title: Alteration of the transcriptional program in dendritic cells by GOLPH2

city: shanghai

first: wei

last: zhang

address: 800 Dongchuan Road. Minhang

institute: shanghai jiaotong university

summary: To explore the immune functions of GOLPH2 in dendritic cells in a comprehensive way, we performed global gene expression analysis by RNA-Seq on Illumina HiSeq 2000 in activated BMDCs from WT and GOLPH2 KO mice.

overall_design: mRNA profiles of BMDCs from WT and GOLPH2 KO mice with or without IFN-gamma and LPS stimulation

first: Wei

last: Zhang

first: Xiaojing

last: Ma


title: Gene expression patterns in caecal lamina propria mononuclear cells and epithelial cells following preventive administration of T. suis ova in a rabbit model of DSS colitis

status: Public on Oct 31 2017

city: Zurich

first: Isabelle

last: Frey-Wagner

address: Raemistr. 100

department: Division of Gastroenterology

country: Switzerland

institute: University hospital Zurich

type: Expression profiling by high throughput sequencing

summary: We describe the transcriptional changes occurring in lamina propria mononuclear cells (LPMC) and intestinal epithelial cells (IEC) upon Trichuris suis ova (TSO) treatment in a rabbit model of DSS colitis

overall_design: NZW rabbits received 3x2500 TSO or vehicle at day 1, 14, 21, i.g. Colitis was induced at day 26 with 0.1% DSS for 5 days, control animal received water. Rabbits were sacrificed at day 35. Caecal lamina propria mononuclear cells (LPMC) and epithelial cells (EC) were isolated for RNA extraction and genome wide expression analysis by  RNAseq. N=3 per group

first: Irina

last: Leonardi


title: Effect of atrazine exposure on D. magna gene expression

status: Public on Oct 30 2017

city: Clemson

first: William

middle: S

last: Baldwin

state: South Carolina

address: 230 Parkway Dr

department: Biological Sciences

country: USA

institute: Clemson University

summary: We report exposure to 40 µM atrazine, a probable HR96 activator in D. magna, induced detoxification and sphingolipid metabolism genes, consistent with previous work on HR96 activation.

overall_design: 7-day old D. magna exposed to 40 µM atrazine for 96 hours. 5 samples consisted of 3 daphnids each.

first: Allison

last: Schmidt

first: Namrata

last: Sengupta

first: Rooksana

last: Noorai

first: Chris

last: Saski


title: Sarcoma RNAseq

city: Nashville

first: Yan

last: Guo

state: TN

address: 639 Preston Research Bld

institute: Vanderbilt Cancer Center

summary: Ewing sarcomas (ES) are aggressive bone and soft tissue cancers associated with aberrant activation of the EWS-FLI1 oncogene. Paradoxically, EWS-FLI1 does not induce ES in mice, thus the absence of a genetically defined model has hindered greater understanding of tumor pathogenesis. Here, we report PCG2, a novel mouse in which human GLI2A, an activator of Hedgehog (Hh) signaling, induces fast-growing, soft tissue tumors. Comprehensive analysis revealed remarkable similarity between PCG2 and ES at the pathology, immuno-phenotype, ultra-structure, and transcriptome levels. Moreover, we show that PCG2 tumors originate in bi-potent mesenchymal progenitors, providing insight into the elusive ES cellular origin. The striking PCG2 phenotype, which was strongly dependent on Gli1 dosage, suggests a greater role for oncogenic Hh signaling in ES etiology than previously recognized.

overall_design: Six samples in total are included. Three TA muscle RNAs were sequenced and used for comparison with RNA from three primary tumors.

first: Joathan

last: Fleming

first: Chin

last: Chiang


title: AML1-ETO-induced FOXO1 activates a self-renewal program in pre-leukemia stem cells

city: Birmingham

first: Salam

middle: Adli

last: Assi

address: IBR

department: Institute for Cancer and Genomic Sciences

country: United Kingdom

institute: University of Birmingham

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Blocking the self-renewal of pre-leukemia stem cells could prevent AML relapse. In this study we show that FOXO1 is an essential self-renewal factor in leukemic and pre-leukemic cells expressing the t(8;21)-associated oncogene AML1-ETO (AE). FOXO1 is consistently upregulated in t(8;21) AML and functions as a critical oncogenic mediator rather than a tumor suppressor. Expression of FOXO1 in human CD34+ cells promotes a pre-leukemic state, partially phenocopying the cellular and transcriptional effects of AE expression. The DNA binding ability of FOXO1 is essential for these features. AE and FOXO1 co-occupy the majority of their binding sites, whereby FOXO1 binds to multiple crucial self-renewal genes and is required for their activation. In concordance with this observation, loss of FOXO1 inhibits the long-term proliferation and clonogenicity of AE cells. Thus, increased FOXO1 represents a new mechanism for acquiring aberrant self-renewal by pre-leukemia stem cells and provides a novel target for therapeutic intervention.

overall_design: AE and FOXO1 ChIP-seq expreiment have been used to study their activates in pre-leukemia stem cells

first: Shan

last: Lin

first: Anetta

last: Ptasinska

first: Xiaoting

last: Chen

first: Mahesh

last: Shretha

middle: A

first: Paulynn

last: Chin

first: Maria

middle: R

last: Imperato

first: Bruce

last: Aronow

first: Jingsong

first: Matthew

middle: T

last: Weirauch

first: Constanze

last: Bonifer

first: James

middle: C

last: Mulloy


title: Single-nucleotide mapping of N1-methyladenosine reveals a tissue-specific role in translational repression

city: Rehovot

first: Schraga

last: Schwartz

state: Choose a State or Province

address: Herzl 234, Department of Molecular Genetics

country: Israel

institute: WEIZMANN INSTITUTE OF SCIENCE

summary: Following synthesis, RNA can be modified with over 100 chemically distinct modifications, and in recent years it was shown that processing, localization, stability and translation of mRNAs can be impacted by an increasing number of these modifications. An emerging modification, present across all three domains of life, is N1-methyladenosine (m1A). m1A is of particular interest, as its methyl group disrupts Watson-Crick base pairing and it thus harbors substantial regulatory potential. Recent studies have suggested this modification to be relatively common in mammalian mRNA, but lacked the resolution of identifying individual m1A containing bases, and did not identify specific sequence motifs required for their modification or the enzymatic machinery catalyzing them. This rendered it challenging to validate the putative substrates and to address their function and mechanisms of action. Here we develop a highly sensitive and specific approach allowing the semi-quantitative mapping of m1A at single nucleotide resolution and in a transcriptome-wide manner. We found m1A to be present in cytosolic and mitochondrial mRNAs. In the cytosol m1A is present in a low number of mRNAs, typically at very low stoichiometry, almost invariably in the loop of hairpin structures, where it is introduced by the TRMT6/TRMT61A complex. In contrast, we found a single site in the mitochondrial ND5 mRNA, catalyzed by TRMT10C, with tightly regulated methylation levels in human development, ranging from nearly 100% up to the 8-cell stage and down to ~20% at the late blastocyst stage. We find that methylation at this site is the hallmark of hyper-stable transcripts, which are maternally transmitted and persist until the onset of zygotic mitochondrial transcription. Finally, we found that polysomes are strongly depleted from methylated mRNAs and that reporters harboring m1A in regions encountered by ribosomes (5’ UTR and CDS), but not in 3’ UTRs, are translated at reduced rates. Our findings suggest that m1A on mRNA, likely due to its dramatic impact on base pairing, lead to repression of translation which is by and large avoided by cells, while revealing one case - in mitochondria - where tight spatiotemporal control over m1A levels was adopted by cells as a potential means of post-transcriptional regulation.

overall_design: M1A measurements in HEK293 cells based on (1) two distinct reverse transcriptase, (2) before and after immunoprecipitation using an anti-m1A antibody, (3) with and without a Dimroth rearrangement, and (4) with or without overexpression of TRMT6/TRMT61A.

first: Modi

last: Safra


title: RNA-seq transcriptome analysis OF formalin-fixed paraffin-embedded canine meningioma

city: Ithaca

first: Jennifer

middle: K

last: Grenier

state: NY

address: 526 Campus Rd

department: Biomedical Sciences

institute: Cornell University

summary: Meningiomas are the most commonly reported primary intracranial tumor in dogs and humans.  Canine meningiomas closely resemble human meningiomas in histological appearance as well as biological behavior.  Because of the similarities between canine and human meningiomas, dogs have been proposed as models and surrogates for studying and treating human cancers including meningioma.  However, little is known about specific pathways and individual genes that are involved in the development and progression of canine meningioma. In addition, there is a paucity of suitable fresh material available for studies of differential expression (DE) of genes in cases of veterinary neoplasia.  We report here the use of formalin-fixed paraffin embedded (FFPE) specimens as much as a decade old, to provide RNA suitable for transcriptome analysis using next-generation sequencing (NGS).  RNA was extracted from 13 canine meningiomas – 12 from (FFPE) and one flash-frozen. These represented 6 grade I and 7 grade II/III. RNA was also collected from flash-frozen meningeal tissue (arachnoid) from 3 control dogs.  RNA from FFPE was of sufficient quality to successfully identify 125 significantly DE genes, the majority of which were related to oncogenic processes.  12 genes (AQP1, BMPER, FBLN2, FRZB, MEDAG, MYC, PAMR1, PDGFRL, PDPN, PECAM1, PERP, ZC2HC1Cc) were validated using qPCR.  Among the DE genes were oncogenes, tumor suppressors, transcription factors, VEGF-related genes, and members of the WNT pathway.  Our work demonstrates that RNA of sufficient quality can be extracted from FFPE samples to provide biologically relevant transcriptome analyses using a NGS technique, such as RNA-seq.

