title: Transcriptional profiling and therapeutic targeting of oxidative stress in neuroinflammation (scRNA-seq dataset)

overall_design: To obtain ROS+ innate immune cells, all live cells isolated from spinal cord were stained for intracellular ROS ex vivo using 2′,7′–dichlorofluorescein diacetate (DCFDA) and the innate immune cell fraction was collected by CD11b+ fluorescence-activated cell sorting. For Tox-seq, we analyzed the transcriptomes of 8,701 CD11b+ cells labelled for ROS production via scRNA-seq from the spinal cords of healthy mice or at the onset of disease (score 1) of MOG35-55 EAE mice, an autoimmune animal model for MS with paralysis and inflammatory demyelination.


title: Differential expression of exosomal miRNAs between medulloblastoma patients and healthy controls

status: Public on Apr 09 2020

city: Shanghai

first: Saihua

last: Huang

address: 399 Wanyuan Rd, Minhang, Shanghai

country: China

institute: Children’s Hospital of Fudan University

type: Non-coding RNA profiling by high throughput sequencing

summary: We characterized circulating exosomal miRNA profiles by miRNA-seq to identify those differentially expressed in children with MB relative to heathy controls

overall_design: Plasma samples from 4 medulloblastoma patients and 4 healthy controls were enrolled in the experiment. Exosomes were extracted, total RNA were isolated from the identified exosomes.miRNA profilings were performed.

first: Ping

last: Xue

first: Yufeng

last: Zhou


title: Selective retrieval of individual cells from microfluidic arrays combining dielectrophoretic force and directed hydrodynamic flow

city: Lausanne

first: Joern

last: Pezoldt

address: Station 19, SV 3818.A

department: SV

country: Switzerland

institute: EPFL

type: Expression profiling by high throughput sequencing

summary: Hydrodynamic-based microfluidic platforms enable single-cell arraying and analysis over time. Despite the advantages of established microfluidic systems, long term analysis and proliferation of cells selected in such devices require off-chip recovery of cells as well as an investigation of on-chip analysis on cell phenotype; requirements still largely unmet. Here, we introduce a device for single-cell isolation, selective retrieval and off-chip recovery. To this end, singularly addressable three-dimensional electrodes are embedded within a microfluidic channel, allowing, through application of a negative dielectrophoretic (DEP) force, the selective release of single cells from their trapping site. Selective capture and release is carried out in standard culture medium and cells can be subsequently single cell mitigated towards a recovery well using hybrid SU-8/PDMS pneumatic valves. Importantly, transcriptional analysis of recovered cells revealed only marginal alteration of the molecular profile upon DEP application, underscored by equivocal minor transcriptional changes induced upon injection into the microfluidics device. Therefore, the established microfluidic system combining targeted DEP manipulation with down-stream hydrodynamic coordination of single cells, provides the means to handle and manipulate individual cells within one device.

overall_design: Jurkat T-cells were injected and either passed through the microfluidics setup in absence or in the presence of DEP forces. After retrieval, cells were collected and cultured for three hours to permit potential alterations by the DEP field or the fluidic forces to be represented transcriptionally. Input cells solely cultured served as negative control (Input), whilst cells cultured for three hours under Phorbol-12-myristate 13-acetate and Ionomcyin activation (PMA/Iono), globally activating transcription based on protein kinase C (PKC) activation and calcium ion influx 29, served as positive control. The chip associated conditions encompassed DEP (Chip-DEP) or solely injected in the chip (Chip-Ctrl).

first: Pierre

middle: E

last: Thiriet

first: Carlotta

last: Guiducci


title: Analysis of gene expression differences in lymph node B cell populations of HIV-infected and uninfected controls

city: Bethesda

first: James

middle: Wesley

last: Austin

state: MD

address: 9000 Rockville Pike, Bldg 10, Room 6A05

country: USA

institute: NIH

summary: This study examines the gene expression profiles of resident lymph node B cell populations in HIV-infected and uninfected controls.

overall_design: 8 different B cell subsets were sorted from lymph nodes of HIV-uninfected and infected individuals and compared by RNA-seq

middle: W

first: Andrew

middle: J

last: Martins

first: John

middle: S

last: Tsang

first: Susan

last: Moir


title: Rat muscle atrophy

city: San Diego

first: Livia

middle: Soares

last: Zaramela

state: California

address: 9500 Gilman Drive

department: Pediatrics

institute: University of San Diego

summary: Transcriptional profiling of castrated rat cells (C3d) treated or not with testosterone for 8h (C3dpt8h) or 24h (C3dpt24h).

overall_design: Three-condition experiment, C3d vs. C3dpt8h cells and C3d vs. C3dpt24h. Biological replicates: 4 replicates for each sample (dye-swap) .

first: Marcelo

last: Damário Gomes

first: Priscila

last: Coelho

first: Flávia

last: Guarnier


title: Transcriptomic analysis reveals the key regulators and molecular mechanisms underlying myometrial activation during equine placentitis

city: Lexington

first: Barry

middle: A.

last: Ball

state: Kentucky

address: 108 Gluck Equine Research Center,

department: Veterinary Scinece

institute: University of Kentucky

summary: Placentitis was induced in five mares at approximately 290d of gestation (placentitis group), four mares with gestationally age-matched (290 d) pregnancies did not receive any treatment (control group), and the remaining three mares were maintained until approximately 330 d of gestation (prepartum group). For induction of placentitis in the former group, Streptococcus equi subsp. zooepidemicus was introduced intracervically.

overall_design: Myometrial samples were collected from the caudal pole of the placenta from mares with experimentally induced placentitis (290 d GA, n =5), normal pregnant mares (290 d GA, n=4), and prepartum mares (330d GA, n=3). Total RNA was isolated from all myometrial samples using RNeasy Mini Kit (#74104; Qiagen), and DNA digestion was performed on-column using RNase-free DNase I (#79254: Qiagen), followed by cleanup procedures. Paired-end reads with 150 nucleotides in length were produced. A TruSeq Stranded mRNA library prep kit (Illumina, San Diego, CA) was used to prepare libraries for mRNA sequencing. Libraries were loaded onto an Agilent DNA 1000 chip and validated on an Agilent 2100 Bioanalyzer (Agilent). Quantitation was performed with the Illumina Library Quantification Kit, ABI Prism qPCR Mix from Kapa Biosystems. Libraries were run on a NextSeq 500 v2 (Illumina) 300cycles High Output kit in a 2x150 base pairs with paired-end reads. The Fastq files were evaluated for read quality using FastQC 0.11.4. Subsequently, Trim Galore 0.4.1 was used for the adapter and read quality trimming (Phred score threshold of 30). Reads were mapped to the Equus caballus reference genome (EquCab 3.0) using the software STAR 2.5.3a, then annotated with the equine reference annotation from NCBI using Cufflinks 2.2.1. Fragments per kilobase per million (FPKM) was used to determine the expression level of genes. Lastly, we used Cuffdiff 2.2.1 to calculate differentially expressed genes (DEG) between samples from the control and urea groups. The significance level was set at the FDR-adjusted p-value of the test statistic < 0.05 using the Benjamini-Hochberg correction.

first: Hossam

last: El-Sheikh Ali

first: Yatta

middle: L

last: Boakari

first: Shavahn

middle: C

last: Loux

first: Pouya

last: Dini

first: Kirsten

last: Scoggin

first: Alejandro

last: Esteller-Vico

first: Ted

last: Kalbfleisch

middle: A


title: Platelet pathogen reduction technologies alter the microRNA profile of platelet-derived microparticles

city: Quebec City

first: Patrick

last: Provost

state: QC

address: 2705 Blvd Laurier, Room T1-65

department: CHUQ Research Center / CHUL Pavilion

country: Canada

institute: Université Laval

summary: The aim of this project was to elucidate the microRNA profile of platelets and of platelet-derived microparticles isolated from clinical platelet concentrates treated or not with pathogen reduction technologies.

overall_design: Platelets and platelet-derived microparticles (MPs) were isolated from a pool of clinical platelet concentrates (PCs) prepared in Additive solution or treated (or not) with Mirasol or Intercept.

first: Abderrahim

last: Benmoussa

first: Idrissa

last: Diallo


title: Transcriptional profiling and therapeutic targeting of oxidative stress in neuroinflammation

city: San Francisco, CA

first: Katerina

last: akassoglou

state: CA

address: 1650 Owens st

institute: Gladstone Institutes

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

overall_design: Refer to individual Series


title: RNA-seq Analysis of Kidney versus Splenic CD4+ and CD8+ T cells in MRL/lpr Lupus Mice

status: Public on Apr 08 2020

city: New Haven

first: Ping-Min

last: Chen

state: CT

address: 333 Cedar Street

department: Immunobiology

institute: Yale University

summary: Purpose: To understand the differences in gene expression of lupus T cells in secondary lymphoic organ versus site of organ damage

overall_design: Methods: CD4+ and CD8+ T cells from spleen and kidney of 14-week-old MRL/lpr mice were sorted, and their RNA extracted for deep sequencing, in duplicate. Sequenced reads were aligned to MM9 mouse genome using Star and Bowtie.

first: Joe

last: Craft


title: The long non-coding RNA PIK3CD-AS2 promotes lung adenocarcinoma progression via YBX1-mediated suppression of p53 pathway

city: nanjing

first: Rong

last: Yin

state: -- None selected --

address: 42 baiziting

institute: Jiangsu Cancer Hospital

summary: The underlying mechanisms of long non-coding RNAs (lncRNA) participating in the progression of lung cancers are largely unknown. We found a novel lncRNA, PIK3CD antisense RNA 2 (PIK3CD-AS2), that contributes to lung adenocarcinoma (LUAD) progression. The expression characteristics of PIK3CD-AS2 in LUAD were analyzed using microarray expression profile, The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets, and validated in 92 paired LUAD tissues by chromogenic in situ hybridization. Our data confirmed that PIK3CD-AS2 expression is a crucial regulator of LUAD progression and associated with shorter patient survival. In vitro studies showed that PIK3CD-AS2 increased cell growth and slowed apoptosis in p53wt cells but not in p53null cells. Mechanically, it is demonstrated that PIK3CD-AS2 bound to and maintained the stability of Y-box binding protein 1 (YBX1), a potent destabilizer of p53, by impeding its ubiquitination and degradation. Downexpression of YBX1 reversed PIK3CD-AS2-mediated inhibition of p53 signaling. Additionally, the therapeutic effect evaluation of a Locked Nuclear Acid (LNA) specifically targeting PIK3CD-AS2 showed an anti-tumor activity in mice with A549 cells xenograft and p53 wild-type LUAD patient-derived tumor xenograft (PDTX) model. Clinically, the high expression of PIK3CD-AS2 showed a poor disease-free survival in p53 wild-type patients in TCGA database. Our findings suggest that PIK3CD-AS2 regulates LUAD progression and elucidate a new PIK3CD-AS2/YBX1/p53 signaling axis, providing a potential lncRNA-directed therapeutic strategy especially in p53 wild-type LUAD patients.

