosenthal


title: IL-17 Signaling in Steatotic Hepatocytes and Macrophages Promotes Alcoholic Liver Disease-induced Hepatocellular Carcinoma

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

overall_design: Refer to individual Series


title: Transcriptome analysis of in vitro hematopoietic stem cells (HSC) and stage 3 (ST3) NK cell progenitors cells expressing a TXNIP-specific shRNA.

city: Ghent

first: Georges

last: Leclercq

address: C. Heymanslaan

institute: Ghent University

summary: To investigate the function of TXNIP in the regulation of natural killer (NK) cell differentiation, we established in vitro NK cell differentation cultures starting with cordblood derived HSC in which TXNIP has been knocked down with shRNA by lentiviral transduction. We then performed transcriptome analysis of the HSC population at day 3 and ST3 population at day 7.

overall_design: mRNA profile of HSC (d3) and ST3 (d7) transduced with shTXNIP in comparison to control transduced cells

first: Eva

last: Persyn

first: Wouter

last: Van Loocke


title: Whole-transcriptome sequencing and ceRNA interaction network construction for temporomandibular joint osteoarthritis [RNA-Seq]

first: Yanxin

last: An

first: Jing

last: Wang

first: Gaoyi


title: IL-17 Signaling in Steatotic Hepatocytes and Macrophages Promotes Alcoholic Liver Disease-induced Hepatocellular Carcinoma [I]

overall_design: IL-17RA-/- and WT mice (C57BL/6, 2 weeks old)were injected i.p. with DEN (25mg/kg body weight, Sigma).  DEN-challenged mice were subjected to isocaloric liquid EtOH feeding, or pair-fed for 18 weeks.


title: Whole transcriptome analysis of neuroblastoma cell lines after ERK5 silencing

status: Public on Oct 29 2022

city: Barcelona

first: Carlos

last: Jimenez

state: Barcelona

address: Pg. Vall dHebron 119-129, Edificio Collserola, lab 207

department: Pediatric Oncology

institute: Vall d'Hebron Institut de Recerca

summary: The transcriptomic network modulated after the depletion of the tyrosin kinase ERK5 through shRNA-mediated silencing was analyzed in SK-N-BE(2) and CHLA-90 neuroblastoma cell lines, in order to characterize and reveal any relevant role of this kinase at the transcriptional level.

overall_design: SK-N-BE(2) and CHLA-90 cells were transduced with lentiviral particles carrying two different shRNA for ERK5 silencing and 72 h later RNA was extracted in biological triplicates for expression microarray analysis.

last: Jiménez

first: Laia

last: París-Coderch

first: Aroa

last: Soriano

first: Miguel

middle: F

last: Segura

first: Nora

last: Diéguez-Martínez

first: Idoia

last: Bolinaga-Ayala

first: Jose

last: Lizcano


title: Effect of SMYD3 on MCF7 breast cancer cells (RNA-seq)

city: Seoul

first: Hee-Joo

last: Choi

address: 222 Yangshimri-ro, Seongdonggu

country: South Korea

institute: Hanyang University

summary: RNA-sequencing analysis of control and SMYD3-overexpressed MCF7 cell lines. SMYD3 (also known as KMT3E), a hisone H3 lysine K4 methyltransferase, is highly expressed in several human cancers, including colorectal and breast carcinomas. Results provide insight into the transcriptional regulation of SMYD3 in breast cancer.

overall_design: MCF7 cells were stably infected with lentiviruses encoding either control (pLVX vectror) or SMYD3 cDNA (pLVX-SMYD3) and selected using puromycin. Total RNA was isolated from control- and SMYD3-overexpressed MCF7 stable cells using Trizol reagent. For each of the 2 conditions, 3 biological replicates were included. In total, 6 RNA-sequencin samples were analyzed; 3 controls and 3 SMYD3 overexpressed MCF7 cells.

first: Jeong-Yeon

last: Lee

first: Gu

last: Kong


title: RNA-Seq of injured mouse hearts depleted for myofibroblast Yap [I]

city: Wauwatosa

first: Michael

middle: Andrew

last: Flinn

state: WI

address: 8701 W Watertown Plank Rd

department: Physiology

institute: Medical College of Wisconsin

summary: A myofibroblast specific tamoxifen inducible Cre was used to assess the contribution of Yap in the mouse heart after myocardial infarction

overall_design: We implemented a Cre-lox system whereby inducible Cre expressed under the myofibroblast specific Periostin promoter is crossed with Yap floxed animals, facilitating inducible depletion of Yap. Mice were siblings with floxed Yap alleles and either a copy of MerCreMer under the endogenous periostin promote or wildtype Periostin. Permenant ligation of the left anterior descending artery or sham surgeries were conducted. Mice were administered tamoxifen citrate diet ad libitum immediately after surgery to promote excession of myofibroblast yap and left ventricles were collected 4 days post injury.

first: M

first: C

last: O'Meara

last: Patterson


title: RNA-seq of injured mouse hearts depleted for myofibroblast Yap or Yap and Wwtr1


title: RNAseq analysis for transcriptomes of colon cancer cell line HCT116 upon p53 and/or iASPP knockdown with or without nutlin treatment

city: Shanghai

first: Jiale

last: Wu

address: Room 707, Science and Education Plaza  197 Rui Jin Er Road

institute: State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Rui Jin Hospital, Shanghai Jiaotong University

summary: The tumor suppressor p53 plays a critical role in the cellular response to various stresses, including DNA damage, hypoxia, nutrition starvation, and oncogene activation. However, wild-type p53 function was largely impaired in cancer cells, one of the reasons is the inhibition by p53 negative regulating proteins (iASPP, MDM2 etc.). To globally evaluate the transcriptome inhibited by iASPP and the potent synergy of co-inhibiting MDM2, we performed RNAseq analysis in colon cancer cell line HCT116 upon p53 or iASPP knockdown with or without Nutlin-3 treatment.

overall_design: RNAseq to evaluate p53 transcriptional activity upon indicated treatments.

first: Min

last: Lu


title: Transcriptome data of co-culture of Brevundimonas diminuta R79 and Pseudomonas balearica R90 in domestication medium

city: Jinan

first: Boya

last: Liang

address: No.336, West Nanxinzhuang Road, Qixian Street

institute: University of Jinan

summary: It is a cost-effective production method to synthesize polyhydroxyalkanoate (PHA) through mixed bacterial consortium fermentation. Pseudomonas balearica R90 and Brevundimonas diminuta R79, which represent the species of abundance increase in the propylene oxide activated sludge, were selected as the model to study the interaction mechanism of PHA synthesis by co-culture between strains. RNA-Seq analysis showed that the expression of acs and phaA genes of R79 and R90 increased in the mixed culture group, which enhanced their ability of acetic acid utilization and poly-β-hydroxybutyrate (PHB) synthesis. So the dry cell weight and the yield of PHB in the mixed culture group was prominently higher than that in the pure culture group. In addition, two-component system genes, quorum- sensing genes, flagellar synthesis related genes and chemotaxis related genes in R90 were enriched at 4 days, so R90 could adapt to the domestication environment more quickly, making the proportion of R90 higher than that of R79 at 4 days. However, the acs gene expression of R79 was higher than that of R90. Therefore, R79 can make better utilize acetate in the domestication solution environment, thus occupying the final dominant position.

sample_organism:
Brevundimonas diminuta
Stutzerimonas balearica

overall_design: The transcriptional group information was detected at 0, 4 and 7 days after mixed culture in the experimental group and single group in the control group.

first: Xiujun

last: Zhang

first: Qiang

last: Li

first: Xiangyu

last: Fan

first: Fang

last: Wang

first: Changfeng

last: Miao

first: Yan

last: Ji

first: Zhaosong

last: Hang

first: Pengfei

last: Gu

first: Xiaoli

last: Liu


title: The Preexisting T Cell Landscape Determines Response to T Cell-Engagers Therapy

status: Public on Oct 28 2022

city: Heidelberg

last: Kilian

address: Im Neuenheimer Feld 280

country: Germany

institute: German Cancer Research Center (DKFZ)

summary: Adaptive immunotherapy including bispecific T cell engagers (TCE) has shown promise in the treatment of various cancers, but clinical responses are heterogeneous and often not durable. As response to TCE is suggested to be independent of tumor recognition and T cell state, molecular determinants or mediators of primary and acquired resistance towards TCE remain poorly understood.   Here, we identify conserved behaviors of bone marrow residing CD4+ and CD8+ T cells in multiple myeloma patients undergoing TCE therapy. We show that the bone marrow immune landscape reacts to TCE therapy with cell state-dependent clonal T cell expansion and herewith infer coupling of tumor recognition via MHC-I, T cell exhaustion and clinical response. While we find the abundance of exhausted-like memory CD8+ T cell clones to be associated with clinical response failure, we describe loss of target epitope and MHC class I expression as tumor-intrinsic mechanisms of acquired resistance to TCE.