overall_design: RNAseq was performed on 13 meningioma samples (FFPE) and 3 normal controls.

first: Andrew

last: Miller


title: Effects of Wnt3A on the transcriptome of CCD-18Co human colon fibroblasts

city: Madrid

first: Nuria

last: Niell

address: C/Arturo Duperier 4

country: Spain

institute: Instituto de Investigaciones Biomédicas Alberto Sols

summary:
Purpouse: To compare the transriptome of CCD-18Co human colon fibroblasts treated with vehicle or Wnt3A.
Methods: We treated triplicate plates of CCD-18Co cells with vehicle or Wnt3A during 24 h. Afterwards, we obtained total RNA and used it in RNA-seq experiments.
Results: Our analysis rendered a total of 1136 differentially expressed genes (FDR<0.05), of which 662 were up-regulated and 474 were downregulated in response to Wnt3A.
Conclusions: Wnt3A regulates a wide set of genes in CCD-18Co human colon fibroblasts

overall_design: Study of gene expression profile of CCD-18Co human colon fibroblasts in response to Wnt3A

first: José

middle: M

last: González Sancho

first: Núria

middle: N

last: Garolera


title: De Novo Transcriptome of tobacco seedlings and Identification of early response gene network under low potassium stress

city: Chengdu

first: li

middle: li

last: qin

state: sichuan province

address: wenjiang district huiming 211road

country: China

institute: Sichuan Agricultural University

summary: We used solexa sequencing technology to analysis transcriptome of tobacco seedings under low potassium stress for 6 h,12 h and 24h treatment. Further analysis suggested that 732 differentially expressed genes (DEGs) were up-regulated and 302 DEGs were down-regulated after potassium deficiency. Our results provided comprehensive analysis of gene regulatory network under low potassium stress of tobacco seedings.

overall_design: Examination of 2 different tobacco seedings samples (CK and LK)

first: liqin

last: li

first: liming

last: lu


title: GC-rich coding sequences reduce transposon-like sRNA-mediated transgene silencing in Arabidopsis and maize

city: St. Louis

first: Blake

middle: C.

last: Meyers

state: MO

address: 975 N Warson Road

institute: Donald Danforth Plant Science Center

type: Methylation profiling by high throughput sequencing

type: Non-coding RNA profiling by high throughput sequencing

summary: The molecular basis of transgene susceptibility to silencing is poorly characterized in plants, thus we evaluated several transgene design parameters as means to reduce heritable sRNA-mediated transgene silencing. Analyses of Arabidopsis plants with transgenes encoding a microalgal polyunsaturated fatty acid (PUFA) synthase revealed that small RNA (sRNA)-mediated silencing, combined with the use of repetitive regulatory elements, led to aggressive transposable element (TE)-like silencing of canola-biased PUFA transgenes. Diversifying regulatory sequences and using native microalgal coding sequences (CDSs) with higher GC content improved transgene expression and resulted in remarkable trans-generational stability via reduced accumulation of sRNAs and DNA methylation. Further experiments in maize with transgenes individually expressing three Bacillus thuringiensis (Bt) crystal proteins tested the impact of CDSs recoding using different codon bias tables. Transgenes with the higher GC content exhibited increased transcript and protein accumulation. These results demonstrate that the sequence composition of transgene CDSs can directly impact silencing providing design strategies for increasing transgene expression levels and reducing risks of heritable loss of transgene expression.

overall_design: For Arabidopsis data in this series, genome-wide small RNA, transcriptome, methylone profilings were done by Illumina TruSeq sample preparation or in-house protocol (methyl C-seq) followed by high-throughput sequencing with Illumina HiSeq 2000 platform. Data for maize small RNA studies are under a separate GEO series GSE103037.

first: Lyudmila

middle: V

last: Sidorenko

first: Tzuu-fen

last: Lee


title: Myostatin inhibition prevents skeletal muscle pathophysiology in Huntington’s disease mice.

status: Public on Oct 29 2017

city: Princeton

first: Jeff

last: Aaronson

state: New Jersey

address: 155 Village Boulevard, Suite 200

department: Discovery & Systems Biology

institute: CHDI

summary: Huntington’s disease (HD) is an inherited neurodegenerative disorder of which skeletal muscle atrophy is a common feature, and multiple lines of evidence support a muscle-based pathophysiology in HD mouse models. Inhibition of myostatin signaling increases muscle mass, and therapeutic approaches based on this are in clinical development. We have used a soluble ActRIIB decoy receptor (ACVR2B/Fc) to test the effects of myostatin/activin A inhibition in the R6/2 mouse model of HD.  Transcriptional profiling of muscle in treated and untreated wild-type and R6/2 mice was performed to analyze the effect of the ActRIIB decoy on genes and pathways involved in maintaining normal muscle physiology as well as those dysregulated due to the mutant HTT gene mutation.

overall_design: RNAseq was performed on tibialis muscle from wild-type, wildtype + decoy, R6/2 and R6/2 + decoy; N = 10 per group.  RNAseq was done on an Illumina Hi-seq 2000. Paired-end sequencing was obtained, 4-plexed across lanes for a minimum of 38 million 50mer paired reads per sample

first: Jim

last: Rosinski


title: Role of GDF10 for axonal sprouting and functional recovery after stroke

status: Public on Oct 28 2017

city: Los Angeles

first: Riki

last: Kawaguchi

state: CA

address: 760 Westwood Plaza, Room 37-420

department: Department of Neurology and Department of Psychiatry

institute: University of California Los Angeles

summary: GDF10 controls a unique transcriptome, which coordinately regulates several molecular signaling systems that provide insights into how this molecule induces a neuronal growth state and is distinct from other developmental and adult plasticity phenotypes.

overall_design:
4 conditions with three replicates:
P4: animal control
WT: adult animal control
PT: adult animal stroke
PT-GDF10: GDF10 siRNA adult animal stroke

first: Songlin

last: Li

first: Esther

last: Nie

first: Yuqin

last: Yin

first: Larry

middle: I

last: Benowits

first: Spencer

last: Thung

first: Harry

last: Vinters

first: Mary

middle: P

last: Stenzel-Poore

first: Giovanni

last: Coppola

first: Thomas

last: Carmichael


title: RNAseq of wild type and Toddler mutant zebrafish embryos

city: Salt Lake City

first: James

last: Gagnon

state: UT

address: 1390 Presidents Circle, Crocker Science Center Receiving, Crocker Science Center Receiving

institute: University of Utah

summary: Goal of this study is differential gene expression between wild type and Toddler mutant during early zebrafish embryogenesis

overall_design: Four timepoints - 4 hours post fertilization (hpf), 5 hpf, 6 hpf, and 7 hpf; one replicate of wild type at each time point, one replicate Toddler mutant at each time point

first: Andrea

last: Pauli

first: Alexander

middle: F

last: Schier


title: Identification of differentially expressed microRNAs in OLF

status: Public on Oct 27 2017

city: Tianjin

first: Kun

last: Zhang

address: Qixiangtai Road NO.22

department: Department of Histology and Embryology

institute: Tianjin medical university

summary: Ossification of the ligamentum flava (OLF) is a common spinal disorder among the elderly that causes myelopathy and radiculopathy. Although studies have identified several genes that correlated with OLF, the underlying regulation network is far from clear. To identify transcriptional regulators for OLF, we compared the microRNA expression of the ligamentum flava tissues from OLF patients and healthy volunteers through microRNA sequencing.

overall_design: The miRNA expression profile of four OLFs and 4 normal LF tissues were analyzed by Illumina NextSeq 500 sequcening.

first: Wei

last: Hong

first: Yuan

last: Xue

first: Yawei

last: Han

first: Liandong


title: Syndecan-1 controls lung tumorigenesis by regulating microRNAs packaged in exosomes [A549]

first: Tanyalak

last: Parimon

address: 127 San Vicente

department: Medicine

institute: Cedars-Sinai Medical Center

summary: We evaluated the effect of syndecan-1 in various cell-based and animal models of lung cancer and found that lung tumorigenesis was promoted when cells lose syndecan-1 expression. We also demonstrate that syndecan-1 (or lack thereof) alters the microRNA (miRNA) cargo carried within exosomes exported from lung cancer cells. Analysis of the changes in miRNA expression identifies a distinct shift toward augmented pro-cancerous signaling, which are consistent with the changes found in lung adenocarcinoma. In all, our work identifies syndecan-1 as an important factor on lung cancer cells that control its ability to shape the lung tumor microenvironment through alterations in miRNA packaging within exosomes.