overall_design: A549 cells were transfected with PIK3CD-AS2 siRNA or control, respectively. 48 hours after transfection, total RNA of A549 cells was harvested and analyzed by RNA sequencing (RNA-seq)

first: Xiufen

last: Zheng


title: Microarray Analysis of ttg1 versus Wild-Type Developing Seeds

city: Bundoora, Melbourne

first: Song

middle: F

last: Li

state: VIC

address: Kingsbury Dr

department: Botany

country: Australia

institute: La Trobe University

summary: MYB-bHLH-TTG1 regulates Arabidopsis seed coat biosynthesis pathways directly and indirectly  via multiple tiers of transcription factors

overall_design: Four ttg1 mutant developing seed samples vs four wild-type Arabidopsis seed samples using Affymetrix ATH1 chips


title: Domain model explain propagation dynamics and stability of K27 and K36 methylation landscapes

city: Copenhagen

first: Anja

last: Groth

address: Blegdamsvej 3B

country: Denmark

institute: Novo Nordisk Foundation Center for Protein Research

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Chromatin states must be stably maintained during cell proliferation to uphold cellular identity and genome integrity. Inheritance of histone modifications across cell division is thought to be central in this process. However, the histone modification landscape is challenged by the incorporation new unmodified histones during each cell cycle and the principles that govern heritability remain poorly defined. Here, we take a quantitative approach and develop a reusable computational model that describes propagation of K27 and K36 methylation states. We measure combinatorial K27 and K36 methylation patterns by quantitative mass spectrometry on subsequent generations of histones in the presence and absence of enzymatic inhibition. Our modelling rejects active global demethylation and invoke the existence of 8 domains defined by distinct methylation endpoints. We find that K27me3 on pre-existing histones stimulates the rate of de novo K27me3 establishment, supporting a read-write mechanism in timely chromatin restoration. Finally, we provide a detailed, quantitative picture of the mutual antagonism between K27 and K37 methylation, and propose that this antagonism enhance the stability of epigenetic states across cell division.

overall_design: Quantitative ChIP-seq analysis of H3K36me2 and H3K27me3 distribution and abundance upon 7 days treatment with DMSO or EZH2 inhibitor (EPZ-6438) in E14 mESCs cells. All experiments were done in duplicates. Chromatin of Drosophila melanogater S2 cells were used as spike-in for normalization purpose. Standard ChIPseq was performed on the same cells for H3K36me3, H3K27me1, H3K27me2 and H3K27me3 to determine regions of enrichment for each of the marks.

first: Constance

last: Alabert

first: Simona

last: Graziano

first: Nazaret

last: Reverón-Gómez


title: Gene expression data from multiple myeloma cell lines treated with Novel Anti-B-cell Maturation Antigen α-Amanitin Antibody-drug Conjugate, HDP-101.

city: Houston

first: Ram Kumar

last: Singh

state: Texas

address: 1515 Holcombe Blvd

department: Lymphoma and Myeloma

institute: MD Anderson Cancer Centre

summary:
Deletion (Del) of 17p involving the TP53 tumor suppressor remains an adverse prognostic factor in multiple myeloma, and more effective targeted therapies are needed for these patients.  Genomic studies revealed that del17p was associated with reduced copy number and mRNA expression of RNA polymerase II subunit alpha (POLR2A), which is located near TP53.  We therefore studied HDP-101, an anti-B-cell maturation antigen (BCMA) antibody drug conjugate (ADC) with the POLR2A poison α-amanitin, which showed potent anti-proliferative and pro-apoptotic activity against cell lines and primary samples.  POLR2A knockdown (KD) in both TP53 wild-type (WT) and knockout (KO) cells, with the latter being a model of del17p, enhanced sensitivity to HDP-101 compared to POLR2A WT cells.  Gene expression profiling and proteomic studies showed evidence for activation of endoplasmic reticulum stress and the unfolded protein response, as well as a reduction of anti-apoptotic proteins such as Myeloid cell leukemia (MCL)-1.  Bortezomib enhanced the activity of HDP-101, as did a gamma-secretase inhibitor, and this ADC overcame resistance both due to microenvironmental factors and in acquired drug resistance models.  Finally, HDP-101 was well tolerated in vivo, reduced disease burden with single, 2-4 mg/kg doses, and no evidence of relapse was seen out to 100 days, even in xenografts that modeled del17p through dual TP53 KO/POLR2A KD, which grew more aggressively without treatment.  Together, the data validate the efficacy of a new BCMA ADC that is ready for clinical translation, and suggest that it could be equipotent, or perhaps even more effective against myeloma with del17p.
We used microarray to investigate the global changes caused by HDP-101 across p53 Wt and p53 KO multiple myeloma cell lines

overall_design: H929 and MM1.S TP53 WT and KO cells were treated with HDP-101 at 200 pM for 24 hours, and then subjected to gene expression profiling to monitor global changes across the sample compared to their respective controls ; PBS, Ab alone, Non-target ADC (NTC). The experiments were performed in two replicates followed by  RNA extraction and hybridization on Affymetrix microarrays. Differential gene expression (Gene + Exon) was analysed across p53 WT or KO control samples  versus HDP-101 treatment. Genome version hg19 (Homo Sapiens), Annotation HTA-2_0.r3.na36.hg19.a1.transcript.csv;  Gene-Level Fold Change < -2 or > 2 with significance calculated at P-Value < 0.05. Heatmaps were generated for MM1.s WT ctrl vs MM1.S WT_HDP-101;MM1 KO_CTR vs MM1  KO_HDP101; H929 WT-Control vs H929 WT-HDP 101; H929 KO_CTR vs H929  KO_HDP101

first: Ram

middle: K

first: Robert

middle: Z

last: Orlowski


title: Transcriptome changes initiated by carbon starvation in Aspergillus nidulans (Microbiology-SGM, 2013, Vol:159)

city: Debrecen

first: Istvan

last: Pocsi

address: Egyetem tér 1.

department: Dept.of Microbiology and Biotechnology

country: Hungary

institute: University of Debrecen

summary: Transcriptional profiling of Aspergillus nidulans comparing control (growing on glucose) and carbon starving cultures.

overall_design: Total RNA was isolated from mycelia after 4 h carbon starvation and from growing mycelia. RNA samples from three parallel experiments were pooled in 1 : 1 : 1 ratios.

first: Melinda

last: Szilaágyi

first: Márton

last: Miskei

first: Zsolt

last: Karányi

first: Béla

last: Lenkey

first: István

last: Pócsi

first: Tamás

last: Emri


title: Identification of Differentially Expressed MicroRNAs and Target Genes of Sunflower Leaves and Roots Under Drought Stress

city: Guiyang

first: Chunbo

last: Liang

state: Guizhou

address: Dongqingnan road

institute: Guizhou University of tradional Chinese Medicine

summary: small RNA sequencing was performed to investigate the the response mechanism of sunflowe seedling  to drought

overall_design: small RNA profiles of  leaves and roots of R5 (tolerant to drought)  were generated by deep sequencing. The sequence reads that passed quality filters were analyzed at the transcript.

first: Xutang

last: Huang


title: Swine intestinal microbiota perturbation by antibiotic treatment is linked to a reduced number of necrotic epithelial cells and up-regulation of immune-associated pathways using an in vitro Salmonella Typhimurium challenge model

city: Saint Paul

first: Matheus

last: Costa

address: 1988 Fitch avenue

institute: University of Minnesota

summary: Salmonella enterica serovar Typhimurium is an animal welfare and public health concern due to its ability to parasite livestock and potentially contaminate meat products. In pigs, it is associated with enterocolitis and diarrhea, whereas some individuals may become life-long carriers. To reduce Salmonella shedding and the risk of pork contamination, antibiotic therapy is used and can contribute to antimicrobial resistance. Here we hypothesized that immune system education by the microbiota can play a role in intestinal resilience to infection. We used amoxicillin (15mg/Kg) to modulate the intestinal microbiome of 10 piglets, paired with same age pigs that received a placebo (n=10) from 0 to 14 days of age. Animals were euthanized when 4-weeks old. Each pig donated colon sections for ex vivo culture (n=20 explants/pig). Explants were inoculated with S. Typhimurium, PBS or LPS. The gut bacteriome was characterized by sequencing of the 16S rRNA at 7, 21 days of age, and upon in vitro culture. In vivo antibiotic treatment led to b-diversity differences between groups at all times (P<0.05), while a-diversity did not differ between amoxicillin and placebo groups on day 21 and at euthanasia (P<0.03 on day 7). Explant microbiomes were not different from in vivo. No significant differences in epithelial cell necrosis scores were observed between amoxicillin and placebo groups after exposure to Salmonella, even though median scores were lower in the amoxicillin group. Both groups did have significantly higher necrosis scores than the PBS group (P<0.05). Activation of immune-related cascades in control explants from the amoxicillin group was observed, whereas Salmonella exposure activated specific cellular repair, wound healing and macrophage pathogen inhibition pathways that were significantly different from placebo pigs. These suggest that immune education by the microbiota may be developed as a tool to mitigate intestinal lesions following pathogen exposure.

overall_design: Transcriptome analysis of colon explants following salmonella challenge.

first: John

last: Harding


title: Host-pathogen interactions in human polyomavirus 7 (HPyV7)-associated skin disease

status: Public on Apr 07 2020

first: Rachel

last: Rosenstein

address: 10 Center Drive, 12N240

summary: The recently discovered polyomavirus HPyV7 is emerging as a cause for intensely itchy skin eruptions in immunocompromised hosts. We performed an in-depth investigation of a renal transplant recipient with HPyV7-associated eruption that resolved with reduction of immunosuppression and treatment with acitretin. RNA sequencing of diseased skin revealed a strong interferon response that decreased upon clinical resolution, correlating with cessation of viral protein expression and seroconversion for HPyV7-specific antibodies. Sequencing of HPyV7 revealed a mutagenic hotspot within a previously undetected agnoprotein gene. The cytosine deaminases APOBEC3A and APOBEC3B were significantly upregulated in affected skin, and the observed viral sequence modifications were consistent with APOBEC activity, suggesting that it may play a role in viral evolution in diseased skin. Through this multi-omic approach, we confirm a pathogenic role for HPyV7, identify signature components of the host response, and highlight the complex interplay between the skin immune microenvironment and viral mutagenesis.

overall_design: 3 skin biopsy RNA-seq samples were analyzed: less affected skin biopsy (3 replicates: 2 technical replicates first and a 3rd replicate done during the late-treatment run), more affected skin biopsy (3 replicates: 2 technical replicates first and a 3rd replicate done during the late-treatment run), late-treatment skin biopsy (1 sample).

first: Diana

middle: V

last: Pastrana

first: Gabriel

last: Starrett

first: Matthew

middle: R

last: Sapio

first: Natasha

middle: T

last: Hill

first: Jay-Hyun

last: Jo

first: Chyi-Chia

last: Lee

first: Michael

last: Iadarola

first: Christopher

middle: B

last: Buck

first: Heidi

middle: H

last: Kong

first: Isaac

last: Brownell

first: Edward

last: Cowen


title: WGBS and RNA-seq of mouse livers and human Hep3B cells

city: Xi’an

first: Yi

last: Wu

state: Shaanxi

address: No.28, Xianning West Road

institute: Xi'an Jiaotong University

type: Methylation profiling by high throughput sequencing

summary: We detected the contributions of CpG methylation in gene promoter to the expression of acute phase proteins in livers

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Gene expression profiles of Hep3B cells with or without IL-6 and IL-1β (10 ng/ml rhIL-6, 1 ng/ml rhIL-1β ) treatment for 24 h were determined with RNA sequencing using illumina Novaseq.  The resting liver tissues were excised from normal mice. After one week recover,100ul turpentine was subcutaneously injected to the every hind limb.Obtaining the turpentine-induced liver tissues two days later.Transcriptome and methylome of prepared mouse liver tissues were determined with RNA sequencing and whole genome bisulfite sequencing using  illumina Novaseq.

first: Shi-Chao

last: Zhang

first: Ming-Yu

last: Wang

first: Jun-Rui

last: Feng

first: Yue

last: Chang

first: Shang-Rong

last: Ji


title: RNA-seq of donor matched freshly FACS-sorted Tregs (CD4+CD127loCD25hi) and Tconvs (CD4+CD127hiCD25lo) to compare both the protein-coding and non-coding transcriptomes from three different healthy donors (HD)

first: Stefan

last: Muljo

address: 10 CENTER DR RM 11N306

institute: NIH/NIAID

summary: The major goal of this study was to perform an in depth characterization of the “gene signature” of human FoxP3+ T regulatory cells (Tregs). Highly purified Tregs and T conventional cells (Tconvs) from multiple healthy donors (HD), either freshly explanted or activated in vitro, were analyzed via RNA sequencing (RNA-seq) and gene expression changes validated using the nCounter system. Additionally, we analyzed microRNA (miRNA) expression using TaqMan low-density arrays. Our results confirm previous studies demonstrating selective gene expression of FoxP3, IKZF2, and CTLA4 in Tregs. Notably, a number of yet uncharacterized genes (RTKN2, LAYN, UTS2, CSF2RB, TRIB1, F5, CECAM4, CD70, ENC1 and NKG7) were identified and validated as being differentially expressed in human Tregs. We further characterize the functional roles of RTKN2 and LAYN by analyzing their roles in vitro human Treg suppression assays by knocking them down in Tregs and overexpressing them in Tconvs. In order to facilitate a better understanding of the human Treg gene expression signature, we have generated from our results a hypothetical interactome of genes and miRNAs in Tregs and Tconvs

overall_design:
Conventional T cells (Tconvs) or Regulatory T cells (Tregs) isolated from peripheral blood of three healthy donors: 1HD (Healthy Donor 1, Male), 2HD (Healthy Donor 2, Female), 3HD (Healthy Donor 3, Male). Samples were recovered either upon fresh explantation (0hr) or after further in vitro activation at longer timepoints (6hr, 24hr, 7d) for Healthy Donor 3HD.