overall_design:
Bone marrow resident CD3 and CD45 cells were isolated by fluorescence-activated cell sorting (FACS) and analyzed using 10x Genomics 5' RNA/TCR sequencing.
**The submitter declares that the raw data were deposited to EGA (EGAD00001007788) due to data protection regulations.**

first: Mirco

last: Friedrich

first: Niklas

last: Kehl

first: Julius

last: Michel


title: Reprogramming Landscape Highlighted by Dynamic Transcriptomes in Therapy-induced Neuroendocrine Differentiation [CUT&RUN]

city: West Lafayette

first: Changdeng

last: Hu

state: IN

address: 575 Stadium Mall Drive

department: Dept. of Medicinal Chemistry and Molecular Pharmacology

institute: Purdue University

summary: Metastatic and locally advanced prostate cancer is treated by pharmacological targeting of androgen synthesis and androgen response via androgen signaling inhibitors (ASI), most of which target the androgen receptor (AR). However, ASI therapy invariably fails after 1-2 years. Emerging clinical evidence indicates that in response to ASI therapy, the AR-positive prostatic adenocarcinoma can transdifferentiate into AR-negative neuroendocrine prostate cancer (NEPC) in 17-25% treated patients, likely through a process called neuroendocrine differentiation (NED). Despite high clinical incidence, the epigenetic pathways underlying NED and ASI therapy-induced NED remain unclear. By utilizing a combinatorial single cell and bulk mRNA sequencing workflow, we demonstrate in a time-resolved manner that following AR inhibition with enzalutamide, prostate cancer cells exhibit immediate loss of canonical AR signaling activity and simultaneous morphological change from epithelial to NE-like (NEL) morphology, followed by activation of specific neuroendocrine (NE)-associated transcriptional programs. Additionally, we observed that activation of NE-associated pathways occurs prior to complete repression of epithelial or canonical AR pathways, a phenomenon also observed clinically via heterogenous AR status in clinical samples. Our model indicates that, mechanistically, ASI therapy induces NED with initial morphological change followed by deactivation of canonical AR target genes and subsequent de-repression of NE-associated target genes, while retaining AR expression and transcriptional shift towards non-canonical AR activity. Coupled with scRNA-seq and CUT&RUN analysis, our model system can provide a platform for screening of potential therapeutic agents that may prevent ASI-induced NED or reverse the NED process.

overall_design: CUT&RUN experiment and analysis was performed on two samples of LNCaP cells exposed to enzalutamide for 14 days or LNCaP cells exposed to DMSO control. Cells were grown in complete RPMI 1640 in 2D culture dishes, exposed to enzalultamide (or DMSO control), then harvested wth nuclei isolation following trypsin dissociation from plate. Samples were then sent to EpiCypher for CUT&RUN assay for H3K4me3, H3K27me3, and H3K27ac.

first: Andrew

last: Asberry

first: Sheng

first: Hye

last: Nam

first: Xuehong

last: Deng

first: Jun

last: Wan

first: Chang-Deng


title: Effect of depletion of AIM2 on gene expression in psoriatic NETs-treated primary human keratinocytes

city: Xi'an

first: Tianyu

last: Cao

address: Changle Road NO.127

institute: Fourth Military Medical University

summary: To investigate the function of the NET-AIM2 axis on keratinocyte activation during psoriasis, we established psoriatic NETs-treated primary human keratinocytes in which AIM2 has been knocked down by siRNA

overall_design: Comparative gene expression profiling analysis of RNA-seq data for primary human keratinocytes treated with psoriatic NETs and AIM2 siRNA, psoriatic NETs and NC siRNA, or NC siRNA as negative control respectively.

first: Xu

last: Yuan

first: Shuai

last: Shao


title: Biotoxic effects and gene expression regulation of urban PM2.5 in southwestern China

status: Public on Oct 30 2022

city: Nanchong

first: Qin

last: Zhang

address: No. 234, Fujiang Road, Shunqing District, Nanchong, Sichuan

institute: North Sichuan medical college

summary: Atmospheric fine particulate matter (PM2.5) causes severe haze in China and is regarded as a threat to human health. The health effects of PM2.5 vary location by location due to the variation in size distribution, chemical com position, and sources. In this study, the cytotoxicity effect, oxidative stress, and gene expression regulation of PM2.5 in Chengdu and Chongqing, two typical urban areas in southern China, were evaluated. Urban PM2.5  in summer and winter significantly inhibited cell viability and increased reactive oxygen species (ROS) levels in A549 cells. Notably, PM2.5 in winter exhibited higher cytotoxicity and ROS level than summer. Moreover, in this study, PM2.5 commonly induced cancer-related gene expression such as cell adhesion molecule 1(PECAM1), interleukin 24 (IL24), and cytochrome P450 (CYP1A1); meanwhile, PM2.5 commonly acted on cancer-related biological functions such as cell-substrate junction, cell-cell junction, and focal adhesion. In partic ular, PM2.5 in Chengdu in summer had the highest carcinogenic potential among PM2.5 at the two sites in summer and winter. Importantly, cancer-related genes were uniquely targeted by PM2.5, such as epithelial splicing regu latory protein 1 (ESRP1) and membrane-associated ring-CH-type finger 1 (1-Mar) by Chengdu summer PM2.5; collagen type IX alpha 3 chain (COL9A3) by Chengdu winter PM2.5; SH2 domain-containing 1B (SH2D1B) by Chongqing summer PM2.5; and interleukin 1 receptor-like 1 (IL1RL1) and zinc finger protein 42 (ZNF423) by Chongqing winter PM2.5. Meanwhile, important cancer-related biological functions were specially induced by PM2.5, such as cell cycle checkpoint by Chengdu summer PM2.5; macromolecule methylation by Chengdu win ter PM2.5; endoplasmic reticulum-Golgi intermediate compartment membrane by Chongqing summer PM2.5;and cellular lipid catabolic process by Chongqing winter PM2.5. Conclusively, in the typical urban areas of southern China, both summer and winter PM2.5 illustrated significant gene regulation effects. This study contrib utes to evaluating the adverse health effects of PM2.5 in southern China and providing public health suggestions for policymakers.

overall_design: mRNA pofiles of the A549 cells treated with CDWIN-PM2.5(100 μg/mL),CDSUM-PM2.5 (100 μg/mL), CQWIN-PM2.5 (100 μg/mL),and CQSUM-PM2.5 (100 μg/mL), the same volumes of DMSO,were generated by deep sequencing,in triplicate,using the NEBNext® Ultra™ RNA Library Prep Kit for Illumina® (NEB,USA).

first: Shumin

first: Jingping

first: Dongmei

last: Guo

first: Yang

last: Chen


title: Nuclear functions of KaeA, the subunit of KEOPS complex in Aspergillus nidulans.

city: Warsaw

first: Agnieszka

last: Dzikowska

address: Pawinskiego 5A

department: Biology

country: Poland

institute: University of Warsaw

summary: The aim of this project is to confirm that KaeA a subunit of highly conserved KEOPS/EKC complex, participates in the transcription regulation in Aspergillus nidulans. To identify genes directly or indirectly regulated by KaeA, the RNA-seq experiments were performed using kaeA mutants and the wild type kaeA+ strain.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for kaeA19 and kaeA25 mutants and their isogenic wild-type strains, grown in minimal medium in three biological replicates.

first: Gawlik

last: Joanna

first: Koper

last: Michal

first: Bogdanowicz

last: Albert

first: Dzikowska

last: Agnieszka


title: Reprogramming Landscape Highlighted by Dynamic Transcriptomes in Therapy-induced Neuroendocrine Differentiation [scRNA-seq]

first: Changdeng

overall_design: Single cell RNA-seq performed on four samples of LNCaP cells exposed to enzalutamide for 4, 7, and 14 days or LNCaP cells exposed to DMSO control. Cells were grown in complete RPMI 1640 in 2D culture dishes, exposed to enzalultamide (or DMSO control) for given time period, then harvested following trypsin dissociation from plate.