overall_design: Examiniation of exosomal microRNA profile in 2 sets of human non-small cell lung cancer cell lines (A549 cell line); The first set is scramble (wild-type; A549.Scrb) cells and syndecan-1 knock-down (A549.1735) cells

first: Peter

last: Chen


title: Curcumin affects gene expression and reactive oxygen species via a PKA dependent mechanism in Dictyostelium discoideum

city: Houston

first: Gad

last: Shaulsky

state: TX

address: One Baylor Plaza

department: Molecular and Human Genetics

institute: Baylor College of Medicine

summary: Botanicals are widely used as dietary supplements and for the prevention and treatment of disease.  Despite a long history of use, there is generally little evidence supporting the efficacy and safety of these preparations.  Curcumin has been used to treat a myriad of human diseases and is widely advertised and marketed for its ability to improve health, but there is no clear understanding how curcumin interacts with cells and affects cell physiology.  D. discoideum is a simple eukaryotic lead system that allows both tractable genetic and biochemical studies.  The studies reported here show novel effects of curcumin on cell proliferation and physiology, and a pleiotropic effect on gene transcription.  Transcriptome analysis showed that the effect is two-phased with an early transient effect on the transcription of approximately 5% of the genome, and demonstrates that cells respond to curcumin through a variety of previously unknown molecular pathways.  This is followed by later unique transcriptional changes and a protein kinase A dependent decrease in catalase A and three superoxide dismutase enzymes.  Although this results in an increase in reactive oxygen species (ROS; superoxide and H2O2), the effects of curcumin on transcription do not appear to be the direct result of oxidation.  This study opens the door to future explorations of the effect of curcumin on cell physiology.

overall_design: Total 48 samples were used for this analysis. Transcriptomes of AX4 strain treated with curcumin at multiple concentrations (0, 2.5, 5.0, 7.5 and 10.0 µg/ml) for different durations (0, 4, 8 and 12 hour) were analyzed with 3 biological replicates.

first: Mariko

last: Katoh-Kurasawa

first: William

last: Swatson

first: Stephen

last: Alexander


title: Defining a microRNA-mRNA targetome for calcineurin inhibitor induced nephrotoxicity

city: Boston

first: Christopher

middle: J

last: Benway

state: MA

address: 300 Longwood Ave, Enders 510

department: Nephrology

institute: Children's Hospital

summary: MicroRNAs have been implicated in the molecular pathogenesis of calcineurin inhibitor nephrotoxicity. However, identification of bona fide physiologically relevent miRNA/mRNA targeting interactions remains a challenge. To define a comprehensive miRNA/mRNA targetome and determine the role of miRNAs in cyclsporine-induced nephrotoxicity, we performed PAR-CLIP (Photoactivatable-Ribonucleoside-Enhanced Crosslinking and Immunoprecipitation) against endogenous Argonaute 2 (AGO2) protein in human proximal tubule cells treated with cyclosporine A (CsA) or vehicle control. Statistically significant mRNA targets of miRNAs in the RNA Inducing Silencing Complex (RISC) complex were identified by PIPE-CLIP, a bioinformatic framework based on a zero-truncated negative binomial model. Further, we determined the total cellular differential expression of miRNAs and mRNAs by conventional deep sequencing methods. Our data indicate that CsA causes specific changes in miRNAs and mRNAs associated with the RISC complex.  A relatively small fraction of the miRNAs and mRNAs identified by total cell RNA-seq were also found in the RISC complex suggesting that changes in targeting by miRs are not necessarily reflected in changes observed in total cellular RNA. Pathway enrichment analysis after integrating miRNA-seq, mRNA-seq, and PAR-CLIP datasets identified canonical pathways specifically under regulation by miRNAs following CsA treatment. Our analysis indicates that miRNAs play an integral role in regulating widespread dysregulation of the proximal tubule cell gene program, contributing to alterations in cell-cell adhesion, integrin-cytoskeleton signaling, and calcium signaling. Analysis of high confidence 3'UTR targets revealed a specific role for miR-101-3p in regulating MAPK signaling which may contribute to the pathogenesis of cyclosporine-induced nephrotoxicity in a calcineurin-independent manner.

overall_design: AGO2-PAR-CLIP, mRNA-seq, and miRNA-seq of a human kidney proximal tubule cell line (HK-2) treated with cyclosporine A or vehicle control was performed and sequenced by Illumina HiSeq 2500. Two replicate AGO2-PAR-CLIP samples in each condition and four replicates in each condition for mRNA-seq and miRNA-seq were obtained.

first: John

last: Iacomini


title: DNase I hypersensitivity with capture in mES cells

city: Lincoln

first: Logan

middle: G

last: Engstrom

address: 27 Old Farm Rd

summary: This dataset introduces a new protocol called DNase-capture, a method that focuses DNase-seq analysis on selected genomic regions, resulting in a substantial increase in region-specific sequencing coverage. DNase-seq takes advantage of the preferential cutting of DNase I. DNase-capture enhances the resolution of DNase-seq by mixing a DNase-seq library with biotin-tagged bait RNA sequences that are complementary to regions of interest. In a hybridization reaction, target DNA is captured away from background DNA through streptavidin bead binding, and the captured target DNA is sequenced.

overall_design: This dataset includes DNase-capture hypersensitivity data from the mES cell type. It also includes a genomic baseline.

first: Daniel

last: Kang

first: Richard

last: Sherwood

first: Amira

last: Barkal

first: Tatsunori

last: Hashimoto

first: David

last: Gifford


title: Transcriptomic analysis of octanoic acid response in Drosophila sechellia using RNA-sequencing

city: Middletown

first: Joseph

last: Coolon

state: CT

address: 52 Lawn Avenue Biology Department

department: Biology

institute: Wesleyan University

summary: The dietary specialist fruit fly Drosophila sechellia has evolved to specialize on the toxic fruit of its host plant Morinda citrifolia. Toxicity of Morinda fruit is primarily due to high levels of octanoic acid (OA). Using RNA interference (RNAi), prior work found that knockdown of Osiris family genes Osiris 6 (Osi6), Osi7, and Osi8 led to increased susceptibility to OA in adult D. melanogaster flies, likely representing genes underlying a Quantitative Trait Locus (QTL) for OA resistance in D. sechellia. While genes in this major effect locus are beginning to be revealed, prior work has shown at least five regions of the genome contribute to OA resistance. Here, we identify new candidate OA resistance genes by performing differential gene expression analysis using RNA sequencing (RNA-seq) on control and OA-exposed D. sechellia flies. We found 104 significantly differentially expressed genes with annotated orthologs in D. melanogaster, including six Osiris gene family members, consistent with previous functional studies and gene expression analyses. Gene ontology (GO) term enrichment showed significant enrichment for cuticle development in upregulated genes and significant enrichment of immune and defense responses in downregulated genes suggesting important aspects of the physiology of D. sechellia that may play a role in OA resistance. In addition, we identified 5 candidate OA resistance genes that potentially underlie QTL peaks outside of the major effect region, representing promising new candidate genes for future functional studies.

overall_design: Differential gene expression analysis of Drosophila sechellia exposed to control food and food containing 0.7% octanoic acid using RNA-sequencing.

middle: D

last: Lanno


title: Hepatic Expression of Ectodysplasin (ED) A Increases in Obesity and Impairs Insulin Sensitivity in Skeletal Muscle

city: Tokyo

first: Motoharu

last: Awazawa

address: 1-21-1 Toyama, Shinjuku

country: Japan

institute: National Institute for Global Health and Medicine

summary: We screened intronic microRNAs dysregulated in liver of obese mouse models to identify previously uncharacterized coding host genes that may contribute to the pathogenesis of obesity-associated insulin resistance and type 2 diabetes mellitus. Our approach identified the expression of Ectodysplasin A (Eda), the causal gene of X-linked hypohidrotic ectodermal dysplasia (XLHED; MIM 305100) was strongly increased in liver of obese mouse models both in rodents and humans.Eda expression in murine liver is controlled via PPARγ activation, increases in circulation and promotes JNK activation and inhibitory serine phosphorylation of IRS1 in skeletal muscle. Consistently, bi-directional modulation of hepatic Eda expression in mouse models affects systemic glucose metabolism with alterations of muscle insulin signaling, revealing a novel role of EDA as an obesity-associated hepatokine, which impairs insulin sensitivity in skeletal muscle.

overall_design: Soleus muscle mRNA profiles of db/db mice at 3 weeks after injection of AAV encoding shRNA targeting mouse Eda or the control scrambled shRNA sequence at the titer of 2-3x10e10 particles/body.

first: Paula

last: Gabel

first: Eva

last: Tsaousidou

first: Hendrik

last: Nolte

first: Marcus

last: Krüger

first: Joel

last: Schmitz

first: P

last: Ackermann

first: Claus

last: Brandt

first: Jan-Wilhelm

last: Kornfeld

first: F

last: Wunderlich

first: Matthias

last: Blüher

first: Jen

last: Brüning


title: Global transcriptome analysis of Aedes aegypti mosquitoes in response to Zika virus infection

city: St Lucia

first: Kayvan

last: Etebari

state: QLD

address: Building No 8

department: School of Biological Sciences

country: Australia

institute: The University of Queensland

summary: Zika virus (ZIKV) of the Flaviviridae family is a recently emerged mosquito-borne virus that has been implicated in the surge of the number of microcephaly instances in south America. The virus is transmitted mainly by the mosquito Aedes aegypti that also vectors dengue virus. Considering rather recent rapid spread of the virus and its declaration as a global health emergency by the World Health Organization, little is known about the interactions of the virus with the mosquito vector. In this study, we investigated the transcriptome profiles of whole Ae. aegypti mosquitoes in response to ZIKV infection at 2, 7 and 14 days post-infection using deep sequencing. Results showed a large number of transcripts were altered at each time point following infection, but 18 transcripts were commonly changed at the three time points. The outcomes provide a basic understanding of Ae. aegypti responses to ZIKV and help determining host factors involved in replication or anti-viral response against the virus.