Please note that each *Tconvs_vs_Tregs_DEGseq_merged_score.tsv contains both Tconvs_count and Tregs_count data from each donor (as indicated in the file name) and is linked to the corresponding *Tconvs sample records.

first: Ravikiran

last: Bhairavabhotla

first: Cuong

last: Nguyen

first: Gokhul

last: Kilaru

first: Ethan

middle: M

last: Shevach


title: RNA-sequencing data of intestinal tissue of pigs fed milk replacer with added starch

city: Frederiksberg C

first: Andrew

last: Williams

state: --- Select One ---

address: Dyrlægevej 100

institute: University of Copenhagen

summary: We show here the transcriptional response in the distal small intestine of piglets fed either normal milk replacer, or milk replacer with added starch.

overall_design: RNA was obtained from the tissue of 10 piglets fed normal milk replacer and 11 piglets fed milk replacer with starch.


title: Exonuclease combinations reduce noises in 3D genomics technologies

city: Shenzhen

first: Qing

last: Li

address: No 7,Pengfei Road,Dapeng District

institute: Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences,

type:
Other
Third-party reanalysis

summary: Chromosome conformation-capture technologies are widely used in 3D genomics; however, experimentally, such methods have high-noise limitations and, therefore, require significant bioinformatics efforts to extract reliable distal interactions. Miscellaneous undesired linear DNAs, present during proximity-ligation, represent a main noise source which needs to be minimized or eliminated. In this study, different exonuclease combinations were tested to remove linear DNA fragments from a circularized DNA preparation. This method efficiently removed linear DNAs, raised the proportion of annulation and increased valid-pairs ratio from 30-40% to 70-80% for enhanced interaction detection in standard Hi-C. This strategy is applicable for development of various 3D genomics technologies, or optimization of Hi-C sequencing efficiency.

overall_design: For dilution system, LIC-Hi-C treatments mean the noises of Hi-C were removed by “Lambda and Exonuclease I” exonuclease combination for 1h, which has three replicates (LIC-Hi-C-1,LIC-Hi-C-2,LIC-Hi-C-3). LRC-Hi-C-1, which means the noises of Hi-C were removed by “Lambda and RecJF” exonuclease combination for 1h.LRC-Hi-C 2-4(three replicates), which means the noises of Hi-C were removed by “Lambda and RecJF” exonuclease combination for 1 min. The formers are belong to Exo-Hi-C. Hi-C 1-3 (three replicates) are Exo-Hi-C control without exonuclease combination treatment. GSM862721(Standard Hi-C 1),GSM1718027(Standard Hi-C 2) and GSM862720(Standard Hi-C 3) are also set as control groups.We have downloaded these three data.We re-analyzed and named them as Standard Hi-C 1, Standard Hi-C 2 and Standard Hi-C 3 in our papers. For in situ system, IIIIC-in situ Hi-C 4-6 (three replicates) and 10-12 (another three replicates) treatments mean in situ Hi-C in this study were treated by  “Exonuclease I and Exonuclease III” exonuclease combination for 1 min. LIC-in situ Hi-C 4-6 (three replicates) and 10-11 (another two replicates)  treatments mean in situ Hi-C in this study were treated by  “Lambda and Exonuclease I” exonuclease combination for 1 min. The formers are belong to In situ exo-Hi-C.In situ Hi-C 1-3 (three replicates) and 12-14 (another three replicates) are in situ exo-Hi-C control without exonuclease combination treatment (named as in situ Hi-C). HIC088,HIC094,HIC096 are also set as control groups.We have downloaded these three data.We re-analyzed and named them as Rao et al. insitu Hi-C in our papers.

first: Siyuan

first: Gaolin

first: Qiujia

first: Qitong

last: Huang

first: Lei

first: Hui

first: Yinghua

first: Yanling

last: Peng

first: Baoming

last: Qin

first: Yubo


title: Effect of FBXW7 loss and concomitant FBXW7-KMT2D loss on mRNA levels

city: Philadelphia

first: Luca

last: Busino

state: PA

address: 421 Curie Blvd, 705 BRB II/III

department: Cancer Biology

institute: Luca Busino

summary: We assessed the role of the E3 ligase FBXW7 in mature B-cell neoplasms. This experiment assesses the role of the FBXW7-KMT2D axis in regulating gene expression in OPM-1 cells.

overall_design: OPM-1 stably expressing RNAs targeting Luciferase, FBXW7 or KMT2D. RNA was collected from three independent biological replicates per condition.

first: Rizwan

last: Saffie


title: Proteomic and transcriptomic studies of BCG823 cells stimulated with Helicobacter pylori isolates from gastric MALT lymphoma

city: Beijing

first: Qinghua

last: Zou

address: No.38, Xueyuan Rd

institute: Peking university health science center

summary: We performed both transcriptomic and proteomic analyses on gastric cancer cells infected by H. pylori isolates from GML patients and the gastric ulcer strain 26695 to investigate the differentially expressed molecular signatures that were induced by GML isolates. Transcriptomicd analysis revealed fifteen pathways, including the Wnt signaling pathway, the mTOR signaling pathway, the NOD-like receptor signaling pathway and the Hippo signaling pathway, were revealed to be related to GML isolates.

overall_design: Compare the transcriptome of BCG823 cells stimulated with Helicobacter pylori GML isolates and gastric ulcer isolate 26695

first: Di

last: Xiao


city: Ann Arbor

first: qin

last: wang

state: MI

address: 109 Zina Pitcher Place

department: neurology

institute: university of michigan

summary: Siponimod selectively enriched regulatory T and B lymphocytes in active secondary progressive multiple sclerosis patients: 20 SPMS baseline including 3 repeats, 19 treated with 5 placebo and 14 siponimod treated.

overall_design: 20 SPMS baseline including 3 repeats (2 samples were dried out, so no data available), 19 treated with 5 placebo and 14 siponimod treated

first: Qi

last: Wu

first: Elizabeth

last: Mills

first: Qin

last: Wang

first: Catherine

last: Dowling

first: Caitlyn

last: Fisher

first: Britany

last: Kirch

first: Steven

last: Lundy

first: David

last: Fox

first: Yang

last: Mao-Draayer


title: Beta cell-specific CD8+ T cells maintain stem-cell memory-associated epigenetic programs during type 1 diabetes (WGBS)

city: memphis

first: yiping

last: fan

state: tn

address: 262 Danny Thomas Place

institute: st jude children's hospital

summary: The pool of beta cell-specific CD8+ T-cells in type 1 diabetes (T1D) sustains an autoreactive potential despite having access to a constant source of antigen. To investigate the long-lived nature of these cells, we established a DNA methylation-based T cell “multipotency index” and found that beta cell-specific CD8+ T-cells retained a stem-like epigenetic multipotency score. Single cell ATAC-seq analysis confirmed the co-existence of naive and effector-associated epigenetic programs in individual beta cell-specific CD8+ T-cells. Assessment of beta cell-specific CD8+ T-cell anatomical distribution and the establishment of stem-associated epigenetic programs revealed that self-reactive CD8+ T-cells isolated from murine lymphoid tissue retained developmentally plastic phenotypic and epigenetic profiles relative to the same cells isolated from the pancreas. Collectively, these data provide new insight into the longevity of beta cell-specific CD8+ T cell responses, and document the utility of this novel methylation-based multipotency index for investigating human and mouse CD8+ T-cell differentiation.

overall_design: Human naïve, TEM, TCM, and TSCM polyclonal CD8 T cells were sorted from healthy donors. Naive and Tetramer+ CD8 T cells were sorted from HIV HAART and T1D patients. whole-genome DNA methylation analysis was performed as previously described (Abdelsamed, et al. JEM 2017, PMID: 28490440). Naïve and NRP-V7 tetramer+ CD8 T cells were sorted from pancreatic islets, lymphnodes, and spleen of NOD mice. whole-genome DNA methylation analysis was performed as previously described (Ghoneim, et al. Cell 2017, PMID: 28648661). Single cell ATACseq was performed using the 10X Genomics platform per the manufacturers instructions.

first: Hossam

last: Abdelsamed

first: Caitlin

last: Zebley

first: Hai

last: Nguyen

first: Rachel

last: Rutishauser

first: Yiping

last: Fan

first: Hazem

last: Ghoneim

first: Jeremy

last: Chase Crawford

first: Francesca

last: Alfei

first: Shanta

last: Alli

first: Susam

last: Pereira Riberio

first: Ashely

last: Castellaw

first: Maureen

last: McGargill

first: Honglian

last: Jin

first: Shannon

last: Boi

first: Cate

last: Speake

first: Elisavet

last: Serti

first: Laurence

last: Turka

first: Michael

middle: E

last: Busch

first: Mars

last: Stone

first: Steve

middle: G

last: Deeks

first: Rafick-Pierre

last: Sekaly

first: Dietmar

last: Zehn

first: Eddie

last: James

first: Gerald

last: Nepom

first: Ben

last: Youngblood


title: Urinary Cell Transcriptomics and Acute Rejection in Human Kidney Allografts

city: New York

first: Akanksha

last: Verma

state: New York

address: 1300, York Avenue

department: Department of Physiology and Biophysics

institute: Weill Cornell Medical College

summary: RNA-sequencing (RNA-Seq) is a precise tool to analyze global transcriptional changes, develop biomarkers, and decipher pathogenic mechanisms. We performed RNA-Seq of urinary cells to investigate gene expression patterns and pathways and whether urinary cell mRNA transcriptional profiles are enriched for biopsy transcriptional profiles.