first: Andrew

first: Sheng

last: Liu

first: Hye


title: Anti-MN1 sdAb screening and its function in vivo

first: Zhenyi

last: Ma

address: No.22，Qixiangtai Road

institute: Tianjin Medical University

summary: To study the function of anti-MN1 sdAb in MN1-positive tumour cells, we treated U2OS cells with anti-MN1 sdAb and performed RNA-seq.

overall_design: Comparative gene expression profiling analysis of RNA-seq data using U2OS cells treated with anti-MN1 sdAb, compared with the sdAb con.

first: Mingchen

last: Li

first: Jinyi

first: Zhe


title: Reprogramming Landscape Highlighted by Dynamic Transcriptomes in Therapy-induced Neuroendocrine Differentiation [mRNA-seq]

last: Hu

overall_design: mRNA-seq performed on six samples of LNCaP cells exposed to enzalutamide for 14 days or LNCaP cells exposed to DMSO control. Cells were grown in complete RPMI 1640 in 2D culture dishes, exposed to enzalultamide (or DMSO control), then harvested following trypsin dissociation from plate.

last: Asberry

last: Nam

first: Xuehong

first: Jun

first: Chang-Deng


title: Monocyte responses associate with MAC lung disease

city: Seattle

first: Kimberly

last: Dill-McFarland

state: WA

address: 750 Republican St

department: Allergy and Infectious Diseases

institute: University of Washington

summary: To understand nontuberculous mycobacterial (NTM) pathogenesis, we evaluated immune responses to Mycobacterium avium (Mav) in asymptomatic individuals with a previous history of M. avium complex lung disease (MACDZ). We analyzed global gene expression in paired Mav-infected and uninfected peripheral blood monocytes from 17 MACDZ and 17 healthy controls.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for peripheral blood monocytes infected with M. avium or media controls.

first: Cecilia

last: Arlehamn

first: Basilin

last: Benson

first: Rebecca

last: Kuan

first: Kimberley

last: Dill-Mcfarland

first: Glenna

last: Peterson

first: Sinu

last: Paul

first: Felicia

middle: K

last: Nguyen

first: Robert

middle: H

last: Gilman

first: Mayuko

last: Saito

first: Randy

last: Taplitz

first: Matthew

last: Arentz

first: Christopher

last: Goss

first: Moira

last: Aitken

first: David

last: Horne

first: Javeed

last: Shah

first: Alessandro

last: Sette

first: Thomas

last: Hawn


title: Reprogramming Landscape Highlighted by Dynamic Transcriptomes in Therapy-induced Neuroendocrine Differentiation

first: Changdeng

last: Hu

overall_design: Refer to individual Series


title: Host cell transcriptomic response to the multidrug-resistant Mycobacterium tuberculosis clonal outbreak Beijing strain reveals its pathogenic features

city: Bangkok

first: Marisa

last: Ponpuak

address: 272 Rama 6 Road

country: Thailand

institute: Department of Microbiology, Faculty of Science, Mahidol University

summary: The upsurge of multidrug-resistant infections has rendered tuberculosis the principal cause of death among infectious diseases. A clonal outbreak multidrug-resistant triggering strain of Mycobacterium tuberculosis was identified in Kanchanaburi Province, designated “MKR superspreader”, which was found to subsequently spread to other regions, as revealed by prior epidemiological reports in Thailand. Herein, we showed that the MKR displayed a higher growth rate upon infection into host macrophages in comparison with the H37Rv reference strain. To further elucidate the MKR’s biology, we utilised RNA-Seq and differential gene expression analyses to identify host factors involved in the intracellular viability of the MKR. A set of host genes function in the cellular response to lipid pathway was found to be uniquely up-regulated in host macrophages infected with the MKR, but not those infected with H37Rv. Within this set of genes, the IL-36 cytokines which regulate host cell cholesterol metabolism and resistance against mycobacteria attracted our interest, as our previous study revealed that the MKR elevated genes associated with cholesterol breakdown during its growth inside host macrophages. Indeed, when comparing macrophages infected with the MKR to H37Rv-infected cells, our RNA-Seq data showed that the expression ratio of IL-36RN, the negative regulator of the IL-36 pathway, to that of IL-36G was greater in macrophages infected with the MKR. Furthermore, the intracellular survival of MKR was diminished with decreased IL-36RN expression. Overall, our results indicate that IL-36RN is critical for MKR intracellular survival and could serve as a new target against this emerging multidrug-resistant M. tuberculosis strain.

overall_design: Raw macrophages were infected with either Mycobacterium tuberculosis reference strain H37Rv or multidrug-resistant Mycobacterium tuberculosis strian MKR for 0 and 4 hr. Total RNAs were then collected and subjected to RNA-Seq analyses. stravation for 2 hr. Total RNAs were then collected and subjected to RNA-Seq analyses.

first: Pinidphon

last: Prombutara

first: Tegar

middle: A

last: Siregarc

first: Thanida

last: Laopanupong

first: Phongthon

last: Kanjanasirirate

first: Tanawadee

last: Khumpanied

first: Suparerk

last: Borwornpinyo

first: Angkana

last: Chaiprasert

first: Prasit

last: Palittapongarnpim


title: Nuclear functions of KaeA, the subunit of KEOPS complex in Aspergillus nidulans

first: Agnieszka

last: Dzikowska

summary: The aim of this project is to confirm that KaeA, the subunit of highly conserved KEOPS/EKC complex, participates in the transcription regulation in Aspergillus nidulans.The ChIP-seq experiment was performed to identify chromatin regions directly or indirectly bound by KaeA.

overall_design: Chip-seq experiment based on immunoprecipitation of chromatine fragments bound to KaeA-HA fussion protein. Experiment was carried out on 6 samples: 3 control biological replicates (input) and 3 biological replicates after immunoprecipitation treatment (IP). Bioinformatical comparison between both groups was performed.

first: Joanna

last: Gawlik

first: Michal

last: Koper


title: Large 22q13.3 deletions perturb peripheral transcriptomic and metabolomic profiles in Phelan-McDermid syndrome

city: New York

first: Michael

last: Breen

state: NY

address: 1468 Madison Ave

department: Depts. of Psychiatry, Genetics and Genomic Sciences

institute: Ichan School of Medicine at Mount Sinai

summary: Peripheral blood transcriptomic data were generated across 68 PMS participants, including Class I sequence variants and mutations (n=33) and Class II mutations (n=35), as well as an age and sex matched control group (n=24), which largely consisted of unaffected siblings (~91%).

overall_design: Examination of peripheral blood gene expression profiles between PMS participants with Class I and Class II 22q13.3 mutations.


title: Transcriptome changes in embryonic and postnatal mouse hearts

city: Nanjing

first: Danyang

last: Chong

state: Jiangsu

address: 101 Longmian Avenue, Jiangning District, Nanjing

institute: Nanjing Medical University

summary: To investigate the transcriptome changes in embryonic and postnatal mouse hearts, we performed gene expression profiling analysis using data obtained from RNA-seq of C57BL/6J mouse hearts at embryonic day 18.5 (E18.5d), postnatal 1st day (P1d) and postnatal 7th day (P7d).

overall_design: Comparative gene expression profiling analysis of RNA-seq data for C57BL/6J mouse hearts at E18.5d, P1d and P7d.

first: Yayun

last: Gu


title: SARS-COV-2 N protein hijacks host NPM1-snoRNA to enhance rRNA 2’-O-Me modification and facilitate replication

city: Hangzhou

first: Jiang

last: Penglei

address: Yuhangtang Road 866

department: School of basic medicine science

institute: Zhejiang University

summary: SARS-COV-2 caused COVID-19 has caused unprecedented global health crisis. Coronavirus have developed a variety of mechanisms to interfere host translation machinery to facilitate virus protein production. Here, we conducted Ribometh-seq to explore the effects of ectopic expression of SARS-COV-2 N protein on rRNA 2'-O-me modification profiles of host cells.

overall_design: Examination of rRNA 2’-O-me modification in HEK293T cells with or without ectopic expression of SARS-COV-2 N protein.