overall_design: Briefly, 4-6 day old female Ae. aegypti (Galveston strain) were orally infected with ZIKV (Mex 1-7 strain) at 2 x 105 focus forming units (FFU)/ml) in a sheep blood meal (Colorado Serum Company). Infected mosquitoes were collected at 2, 7 and 14 days post-infection (dpi) from which RNA was extracted using the mirVana RNA extraction kit (Life Technologies) applying the protocol for extraction of total RNA. Viral infection in mosquitoes was confirmed by Taqman qPCR on ABI StepOnePlus machine (Applied Biosystems). For all time points, three independent pools were used to create libraries for infected and uninfected samples. Uninfected mosquitoes were fed with ZIKV-free blood, collected at the same time points and processed as above.

first: Sassan

last: Asgari

first: Grant

middle: L

last: Hughes


title: H3.3K27M cooperates with p53 loss and Pdgfra gain in mouse embryonic neural progenitor cells to induce invasive high-grade gliomas [Mouse WES]

city: Montreal

first: Nada

last: Jabado

state: Québec

address: 1001 Décarie Boulevard

department: Department of Pediatrics

country: Canada

institute: McGill University

summary: Gain-of-function mutations in histone 3 (H3) variants are found in a large proportion ofpediatric high-grade gliomas (pHGG) and are often associated with p53 loss and PDGFRA amplification. However, a lack of faithful models has hampered investigation of disease mechanisms and preclinical development. Here, we describe a somatic mouse model of H3.3K27M-driven HGG, which faithfully recapitulates human H3.3K27M pHGG. H3.3K27M and p53 loss are sufficient for neoplastic transformation but only within a specific window of brain development. In this model, H3.3K27M primes the PDGFRA pathway during transformation, and accordingly gain of wild-type PDGFRA decreases latency and increases invasion. Finally, we reveal a previously underappreciated dynamic regulation of H3K27 trimethylation at specific loci. Overall, this experimental model provides key insights into oncohistone-driven pHGG pathogenesis and will enable investigations of future therapies.

overall_design: We performed whole-exome sequencing (WES) of 10 spatial biopsies of a K27M-AP tumor (H3.3K27M, Trp53-/- and Atrx shRNA). We employed in utero electroporation and a piggyBac transposon-based system to deliver mutant H3.3K27M, Atrx shRNA and Trp53 CRISPR/Cas9 into developing NPCs – and all their successive progeny – during embryonic neurogenesis in vivo.

first: Manav

last: Pathania

first: Nicolas

last: De Jay

first: Nicola

last: Maestro

first: Ashot

middle: S

last: Harutyunyan

first: Justyna

last: Nitarska

first: Pahlavan

last: Pirasteh

first: Stephen

last: Henderson

first: Leonie

last: Mikael

first: Angela

last: Richard-Londt

first: Ying

last: Zhang

first: Joana

last: Coasta

first: Steven

last: Hebert

first: Sima

last: Khazaei

first: Nisreen

last: Samir Ibrahim

first: Javier

last: Herrero

first: Antonella

last: Riccio

first: Steffen

last: Albrecht

first: Robin

last: Ketteler

first: Sebastian

last: Brandner

first: Claudia

last: Kleinman

first: Paolo

last: Salomoni


title: H3.3K27M cooperates with p53 loss and Pdgfra gain in mouse embryonic neural progenitor cells to induce invasive high-grade gliomas [Mouse ChIP-Seq]

first: Nada

last: Jabado

overall_design: We performed genome-wide H3K27me3 profiling by next-generation sequencing technology (ChIP-seq) of GFP+ cells sorted and expanded from embryonic cortices of electroporated mice at 72 hours (preneoplastic) and 5-9 months (tumor) post-IUE for a total of 9 samples. We employed in utero electroporation and a piggyBac transposon-based system to deliver mutant H3.3K27M, Pdgfra, Atrx shRNA and Trp53 CRISPR/Cas9 into developing NPCs - and all their successive progeny - during embryonic neurogenesis in vivo.  We produced 1 replicate per condition.  Preneoplastic conditions include baseline controls (EV ctl, EV ctl PDGFRA), controls with Trp53-/- and Atrx shRNA (EV-AP, EV-APP), controls overexpressing wild-type H3.3 with Trp53-/- and Atrx shRNA (WT-AP, WT-APP), K27M expressing cells with Trp53-/- and Atrx shRNA (K27M-AP, K27M-APP).  Tumor conditions include tumors with H3.3K27M and Trp53-/- (K27M-P T), tumors with H3.3K27M, Trp53-/- and Atrx shRNA (K27M-AP T), and tumors with H3.3K27M, Trp53-/-, Atrx shRNA and Pdgfra (K27M-APP T). For each sample, we also obtained genomic DNA for use an input for subsequent analyses.

first: Manav

last: Pathania

first: Nicolas

last: De Jay

first: Nicola

last: Maestro

first: Ashot

last: Harutyunyan

first: Justyna

last: Nitarska

middle: R


title: Transcriptomes of Nfi deficient and wildtype mouse neocortical tissue at E16

first: Jens

last: Bunt

address: QBI Building 79

department: Queensland Brain Institute

institute: University of Queensland

summary: Here, we generated transcriptomes of microdissected neocortex of Nfia knockout, Nfib knockout and wildtype littermate embryos at embryonic day 16.

overall_design: mRNA profiles of microdissected mouse neocortex

first: Jonathan

middle: W

last: Lim

first: Timothy

last: O'Connor

first: Linda

last: Richards

first: Janette

last: Edson

first: Zong

middle: H

last: Zhang

first: Qiong-Yi

last: Zhao


title: Sex-specific differences in the pulmonary transcriptome in neonatal hyperoxic lung injury

first: Krithika

last: Lingappan

address: 6621 Fannin

summary: Changes in the pulmonary transcriptome in male and female mice on PND7 and PND21 exposed to room air or hyperoxia

overall_design: Examination of the effect of hyperoxia on the lung transcriptome and sex-specific differences

first: Cristian

last: Coarfa


title: Isoform-specific localization of DNMT3A regulates DNA methylation fidelity at bivalent CpG islands [WGBS]

city: Utrecht

first: Tuncay

last: Baubec

address: Padualaan 8

department: Department of Biology

country: Netherlands

institute: Utrecht University

summary: DNA methylation is a prevalent epigenetic modification involved in transcriptional regulation and essential for mammalian development. While the genome-wide distribution of this mark has been studied to great detail, the mechanisms responsible for its correct deposition, as well as the cause for its aberrant localization in cancers, have not been fully elucidated. Here we have compared the activity of individual DNMT3A isoforms in mouse embryonic stem and neuronal progenitor cells and report that these isoforms differ in their genomic binding and DNA methylation activity at regulatory sites. We identify that the longer isoform DNMT3A1 preferentially localizes to the methylated shores of bivalent CpG island promoters in a tissue-specific manner. The isoform-specific targeting of DNMT3A1 coincides with elevated hydroxymethylcytosine (5-hmC) deposition, suggesting an involvement of this isoform in mediating turnover of DNA methylation at these sites. Through genetic deletion and rescue experiments, we demonstrate that this isoform-specific recruitment plays a role in maintenance of DNA methylation at CpG island shores, with implications on H3K27me3 deposition and regulation of developmental genes.

overall_design: Whole-genome bisulphite sequencing in Dnmt3a, Dnmt3b, Dnmt1-triple KO cell lines re-expressing DNMT3A1 (TKO-Dnmt3A1)

first: Massimiliano

last: Manzo


title: Antagonistic modulation of NPY/AgRP and POMC neurons in the arcuate nucleus by noradrenaline

status: Public on Oct 26 2017

city: Cologne

first: Ismene

last: Karakasilioti

state: NRW

address: Gleueler str. 50

country: Germany

institute: Max Planck Institute for Metabolism Research

summary: The arcuate nucleus of the hypothalamus (ARH) is one key structure controlling energy homeostasis. While it has been shown that the biogenic amines dopamine and serotonin modulate food intake controlling NPY/AgRP and/or POMC neurons in the ARH, the neural substrates that mediate the effect of noradrenaline (NA) on energy homeostasis remain elusive. By electrophysiological recordings and cell type-specific transcriptomics we show that the main neuronal populations in the ARH, NPY/AgRP and POMC neurons express a combination of excitatory and inhibitory adrenergic receptors (ARs). Surprisingly, NA had a clear differential effect on these neurons. Activation of NPY/AgRP neurons is mediated by _1A - and _- ARs, while POMC neurons are inhibited via _2A ARs. Collectively, our data indicate an orexigenic influence of NA on the ARH circuitry that controls energy balance

overall_design: We have isolated NPY- and POMC-expressing neuronal populations by means of FACS-sorting green fluorescent protein expressed under the Npy or Pomc gene promoter, from the hypothalami of 6-week-old mice. We have extracted total RNA and prepared libraries from these samples, sequenced and identified differentially expressed genes between the two neuronal populations, in order to identify in an unbiased way, which and how agrenergic receptor genes are differentially expressed under these conditions.