overall_design: We performed RNA-Seq of 57 urinary cell pellets of kidney allograft recipients obtained at the time of biopsy diagnosis of T cell mediated rejection (N=22), antibody mediated rejection (N=8), or Normal/nonspecific changes/no rejection (N=27)

first: Olivier

last: Elemento

first: Manikkam

last: Suthanthiran


title: Beta cell-specific CD8+ T cells maintain stem-cell memory-associated epigenetic programs during type 1 diabetes

first: yiping

last: fan

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

overall_design: Refer to individual Series


title: Genome-wide expression analysis of C. elegans nematodes after feeding RNAi impairment of the transcription factors lin-32 and hlh-2

city: Jena

first: Marco

last: Groth

address: Beutenbergstraße 11

department: Core Facility - Next Generation Sequencing

country: Germany

institute: Leibniz Institute on Aging - FLI

summary: Physiological aging is a complex process, influenced by a plethora of genetic and environmental factors. While being far from fully understood, a number of common aging hallmarks have been elucidated in recent years. Among these, transcriptomic alterations are hypothesized to represent a crucial early manifestation of aging. Accordingly, several transcription factors (TFs) have previously been identified as important modulators of lifespan in evolutionarily distant model organisms. Based on a set of TFs conserved between nematodes, zebrafish, mice, and humans, we here perform a RNA interference (RNAi) screen in C. elegans to discover evolutionarily conserved TFs impacting aging. We identify a basic helix-loop-helix TF, named HLH-2 in nematodes (Tcf3/E2A in mammals), to exert a pronounced lifespan-extending effect in C. elegans upon impairment. We further show that its impairment impacts cellular energy metabolism, increases parameters of healthy aging, and extends nematodal lifespan in a ROS-dependent manner. We then identify arginine kinases , orthologues of mammalian creatine kinase, as a target of HLH-2 transcriptional regulation, serving to mediate the healthspan-promoting effects observed upon impairment of hlh-2 expression. Consistently, HLH-2 is shown to epistatically interact with core components of known lifespan-regulating pathways, i.e. AAK-2/AMPK and LET-363/mTOR, as well as the aging-related TFs SKN-1/Nrf2 and HSF-1. Lastly, single-nucelotide polymorphisms (SNPs) in Tcf3/E2A are associated with exceptional longevity in humans. Together, these findings demonstrate that HLH-2 regulates energy metabolism via arginine kinases and thereby affects the aging phenotype dependent on ROS-signaling and established canonical effectors.

overall_design: In total eight samples, all derived from C. elegans wild-type N2 nematodes, were analysed - two from feeding with the empty plasmid L4440, three from feeding with a lin-32 RNAi plasmid, and three from feeding with a hlh-2 RNAi plasmid.

first: Leonid

last: Rozanov


title: Beta cell-specific CD8+ T cells maintain stem-cell memory-associated epigenetic programs during type 1 diabetes (scATAC-seq)

overall_design: Single cell ATACseq was performed using the 10X Genomics platform per the manufacturers instructions.

first: Hossam

last: Abdelsamed

first: Caitlin

last: Zebley

first: Hai

last: Nguyen

first: Rachel

last: Rutishauser

first: Yiping

last: Fan

first: Hazem

last: Ghoneim

first: Jeremy

last: Chase Crawford

first: Francesca

last: Alfei

first: Shanta

last: Alli

first: Susam

last: Pereira Riberio

first: Ashely

last: Castellaw

first: Maureen

last: McGargill

first: Honglian

last: Jin

first: Shannon

last: Boi

first: Cate

last: Speake


title: ZBTB7A prevents RUNX1-RUNX1T1 dependent clonal expansion of human hematopoietic progenitor cells

city: Munich

first: Enric

last: Redondo Monte

state: Bavaria

address: Max-Lebsche-Platz 30

department: Internal Medicine 3

institute: Ludwig-Maximilians University Munich

summary: ZBTB7A is frequently mutated in acute myeloid leukemia (AML) with t(8;21) translocation. However, the oncogenic collaboration between mutated ZBTB7A and the RUNX1-RUNX1T1 fusion gene in AML t(8;21) remains unclear. Here, we investigate the role of ZBTB7A and its mutations in the context of normal and malignant hematopoiesis.

overall_design: RNA-seq of control and ZBTB7A in K562 cell lines.

first: Johannes

last: Bagnoli


title: DNA methylation clocks as a predictor for ageing and age estimation in naked mole-rats, Heterocephalus glaber

city: London

first: Amy

middle: Frances

last: Danson

state: Greater London

address: 2 Newark St

department: Centre for Genomics and Child Health

country: United Kingdom

institute: The Blizard Institute

summary: The naked mole-rat, Heterocephalus glaber (NMR), the longest-lived rodent with a maximum possible lifespan exceeding 33 years, is emerging as an important non-model organism for the study of longevity and healthspan. As such it is of significance and interest in the study of biomarkers for ageing in mammals. Recent breakthroughs in this field have indicated that ‘epigenetic clocks’ based on the temporal accumulation of DNA methylation at specific genomic sites can enable accurate age estimates for tissues across the lifespan of an individual. Here, we validate the hypothesis of an epigenetic clock in NMRs, and create a method for predicting the age of naked mole-rats based on changes in methylation of targeted CpG sites in regions known as ageing-associated differentially methylated positions (aDMPs). In the discovery phase, we performed a targeted analysis of 51 different CpGs in 24 different NMR livers spanning an age range from 39 weeks to 1,144 weeks. Of these 51 different sites, 23 were found to be significantly associated with age (p < 0.05). We then built a predictor of age using the 23 sites that showed an association with age. To test the accuracy of this model, we predicted age in an additional test set of 19 different livers spanning an age range 43 to 1,196 weeks. Our model was able to successfully predict age in the test with a root mean squared error (RMSE) of 166.11 weeks. We also profiled a 20 skin samples with the same age range and found a striking correlation between the predicted age of these samples versus their actual age (R=0.93). However, this correlation when compared to the liver samples showed a lower predicted age than actual age, suggesting that skin tissue ages slower than the liver in NMRs. Finally, we have produced freely available software tool that will take in raw sequencing data and produce an age prediction for new NMR samples. Our model will enable the prediction of age in wild caught naked mole-rats and captive animals of unknown age, and will be invaluable for further mechanistic studies of mammalian ageing.

overall_design: DNA methylation at age-related differentially methylated sites was measured in naked mole rat (Heterocephalus glaber) liver and skin in animals of different ages to test whether the DNA methylation aging clock seen previously in liver applies to skin, allowing for age-typing of wild animals in future research.

first: Robert

last: Lowe


title: Bacterial nucleoside catabolism controls quorum sensing and commensal-to-pathogen transition in the Drosophila gut

city: Seoul

first: Do Young

last: Hyeon

state: Select State

address: 1 Gwanak-ro, Gwanak-gu

department: School of Biological Sciences

country: South Korea

institute: Seoul National University

summary: Although gut microbiomes are generally symbiotic or commensal, some of microbiomes become pathogenic under certain circumstances, which is one of key processes of pathogenesis. However, the factors involved in these complex gut-microbe interactions are largely unknown. Here we show that bacterial nucleoside catabolism using gut luminal uridine is required to boost inter-bacterial communications and gut pathogenesis in Drosophila. We found that uridine-derived uracil is required for DUOX-dependent ROS generation on the host side, whereas uridine-derived ribose induces quorum sensing and virulence gene expression on the bacterial side. Importantly, genetic ablation of bacterial nucleoside catabolism is sufficient to block the commensal-to-pathogen transition in vivo. Furthermore, we found that major commensal bacteria lack functional nucleoside catabolism, which is required to achieve gut-microbe symbiosis. The discovery of a novel role of bacterial nucleoside catabolism will greatly help to better understand the molecular mechanism of the commensal-to-pathogen transition in different contexts of host-microbe interactions.

overall_design: mRNA expression profiles of wild type (Ecc15) and nucleoside hydrolase mutant (Ecc15_delNH) E. carotovora carotovora15 strain were examined by Illumina Hi-seq 2500.

first: Won

middle: J

last: Lee

first: Daehee

last: Hwang


title: Effect of neuropathy-associated MCM3AP variants on gene expression in fibroblasts

city: Helsinki

first: Jouni

middle: Antero

last: Kvist

state: Uusimaa

address: Haartmaninkatu 8

department: Research Program for Molecular Neurology

country: Finland

institute: University of Helsinki

summary: An RNA sequencing analysis of fibroblasts derived from affected individuals with neuropathy, who carry biallelic variants in MCMC3AP gene. The expression levels are compared with healthy controls.

overall_design: Fibroblasts from 5 affected individual, 1 healthy carrier and 2 unrelated controls

first: Rosa

last: Woldegebriel

first: Emil

last: Ylikallio

first: Henna

last: Tyynismaa


title: Transcriptional changes in soleus muscle for rats exposed to different activities after contusion injury to the spinal cord and transcriptional changes in soleus muscle with complete spinal cord transection injury

city: Louisville

first: Eric

middle: Christian

last: Rouchka

state: Kentucky

address: 522 East Gray Street

department: Biochemistry and Molecular Genetics

institute: University of Louisville

summary: Spinal cord injury (SCI) is a devastating clinical condition resulting in significant disabilities for affected individuals. Apart from local injury within the spinal cord, SCI patients develop a myriad of complications characterized by multi-organ dysfunction. Disorders, such as lung injury, cardiovascular disease, liver damage, kidney and urinary tract dysfunction, alterations in gut microbiome, neuropathic pain, depression and altered immune responses are common in SCI patients. Such whole body, systemic responses hinder the functional recovery and can be life-threatening in SCI population. Investigations of organ specific gene expression analyses can provide a better understanding of the injury response and identify molecular targets. Consequently, this can be used to develop treatment for SCI, promoting functional recovery and overall quality of life.

overall_design: Rats were subjected to a single level laminectomy at T2 vertebrae before receiving a complete transection injury or moderately-severe contusion injury (25 g-cm SCI) at the T2 spinal cord level using the NYU Impactor (W.Young, Rutgers University, Newark, NJ). After four days of recovery, all animals were housed two per cage in tiny cage (7.5” x 8.5” x 8”) as opposed to standard cage (22” x 12.5” x 8”) to restrict their motion for the duration of the study. The subjects were then randomized into one of four groups: 1) Contusion SCI + swimming (SWIM), 2) Contusion SCI + shallow water walking (SWW), 3) Contusion SCI, un-exercised, 4) Complete Transection, un-exercised and 5) un-injured and un-exercised control group. Swimming and shallow water walking as exercise intervention, began 2.5 weeks post injury in T2 contused group and was conducted 5 days a week for 10 weeks. Animals were sacrificed at 13.5 weeks post-injury for contusion SCI+Exercise, at 11.5 weeks post-injury for contusion SCI alone, and 8.5 weeks post-injury for transection SCI. Soleus muscle tissue was retrieved from each animal and total RNA was extracted for Illumina NextSeq RNA sequencing.

first: Julia

last: Chariker

first: Sujata

middle: S

last: Ohri

first: Cynthia

last: Gomes

first: Fiona

last: Brabazon

first: Kathryn

last: Harman

first: David

last: Magnuson

first: Michal

last: Hetman

first: Jeffrey

last: Petruska

first: Scott

last: Whittemore


title: Combined Cohesin-Runx1 Deficiency Synergistically Perturbs Chromatin Looping and Causes Myelodysplastic Syndromes

city: Kyoto

first: Yotaro

last: Ochi

address: Yoshida-Konoe-cho

department: Department of Pathology and Tumor Biology

country: Japan

institute: Kyoto Univiersity


title: Hippo signaling coordinates cellular quiescence with terminal maturation in iNKT cell development and fate decisions [MoGene-2_0]

city: Memphis

first: Hongbo

last: Chi

state: TN

department: Immunology

institute: St Jude Children's Research Hospital

summary:
Hippo kinases Mst1 and Mst2 act as molecular rheostats for the terminal maturation and effector differentiation programs of iNKT cells.
iNKT developmental stages 1, 2, and 3 (S1, S2, S3) were sorted from the thymus of WT (n = 3) and Cd4CreMst1fl/fl (n = 3) mice

overall_design: In total 18 samples were analyzed: n=3 for each iNKT developmental stages were sorted from the thymus of WT (n = 3) and Cd4CreMst1fl/fl (n = 3) mice.

first: Jana

middle: L

last: Raynor

first: Yogesh

last: Dhungana


title: Blockade of lL17 signaling reverses alcohol-induced liver injury, and excessive alcohol drinking in mice.