first: Hui

last: Wang

first: Penglei

last: Jiang

first: Pengxu

last: Qian


title: Direct reprogramming of human fetal retinal pigment epithelial cells into photoreceptor-like cells [RNA-seq]

city: los angeles

first: Guoping

last: Fan

state: ca

address: 695 Charles E Young Drive South

department: Human Genetics

institute: university of california, los angeles

summary: RNAseq profiles for the  CiPCs induction

overall_design: fRPE cells were plated on 0.1% gelatin coated plates at a density of 3 x 104 cells/cm2 and cultured in fRPE medium on Day 0 (D0). The next Day (D1), medium was changed to photoreceptor induction medium 1 (PIM1) containing DMEM/F12, 10% knockout serum replacement, 2% B27, 5 ng/mL Noggin, 5 ng/mL IGF-1, in combination with 5 small molecule factors (5F): 0.5 mM VPA, 4.8 μM CHIR99021, 2 μM Repsox, 10 μM Forskolin and 10 μM IWR1. To promote and support the formation of photoreceptors, 3 nM sonic hedgehog, 100 μM taurine, 1 μM retinoic acid (STR), 1% N2 and 5 ng/mL bFGF were added in the medium (PIM2) along with 5F from D5 to D10.  For HDF reprogramming, cells were seeded in growth medium. On D1, PIM1 containing 5F (at the same concentrations) was added, and PIM2 containing STR and 5F was added on D5. For PTBP1 ASO treatment, Cells were seeded on D0 and cultured in growth medium to reach a confluency at around 70%-80% 24 hours later. On D1, in addition to medium change of PIM1 with 5F, PTBP1 ASO was transfected with Lipofectamine RNAimax (ThermoFisher Scientific). We used 3.75 μL of RNAimax, 37.5 pmol ASO in 1 ml of culture medium. 48 hours after ASO treatment, medium was replaced by fresh PIM1 containing 5F and the following process was the same as described above.

first: Jing


title: NOS1AP is a novel molecular target and critical factor in TDP-43 pathology.

city: Trieste

first: Maurizio

last: Romano

address: Via A. Valerio 28

department: Department of Life Sciences

institute: University of Trieste

summary: Effects of hnRNPD and hnRNPU silencing on gene expression in SH-SY5Y cells.

overall_design: SH-SY5Y cells were treated with siRNA anti-hnRNPD (n=3), or anti-hnRNPU  (n=3), or anti-Luciferase  (n=3)

first: Emanuele

last: Buratti


title: Direct reprogramming of human fetal retinal pigment epithelial cells into photoreceptor-like cells [scRNA-seq]

summary: single cell RNAseq for the  CiPCs induction

overall_design: fRPE cells were plated on 0.1% gelatin coated plates at a density of 3 x 104 cells/cm2 and cultured in fRPE medium on Day 0 (D0). The next Day (D1), medium was changed to photoreceptor induction medium 1 (PIM1) containing DMEM/F12, 10% knockout serum replacement, 2% B27, 5 ng/mL Noggin, 5 ng/mL IGF-1, in combination with 5 small molecule factors (5F): 0.5 mM VPA, 4.8 μM CHIR99021, 2 μM Repsox, 10 μM Forskolin and 10 μM IWR1. To promote and support the formation of photoreceptors, 3 nM sonic hedgehog, 100 μM taurine, 1 μM retinoic acid (STR), 1% N2 and 5 ng/mL bFGF were added in the medium (PIM2) along with 5F from D5 to D10. For PTBP1 ASO treatment, Cells were seeded on D0 and cultured in growth medium to reach a confluency at around 70%-80% 24 hours later. On D1, in addition to medium change of PIM1 with 5F, PTBP1 ASO was transfected with Lipofectamine RNAimax (ThermoFisher Scientific). We used 3.75 μL of RNAimax, 37.5 pmol ASO in 1 ml of culture medium. 48 hours after ASO treatment, medium was replaced by fresh PIM1 containing 5F and the following process was the same as described above.


title: Direct reprogramming of human fetal retinal pigment epithelial cells into photoreceptor-like cells [Methyl-seq]

type: Methylation profiling by high throughput sequencing

summary: DNA methylation profiles for the  CiPCs induction


title: Direct reprogramming of human fetal retinal pigment epithelial cells into photoreceptor-like cells

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


title: Tripartite target-agnostic combination immunotherapy cures established poorly immunogenic tumors

city: Cologne

first: Sven

last: Borchmann

address: Weyertal 115c

institute: University Of Cologne

summary: Single-agent immunotherapy, such as immune checkpoint inhibition, has shown remarkable efficacy in selected cancer entities and individual patients. However, most patients fail to respond. This is likely due to diverse immunosuppressive mechanisms acting in a concerted way to suppress the host anti-tumor immune response reducing the efficacy of single-agent immunotherapy. Combination immunotherapy approaches that are effective in such poorly immunogenic tumors mostly rely on precise knowledge of immunological targets on tumor cells by vaccinations or antibodies engineered to directly target those. Thus, creating a target-agnostic combination immunotherapy that is effective in poorly immunogenic tumors for which an immunological target is not known is a major challenge. We show that combined adoptive cellular therapy (ACT) with lymphokine-activated killer cells (LAKs), cytokine-induced killer cells (CIKs), Vγ9Vδ2-T-cells (γδ-T-cells) and adaptive, tumor-specific T-cells (CTLs) display synergistic anti-tumor treatment effects, which is further enhanced by co-treatment with anti-PD1 antibodies. Most strikingly, combination of this ACT with anti-PD1 antibodies, local immunotherapy of agonists against Toll-like receptor 3, 7 and 9 and pre-ACT lymphodepletion, a protocol we named TRI-IT, eradicates established, poorly immunogenic tumors and induces durable anti-tumor immunity in a variety of poorly immunogenic syngeneic, autochthonous, as well as autologous humanized patient-derived models. Mechanistically, we show that TRI-IT co-activates adaptive cellular and humoral, as well as innate anti-tumor immune responses to mediate its anti-tumor effect without inducing off-target toxicity. Our data demonstrate the efficacy of a target-agnostic combination immunotherapy that eradicates and potentially cures established poorly immunogenic tumors.

overall_design: Comparison of gene expression in differently treated tumors


title: PPIB-regulated alternative splicing of cell cycle gene contributes to its regulation of cell proliferation

city: Wuhan

first: Dong

last: Chen

state: Hubei

address: 388 GaoXin 2nd Road, East Lake Hi-Tech Development Zone

department: Center for Genome Analysis

institute: ABLife, Inc.

summary: Background: Peptidylprolyl cis-trans isomerase B (PPIB) plays an important function in the process of inflammation through binding RNA, but the clear molecular pathogenesis is not completely understood. The objective of this study was to investigate the PPIB-regulated gene expression and alternative splicing.

overall_design: transcrptional analysis of PPIB knockdown and control in Hela cells

first: Yuan

last: Zhang

first: Shitao

first: Minghui

last: Zhou


title: Acute deletion of TET enzymes results in aneuploidy in mouse embryonic stem cells through decreased expression of Khdc3

city: La Jolla

first: Hugo

last: Sepulveda

state: California

address: 9420 Athena Circle

department: Division of Signaling and Gene Expression

institute: La Jolla Institute for Immunology

summary: Gene expression with RNA-seq for inducible Tet TKO (Tet iTKO) mESCs compared with control mouse ESCs (mESC) after 6.5 days in vitro culture after tamoxifen treatment

overall_design: For transcriptional profiling using RNA-seq, 100,000 cells were sorted to isolate the Live/Dead dye and Thy1.2 negative CD326+GFP+ population representing the mESCs populations responsive to the tamoxifen treatment. The cells were resuspended in FACS buffer and filtered with a 70 µM filter before sorting.

first: Romain

last: Georges

first: Anjana

last: Rao


title: scRNA-seq generates a molecular map of emerging cell subtypes after sciatic nerve injury in rats

status: Public on Oct 27 2022

city: West Point

first: Ditte

last: Lovatt

address: 770 Sumneytown Pike

institute: Merck

summary: Patients with peripheral nerve injury, viral infection or metabolic disorder often suffer neuropathic pain due to inadequate pharmacological options for relief. Developing novel therapies has been challenged by incomplete mechanistic understanding of the cellular microenvironment in sensory nerve that trigger the emergence and persistence of pain. In this study, we report a high resolution transcriptomics map of the cellular heterogeneity of naïve and injured rat sensory nerve covering more than 110,000 individual cells. Annotation reveals distinguishing molecular features of multiple major cell types totaling 45 different subtypes in naïve nerve and an additional 23 subtypes emerging after injury. Ligand-receptor analysis revealed a myriad of potential targets for pharmacological intervention. This work forms a comprehensive resource and unprecedented window into the cellular milieu underlying neuropathic pain and demonstrates that nerve injury is a dynamic process orchestrated by multiple cell types in both the endoneurial and epineurial nerve compartments.

overall_design: Single-cell RNA-seq of acutely dissociated rat sciatic nerve from naïve and CCI injured animals.