first: Lars

last: Paeger

first: Peter

last: Frommolt

last: Kloppenburg

middle: C

last: Brüning


title: H3.3K27M cooperates with p53 loss and Pdgfra gain in mouse embryonic neural progenitor cells to induce invasive high-grade gliomas [Mouse RNA-Seq]

first: Nada

last: Jabado

overall_design: We performed genome-wide transcriptional profiling by next-generation sequencing technology (RNAseq) of GFP+ cells sorted and expanded from embryonic cortices of electroporated mice at 72 hours (preneoplastic; n = 16) and 5-9 months (tumor; n = 5) post-IUE for a total of 21 samples. We employed in utero electroporation and a piggyBac transposon-based system to deliver mutant H3.3K27M, Pdgfra, Atrx shRNA and Trp53 CRISPR/Cas9 into developing NPCs - and all their successive progeny - during embryonic neurogenesis in vivo.  Except in the case of K27M-P T, we produced 2 replicates per condition.  Preneoplastic conditions include baseline controls (EV ctl, EV ctl PDGFRA), controls with Trp53-/- and Atrx shRNA (EV-AP, EV-APP), controls overexpressing wild-type H3.3 with Trp53-/- and Atrx shRNA (WT-AP, WT-APP), K27M expressing cells with Trp53-/- and Atrx shRNA (K27M-AP, K27M-APP).  Tumor conditions include tumors with H3.3K27M and Trp53-/- (K27M-P T, n = 1), tumors with H3.3K27M, Trp53-/- and Atrx shRNA (K27M-AP T), and tumors with H3.3K27M, Trp53-/-, Atrx shRNA and Pdgfra (K27M-APP T).

first: Manav

last: Pathania

first: Nicolas

last: De Jay

first: Nicola

last: Maestro

last: Harutyunyan

last: Nitarska

first: Pahlavan

last: Pirasteh

first: Stephen

last: Henderson

first: Leonie

last: Mikael

first: Angela

last: Richard-Londt

first: Ying

first: Joana

last: Coasta

first: Steven

last: Hebert

first: Sima

last: Khazaei

first: Nisreen

last: Samir Ibrahim

first: Javier

last: Herrero

first: Antonella

last: Riccio

first: Steffen

last: Albrecht

first: Robin

last: Ketteler

first: Sebastian

last: Brandner

first: Claudia

last: Kleinman

first: Paolo

last: Salomoni


title: Isoform-specific localization of DNMT3A regulates DNA methylation fidelity at bivalent CpG islands [RRBS]

first: Tuncay

last: Baubec

overall_design: Reduced-representation bisulphite sequencing in WT, Dnmt3a KO and Dnmt TKO cell lines.

first: Massimiliano

last: Manzo


title: H3.3K27M cooperates with p53 loss and Pdgfra gain in mouse embryonic neural progenitor cells to induce invasive high-grade gliomas [Human RNA-Seq]

first: Nada

last: Jabado

summary: Gain-of-function mutations in histone 3 (H3) variants are found in a large proportion of pediatric high-grade gliomas (pHGG) and are often associated with p53 loss and PDGFRA amplification. However, a lack of faithful models has hampered investigation of disease mechanisms and preclinical development. Here, we describe a somatic mouse model of H3.3K27M-driven HGG, which faithfully recapitulates human H3.3K27M pHGG. H3.3K27M and p53 loss are sufficient for neoplastic transformation but only within a specific window of brain development. In this model, H3.3K27M primes the PDGFRA pathway during transformation, and accordingly gain of wild-type PDGFRA decreases latency and increases invasion. Finally, we reveal a previously underappreciated dynamic regulation of H3K27 trimethylation at specific loci. Overall, this experimental model provides key insights into oncohistone-driven pHGG pathogenesis and will enable investigations of future therapies.

overall_design: We performed genome-wide transcriptome profiling (RNAseq) of 12 samples derived from human patients: matched normal brain controls (normal brain tissue from pediatric brain tumor patients; n = 3), pediatric high-grade gliomas (pHGG) that are wild-type for H3.3 and TP53 (n = 4), pHGG with H3.3K27M and loss-of-function TP53 mutations (n = 5).

first: Manav

last: Pathania

first: Nicolas

last: De Jay

first: Nicola

last: Maestro

first: Ashot

last: Harutyunyan

first: Justyna

last: Nitarska

first: Pahlavan

last: Pirasteh

first: Stephen

last: Zhang


title: Warm sensor protein TRPM2 is required for brain development via β-catenin in hyperthermia

city: Beijing

first: Jianwei

last: Jiao

state: Beijing

address: 1 Beichen West Road

department: State Key Laboratory of Reproductive Biology

institute: Institute of Zoology, Chinese Academy of Sciences

summary: Next-generation sequencing (NGS) has revolutionized systems-based analysis of gene expression. The goals of this study are to compare the different transcripts between TRPM2 knockdown and control in the neural progenitor cells when the maternal hyperthermia was induced.

overall_design: Methods: the in utero electroporation was employed to introduce the TRPM2 knockdown or control plasmids into the E13 embryonic cortex. and then the GFP+ neural progenitor cell isolated from E15 mice by using FACS. RNA utilized for global transcriptome analysis were extracted from these GFP+ neural stem cells and sequenced by Hiseq 2500. Significantly differentially expressed genes were identified when we compared Normalized Reads Count between groups with p < 0.05 and |Log2FoldChange| > 1.

first: Yanxin

last: Li


title: Identification of RNAs that co-purify with the Caulobacter sRNA, GsrN

city: East Lansing

first: Sean

last: Crosson

state: Michigan

address: 567 Wilson Rd

department: Dept. Microbiology and Molecular Genetics

institute: Michigan State University

summary:
Purpose: To identify RNAs that interact with GsrN, a small regulatory RNA from Caulobacter crescentus.
Methods: Pseudomonas phage 7 (PP7) viral coat protein fused to maltose binding protein (MBP) was immobilized on amylose resin. PP7 coat protein binds to PP7 RNA hairpins (PP7hp).  A strain expressing GsrN tagged with a genetically encoded PP7hp at base 37 (GsrN(37)-PP7hp) was captured on this column, washed, and eluted in biological triplicate (pos_rep). As a negative control, we incubated the PP7 coat protein column with independent duplicate lysates from a Caulobacter strain expressing PP7hp fused to a non-functional 3' isoform of GsrN (mock). We generated RNA-seq libraries for each of three independent GsrN(37)-PP7hp fractions, and the duplicate mock fractions.
Results: We quantified levels of RNAs in the GsrN(37)-PP7hp (pos) fractions with fractions from parallel PP7hp-3'GsrN(mock) pull-downs by RNA-seq. From these data, we identified a group of RNAs that were enriched in the GsrN(37)-PP7hp fraction.

overall_design:
For Rockhopper analysis:
RNA-seq reads of three replicate GsrN(37)-PP7hp (pos) purifications and duplicate (mock) PP7hp-GsrN purifications were quantified and analyzed with Rockhopper 2.0 (Tjaden, 2015). Reads were mapped to modified Caulobacter NA1000 genome files (FASTA, PTT, RNT) where the gsrN locus was replaced with the sequence of gsrN(37)-PP7hp. We pruned the data set to find genes that had a low FDR values (“qValue” < .05), were specifically enriched in the GsrN(37)-PP7 (“Expression GsrN(37)-PP7hp” > “Expression PP7hp”), and had a high level of reads mapped to the gene in the GsrN(37)::PP7 (“Expression GsrN(37)-PP7hp” >1000).