city: La Jolla

first: Tatiana

last: Kisseleva

state: CA

address: 9500 Gilman Drive

institute: University of California, San Diego

summary: Chronic alcohol abuse has a detrimental effect on the brain and liver. There is no effective treatment for these patients and the mechanism underlying alcohol addiction and consequent alcohol-induced damage of the liver/brain axis remains unresolved.  We compared experimental models of alcoholic liver disease (ALD) and alcohol dependence in mice and demonstrated that genetic ablation of IL17 Receptor A (IL17ra-/-), or pharmacological blockade of IL17 signaling effectively suppressed the increased voluntary alcohol drinking in alcohol-dependent mice, and blocked alcohol-induced hepatocellular and neurological damage. The level of circulating IL17A positively correlated with the alcohol use in excessive drinkers, and was further increased in patients with ALD as compared to healthy individuals. Our data suggest that IL17A is a common mediator of excessive alcohol consumption and alcohol-induced liver/brain injury, and targeting IL17A may provide a novel strategy for treatment of alcohol-induced pathology.

overall_design: Hippocampus were dissected from brains of Air (n=3) and CIE ± anti-IL17A Ab mice (n=3/group) and analyzed by RNA-Seq.

first: Jun

last: Xu

first: Sara

last: Rosenthal


title: Identification of miR181ab1 targets in mutant Kras lung cancer cells

city: San Francisco

first: Alex

last: Lee

address: 1550 Fourth St.

institute: UCSF

summary: RNAseq comparison of miR181ab1-knockout and miR181ab1-reconstituted mouse lung cancer cells (KLA)

overall_design: KLA cells derived from KrasLA2 ; miR181ab1f/f mice transduced with a control plasmid (mut/mut) or a plasmid expressing exogenous miR181ab1 (wt/wt) were treated with adenoviral Cre recombinase to deplete endogenous miR181ab1 expression

first: Vicent

last: Silvestre

first: Sweet-Cordero

last: Alejandro


title: Genome-wide analysis of gene expression in normal and fibrotic mouse kidneys and normal and fibrotic mouse lungs

city: Houston

first: Valerie

last: LeBleu

state: TX

address: 1881 East Road

institute: MDACC

summary: In this study, adult virgin female BALB/C  mice were kidney and lungs were harvested for RNA extraction (healthy kidney and lung). Adult virgin female BALB/C  mice were subjected to unilateral ureter obstruction (UUO) to induce kidney fibrosis and the fibrotic kidney was harvested for RNA extraction. Adult virgin female BALB/C  mice were subjected to intratracheal administration of bleomycine to induce lung fibrosis and the fibrotic lungs was harvested for RNA extraction.

overall_design: Total RNA was isolated from the kidney and lung of healthy mice (n=3 mice), from the kidney of mice with kidney fibrosis (n=2 mice), and from the lung of mice with lung fibrosis (n=3 mice).


title: Genomic landscape of endothelial cell-glucocorticoid receptor interactions: Regulation of the Wnt signaling pathway

city: New Haven

first: Julie

last: Goodwin

address: 333 Cedar St

institute: Yale University


title: Genomic landscape of endothelial cell-glucocorticoid receptor interactions: Regulation of the Wnt signaling pathway [RNA-seq]

summary: Vascular inflammation is present in many cardiovascular diseases and exogenous glucocorticoids have traditionally been used as a therapy to suppress inflammation. However, recent data has shown that endogenous glucocorticoids, acting through the endothelial glucocorticoid receptor, act as negative regulators of inflammation. Here we performed chromatin immunoprecipitation for the glucocorticoid receptor followed by next-gen sequencing in mouse endothelial cells to investigate how the endothelial glucocorticoid receptor regulates vascular inflammation. We identified a novel role of the Wnt signaling pathway in this setting and show that loss of the endothelial glucocorticoid receptor results in up regulation of Wnt signaling both in vitro and in vivo using our validated mouse model. Further we demonstrate glucocorticoid receptor regulation of a key gene in the Wnt pathway via a novel glucocorticoid response element gleaned from our genomic data. These results suggest a novel role for endothelial Wnt signaling modulation in states of vascular inflammation.

overall_design: Examination of RNA-seq in endothelial cells with and without the glucorticoid receptor, either unstimulated or treated with dexamethasone (4 conditions in triplicate)

first: Han

last: Zhou

first: Sameet

last: Mehta

first: Kariona

last: Grabinska

first: Chris

last: Wong

first: Ahmad

middle: F

last: Hedayat

first: Paola

last: Perrotta

first: William

middle: C

last: Sessa


title: Genomic landscape of endothelial cell-glucocorticoid receptor interactions: Regulation of the Wnt signaling pathway [ChIP-seq]

overall_design: Examination of ChIP-seq in endothelial cells with and without the glucorticoid receptor, either unstimulated or treated with dexamethasone (4 conditions) with appropriate IgG and whole cell input controls


title: Sub-region-Specific Optic Nerve Head Glial Activation in Glaucoma

city: Madison

first: Kazuya

last: Oikawa

state: WI

address: 1300 University Ave

institute: University of Wisconsin-Madison

summary: Glaucoma, a multifactorial neurodegenerative disease characterized by progressive loss of retinal ganglion cells and their axons in the optic nerve, is a leading cause of irreversible vision loss. Intraocular pressure (IOP) is a risk factor for axonal damage, which initially occurs at the optic nerve head (ONH). Complex cellular and molecular mechanisms involved in the pathogenesis of glaucomatous optic neuropathy remain unclear. Here we define early molecular events in the ONH in an inherited large animal glaucoma model in which ONH structure resembles that of humans. Gene expression profiling of ONH tissues from rigorously phenotyped feline subjects with early-stage glaucoma and precisely age-matched controls was performed by RNA-sequencing (RNA-seq) analysis and complementary bioinformatic approaches applied to identify molecular processes and pathways of interest. Immunolabeling supported RNA-seq findings while providing cell-, region-, and disease stage–specific context in the ONH in situ. Transcriptomic evidence for cell proliferation and immune/inflammatory responses is identifiable in early glaucoma, soon after IOP elevation and prior to morphologically detectable axon loss, in this large animal model. In particular, proliferation of microglia and oligodendrocyte precursor cells is a prominent feature of early-stage, but not chronic, glaucoma. ONH microgliosis is a consistent hallmark in both early and chronic stages of glaucoma. Molecular pathways and cell type–specific responses strongly implicate toll-like receptor and NF-κB signaling in early glaucoma pathophysiology. The current study provides critical insights into molecular pathways, highly dependent on cell type and sub-region in the ONH even prior to irreversible axon degeneration in glaucoma.

overall_design: Optic nerve head mRNA profiles of feline congenital glacoma cats and age-matched normal cats were generated, using illumina Hiseq 2000.

first: K

first: J

middle: N

last: Ver Hoeve

first: L

last: Teixeira

last: Snyder

first: E

middle: A

last: Hennes-Beean

first: C

last: Rasmussen

last: Kiland

first: N

last: Ellinwood

first: G

last: McLellan


title: A novel subclass of exon-derived microRNA is widespread in the mammalian genome

city: Brisbane

first: Selene

middle: Lizbeth

last: Fernandez-Valverde

state: QLD

address: Goddard Building 8 University of Queensland

institute: University of Queensland

summary: Abstract: Argonaute-2, the primary effector molecule of the RNA Induced Silencing Complex, loads both canonical miRNAs and a wide variety of other non-canonical miRNA-like species that enable base pair mediated transcript regulation. Here, using ultra-deep RNA immunoprecipitation and sequencing of nuclear and cytoplasmic hAGO2 in human breast cancer-derived MCF-7 cells, we have identified over one thousand novel AGO2-associated small RNAs. These include a wide variety of isomiRs, in excess of 100 mirtron loci and H/ACA snoRNA and HY3 repeat-derived small RNAs. Unexpectedly, we also discovered 298 AGO2-loaded exon-derived miRNAs (emiRs). These conserved small RNAs are encoded within protein-coding exons and 3’UTRs, have a 5’ end adenosine bias (in contrast to the 5’ U observed in canonical miRNAs), are DICER-1 dependent, processed from mature mRNAs post-splicing and derived from a wide variety of genes involved in differentiation and development including SOX4, JUN, c-MYC and AGO2 itself. We find evidence of emiR expression in human brain and other peripheral tissues, and demonstrate that human emiRs are conserved and detected in murine Ago2 small RNA libraries. Five human emiR loci coincide with known Mendelian disease-causing mutations, and the expression of emiRs is altered in human breast cancer, which may indicate that these species can play a role in disease etiology and progression. We propose that emiRs are the small RNA complement to the competing endogenous RNA (ceRNA) system.

overall_design: Small RNAs and AGO2-bound small RNAs and in whole cell, nuclear and cytoplasmic compartments of MCF-7 cells.

first: John

last: Mattick

first: Ryan

last: Taft


title: Gene expression of primary breast cancers from patients before and after neo-adjuvant Tamoxifen treatment

status: Public on Apr 06 2020

city: Amsterdam

first: Wilbert

last: Zwart

state: Noord-Holland

address: Plesmanlaan 121

department: Oncogenomics

country: Netherlands

institute: Netherlands Cancer Institute

summary:
Tumor gene expression data (microarray from FFPE) was obtained from breast cancer patients enrolled in a pre-operative window trial (ClinicalTrials.gov Identifier: NCT00738777). Patients received an oral loading dose of 40 mg of tamoxifen twice daily for the first seven days, followed by a daily dose of 20 mg until surgery. A core needle biopsy of the tumor was taken prior to treatment (n=62) and post-treatment tumor material (n=40) was obtained during surgery 20.7 (±9.6) days later. Paired material was available for 27/74 patients.
Differential analysis comparing gene expression before and after Tamoxifen treatment implicated activation of the NFκB pathway and an enrichment of EMT/stemness features upon Tamoxifen treatment. In line with these findings, exposure of ER+ breast cancer cell lines to tamoxifen, in vitro and in vivo, gives rise to a tamoxifen-tolerant population with similar NFκB activity and EMT/stemness characteristics as described in the corresponding publication.

overall_design: FFPE tumor material was sent to Agendia Inc. RNA was isolated from samples with sufficient tumor cell content (>30%) and analyzed on a custom Agilent array. Feature Extraction software v11.5.1.1 was used to quantify fluorescent intensities and those were normalized using DataPrint software v1.15. Downstream data processing was subsequently done at the Netherlands Cancer Institute including missing values impution with knn=10 and batch correction for date of RNA extraction using ComBat from the R package sva, using all available patient material from the trial (ClinicalTrials.gov Identifier: NCT00738777). Here we deposited samples used for the Tamoxifen focused analysis described in the cited paper.

first: Stacey

last: Joosten

first: Annuska

last: Glas

first: Sabine

last: Linn


title: Affymetrix SNP array data for esophageal squamous cell carcinoma samples

city: Johannesburg

first: Jacqueline

last: Brown

state: Gauteng

address: 7 York Rd Parktown

department: Molecular Medicine and Haematology

country: South Africa

institute: National Health Laboratory Services

type:
SNP genotyping by SNP array
Genome variation profiling by SNP array

summary:
Esophageal squamous cell carcinoma (ESCC) is an aggressive cancer with one of the highest world incidences in the Eastern Cape region of South Africa. Several genome wide studies have been performed on ESCC cohorts from Asian countries, North America, Malawi and other parts of the world but none has been conducted on ESCC tumors from South Africa to date, where the molecular pathology and etiology of this disease remains unclear. We report here tumor associated copy number changes observed in 51 ESCC patients’ samples from the Eastern Cape province of South Africa.