first: Alex

last: Tamburino

first: Alicja

last: Krasowska-Zoladek

first: Raul

last: Sanoja

first: Lixia

last: Li

first: Vanessa

last: Peterson

first: Xiaohai

first: Jason

last: Uslaner


title: Next-generation sequencing of Tfh cells from CSF compared to paired blood in multiple sclerosis

city: RENNES

first: Laure

last: Michel

address: 2 rue Henri Le Guilloux

department: Neurology

country: France

institute: CHU Pontchaillou

summary: Tertiary lymphoid structures are reported in the meninges of patients with multiple sclerosis, especially at the progressive stage and are strongly associated to cortical lesions and disability. Besides B cells, these structures comprise follicular helper T cells (Tfh) that are crucial to support B cell differentiation. Tfh play a pivotal role in amplifying autoreactive B cells and promoting autoantibody production in several autoimmune diseases but very few is known in multiple sclerosis. Here we reporter transcriptomic profile of CSF infiltrating Tfh compared with paired blood in RRMS patients.

overall_design: RNAseq analysis of Tfh from CSF and Tfh from blood in multiple sclerosis patients

first: Marion

last: Mandon

first: Stéphane

last: Rodriguez


title: TCR sequencing data from responders and progressors to cyclophosphamide chemotherapy

city: Perth

first: Caitlin

last: Tilsed

address: QQ Block

institute: University of Western Australia

summary: The difference in the TCR between responders and progressors to cyclophosphamide is unknown. Here we performed TCR sequencing on the RNA of tumors from mice bearing AB1-HA. Mice were catagorised as responders and non-responders.

overall_design: BALB/c mice bearing bilateral AB1-HA murine mesothelioma were treated 200 mg/kg cyclophosphamide. One tumor was surgically excised pre-treatment (one day prior to cyclophosphamide, day-1) or post-treatment (three or seven days after cyclophosphamide, day+3 or day+7) and RNAseq performed. The remaining tumor was used as a readout of response.n=5 for all groups. Groups are as follows: responder day -1, progressor day-1, responder day +3, progressor day+3, responder day +7, progressor day +7.

first: W

last: Lesterhuis


title: Transcriptomic choreography in response to light quality variation reveals metabolic acclimation in marine Nannochloropsis oceanica.

city: Haikou

first: Li

last: Wei

state: Hainan

address: No. 99 Longkun South Road, Haikou

department: Colleage of life science

institute: Hainan normal university

summary: We report the transcriptomic dynamics and metabolic adaptation of Nannochloropsis oceanica to blue (410nm) and red (680nm) light by high-throghout Next-generation sequencing (NGS). Preferential excitation of different light spectra induces massive reprogramming of the Nannochloropsis transcriptome.

overall_design: Nannochloropsis oceanica IMET1 was inoculated into modified f/2 liquid medium containing 30 g/L sea salt, 10 mM Tris-HCl (pH 7.6), 427.5 mg/L NaNO3, 30 mg/L NaH2PO4·H2O, 5 mg/L trace metal mixture (4.36 g/L Na2EDTA·2H2O, 3.15 g/L FeCl3·6H2O, 10 mg/L CoCl2·6H2O, 22 mg/L ZnSO4·7H2O, 180 mg/L MnCl2·4H2O, 9.8 mg/L CuSO4·5H2O, 6.3 mg/L Na2MoO4·2H2O), and 2.5 mg/L vitamin stock solution (1 mg/L vitamin B12, 1 mg/L biotin, 200 mg/L thiamine). The cells were cultivated in liquid cultures using column bioreactor under continuous light (approximately 80 ± 5 µmol photons m-2 s-1) at 25˚C and aerated by bubbling with air-level CO2 (0.04%) at 0.6 vvm (volume gas per volume medium per minute) under white, red and blue light..After the switch from white light to red and blue light, cell aliquots were taken at 0 (white light), 12 (red and blue light), and 24h (red and blue light) from each column by syringe for transcriptomic profiling.

first: Jian

last: Xu


title: Genome-wide maps of gene transcription level in BMDMs infected with recombinant Mycobacterium tuberculosis H37Ra strains.

city: WuHan

first: Yugang

address: shizishan street

institute: Huazhong Agricultural University

summary: We report the application of RNA-seq technology for high-throughput profiling of gene transcription in BMDMs. By obtaining over six billion bases of sequence from mRNA, we generated genome-wide gene transcription maps of BMDMs infected with recombinant Mycobacterium tuberculosis H37Ra strains. We find that a group of genes is significantly affected by MpbR. This finding indicates that MpbR regulates the host immune.

overall_design: Examination of gene expression level in 3 H37Ra strains infected BMDM cells.

first: Zhengguo

last: He


title: miR-223 Plays A Critical Role in Obesogen-Enhanced Adipogenesis in Mesenchymal Stem Cells and Transgenerational Obesity

city: Irvine

first: Richard

middle: Cheng-An

last: Chang

address: 4311 Nature Science II

institute: University of California Irvine

summary: Exposure of pregnant F0 mouse dams to the obesogen tributyltin (TBT) predisposes unexposed male descendants to obesity and diverts mesenchymal stem cells (MSCs) toward the adipocytic lineage. TBT also promotes adipogenic commitment and differentiation of MSCs, in vitro. We sought to identify TBT-induced factors predisposing MSCs toward the adipocytic fate. We exposed mouse MSCs to TBT, the PPARγ-selective agonist rosiglitazone or the RXR-selective agonist LG-100268 and determined their transcriptomal profiles to determine candidate microRNAs (miR) regulating adipogenic commitment and differentiation. Of the top 10 candidate microRNAs predicted by Ingenuity Pathway Analysis, miR-21, miR-33 and miR-223 were expressed to regulate genes differentially expressed in adipogenesis. After exposing to 50 nM TBT for 24 hours, miR-223 levels of MSCs were increased and expression of its target genes ZEB1, NFIB, and FOXP1 decreased. Both ROSI and TBT increased miR-223 levels, and this induction was inhibited by PPARγ antagonists (T0070907) but not RXR antagonists (HX531, UVI3003), placing miR-223 downstream of PPARγ. Chromatin immunoprecipitation confirmed TBT-induced binding of PPARγ to regulatory elements in the miR-223 promoter. miR-223 levels were elevated in ancestral TBT exposed F2 and F3 male adipose tissues and further increased when animals were fed with a high fat diet. TBT induced miR-223 expression and adipogenesis in MSCs through the PPARγ pathway and promoted elevated miR-223 expression in white adipose tissue of F2 and F3 male descendants of F0 treated dams. This shows that transgenerationally increased expression of miR-223 plays an important role in the transmission of the obese phenotype after TBT exposure.

overall_design: We generated RNA-Seq data in MSCs differentiated in the presence of an adipogenic induction cocktail (0.5 mM isobutylmethylxanthine, 1 uM dexamethasone, 5 ug/mL insulin )treated with DMSO (0.1%) or tributyltin (TBT, 5, 50, 100 nM) for 0, 4, 7, or 14 days.

first: R

first: B

last: Shoucri

first: T

last: Shioda

last: Blumberg


title: RNA-seq in LX-2Vector and LX-2FAP cells

city: Guangzhou

first: Ming

last: Qi

email: 756410656@qq.com, qiming561@gmail.com

state: Guangdong

address: No.601 West Huangpu Avenue

institute: Jinan University

summary: To investigate the underlying mechanism by which FAPα in HSCs promoted tumor cell EMT

overall_design: We performed gene expression profiling analysis using data obtained from RNA-seq of 2 different LX-2 cells.

first: Dongmei

last: Zhang

first: Minfeng

last: Chen

first: Shuran

last: Fan


title: Blocking LAIR1 signaling in immune cells inhibits tumor development

city: Dallas

first: kenian

last: chen

state: TX

address: 5323 Harry Hines Boulevard

department: Population and Data Science

institute: UTsouthwestern

summary: LAIR1 is an inhibitory immune cell receptor. We used single cell RNA sequencing (scRNA-seq) to analyze the immune cell distribution in the implanted B16 tumor tissues of Vav-cre human LAIR1 transgenic and LAIR1-/- C57bl/6j mice after control or anti-LAIR1 blocking antibody treatment.

overall_design: mCD45+ cells from subcutaneous inoculated B16 tumors in Vav-cre human LAIR1 transgenic and LAIR1-/- C57bl/6j mice were isolated by Fluorescence-activated cell sorting (FACS) and analyzed by scRNA-seq.