For sliding window analysis:
Read quantification across the three independent GsrN(37)-PP7hp fractions showed some differences. In sample 1 (pos_rep1) 2.69% reads mapped to gsrN(37)-PP7hp, while 15.78% and 14.04% mapped to GsrN in samples 2 (pos_rep2) and 3 (pos_rep3) respectively. We observed several genes that were strongly enriched in sample 1 but not in sample 2 and 3. Thus we employed a metric to balance the discrepancies between the three independent purifications. To minimize potential false positives, we calculated the average of all three samples and the average of samples 2 and 3. If the total average was 1.5 times greater than the sample 2 and 3 average, we assumed that the sample 1 artificially raised the average RPKM value and did not consider any data from any of the purifications in that specific window.

first: Matthew

middle: Z

last: Tien

first: Aretha

last: Fiebig


title: A p53 super-tumor suppressor reveals a tumor suppressive p53-Ptpn14-Yap axis in pancreatic cancer

city: Stanford

first: Stephano

last: Spano Mello

address: 269 Campus Drive

institute: Stanford University

summary: The p53 transcription factor is a critical barrier to pancreatic cancer progression. To unravel mechanisms of p53-mediated tumor suppression, we analyzed pancreatic cancer predisposition in mice expressing p53 transactivation domain (TAD) mutants. Surprisingly, we observed that p53 TAD2 mutant behaves as a “super-tumor suppressor”, with an enhanced capacity to suppress pancreatic cancer and to activate a subset of novel p53 target genes.  One such gene, Ptpn14, is a direct p53-inducible gene encoding a negative regulator of the Yap oncoprotein. To determine the effects of p53 deficiency on Yap target gene expression in pre-malignant mouse pancreatic intraepithelial neoplasia (PanIN) lesions, we sorted the CD133-positive ductal epithelial cells that make up the PanINs and used these cells for RNA-sequencing analysis. This analysis revealed that a Yap signature is induced upon p53 deficiency, suggesting that p53 loss promotes the induction of a Yap transcriptional program.

overall_design: RNA-seq was performed to determine the differentially expressed genes in wild-type and p53-/- PanIN cells, sorted from KrasG12D;Pdx1-Cre;p53+/+ and KrasG12D;Pdx1-Cre;p53-/- mice.

last: Mello

first: Laura

last: Attardi


title: Expression data from porcine endometrial epithelial cells induced by seminal exosomes

first: Rulan

last: Bai

address: 1-1-1 Yayoi, Bunkyouku

institute: The University of Tokyo

summary:
Purpose: Seminal fluid (SF) is considered as a regulator on environment establishing in female reproductive tract of various mammal species without mechanism elucidated completely. This study aimed to identified the function of exosome isolated from SF on porcine endometrium.

Methods: Total RNA profiles of porcine endometrial epithelial cells with seminal exosomes treatment (EXO.) or not (CTRL.) were generated by deep sequencing, in triplicate, using HiSeq 2500. Trimmed sequences were analyzed on the basis of the TopHat/Cufflinks pipeline based on the porcine genome and reference annotations obtained from Ensembl genome browser (https://www.ensembl.org).

Results: 10916 transcripts, from which 70 genes were up-regulated and 114 genes were down-regulated with q-values less than 0.05 in EECs with seminal exosome treatment compared to those without exosome treatment.

Conclusions: Through the gene ontology (GO) biological process and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis which revealed significantly enriched or decreased molecular functions, Our work demonstrated that exosomes derived from porcine seminal fluid  induced endometrial immune and inflammatory response via CCL20 and AMCFII regulation specifically, which may facilitate sperm cells survival and activation, and resulting in appropriate environment required for fertilization and even implantation.

first: Zeinab

last: Latifi

first: Kazuya

last: Kusama

first: Kazuhiko

last: Imakawa


title: Inhibition of 12/15-Lipoxygenase Protects Against β Cell Oxidative Stress and Glycemic  Deterioration in Mouse Models of Type 1 Diabetes

city: Indianapolis

first: Raghavendra

last: Mirmira

state: IN

address: 635 Barnhill Drive

department: Biochemistry

institute: Indiana University School of Medicine

summary: Islet β-cell dysfunction and aggressive macrophage activity are early features in the pathogenesis of type 1 diabetes (T1D). 12/15-lipoxygenase (12/15-LOX) is induced in β cells and macrophages during T1D and produces pro-inflammatory lipids and lipid peroxides that exacerbate β-cell dysfunction and macrophage activity. Inhibition of 12/15-LOX provides a potential therapeutic approach to prevent glycemic deterioration in T1D. Two inhibitors recently identified by our groups through screening efforts, ML127 and ML351, have been shown to selectively target 12/15-LOX with high potency. Only ML351 exhibited no apparent toxicity across a range of concentrations in mouse islets, and molecular modeling suggested reduced promiscuity of ML351 compared to ML127. In mouse islets, incubation with ML351 improved glucose-stimulated insulin secretion in the presence of pro-inflammatory cytokines and triggered gene expression pathways responsive to oxidative stress and cell death. Consistent with a role for 12/15-LOX in promoting oxidative stress, its chemical inhibition reduced production of reactive oxygen species in both mouse and human islets in vitro. In a streptozotocin-induced model of T1D in mice, ML351 prevented the development of diabetes, with coincident enhancement of nuclear Nrf2 in islet cells, reduced β-cell oxidative stress, and preservation of β-cell mass. In the non-obese diabetic mouse model of T1D, administration of ML351 during the prediabetic phase prevented dysglycemia, reduced β-cell oxidative stress, and increased the proportion of anti-inflammatory macrophages in the insulitis. Our data provide the first evidence to date that small molecules that target 12/15-LOX can prevent progression of β-cell dysfunction and glycemic deterioration in models of T1D.

overall_design: RNA-seq of Mouse islets treated with vehicle, Proinflammatory cytokine cocktail, and/or ML351 for 24 hours

first: Marimar

last: Hernandez-Perez

first: Gaurav

last: Chopra

first: Jonathan

last: Fine

first: Abass

last: Conteh

first: Ryan

middle: M

last: Anderson

first: Amelia

middle: K

last: Linnemann

first: Chanelle

last: Benjamin

first: Jennifer

middle: B

last: Nelson

first: Kara

last: Benninger

first: Jerry

last: Nadler

first: David

last: Maloney

first: Sarah

middle: A

last: Tersey


title: RNA-Seq gene expression analysis of ΔgsrN, gsrN-OE, and wild-type Caulobacter crescentus

first: Sean

last: Crosson

summary:
Purpose: Define steady state levels of transcripts in different gsrN mutants
Methods: Sequenced total RNA purified from from cell extracts of gsrN mutants
Results: We report differences in transcript levels between wild type, ΔgsrN, and gsrN-overexpression(OE) strains

overall_design: Total RNA was purified from four independent cultures (each) of Caulobacter crescentus ΔgsrN, gsrN-OE, and wild-type strains grown to 0.85-0.90 OD600 in M2-xylose medium. mRNA steady state levels in these strains were determined by mapping reads to the Caulobacter crescentus NA1000 genome (CP001340).

first: Matthew

last: Tien

first: Aretha

last: Fiebig


title: RNA-seq analysis of umbilical cord blood cells upon knockdown of NAP1L3

city: Stockholm

last: Brodin

address: Hälsovägen 7-9

department: Department of Biosciences and Nutrition

country: Sweden

institute: Karolinska Institute

summary: The nucleosome assembly proteins (NAPs) are histone chaperones with an important role epigenetic regulation of gene expression. We find that high gene expression levels of murine Nap1l3 is restricted to hematopoietic stem cells. Loss of function of murine and human NAP1L3 impair maintenance of  hematopoietic stem cells and differentiation both in vitro and in vivo. NAP1L3 inhibition in human hematopoietic cells causes a growth arrest in the G0 phase of cycle progression, and induces gene expression signatures that highly significantly correlate with downregulation of genes involved in cell cycle regulation, including E2F and MYC target genes. In addition, we also show that the HOXA3, HOXA5, HOXA6 and HOXA9 are markedly upregulated when NAP1L3 is suppressed in Human hematopoietic cells. Taken together, our findings establish an important role for NAP1L3 in HSC homeostasis and hematopoietic differentiation.

overall_design: Umbilical cord blood cells were transduced with shRNA targeting NAP1L3 or negative control vectors and RNA was isolated for RNA-seq analysis 72hour post transduction.

first: Julian

last: Walfridsson

first: Yaser

last: Heshmati


title: GATA2/3-TFAP2A/C transcription factor network couples human pluripotent stem cell differentiation to trophectoderm with repression of pluripotency

city: Martinsried

first: Christoph

last: Ziegenhain

state: Bavaria

address: Großhaderner Str. 2

department: Department Biology II

institute: Ludwig-Maximilians University Munich

summary: To elucidate the molecular basis of BMP4-induced differentiation of human pluripotent stem cells (PSCs) toward progeny with trophectoderm characteristics, we produced transcriptome, epigenome H3K4me3, H3K27me3, and CpG methylation maps of trophoblast progenitors, purified using the surface marker APA. We combined them with the temporally resolved transcriptome of the preprogenitor phase and of single APA+ cells. This revealed a circuit of bivalent TFAP2A, TFAP2C, GATA2, and GATA3 transcription factors, coined collectively the “trophectoderm four” (TEtra), which are also present in human trophectoderm in vivo. At the onset of differentiation, the TEtra factors occupy multiple sites in epigenetically inactive placental genes and in OCT4. Functional manipulation of GATA3 and TFAP2A indicated that they directly couple trophoblast-specific gene induction with suppression of pluripotency. In accordance, knocking down GATA3 in primate embryos resulted in a failure to form trophectoderm. The discovery of the TEtra circuit indicates how trophectoderm commitment is regulated in human embryogenesis.

overall_design: hESC cell line H9 was differentiated towards trophoblast lineage using treatment with BMP4 for 3 days. Undifferentiated hESC and cells stained with anti-APA antibody were sorted into 384-well plates at 1 cell per well (1 plate per condition) and subjected to SCRB-seq

first: Dmitry

last: Shaposhnikov


title: Heterogeneity in early lymphoid compartments

city: Lund

first: Shamit

last: Soneji

address: Solvegatan 19

institute: BMC

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

overall_design: Refer to individual Series


title: RNA-Seq study of migratory bird under two seasonal states

status: Public on Oct 25 2017

city: DELHI

first: AAKANSHA

last: SHARMA

state: DELHI

address: CHATTRA MARG

department: ZOOLOGY

country: India

institute: UNIVERSITY OF DELHI

summary: We report the mRNA found in hypothalamus and liver tissue of a migratory bird. The aim of this study was to study how the mRNA makeup of tissue varies under different seasonal states.