We extracted tumor DNA from 51 archived ESCC specimens and interrogated tumor associated DNA copy number changes using Affymetrix® 500K SNP array technology. The Genomic Identification of Significant Targets in Cancer (GISTIC) algorithm was applied to identify significant focal regions of gains and losses. Gains of the top recurrent cancer genes were validated by fluorescence in situ hybridization and their protein expression assessed by immunohistochemistry.

Twenty-three significant focal gains were identified across samples. Gains involving the CCND1, MYC, EGFR and JAG1 loci recapitulated those described in studies on Asian and Malawian cohorts. The two most significant gains involved the chromosomal sub-bands 3q28, encompassing the TPRG1 gene and 11q13.3 including the CTTN, PPFIA1and SHANK2 genes. There was no significant homozygous loss and the most recurrent hemizygous deletion involved the B3GAT1 gene on chromosome11q25. Focal gains on 11q13.3 in 37% of cases (19/51), consistently involved CTTN and SHANK2 genes. Twelve of these cases (23,5%), had a broader region of gain that also included the CCND1, FGF19, FGF4 and FGF3 genes.  SHANK2 and CTTN are co-amplified in several cancers, these proteins interact functionally together and are involved in cell motility. Immunohistochemistry confirmed both Shank2 (79%) and cortactin (69%) protein overexpression in samples with gains of these genes. In contrast, cyclin D1 (65%) was moderately expressed in samples with CCND1 DNA gain.

This study reports copy number changes in a South African ESCC cohort and highlights similarities and differences with cohorts from Asia and Malawi. Our results strongly suggest a role for CTTN and SHANK2 in the pathogenesis of ESCC in South Africa.

overall_design: Affymetrix SNP arrays were performed according to the manufacturer's instructions on DNA extracted from formalin-fixed paraffin-embedded tissue samples. Copy number analysis was performed on Affymetrix 500K SNP data for 51 esophageal squamous cell carcinomas. There were also 30 samples from normal formalin-fixed paraffin-embedded tissue samples from a matched population group that were used as a reference set for copy number inference.

first: P

last: Willem

first: AJ

last: Stepien


title: Arabidopsis thaliana small RNA from epidermis and vasculature tissues of Col-0 and ago1 mutants leaves

city: Zürich

first: Alexis

last: Sarazin

address: Universitätstrasse 2

institute: ETH

summary: We aimed at characterizing the identity of the silencing signal i.e. siRNA or longer dsRNA precursor thereof. We used transgenic dsRNA, endogenous dsRNA or virus infection as sources of siRNAs combined to sophisticated immunoprecipitation-based procedures coupled to deep-sequencing. We found that although they are diluted as they move away from their sites of production, siRNAs population are highly similar between incipient and recipient cells in the three systems. Additionally, a significant depletion of 5’U and 5’A content in the recipient cells suggested Argonaute-loading dependent depletion of these siRNAs during their movement over multiple cell layers. Using the PAZ-domain mutants ago1-18 and ago1-42 confirmed that the observed depletion of mobile siRNAs is the result of RISC loading. The results advocate movement of individual siRNA duplexes as opposed to their precursors and that loading into Argonaut proteins renders those small RNAs cell-autonomous.

overall_design: We examined small RNA from vasculature and epidermis tissus from Arabidopsis thaliana Col0 WT leaves as well as ago1-18 and ago1-42 mutants (3 replicates for each)

first: Emanuel

last: Devers

first: Christopher

last: Brosnan

first: Daniele

last: Albertini

first: Andrea

last: Amsler

first: Florian

last: Brioudes

first: Pauline

last: Jullien

first: Peiqi

last: Lim

first: Gregory

last: Schott

first: Olivier

last: Voinnet


title: The CWC27/CWC22 heterodimer: a spliceosome building block linked to the inflammation response in retinal pigment epithelium

city: Paris

first: Herve

last: Le Hir

address: 46, Rue d’Ulm

country: France

institute: IBENS

summary: Human CWC27 is an uncharacterized splicing factor and mutations in its gene are linked to retinal degeneration and other developmental defects. We identify the splicing factor CWC22 as the major CWC27 partner. Both CWC27 and CWC22 are present in published Bact spliceosome structures, but no interacting domains are visible. Here, the structure of a CWC27/CWC22 heterodimer bound to the Exon Junction Complex (EJC) core component eIF4A3 is solved at 3Å-resolution. According to spliceosomal structures, the EJC is recruited in the C complex, once CWC27 has left. Our 3D structure of the eIF4A3/CWC22/CWC27 complex is compatible with the Bact spliceosome structure but not with that of the C complex, where a CWC27 loop would clash with the EJC core subunit Y14. A CWC27/CWC22 building block might thus form an intermediate landing platform for eIF4A3 onto the Bact complex prior to its conversion into C complex. Knock-down of either CWC27 or CWC22 in immortalized retinal pigment epithelial cells affects numerous common genes, indicating that these proteins cooperate, targeting the same pathways. As the most up-regulated genes encode factors involved in inflammation, our findings suggest a possible link to the retinal degeneration associated with CWC27 deficiencies.

overall_design: 9 RNA-seq samples were analyzed. 3 controls samples, 3 samples with siRNA depletion of CWC22 and 3 samples with siRNA depletion of CWC27.

first: Virginia

last: Busetto

first: Isabelle

last: Barbosa

first: Jérôme

last: Basquin

first: Émelie

last: Marquenet

first: Rémi

last: Hocq

first: Magali

last: Hennion

first: Janio

last: Paternina

first: Abdelkader

last: Namane

first: Elena

last: Conti

last: Bensaude

first: Hervé


title: Hydrogen sulfide dysregulates the immune response by suppressing central carbon metabolism to promote tuberculosis

city: Birmingham

first: Adrie

middle: JC

last: Steyn

state: AL

address: 845 19th Street South

institute: UAB

summary: The ubiquitous gasotransmitter hydrogen sulfide (H2S) has been recognised to play a crucial role in human health.  However, a role for host H2S in  pathogenesis has not yet been demonstrated.  Using cystathionine -lyase (CSE) deficient mice, we demonstrated an unexpected role of H2S in Mtb pathogenesis.  We showed that Mtb-infected CSE-/- mice survive longer than wild-type mice, and support reduced pathology and lower bacterial burdens in the lung, spleen and liver.  Similarly, in vitro Mtb infection of macrophages resulted in reduced colony forming units (CFUs) in CSE-/-cells.  Chemical complementation of infected wild-type and CSE-/-macrophages using the slow H2S releaser GYY3147 and the CSE inhibitor DL-propargylglycine demonstrated that H2S is the effector molecule regulating Mtb survival in macrophages.  Furthermore, we demonstrate that CSE promotes an excessive innate immune response, suppresses the adaptive immune response and reduces circulating IL1β, IL-6, TNFα, and IFN-γ levels in response to Mtb infection.  Notably, Mtb infected CSE-/- macrophages show increased flux through glycolysis and the pentose phosphate pathway thereby establishing a critical link between H2S and central metabolism.  Our data suggest that excessive H2S produced by the infected wild type mice reduce HIF-1α levels, thereby suppressing glycolysis and production of IL-1β, IL-6 and IL-12, and increasing bacterial burden.  Clinical relevance was demonstrated by the spatial distribution of H2S producing enzymes in human necrotic, non-necrotic and cavitary pulmonary TB lesions.  In summary, CSE exacerbates TB pathogenesis by altering immunometabolism in mice and inhibiting CSE or modulating glycolysis are potential targets for host-directed TB control.

overall_design: Total RNA extracted from thioglycollate elicited mice peritoneal macrophages with and without Mtb H37Rv infection. Samples were from two different mouse, CSE wild-type and knock-out. Each samples are in three biological replicates.

first: Md

last: Rahman

first: Bridgette

last: Cumming

first: Kelvin

last: Addicot

first: Hayden

last: Pacl

first: Shannon

last: Russell

first: Kievershen

last: Nargan

first: Threnesan

last: Naidoo

first: Pratistadevi

middle: K

last: Ramdial

first: John

last: Adamson

first: Rui

last: Wang


title: Dnmt3a associates with promoters and enhancers to protect epidermal stem cells from cancer [RNA-seq]

city: Barcelona

first: Lorenzo

last: Rinaldi

state: Spain

address: Carrer Reixac Baldiri 10

department: Oncology

country: Spain

institute: IRB

summary: The de novo DNA methyltransferase Dnmt3a is mutated in human acute myeloid leukemia, and suppresses tumorigenesis in murine models of leukemia and lung cancer. Conversely, deregulation of the other de novo DNA methyltransferase, Dnmt3b, predominantly promotes tumorigenesis. However, the molecular mechanisms underlying the roles of Dnmt3a and Dnmt3b in cancer remain poorly understood. Using conditional knockout mice, here we show that Dnmt3a -- but not Dnmt3b -- strongly protects epidermal stem cells from carcinogen-induced tumor initiation, without affecting the progression of benign lesions to aggressive carcinomas. Only upon combined deletion of Dnmt3a and Dnmt3b, squamous cell carcinomas acquired a more aggressive fate and even became metastatic, indicating that Dnmt3b is tumor-suppressive, rather than pro-tumorigenic, in epidermal neoplasia. Mechanistically, Dnmt3a promotes the expression of epidermal differentiation genes by interacting with their enhancers, and inhibits the expression of lipid metabolism and cell proliferation genes by directly methylating their promoters. Altogether, we demonstrate that Dnmt3a, but not Dnmt3b, is critical for suppressing epidermal tumor initiation, while both enzymes prevent tumor progression.

overall_design: In this experiment, we wanted to study the difference in the genome-wide transcriptome between FACS-sorted tumoral cells derived from skin tumors originated in wild type and Dnmt3a-deficient background.

first: Alexandra

last: Avgustinova

first: Debayan

last: Datta

first: Guiomar

last: Solanas

first: Neus

last: Prats

first: Salvador

last: Aznar Benitah


title: MeDIP-chip for porcine intestinal epithelial cells with ETEC F4ab/ac infection

city: Tai'an

first: Wenwen

address: NO. 61 Daizong street

institute: Shandong Agricultural University

summary:
To better understand the molecular effects of Enterotoxigenic Escherichia coli (ETEC) F4ab/ac infection,  we performed a genome-wide comparison of the changes in DNA methylation in ETEC F4ab/ac infected porcine intestinal epithelial cells.
Our data provides further insight into the epigenetic alterations of ETEC F4ab/ac infected porcine intestinal epithelial cells and may advance the identification of biomarkers and drug targets for predicting susceptibility to and controlling ETEC F4ab/ac induced diarrhea.

overall_design: comparison of ETEC F4ab/ac infected and control IPEC-J2 cells

first: Qin

last: Zhang


title: An MXD1-derived repressor peptide identifies non-coding mediators of MYC-driven cell proliferation

first: Jonathan

middle: Ross

last: Hart

address: 10550 North Torrey Pines Road, BCC239

department: Molecular and Experimental Medicine

institute: The Scripps Research Institute

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

overall_design: Refer to individual Series


title: An MXD1-derived repressor peptide identifies non-coding mediators of MYC-driven cell proliferation [Amplicon-seq]

summary: MYC controls the transcription of large numbers of long non-coding RNAs. Since MYC is a ubiquitous oncoprotein, some of these long non-coding RNAs (lncRNAs) probably play a significant role in cancer. We applied CRISPRi to the identification of MYC-regulated lncRNAs that are required for MYC-driven cell proliferation in the P493-6 and RAMOS human lymphoid cell lines. We identified 320 non-coding loci that play a positive role in cell growth. Transcriptional repression of any one of these lncRNAs reduces the proliferative capacity of the cells. Selected hits were validated by RTqPCR and in CRISPRi-competition assays with individual GFP-expressing sgRNA-constructs. We also showed binding of MYC to the promoter of two candidate genes by chromatin immunoprecipitation. In the course of our studies, we discovered that the repressor domain SID derived from the MXD1 protein is highly effective in P493-6 and RAMOS cells in terms of the number of guides depleted in library screening and the extent of the induced transcriptional repression. In the cell lines used, it is superior to the KRAB repressor domain which serves routinely as transcriptional repressor domain in CRISPRi. The SID transcriptional repressor domain is effective as a fusion to the MS2 aptamer binding protein MCP allowing the construction of a doxycycline regulatable CRISPRi-system that allows controlled repression of targeted genes and will facilitate the functional analysis of growth-promoting lncRNAs.