first: Jingjing

last: Xie

first: Xiaoye

last: Liu


title: The chemokine receptor CXCR4 regulates satellite cell activation, early expansion, and self-renewal, in response to skeletal muscle injury

city: Minneapolis

first: Micah

last: Gearhart

state: MN

address: 6-160 Jackson Hall, 321 Church St.

department: Genetics, Cell Biology and Development

institute: University of Minnesota

summary: Acute skeletal muscle injury is followed by satellite cell activation, proliferation, and differentiation to replace damaged fibers with newly regenerated muscle fibers, processes that involve satellite cell interactions with various niche signals.  Here we show that satellite cell specific deletion of the chemokine receptor CXCR4, followed by suppression of recombination escapers, leads to defects in regeneration and satellite cell pool repopulation in both the transplantation and in situ injury contexts.  Mechanistically, we show that endothelial cells and FAPs are the major source of the ligand, Sdf1α, and that CXCR4 is principally required for proper activation and for transit through the first cell division, and to a lesser extent the later cell divisions.  In the absence of CXCR4, gene expression in quiescent satellite cells is not severely disrupted, but in activated satellite cells a subset of genes normally induced by activation fail to upregulate normally.  These data demonstrate that CXCR4 signaling is essential to normal early activation, proliferation, and self-renewal of satellite cells.

overall_design: Wild type and CXCR4 knockout satellite cells in quiescent and activated conditions analyzed by RNA-seq

first: Ahmed

last: Shams

middle: D

first: Michael

last: Kyba


title: Immune cells and their inflammatory mediators modify beta cells and cause checkpoint inhibitor-induced diabetes

city: New Haven

first: Ana Luisa

last: Perdigoto

state: CT

address: 300 George Street

institute: YALE UNIVERSITY

summary: Checkpoint inhibitors (CPIs) targeting PD-1/PD-L1 and CTLA-4 have revolutionized cancer treatment but can trigger autoimmune complications including CPI-induced diabetes (CPI-DM), which occurs preferentially with PD-1 blockade. We found evidence of pancreatic inflammation in patients with CPI-DM with shrinkage of pancreases, increased pancreatic enzymes, and in a case from a patient who died with CPI-DM, peri-islet lymphocytic infiltration. In the NOD mouse model, anti-PD-L1 but not anti-CTLA-4 induces DM rapidly. RNA sequencing revealed that cytolytic IFNγ+ CD8+ T cells infiltrated islets with anti-PD-L1.  Changes in β cells were predominantly driven by IFNγ and TNFα and included induction of a novel β cell population with transcriptional changes suggesting dedifferentiation. IFNγ increased checkpoint ligand expression and activated apoptosis pathways in human β cells in vitro. Treatment with anti-IFNγ and anti-TNFα prevented CPI-DM in anti-PD-L1 treated NOD mice. CPIs targeting the PD-1/PD-L1 pathway result in transcriptional changes in β cells and immune infiltrates that may lead to the development of diabetes. Inhibition of inflammatory cytokines can prevent CPI-DM, suggesting a strategy for clinical application to prevent this complication.

overall_design: Comparison of immune (CD45+) and islet cells (CD45-) from pancreatic islets from anti-PD-L1 treated, anti-CTLA-4 treated or Control NOD mice.

first: Ana

middle: L

first: Songyan

last: Deng

first: Katherine

last: Du

first: Manik

last: Kuchroo

first: Daniel

last: Burkhardt

first: Alexander

last: Tong

first: Gary

last: Israel

first: Marie

middle: E

last: Robert

first: Stuart

middle: P

last: Weisberg

first: Nancy

last: Kirkiles-Smith

first: Angeliki

last: Stamatouli

first: Harriet

last: Kluger

first: Zoe

last: Quandt

first: Arabella

last: Young

first: Mei-Ling

last: Yang

first: Mark

middle: J

last: Mamula

first: Jordan

last: Pober

last: Anderson

first: Smita

last: Krishnaswamy

first: Kevan

last: Herold


title: RNA-seq performed on LSECs obtained from bevacizumab-sensitive and -resistant HCT116 CRCLM xenografts

first: Ming

last: Qi

summary: To determine the differentially-expressed endothelial genes in explants from the bevacizumab-sensitive and -resistant explants

overall_design: We performed gene expression profiling analysis using data obtained from RNA-seq of 2 different condition mediums cultured lx-2 cells.

first: Dongmei

last: Zhang

first: Minfeng

last: Chen

first: Shuran

last: Fan


title: Dormant SOX9-positive cells facilitate MYC-driven recurrence of medulloblastoma

city: Uppsala

first: Fredrik

middle: Johansson

last: Swartling

address: Dag Hammarskjölds väg 20

department: Immunology, Genetics and Pathology

country: Sweden

institute: Uppsala University

summary: Tumor recurrence is a slow biological process involving therapy resistance, immune escape and metastasis and is the leading cause of death in medulloblastoma, the most frequent malignant pediatric brain tumor. By studying paired primary-recurrent patient samples and patient-derived xenografts we identified significant accumulation of SOX9-positive cells in relapses and metastases. They exist as rare, quiescent cells in Group 3 and Group 4 patients that constitute two thirds of medulloblastoma. To follow relapse at the single cell level we developed an inducible dual Tet Off animal model of MYC-driven MB, where MYC can be directed from treatment-sensitive bulk cells to resistant, dormant SOX9-positive cells. SOX9 promoted immune escape, DNA repair suppression and was essential for recurrence. Tumor cell dormancy was non-hierarchical, migratory and depended on MYC suppression by SOX9 to promote relapse. By using computational modeling and treatment we further showed how doxorubicin and MGMT inhibitors are specifically targeting relapsing cells.

overall_design: We examined tumor recurrence using RNA-seq, single cell RNA-seq and ATAC-seq. In total 27 samples were sequenced by conventional RNA-seq, of which 12 samples (triple replicates) were part of a treatment study (DMSO, DOX). 16 samples were ATAC-sequenced, all in duplicates, and 8 were part of a treatment study (DMSO, DOX). The single cell RNA-seq rendered in 4498 and 4645 cells for each sample respectively.

first: Anna

last: Borgenvik

first: Sara

last: Bolin


title: An integrated SAGA and TFIID PIC assembly pathway selective for poised and induced promoters

city: Ithaca

first: B. Franklin

last: Pugh

address: 465 Biotechnology Building

department: Molecular Biology & Genetics

institute: Cornell University

overall_design: Refer to individual Series


title: An organoids-on-a-chip model of human ARPKD

city: Boston

first: Ryuji

last: Morizane

state: Massachusetts

address: 149 13th Street

department: Nephrology Division

institute: Massachusetts General Hospital

summary: Microarray of kidney organoids derived from PKHD1 mutant human pluripotent stem cells.

overall_design: Total RNA samples were prepared from PKHD1-/- and PKHD1+/- organoids in three different culture conditions: 1. flow, 2. static, or 3. forskolin (FK) on day 35. Gene expression was analyzed using 3D-Gene® Human 25k oligonucleotide microarrays. Sample preparation for array hybridization was carried out as described in the manufacturer's instructions.

first: Tomoya

last: Miyoshi

first: Ken

last: Hiratsuka


first: Ana Luisa

last: Perdigoto

institute: Yale University

overall_design: Comparison of transcriptional changes in pancreatic islet cells from anti-PD-L1 versus anti-CTLA-4 treated NOD mice.

first: Ana

first: Songyan

last: Deng

first: Katherine

middle: C

last: Du

first: Manik

last: Kuchroo

first: Daniel

last: Burkhardt

first: Alexander

last: Tong

first: Gary

last: Israel

first: Marie

last: Robert

first: Stuart

last: Weisberg

first: Nancy

last: Kirkiles-Smith

first: Angeliki

middle: M

last: Stamatouli

first: Harriet

last: Kluger

first: Zoe

last: Quandt

first: Arabella

last: Young

last: Yang


title: Bioinformatics Analysis of miRNAs Germacrone Protection of Diabetic Nephropathy

city: Beijing

first: Shuang

last: Li

state: Beijing

address: Biomedical engineering

department: Biomedical engineering

institute: Beihang university

summary:
The mechanisms of Germacrone in DN remain unknown nevertheless. This study used comprehensive bioinformatics analysis to Critical miRNAs and probable pathways related to Germacrone.
We established a DN mice model and treated with Germacrone in this study and investigated how it alters the microRNA (miRNA) transcriptome of mice kidneys. For that purpose, we have performed RNA sequencing on a DN mice model , with and without Germacrone pre-treatment.