overall_design: Study of total mRNA from hypothalamus and liver under two different seasonal states (short day and long day), using 454 pryrosequencing.

first: Devraj

last: Singh

first: Aakansha

last: Sharma

first: Subhajit

last: Das


title: NR4A1 Inhibition Synergizes with Ibrutinib in Killing Mantle Cell Lymphoma Cells

city: Madison

first: Lixin

last: Rui

state: WI

address: 1111 Highland ave, Room 4053

institute: Wisconsin Ins for Medical Res

summary:
Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to identify NR4A1 targets by RNA-seq and high-throughput data analysis and verify these genes by quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods.
Methods: Jeko/Rec-1 Cas9 control and NR4A1 sgRNA stable cell lines were generated with tet-on system vector, sg RNAs were induced for 48 hours after doxycycline addition, mRNA was extracted and used for RNA sequencing. After TopHat analysis followed by Cufflinks, down/up regulated genes list was generated. qRT–PCR validation was then performed using SYBR Green assays.
Results: Using an optimized data analysis workflow and with a fold change ≥1.3 and p value <0.05, thousands of genes were changed. Altered expression of 6 genes was then confirmed with qRT–PCR, demonstrating the high qulity of the RNA-seq method.

overall_design: Jeko/Rec-1 Cas9 control and NR4A1 sgRNA stable cell lines were generated with tet-on system vector, sgRNAs were induced for 48 hours after doxycycline addition, and total RNA from these cells was then used for RNA-seq analysis.

first: Yangguang

last: Li

first: Li

last: Lu


title: PGAM5 promotes lasting FoxO activation after developmental mitochondrial stress and extends lifespan in Drosophila

city: Novato

first: Martin

last: Borch Jensen

state: California

address: 8001 Redwood Blvd.

institute: Buck Institute for Research on Aging

summary: The mitochondrial unfolded protein response (UPRmt) has been associated with long  lifespan across metazoans. In Caenorhabditis elegans, mild developmental mitochondrial stress  activates UPRmt reporters and extends lifespan. We show that similar developmental stress is  necessary and sufficient to extend Drosophila lifespan, and identify Phosphoglycerate Mutase 5  (PGAM5) as a mediator of this response. Developmental mitochondrial stress leads to activation of  FoxO, via Apoptosis Signal-regulating Kinase 1 (ASK1) and Jun-N-terminal Kinase (JNK). This  activation persists into adulthood and induces a select set of chaperones, many of which have been  implicated in lifespan extension in flies. Persistent FoxO activation can be reversed by a high-  protein diet in adulthood, through mTORC1 and GCN-2 activity. Accordingly, the observed lifespan  extension is prevented on a high-protein diet and in FoxO-null flies. The diet-sensitivity of this  pathway has important implications for interventions that seek to engage the UPRmt to improve  metabolic health and longevity.

overall_design: Three thoracic samples, including one genetic control and two experimental conditions. Also eight fat body samples, four each from adults and larvae, from wild type and PGAM5 mutant flies, with and without RU486 treatment to induce genetic phenotype.

first: Yanyan

last: Qi

first: Rebeccah

last: Riley

first: Liya

last: Rabkina

first: Heinrich

last: Jasper


title: ChIP-seq from adrenal gland (ENCSR899JSO)

first: ENCODE

last: DCC

address: 300 Pasteur Dr

institute: ENCODE DCC

summary:
CTCF ChIP-seq on human adrenal gland

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Heterogeneity in early lymphoid compartments [RNA-Seq]

summary: In order to understand the developmental trajectories of early lymphocyte development it is crucial to prospectively isolate stage and lineage specific cells. It has become clear that early lymphoid progenitor compartments in the bone marrow are molecularly and functionally heterogeneous which warrants further investigation to refine the marker combinations used to isolate these progenitors. An initial antibody screen revealed extensive surface marker heterogeneity amongst early lymphoid progenitors. This heterogeneity was resolved using single cell gene expression assays and single cell in vitro differentiation assays, identifying marker combinations that isolate functionally distinct populations. In addition, using reporter transgenic mice we were able to identify a set of surface markers that can be used alone or in combination with classical targets to identify specific stages of B-cell development. B-cell stages based on transgene expression which were used for screening purposes were verified by RNASeq. The data provides a greater resolution of the complexity of the lymphoid progenitor compartment within the bone marrow than has been understood to date and provides novel tools for the further identification of cell populations in B-lineage development.

overall_design: Investigation of the transcriptome in 7 different bone marrow B-cell compartments by RNASeq (3-4 replicates/cell type)

first: Christina

middle: T

last: Jensen

first: Stefan

last: Lang

first: Mikael

last: Sigvardsson


title: General response of Salmonella enterica serovar Typhimurium to desiccation: A new role for the virulence factors sopD and sseD in survival.

city: St. Cloud

first: Ryan

middle: Cristiano

last: Fink

state: MN

address: 720 4th Ave S

institute: St. Cloud State University

summary: Salmonella can survive for long periods under extreme desiccation conditions.  This stress response poses a risk for food safety, but relatively little is known about the molecular and cellular regulation of this adaptation mechanism. To determine the genetic components involved in Salmonella’s cellular response to desiccation, we performed a global transcriptomic analysis comparing Salmonella Typhimurium cells equilibrated to low water activity (aw 0.11) and cells equilibrated to high water activity (aw 1.0). The analysis revealed that 719 genes were differentially regulated between the two conditions, of which 290 genes were up-regulated at aw 0.11. Most of these genes were involved in metabolic pathways, transporter regulation, DNA replication/repair, transcription and translation, and, more importantly, virulence genes.

sample_organism: Salmonella enterica subsp. enterica serovar Typhimurium str. ATCC 14028

overall_design: S. Typhimurium cells were spotted on 0.2 µm polycarbonate filters and air dried for 24 hours at room temperature. Filters were then equilibrated for 4 days to two different water activitie: aw 1.0 as control condition, and aw 0.11 as low water activity and desiccating condition. Expression profile of cells equilibrated to low water activity (aw 0.11) was compared to the expression profile of cells in control conditions (aw 1.0).

first: Alice

last: Maserati

first: Franciso

last: Diez-Gonzalez


title: RNAseq analysis of genes regulated by GDE2 in neuronal cells

city: Amsterdam

first: Wouter

last: Moolenaar

address: Plesmanlaan 121

institute: Netherlands Cancer Institute

summary: We analyze differentially expressed genes in wild-type versus GDE2 knockdown neuroblastoma cells

overall_design: Stable knockdown of GDE2 in Shep2 neuroblastoma cells, followed by mRNA expression profiling

first: Elisa

last: Matas-Rico

first: Michiel

last: van Veen


title: Neurogenomic  signatures of successes and failures in core life-history transitions in a key insect pollinator

city: Egham

first: Fabio

last: Manfredini

state: Surrey

address: Bourne Lab Room 4-17

institute: Royal Holloway University of London

summary: The switch between biological states during key life-history transitions requires major reprogramming at the behavioural level that is under the control of the brain. In this study we focused on major life-history transitions in bumblebee queens (Bombus terrestris) that involve switching from virgin to mated and reproductively mature. To reveal the molecular processes underpinning the behavioural changes that accompany these transitions, we characterised the neurogenomic state of queens that succeeded or failed in making these transitions. Analyses of shared transcription patterns suggested that failures are associated with larger molecular signatures than successes. This was observed at the level of total numbers of differentially expressed genes (DEGs) and proportions of these genes that were up-regulated, and applies to both mating and reproductive maturation. ‘Failed Reproductive’ queens were the most distinct phenotype, associated with the highest number of DEGs (1,578) and two networks of co-expressed genes. Mating status influenced gene expression the least, followed by the transition between the two successful phenotypes (mating to reproductive maturation) and reproductive maturation. However, this pattern was not mirrored in terms of functional specialisations, for Gene Ontology (GO) terms, KEGG pathways and co-expression networks associated with DEGs. Out of the 21 highly connected (hub) genes associated with co-expression networks, 9 are involved in neural processes and 4 are regulators of gene expression. This study shows that different life-history transitions trigger distinct molecular profiles, within a single caste of a eusocial insect. Failure to surmount key life-history transitions has the largest effect on a queen’s neurogenomic state, and it triggers a massive overall up-regulation of gene expression. Hence, failure is an important outcome that must be taken into account when analysing the molecular regulation of important life-history transitions.