overall_design: CRISPRi dCas9-KRAB, dCas9-SID, and dCas9-KRAB/MCP-SID experiments with an sgRNA library targeted to MYC driven ncRNAs

middle: R

first: Philipp

last: Raffeiner

first: Peter

last: Vogt


title: Whole transcriptome profiling of ESR1 Q375H and R394H mutatons from the human breast cancer MB-231 stable cells

city: RTP

first: NIEHS

last: Microarray Core

state: NC

address: 111 T.W. Alexander Drive

department: DIR

institute: NIEHS

summary:
Estrogeh insensitivity syndrome (EIS) arises from rare mutations in estrogen receptor α (ERα, encoded by ESR1 gene) resulting in the inability of estrogen to exert its biological effects. Due to the rarity, mutations in ESR1 gene and the underlying molecular mechanisms of EIS have not been thoroughly studied.
We used whole transcriptome analysis to comparison of the transcriptome between the WT ESR1 and Q375H and R394H clinical mutants in MB231 stable cell lines.

overall_design: MB231 cells stably exressing the WT, Q and R mutation were tretaed with veh, E2 or DES for 18 hours.

first: Yin

last: Li

first: Kevin

last: Gerrish

first: Tianyuan


title: An MXD1-derived repressor peptide identifies non-coding mediators of MYC-driven cell proliferation [RNA-seq]

overall_design: RNA-seq of Ramos cells


title: RNA seq of femur and humerus bone tissues from Prx1cre driven Piezo1/2 mutant pups at the age of P0

city: Boston

first: Taifeng

last: Zhou

state: Massachusetts

address: 188 Longwood Avenue, REB514B

department: Developmental biology

institute: Harvard University

summary: The Prx1cre driven Piezo1/2 knockout mice showed bone fractures caused by reduced bone formation. In order to understand the underlying mechanism, we performed RNA seq experiments using total RNA from the bone tissue of control and Piezo1/2 mutant P0 pups.

overall_design: Total RNA from P0 femur and humerus bone tissue devoid of bone marrow were prepared using Rneasy Mini Kit. Three different genotypes of mice were examined: Wild type, Piezo1 CKO and Piezo1/2 DKO. 2 replicates for each group.

first: Yingzi

last: Yang

first: Yuchen

last: Liu


title: Identification of deregulated pathways, key regulators, and novel miRNA-mRNA interactions in HPV-mediated transformation. [mRNA cell lines-Agilent]

first: Renske

middle: DM

last: Steenbergen

address: De Boelelaan 1117

department: Pathology

institute: Amsterdam UMC, location VUmc

summary: Next to a persistent infection with high-risk human papillomavirus (HPV), molecular changes are required for the development of cervical cancer. To identify which molecular alterations drive carcinogenesis, we performed a comprehensive and longitudinal molecular characterization of HPV-transformed keratinocyte cell lines. Comparative genomic hybridization, mRNA, and miRNA expression analysis of four HPV-containing keratinocyte cell lines at eight different time points was performed. Data was analyzed using unsupervised hierarchical clustering, integrated longitudinal expression analysis, and pathway enrichment analysis. Biological relevance of identified key regulatory genes was evaluated in vitro and dual-luciferase assays were used to confirm predicted miRNA-mRNA interactions. We show that the acquisition of anchorage independence of HPV-containing keratinocyte cell lines is particularly associated with copy number alterations. Approximately one third of differentially expressed mRNAs and miRNAs was directly attributable to copy number alterations. Focal adhesion, TGF-beta signaling, and mTOR signaling pathways were enriched among these genes. PITX2 was identified as key regulator of TGF-beta signaling and inhibited cell growth in vitro, most likely by inducing cell cycle arrest and apoptosis. Predicted miRNA-mRNA interactions miR-221-3p_BRWD3, miR-221-3p_FOS, and miR-138-5p_PLXNB2 were confirmed in vitro. Integrated longitudinal analysis of our HPV-induced carcinogenesis model pinpointed relevant interconnected molecular changes and crucial signaling pathways in HPV-mediated transformation.

overall_design: Expression profiles of 8 sequential passages of 4 HPV-transformed human foreskin primary keratinocyte cell lines either treated with or without demethylation agent DAC were analyzed using whole human genome oligo microarrays (G4112A, mRNA 4x44K; Agilent).

first: Iris

last: Babion

first: Viktorian

last: Miok

first: Annelieke

last: Jaspers

first: Angelina

last: Huseinovic

middle: D

first: Wessel

last: vanWieringen

first: Saskia

middle: M

last: Wilting


title: Identification of deregulated pathways, key regulators, and novel miRNA-mRNA interactions in HPV-mediated transformation. [mRNA tissues-Agilent]

overall_design: Expression profiles were analyzed in healthy cervical tissues (n=10), high-grade precancerous lesios (CIN2/3, n=15) and cervical squamous cell carcinomas (n=10) using whole human genome oligo microarrays (G4112A, mRNA 4x44K; Agilent Technologies).


title: Identification of deregulated pathways, key regulators, and novel miRNA-mRNA interactions in HPV-mediated transformation. [CGH cell lines-Agilent]

type: Genome variation profiling by genome tiling array

overall_design: Chromosomal profiles of 8 sequential passages of 4 HPV-transformed human foreskin primary keratinocyte cell lines were analyzed using comparative genomic hybridization (CGH) microarrays (SurePrint G3 human CGH microarray 4x180K; Agilent).


title: Chronic rare DUX4 expression in mouse drives transcriptional similarities to human FSHD in whole muscle and fibroadiopgenic progenitors

city: Minneapolis

first: Michael

last: Kyba

state: MN

address: 2231 6th St SE

institute: University of Minnesota

summary: RNA-seq data was obtained on various samples from the iDUX4pA mouse model for FSHD and from control WT littermates.

overall_design: RNA-seq was performed on whole muscle, as well as sorted endothelial cells and fibroadipogenic progenitors at early and late time points in the course of the disease.

first: Darko

last: Bosnakovski

first: Ce

last: Yuan


title: Comprehensive analyses of function and molecular interaction of differential expressed non-coding RNAs and mRNA in Hantaan virus infection

city: Wuhan

first: LI

last: LI

state: Hubei

address: 185 Donghu Road

institute: wuhan university school of basic medical sciences

summary: Hantaan virus (HTNV), the prevalent prototype of the hantavirus in Asia, causes hemorrhagic fever with renal syndrome (HFRS) with high mortality in human being. However, the pathogenesis of HTNV infection remains elusive. Accumulating evidences indicate that non-coding RNAs (ncRNAs), including long non-coding RNA (lncRNA), circular RNA (circRNA) and microRNA (miRNA) play crucial roles in the progression of virus infection. Here, we identified differential lncRNA/miRNA/circRNA and mRNA expression profiles of HTNV-infected  human umbilical vein endothelial cells (HUVECs) compared with mock-infected HUVECs by whole transcriptome sequencing. Subsequently, comprehensive bioinformatics analyses established miRNA-mRNA co-expression, protein-protein interaction and competing endogenous RNA (ceRNA) networks in miRNA-lncRNA-circRNA-mRNA regulatory axis. The trans or cis regulatory roles of identified RNAs on HTNV infection were ascertained by RNA interference and key ceRNA relationships were verified by dual-luciferase reporter experiments. Moreover, gene ontology (GO) enrichment analysis showed that dysregulated RNAs were mostly related to antiviral innate immune response. In conclusion, our findings firstly revealed that circRNAs and ceRNA network were involved in regulating HTNV infection, and also confirmed several key lncRNAs and miRNAs which had vital effects on HTNV infection. The identification and characterization of RNAs provide the new insights on ceRNA networks in HTNV-host interactions, which lays the foundation for future research of the potential roles of ncRNAs in the pathogenesis of HFRS.

overall_design: Mock-infected and Hantaan virus-infected HUVECs were generated by deep sequencing, in triplicate respectively

first: Shuang

last: Lu

first: Fan

last: Luo

first: Wei

last: Hou


title: Identification of deregulated pathways, key regulators, and novel miRNA-mRNA interactions in HPV-mediated transformation.


title: Investigating stromal reprogramming in canine mammary adenoma using next-generation RNA sequencing of FFPE subsections

city: Zurich

first: Enni

last: Markkanen

address: Winterthurerstr. 260

department: Institute of Veterinary Pharmacology and Toxicology

institute: University of Zurich

summary: Cancer-associated stroma (CAS) and matched normal stroma (NS) samples from 13 cases of canine mammary adenoma

overall_design: Spontaneous tumours from patients, formalin-fixed and paraffin embedded. Isolation of stromal areas of interest by LCM, followed by RNA isolation and sequencing.

first: Parisa

last: Amini

first: Sina

last: Nassiri

first: Julia

last: Ettlin

first: Alexandra

last: Malbon


first: Jin

last: Liu


title: Alteration of CTCF associated chromatin neighborhood inhibits TAL1-driven oncogenic transcription program and leukemogenesis

city: Hangzhou

first: Huacheng

state: Zhejiang

address: No. 150, Fucheng Road, Qiantang District

institute: Hangzhou Institute of Medicine (HIM), The Chinese Academy of Sciences

summary: Aberrant activation of the TAL1 oncogene is associated with up to 60% of T-ALL patients and is involved in CTCF mediated genome organization within the TAL1 locus, suggesting the importance of the CTCF boundary in the molecular pathogenesis of T-ALL. Here, we show that deletion of CTCF binding site (CBS) or alternation of CTCF boundary orientation alters expression of the TAL1 oncogene in a cell context dependent manner. Deletion of the CTCF binding site located at -31 Kb upstream of TAL1 (-31CBS) reduces chromatin accessibility in the +51 enhancer and the TAL1 promoter I, and blocks long-range interaction between the +51 erythroid enhancer and TAL1 promoter 1b that inhibits expression of TAL1 in erythroid cells, but not in T-ALL cells. However, in the TAL1 expressed T-ALL primary patient samples or cell line, the T-ALL prone TAL1 promoter IV specifically interacts with the +19 stem cell enhancer that is located 19 kb downstream of the TAL1 promoter and required for TAL1 transcription in the hematopoietic stem cell (HSC) stage. Inversion of -31CBS orientation, but not deletion of -31CBS, alters chromatin accessibility, enhancer/promoter histone modifications, CTCF-mediated topological associated domain (TAD), and enhancer/promoter interaction in the TAL1 locus leading to inhibition of TAL1 oncogene expression and TAL1-driven T cell leukemogenesis. Thus, our data reveal that the TAL1 +19 stem cell enhancer acts not only as stem cell enhancer, but also as a leukemia specific enhancer to activate the TAL1 oncogene in T-ALL. Manipulation of CTCF defined chromatin boundary can alter TAL1 TAD and oncogenic transcription networks in leukemogenesis.

overall_design: We have finished the RNA-SEQ, ATAC-seq, ChIP-seq and HiC-seq to investigate the role of TAL1 transcription  and CTCF boundaries in leukemogenesis. Jurkat leukemia cells and K562 cells were used to perform the RNA-seq, ATAC-seq, 4Cseq, CHIP-seq and HiC-seq analysis.