overall_design: Comparative gene expression profiling analysis of miRNA-seq data for mice model (control group, diabetes nephropathy group and germacrone-treated group).

first: Binqi

last: Wang

first: Wenfang

last: He

first: Jinshi

last: Zhang


title: miRNA for MACF1 regulates osteoblast differentiation

city: xi'an

first: Shanfeng

last: Jiang

state: shaanxi

address: No. 127, West Youyi Road, Beilin District

department: School of Life Sciences

institute: Northwestern Polytechnical University

summary: MC3T3-E1 cells were transfected with short hairpin RNA (shRNA) specifically targeting the murine MACF1 lentivirus vector or with scrambled shRNA, and the stably transfected cell lines were selected using puromycin. After 15 days of selection, all cells were collected for further study.

overall_design:
The collected MC3T3-E1 cells were subjected to sequencing by RiboBio Co., Ltd. (Guangzhou, China) for miRNA  microarray analyses. Total RNA was harvested and quantified, and its quantity and purity were assessed using a K5500 Micro-Spectrophotometer (Beijing Kaiao Technology Development Co., Ltd., Beijing, China). Here, A260/A280 ≥ 1.5 and A260/A230 ≥ 1 indicated acceptable RNA purity and RNA integrity number (RIN) ≥ 7 (based on an Agilent 2200 RNA assay, Agilent Technologies, USA) indicated acceptable RNA integrity. Genomic DNA contamination was evaluated by gel electrophoresis.
**Please note that the original raw data files have been lost and thus are not provided.***

first: shanfeng

last: jiang


title: An integrated SAGA and TFIID PIC assembly pathway selective for poised and induced promoters [ChIP-Exo]

first: B. Franklin

last: Pugh

summary: Genome-wide, little is understood about how proteins organize at inducible promoters before and after in-duction, and to what extent inducible and constitutive architectures depend on cofactors. We report that se-quence-specific transcription factors and their tethered cofactors (e.g., SAGA, Mediator, TUP, NuA4, SWI/SNF, RPD3-L) are already bound to promoters prior to induction (“poised”), rather than recruited upon induction, whereas induction recruits the pre-initiation complex (PIC). Through depletion and/or deletion ex-periments we show that SAGA does not function at constitutive promoters, although a SAGA-independent Gcn5 does acetylate +1 nucleosomes there. At poised promoters, SAGA catalyzes +1 nucleosome acetylation but not PIC assembly. At induced promoters, SAGA catalyzes acetylation, deubiquitylation, and PIC assembly. Surprisingly, SAGA mediates induction by creating a PIC that allows TFIID to stably associate, rather than creating a TFIID-independent PIC, as is generally thought. These findings suggest that inducible systems, where present, evolved on top of constitutive systems.

overall_design: Genome-wide analysis of yeast TFs under heat shcok and mock heat shock conditions using ChIP-exo

first: Chitvan

last: Mittal

first: Olivia

last: Lang

first: Alain

middle: R

last: Bataille

first: William

last: Lai

first: B


title: ChIP-seq H4 and AcH4 in WT and del.ncu09482

status: Public on Oct 26 2022

city: Hanover

first: Bin

state: New Hampshire

address: Vail Loading Dock, Attn: 702 Remsen

department: MSB

institute: Geisel School at Dartmouth

summary: Post-translational modifications (PTMs) on histones have been found to play diverse functions in regulating chromatin events and gene expression. The operation of circadian clocks heavily relies on finely tuned and timely expression of the proteins comprising core oscillators. However, most studies of PTMs’ effects on circadian clocks have been conducted using static systems in which circadian clocks are rendered arrhythmic due to the essential role of PTMs on gene expression. In the Neurospora circadian system, the White Collar Complex (WCC), a heterodimeric transcription factor formed from White Collar-1 (WC-1) and White Collar-2 (WC-2), serves the function of the BMAL1/CLOCK heterodimer in mammals, driving expression of circadian negative arm component(s), a principal one in Neurospora encoded by the gene frequency (frq). FRQ interacts with FRH (FRQ-interacting helicase) and CK-1 forming a stable complex that represses its own expression by inhibiting WCC. In this study, a genetic screen identified a gene, designated as brd-8, that encodes a conserved auxiliary subunit of the NuA4 histone acetylation complex. Loss of brd-8 reduces H4 acetylation and RNA polymerase (Pol) II occupancy at frq and other known circadian genes, and leads to a long circadian period, delayed phase, and defective overt circadian output at some temperatures. In addition to strongly associating with the NuA4 histone acetyltransferase complex, BRD-8 is also found complexed with the transcription elongation regulator BYE-1. Expression of brd-8, bye-1, histone hH2Az, and several NuA4 subunits is controlled by the circadian clock, indicating that the molecular clock both regulates the basic chromatin status and is regulated by changes in chromatin. Taken together, our data identify new auxiliary elements of the fungal NuA4 complex having homology to mammalian components, which along with conventional NuA4 subunits, are required for timely and dynamic frq expression and thereby a normal and persistent circadian rhythm.

overall_design: ChIP-seq histone H4 and acetylated histone H4 in WT at D20 (cultured by shaking in the dark for 20 hrs) and del.ncu09482 at D24 (cultured by shaking in the dark for 26 hrs)

first: Xiaoying

last: Zhou

first: Hugh

last: Mitchell

first: Lye

last: Markillie


title: Regulatin of KDM5C stability and enhancer reprogramming in breast cancer [RNA-seq]

city: Wuhan

first: Qiong

last: Xiao

address: street of luojia mountain

institute: College of Life Sciences, Wuhan University

summary:
Purpose: Purpose:Exploring genes regulated by trim11 and kdm5c in breast cancer
Methods: TRIM11 knock down and KDM5C knock down MDA-MB-231 cell lines were constructed and Trim11 knock down MMTV mice were generated. The RNA-seq libraries of cell lines and mice mammary tumors were sequenced by Illumina Nova-seq platform with pair-end reads of 150 bp.
Results: Quality control of mRNA-seq data was performed using Fatsqc and low-quality bases were trimmed. The adaptor sequence was removed using Cutadapt (version 1.16) to clean RNA-seq raw data. All RNA-seq data were mapped to the human reference genome (hg19) or mouse reference genome (mm10) by HISAT2 (version 2.1.0). The gene expression level was calculated by Cufflinks with default parameters. Differential expressed genes (DEGs) were identified by 1.5-fold change and p-value < 0.05. Gene ontology analysis and KEGG pathways analysis was performed using DAVID (https://david.ncifcrf.gov).
Conclusions: Our study represents biological process and KEGG pathway enrichment analyses of TRIM11 and KDM5C down-regulated genes or up-regulated genes

overall_design: mRNA profiles of control, TRIM11 knockdown, KDM5C knockdown and double knockdown MDA-MB-231 breast cancer cells. mRNA profiles of wide type(WT) and Trim11+/- MMTV mice breast tumors

first: Chen-Yu

first: Chuan

last: Gao

first: Lian-Yun

first: Min

last: Wu


title: Regulatin of KDM5C stability and enhancer reprogramming in breast cancer

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


title: RNA sequencing analysis Reveal Post-Stroke Cognitive Impairment related genes in Hippocampus of Cerebral Ischemic Rat

first: Jiemei

last: Chen

address: Tianhe Road

department: Rehabilitation Medicine

institute: Sun Yat-Sen Unv

summary: In summary, a comprehensive bioinformatics analysis of the possible DEGs and pathways involved in tMCAO rats with cognitive impairment and Sham rats was conducted. DEGs, such as Acta2, Calb2, Cxcl12, as well as the intestinal immune and steroid biosynthesis may play a pivotal role in mechanism of PSCI.

overall_design: Infarct volume was measured using 2,3,5-triphenyltetrazolium chloride (TTC) stain after tMCAO model was established. Morris Water Maze (MWM) and Luxol fast blue staining were performed to assess the cognitive function and white matter (WM) lesion of rats. Furthermore, to explore the underlying mechanism, differentially expressed genes (DEGs) in the hippocampus of rats in the tMCAO group and Sham group were compared using RNA sequencing. Then, gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis and protein-protein interaction (PPI) network analysis, was conducted to elaborate these DEGs. The expression of 6 randomly selected DEGs were validated by qPCR assays.