first: Suming

last: Huang


title: Tumor endothelial up-regulation of IDO1 limits the response to CD40-stimulating immunotherapy

city: Bonn

first: Joachim

last: Schultze

state: NRW

address: Carl-Troll-Strasse 31

department: Genomics and Immunoregulation

institute: LIMES (Life and Medical Sciences Center Genomics and Immunoregulation)

summary: CD40-stimulating immunotherapy elicits potent anti-tumor responses, which are mainly T-cell dependent. Here, we have investigated how tumor endothelial cells respond to CD40-stimulating immunotherapy by isolating endothelial cells from B16.F10 melanoma in anti-CD40 treated or isotype treated mice followed by RNA-sequencing. Gene set enrichment analysis revealed an increase in interferon- related responses in tumor endothelial cells following anti-CD40 therapy. The immunosuppressive enzyme indoleamine 2, 3-dioxygenase 1 (IDO1) was preferentially expressed in endothelial cells, and it was up-regulated upon anti-CD40 treatment. IDO1 expression in tumor endothelium was positively correlated to T-cell infiltration and to increased expression of IFNγ in the tumor microenvironment. In vitro, endothelial cells up-regulated IDO1 in response to T-cell-derived IFNγ, but not in response to CD40-stimulation. Combining agonistic anti-CD40 therapy with the IDO1 inhibitor epacadostat delayed tumor growth and increased survival in B16.F10 tumor-bearing mice, which was associated with increased activation of tumor-infiltrating T-cells. Hereby, we have uncovered an immunosuppressive feedback mechanism, in which tumor vessels limit the efficacy of cancer immunotherapy by up-regulating IDO1 in response to T-cell activation.

overall_design: Analysis of changes in the expression of tumor endothelial cell-specific mRNAs in response to CD40-stimulating immunotherapy.

first: M

last: Georganaki

last: Ramachandran

first: S

last: Tuit

first: N

last: Nunez

first: A

last: Karampatzakis

first: G

last: Fotaki

first: L

last: van Hooren

first: H

first: R

last: Lugano

first: T

last: Ulas

last: Kaunisto

first: E

last: Holland

first: P

last: Ellmark

last: Mangsbo

first: J

last: Essand

last: Tugues

last: Dimberg


title: The profiles of circRNAs, lncRNAs and mRNAs in drug-resistant non-small-cell lung cancer cell lines by RNA sequencing

city: Zhengzhou

first: Xiangzhen

last: Kong

address: No.1 Jianshe road

institute: The First Affiliated Hospital of Zhengzhou University

summary: We detected the expression profiles ofcircRNAs, lncRNAs and mRNAs in two drug-resistant NSCLC cell lines (A549/R and HCC827/R) and their parent cell lines (A549 and HCC827) by RNA sequencing, employed a comprehensive analysis of the dysregulated lncRNAs, miRNAs and mRNAs by bioinformatics methods.

overall_design: The  profiles of circRNAs,lncRNAs and mRNAs in two drug-resistant NSCLC cell lines (A549/R and HCC827/R) and their parent cell lines (A549 and HCC827) were detected by RNA sequencing

first: Shousen

last: Hu


title: Comprehensive analyses of function and molecular interaction of differentially expressed non-coding RNAs and mRNA in Hantaan virus infection

first: LI

last: LI

first: Shuang

last: Lu

first: Fan

last: Luo

first: Wei

last: Hou


title: Different expression of miRNA between the exosomes secreted by monocyte and M2 macrophage

city: Shanghai

first: xiaoduan

last: li

address: Changle road no. 536

institute: Department of Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai , China.

summary: The macrophages in tomor microenvironment in were alike M2 macrophages which contribute to tumor progression and migration. Since macrophages can secret lots of exosomes and M2 macrophage can induce the imbalance of Treg/Th17 ratio in EOC tumor environment, we want to investage the different expression of miRNA between the exosomes secreted by monocyte and M2 macrophage. Thus to see if the microRNA in exosomes secreted from M2 macrophage paly a big role in the T cell imbalance.

overall_design:
Thp-1 cell was induced into M2 macrophage, and exosomes was collected. The Exosome from untreated Thp-1 cells were used as control.
The M2 macrophages were induced by PMA (50 ng/ml) and IL-4 (20 ng/ml) for 24h. Then the culture medium was change into RPMI1640 and culture for 24h. In order to isolate exosomes, we centrifuge the supernatants for two times (1000g × 10min, 3000g × 30min to deplete the cell or fragments), and then add the total exosome isolation kit (Life technology) over night, and then centrifuge for 10000g×1h. Total RNA was extracted by mirVanaTM RNA Isolation Kit (Applied Biosystem p/n AM1556)

first: Xiaoli

last: Wu

first: Xipeng

last: Wang


title: Identification of molecular markers for candidate sleep-promoting neurons in CeA using TRAP-seq

city: Berkeley

first: Chenyan

last: Ma

address: 230E Li Ka Shing Center

institute: UC Berkeley

summary: A crucial step in understanding the sleep-control mechanism is to identify sleep neurons. In principle, a neuron could promote sleep by inhibiting wake-promoting neurons. Using rabies virus (RV)-mediated transsynaptic tracing, we identified several brain regions with GABAergic neurons that broadly inhibit multiple wake-promoting neuronal populations, and the most prominent source of GABAergic inputs was found in a posterior part of the CeA. The CeA is known to contain multiple subtypes of GABAergic neurons with distinct molecular markers, projection targets, and functional properties. Using translating ribosome affinity purification (TRAP) RNA-Seq, we identified molecular markers for the canditate sleep-promoting neurons in CeA.

overall_design: TRAP RNA-Seq profiling identifies transcripts enriched in CeA GABAergic neurons that project to wake-promoting brain regions (LC/PB).

first: Zeke

last: Barger

first: Yang

last: Dan


title: Vimentin knock out mouse neural stem cell RNA sequencing

status: Public on Apr 05 2020

city: Madison

first: Christopher

last: Morrow

state: Wisconsin

address: 1111 Highlange Ave.

institute: University of Wisconsin - Madison

summary: Total RNA sequencing data generated from untreated wild type (NT) and vimentin knock out (KO) mouse hippocampal neural stem cells (NSCs) cultured in vitro

overall_design: 3 wild type and 3 vimentin KO mouse NSC cultures were sent for RNA sequencing

first: Darcie

last: Moore


title: The position and complex genomic architecture of plant T-DNA insertions revealed by 4C

city: Ramat-Gan

first: Ofir

last: Hakim

address: Max and Anna Webb

country: Israel

institute: Bar-Ilan University

summary: The integration of T-DNA to plant genomes is widely used for basic research and agriculture. High heterogeneity in the number of integration events per genome, their configuration and impact on genome integrity highlight both, the critical need and great challenge to detect the genomic locations of T-DNA insertions and their associated chromosomal rearrangements. Here we present ‘4SEE’, a circular chromosome conformation capture (4C) based method for robust, rapid and cost-efficient detection of the entire scope T-DNA locations. Moreover, by measuring the chromosomal architecture at plant genome flanking the T-DNA insertions, 4SEE outlines their associated complex chromosomal aberrations. Applying 4SEE to a collection of confirmed T-DNA lines revealed previously unmapped T-DNA insertions and chromosomal rearrangements such as inversions and translocations. Uncovering such events in feasible, robust and cost-effective manners by 4SEE in any plant of interest have implications for accurate annotation and phenotypic characterization of T-DNA insertion mutants and transgene expression in basic science applications as well as for plant biotechnology.

overall_design: 4C-seq was performed on WT, SALK_011436, SALK_009469, SALK_041474, SALK_064627, SALK_005512 from the SALK stock, and CS68932 from the Arabidopsis Biological Resource Center (ABRC) were used in this study.  There are 118 samples, as follows: three endogenous genes (two replicas each), four SALK lines in a gradient of template amounts: six samples of SALK_063720 and SALK_064627, five samples of SALK_011436 and seven samples of SALK_005512. The remaining SALK lines have 1 sample each. Seventy-two files are on the ADF viewpoint (CS68932), with a gradient of template amounts and reads. The remaining 14 samples are seven viewpoints measured in WT or CS68932 plant, which map the chromosomal rearrangements.

first: Ronen

last: Krispil

first: Miriam

last: Tannenbaum

first: Avital

last: Sarusi-Portuguez

first: Olga

last: Loza

last: Raskina


title: Gene expression analysis of Triple-negative breast tumors from young and aged mice

first: Gregory

middle: James

last: Goreczny

state: MA

address: 4 Blackfan Cir.

institute: Brigham & Women's Hospital

summary: Whole tissue RNA-seq analysis of mammary tumors from old (>12 months) and young (8-10 weeks) of mice after treatment with isotype, anti-CTLA4 or anti-PDL1 treatments.

overall_design: To test in murine mammary tumors from young and old mice for the  effects on gene expression of isotype (negative control), anti-CTLA4 and anti-PDL1 treatments. At least two seven replicates from each treatment were used in both pairwise and difference of differences fashions.

first: Jaclyn

last: Sceneay

first: John

last: Hutchinson

first: Sandra

last: McAllister


title: Tuberculosis-associated IFN-I induces Siglec-1 on microtubule-containing tunneling nanotubes and favors HIV-1 spread in macrophages

status: Public on Apr 04 2020

city: marseille

first: Thien-Phong

last: Vu Manh

address: 163 avenue de Luminy

institute: CIML

summary: To understand the susceptbility of human M(IL-10) macrophages to human immunodeficiency virus, we performed a genome-wide transcriptome analysis in these cells to identify a gene profile responsible for this phenomenon. A distinct 60 gene-transcript signature was defined in M(IL-10) macrophages, using a combination of the expression level, statistical filters and hierarchical clustering; 51 genes were up-regulated and 9 genes were down-regulated in M(IL-10) macrophages compared to control cells. Among the genes upregulated, we identified a interferon-stimulated gene (ISG) signature include SIGLEC-1. We confirmed SIGLEC-1 and other five ISG genes by qPCR, FACS and western blot.

overall_design: Human macrophages were diffentiated from freshly isolated monocytes treated with M-CSF and conditioned media. Conditioned media was generated from Mycobacterium tuberculosis-infected (coMtb) or non-infected (coCtrl) macrophages. Upon confirmation of the M(IL-10) macrophage phenotype induced by coMtb, and susceptbility to HIV-1 infectiion, the transcriptome analyses was performed in these conditioned cells from four independent donors.

first: Shanti

last: Souriant

first: Céline

last: Cougoule

first: Ingrid

last: Mercier

first: Maeva

last: Dupont

first: Christel

last: Vérollet

first: Geanncarlo

last: Lugo-Villarino


title: MiRNA degradation by NS3 of JEV

city: Hohhot

first: Yang

last: yang

state: Inner Mongolia Autonomous Region

address: No. 24 Zhaojun Road, Yuquan District

department: School of Life Sciences

country: China

institute: Inner Mongolia University

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

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

overall_design: Refer to individual Series


title: MiRNA degradation by NS3 of JEV [mRNA]

summary: In order to further determine the changes in gene expression levels of Japanese encephalitis virus (JEV) C57BL / 6 mice after infection, we used the Agilent single-channel expression profile chip as a platform to detect the total brain tissue of mice in the uninfected (control) and experimental groups Compared with the control group, it was found that the gene expression levels of several mice in the experimental group were lower than those in the control group. We selected ten or so genes with significant changes for verification, and the results were consistent.

overall_design: Four week old healthy C57BL / 6 mice were selected. One group was injected with JEV virus as the experimental group. A group of injection medium was used as a control group. After the experimental group showed the corresponding symptoms, the two groups of mice were sacrificed immediately, the brain tissue was separated from the liquid nitrogen and sent to the company for detection of gene expression levels.

last: Yang