first: Jiena

last: Hong

first: Chao

last: Li

first: Mengshu

last: Xie

first: Xue

first: Hongmei

last: Wen


title: Circulating microRNAs in relapsing MS patients treated with dimethyl fumarate in the phase 4 TREMEND trial

city: Copenhagen N

first: Atul

last: Anand

address: Ole Maaløes Vej 5, building 2, 3 floor

department: Department of Pathology

country: Denmark

institute: Rigshospitalet

summary: Dimethyl fumarate (DMF) is an oral drug approved for relapsing multiple sclerosis (MS) that leads to reduction of neurofilament light (NFL).  This may be related to dynamics and persistence of microRNA signatures in the peripheral blood of treatment-naïve MS patients before and after dimethyl fumarate (DMF) at different time points. 210 blood samples were collected from 51 treatment-naïve patients at baseline (BL) and after 1-3, 4-7, 9-15 and 21-27 months of DMF and from 22 controls from the phase IV TREMEND trial. Using microarray, 1,085 miRNAs were two-folds above the background and compared versus NFL. Altered miRNA profiles peaked after 4-7 months. MiR-16-5p and miR-4306, involved in the NF-kB-pathway, were upregulated in low NFL samples, while miR-940 and miR-4665-3p were upregulated in high NFL samples. NFL and miRNA correlations were strongest after 4-7 months DMF. In four patients with blood samples taken at all 5 time points, time-series analysis found miR-146a-5p, the inhibitor of the NF-kB-pathway, increased 1-3 months after treatment. DMF induces dynamic changes in composite miRNA profiles 4-7 months after initiation, several involved in the NF-kB-pathway. Upregulation of miR-16-5p and miR-4306 in low-NFL, while miR-940 and miR-4665-3p in high-NFL samples may indicate a response to DMF treatment.

overall_design: 210 blood samples from the TREMEND (Tecfidera in Relapsing-Remitting Multiple Sclerosis: Endothelial Dysfunction) phase IV clinical trial was divided into six different groups. Controls: blood 22 healthy controls. Baseline: 51 RRMS patients before Tecfidera (DMF) treatment. Early: 45 RRMS patients 1-3 month after DMF treatment. Intermediate: 20 RRMS patients 4-7 month after DMF treatment. 1-year: 49 RRMS patient after 1-year with DMF treatment. Long term: 23 RRMS patients 2 years after start of treatment with DMF.  MicroRNA detections from RNA extracts of the whole blood samples were obtained with miRNA Microarray System.

first: Maria

last: Elkjaer

first: Rikke

last: Lohse

first: Mark

last: Burton

first: Jason

last: Mendoza

first: Mads

last: Thomassen

first: Tobias

last: Sejbaek

first: Zsolt

last: Illes


title: RAS induced senescence of skin keratinocytes is mediated through Rho kinase

city: Bethesda

first: Howard

last: Yang

state: MD

address: 37 CONVENT DR, Room 5120

department: CCR

institute: NCI

summary: This study is to elucidate the role of ROCK in oncogenis RAS induced senescence in mouse keratinocytes.

overall_design: Primary mouse kearinocytes trasduced with oncogenic RAS were cultured with or without ROCK inhibitor Y17632.  RNA sequencing was performed to evaluate the differentially expressed genes iaffected by RAS and Y27632 tratment.

first: Alex

last: Lee

first: Elise

last: Fraser

first: Jee

last: Kim

first: Kenneth

last: Wong

first: Huatian

last: Liu

first: Maxwell

first: Christophe

last: Cataisson

first: Stuart

last: Yuspa

first: Luowei


title: Decoupling the role of RORgt in the differentiation and effector function of Th17 cells

city: Duarte

first: Xiancai

last: Zhong

state: CA

address: 1500 E Duarte Rd

department: Immunology & Theranostics

institute: Beckman Research Institute of City of Hope

summary: RORgt is known to instruct the differentiation of Th17 cells that mediate the pathogenesis of autoimmune diseases. However, it remains unknown whether RORgt plays a distinct role in the differentiation and effector function of Th17 cells. Here we show that mutation of RORgt lysine 256, a ubiquitination site, to arginine (K256R) separates the RORgt role in these two functions. Preventing ubiquitination at K256 via arginine substitution does not affect RORgt-dependent thymocyte development and Th17 differentiation in vitro and in vivo, however, greatly impaired the pathogenesis of Th17 cell-mediated experimental autoimmune encephalomyelitis (EAE). Mechanistically, K256R mutation impairs RORgt to bind to and activate Runx1 expression critical for Th17-mediated EAE. Thus, RORgt regulates the effector function of Th17 cells in addition to Th17 differentiation. This work informs the development of RORgt-based therapies that specifically target the effector function of Th17 cells responsible for autoimmunity.

overall_design: Comparitive gene expression profiling analysis of RNA-Seq data for sorted (EGFP+) WT/IL-17A-EGFP and RORγt-K256R/IL-17A-EGFP mouse CD4+ T cells in vitro differentiated under Th17 polarization condition

first: Hongmin

last: Wu

first: Wencan

last: Zhang

first: Yousang

last: Gwack

first: Weirong

last: Shang

first: Kyle

last: O Lee

first: Noah

last: Isakov

first: Zhiheng

last: He

first: Zuoming

last: Sun


title: RNA-seq Analysis of Sulodexide- and Vehicle-treated TAA induced Fibrotic Mouse Liver Transcriptomes

city: Shanghai

first: xin

last: zhang

address: 415 Fengyang Road

institute: Changzheng hospital

summary: Liver fibrosis is the formation of fibrous scar with the deposition of extracellular matrix (ECM) proteins resulting from persistent liver inflammation and has become a huge global health burden. Sulodexide is a heparinoid compound purified from porcine intestine mucosa, which consists of 80% electrophoretically fast-moving heparin and 20% dermatan sulfate, with endothelium protective function. In this study, we evaluated the therapeutic potential of sulodexide in TAA-induced liver fibrosis model. To determine the mechanism of sulodexide in the treatment of liver fibrosis, we performed high throughput sequencing of mRNA in three groups of liver tissue and identified the protective role of sulodexide on liver sinusoidal endothelial cells.

overall_design: To investigate the effect of sulodexide on liver fibrosis, we subjected mice randomly into three groups: the control group, the vehicle-treated TAA group and sulodexide-treated TAA group. Liver fibrosis in the mice was induced by feeding with TAA water (400mg/L) for 16 weeks.The treatment was started on the beginning of 13th week. 4 weeks later, the mice were sacrificed with liver and serum collected.

first: Ru

last: Huang

first: Juan

last: Deng


title: Intermittent fasting alters the spatiotemporal atlas of transcriptomes

city: Changsha

first: Guolin

last: Li

state: Hunan

address: 177 Lushan Road

department: College of Life Sciences

institute: Hunan Normal University

summary: Transcription factors may orchestrate the health benefits of intermittent fasting through directing the expression of genome. Here, we find intermittent fasting can spin the spatiotemporal profile of transcription factors, and provide an atlas of transcription factors in biological space, time and feeding regimen.

overall_design: The transcriptomic atlas of mice under different feeding regimens was mapped from 600 samples (across 4 metabolic tissues in mice under 5 feeding regimens sampled every 4 hours over 24 hours, in 5 replicates) by deep sequencing using Illumina Novaseq™ 6000 .

first: Fang

last: Wei

first: Lijun

last: Gong

first: Siyu

last: Lu

first: Lin

last: Zheng

first: Yiming

last: Zhou

first: Minzhi

last: Chen

first: Yuhui

last: Xu

first: Rong

last: Xiang

first: Frank

last: Gonzalez


title: Regulatin of KDM5C stability and enhancer reprogramming in breast cancer [ChIP-Seq]

first: Qiong

last: Xiao

summary: We report the high-throughput profiling of histone modifications( H3K4me3 and H3K27ac) inTRIM11 knockdown and KDM5C knockdown MDA-MB-231 cells.  we generated genome-wide chromatin-state maps of MDA-MB-231 cells.This study provides the localization of H3K4me3 and H3K27ac on chromatin in TRIM11 knockdown and KDM5C knockdown MDA-MB-231 cells.

overall_design: Examination of 2 different histone modifications in MDA-MB-231 breast cancer cells.

first: Chen-Yu

last: Wang

first: Chuan

last: Gao

first: Lian-Yun

first: Min

last: Wu


title: Decoupling the role of RORγt in the differentiation and effector function of Th17 cells

first: Xiancai

last: Zhong

first: Hongmin

first: Wencan

last: Zhang

first: Yousang

last: Gwack

first: Weirong

last: Shang

first: Kyle

middle: O

last: Lee

first: Noah

last: Isakov

first: Zhiheng

last: He

first: Zuoming

last: Sun