overall_design: Brain RNA samples for 4 treatments: successfully mated (SM, N=8), failed mated (failed mated, N=9), successfully reproductive (SR, N=8) and failed reproductive (FR, N=8)

first: Alfonso

middle: E

last: Romero

first: Inti

last: Pedroso

first: Alberto

last: Paccanaro

first: Seirian

last: Sumner

first: Mark

last: Brown


title: Single cells transitioning to hematopoietic fate in vivo show pulsatile Gata2 expression

city: Edinburgh

first: Elaine

last: Dzierzak

address: 47 Little France Crescent

department: MRC Centre for Inflammation Research

institute: University of Edinburgh

summary: Cell fate is established through coordinated gene expression programs in individual cells. Regulatory networks that include the Gata2 transcription factor play central roles in hematopoietic fate establishment. Whereas Gata2 is essential to the embryonic development and function of hematopoietic stem cells that form the adult hierarchy, little is known of the in vivo expression dynamics of Gata2 in single cells. Here we examine Gata2 expression in single aortic cells as they establish hematopoietic fate in Gata2Venus mouse embryos. Time-lapse imaging reveals rapid pulsatile level changes in Gata2 reporter expression in cells undergoing endothelial-to-hematopoietic-transition. Moreover, Gata2 reporter pulsatile expression is dramatically altered in Gata2+/- aortic cells, which undergo fewer transitions and are reduced in hematopoietic potential. Our novel finding of dynamic pulsatile expression of Gata2 suggests a highly unstable genetic state in single cells concomitant with their transition to hematopoietic fate. This reinforces the notion that threshold levels of Gata2 influence fate establishment and has implications for transcription factor-related hematologic dysfunctions.

overall_design: At embryonic day 10.5, HP/SC populations (CD31+ckit+) were sorted into Gata2Venus high and intermediate populations.

last: Eich

first: Parham

last: Solaimani Kartalaei


title: Olfactory stem cell-mediated regeneration: horizontal basal cell (HBC) lineage [scRNA-seq]

city: Berkeley

first: Diya

last: Das

address: 265 Life Sciences Addition #3200

department: Molecular & Cell Biology

institute: University of California, Berkeley

summary: The lineage of the horizontal basal cells (HBC) stem cells and their descendants from the olfactory epithelium were profiled by single-cell RNA-Seq to identify differentiated cell types, intermediate stages, transition states, and to infer the lineage trajectories.

overall_design:
Horizontal basal cell (HBC) stem cells from the olfactory epithelium that were either wild-type or mutant for Sox2 were lineage traced, collected by FACS, and profiled by single-cell RNA-seq.  A minimum of two biological replicates were collected for each time-point/experimental condition. A total of 1384 YFP-positive lineage traced cells were used in this analysis. Additional samples from GSE95601 were used in some analyses.

Please note that the GSE95601 samples (total 849 samples) were included and re-analyzed in the current study. The processed data files (linked to the current GSE99251 records) include the re-analyzed data of the GSE95601 samples (total 849 samples), and the raw data (for the re-analyzed samples) are available from the corresponding GSE95601 sample records.

first: Levi

last: Gadye

first: Michael

last: Sanchez

first: Kelly

last: Street

first: Ariane

last: Baudhuin

first: Allon

last: Wagner

last: Cole

first: Yoon

last: Choi

first: Nir

last: Yosef

first: Elizabeth

last: Purdom

first: Sandrine

last: Dudoit

first: Davide

last: Risso

first: John

last: Ngai

first: Russell

last: Fletcher


title: ChIP-seq from Peyer's patch (ENCSR799WDT)

first: ENCODE

last: DCC

state: CA

summary:
CTCF ChIP-seq on human Peyer's patch

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from HEK293 (ENCSR897JCM)

summary:
eGFP-ZNF491 ChIP-seq on human HEK293 cells.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from HEK293 (ENCSR897RVP)

summary:
eGFP-ZNF514 ChIP-seq on human HEK293 cells.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from HepG2 (ENCSR894SXR)

summary:
TCF12 ChIP-seq on human HepG2

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from MCF-7 (ENCSR897JAS)

summary:
CREB1 ChIP-seq on human MCF-7

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from ascending aorta (ENCSR894EKG)

summary:
ChIP-seq on human ascending aorta

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from spleen (ENCSR895OZW)

summary:
ChIP-seq on human spleen

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from transverse colon (ENCSR799YAO)

summary:
ChIP-seq on human transverse colon

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Poised enhancers regulatory activity is topologically facilitated by polycomb [RNA-seq LHX5]

city: Koeln

first: Milos

last: Nikolic

state: Nordrhein-Westfalen

address: Robert Koch Str. 21

institute: Center for Molecular Medicine Cologne

summary: Poised enhancers marked by H3K27me3 in pluripotent cells were previously proposed to facilitate the establishment of somatic expression programs upon embryonic stem cell (ESC) differentiation. However, the functional relevance and mechanism of action of poised enhancers remain unknown. Here, we use genetic deletions to demonstrate that poised enhancers are necessary for the induction of major anterior neural regulators. Mechanistically, poised enhancers enable RNA Polymerase II recruitment to their cognate promoters upon differentiation. Interestingly, poised enhancers already establish physical interactions with their target genes in ESC in a Polycomb repressive complex 2 (PRC2) dependent manner. Loss of PRC2 led to neither the activation of poised enhancers nor the induction of their putative target genes in undifferentiated ESC. In contrast, loss of PRC2 severely and specifically compromised the induction of major anterior neural genes representing poised enhancer targets. Overall, our work illuminates a novel function for polycomb proteins, which we propose facilitate neural induction by providing major anterior neural loci with a permissive regulatory topology.

overall_design: mRNA profiles were generated by RNA-seq from AntNPC derived from mESC: WT AntNPC (four biological replicates),  PE Lhx5(-109)-/- Clon1 AntNPC (two biological replicates) and  PE Lhx5(-109)-/- Clon2 AntNPC (two biological replicates).

first: Sara

last: Cruz-Molina

first: Alvaro

last: Rada-Iglesias


title: ChIP-seq from HEK293 (ENCSR892ZTO)

summary:
eGFP-ZNF548 ChIP-seq on human HEK293 cells.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from esophagus muscularis mucosa (ENCSR891WPD)

summary:
Chip-Seq on muscle layer of esophagus

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from subcutaneous adipose tissue (ENCSR790VEV)

summary:
CTCF ChIP-seq on human adipose tissue

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from breast epithelium (ENCSR794WXG)

summary:
ChIP-seq on human breast epithelium

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from HEK293 (ENCSR892QHR)

summary:
eGFP-PRDM6 ChIP-seq on human HEK293 cells.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from stomach (ENCSR890ONE)

summary:
Chip-Seq on -human (fragmentation date:Tue Aug 30 2016 00:00:00 GMT-0500 (CDT)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from tibial nerve (ENCSR889VXP)

summary:
Chip-Seq on -human (fragmentation date:Tue Nov 08 2016 00:00:00 GMT-0600 (CST)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from K562 (ENCSR796ITY)

summary:
NFIC ChIP-seq on human K562

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from upper lobe of left lung (ENCSR888OWU)

summary:
POLR2A ChIP-seq on human upper lobe of left lung

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from lower leg skin (ENCSR888HXN)

summary:
POLR2A ChIP-seq on human lower leg skin

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from right lobe of liver (ENCSR790UYC)

summary:
ChIP-seq on human right lobe of liver

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from K562 (ENCSR886RYH)

summary:
NONO ChIP-seq on human K562

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from uterus (ENCSR798NVH)

summary:
CTCF ChIP-seq on human uterus

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from HepG2 (ENCSR887LYD)

summary:
SMARCC2 ChIP-seq on human HepG2

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from K562 (ENCSR788RSW)

summary:
SOX6 ChIP-seq on human K562

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from GM12878 (ENCSR784VIQ)

summary:
NR2C1 ChIP-seq on human GM12878

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from HEK293 (ENCSR878DES)

summary:
eGFP-ZNF624 ChIP-seq on human HEK293 cells.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from HepG2 (ENCSR784FYS)

summary:
RBFOX2 ChIP-seq in HepG2

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from GM12878 (ENCSR785OKZ)

summary:
RB1 ChIP-seq on human GM12878

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from esophagus squamous epithelium (ENCSR877OYD)

summary:
POLR2A ChIP-seq on human esophagus squamous epithelium

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from vagina (ENCSR877SNO)

summary:
Chip-Seq on vagina

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: UTX/KDM6A Loss Enhances the Malignant Phenotype of Multiple Myeloma and Sensitizes Cells to EZH2 inhibition

city: Pamplona

first: Teresa

last: Ezponda

state: Navarra

address: Pio XII 55

department: Hematology/Oncology

institute: Center for Applied Medical Research

summary: In this project we analyze the transcriptome of the human multiple myeloma isogenic cell lines ARP-1 (UTX wild-type) and ARD (UTX null). The transcriptome is studied at baseline, upon restoration of UTX levels in ARD cells for 3 and 6 days, and upon treatment of the cell lines with the EZH2 inhibitor GSK343. Moreover, we analyzed the transcriptome of a ARD resistant cell line that we generated.

overall_design: Examination of transcriptome of two cell lines upon restoration of UTX and treatment with EZH2 inhibitors

first: Jonathan

last: Licht


title: ChIP-seq from omental fat pad (ENCSR875UDE)

summary:
Chip-Seq on -human (fragmentation date:Wed Aug 24 2016 00:00:00 GMT-0500 (CDT)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: A Molecular Atlas of the Developing Ectoderm Defines Neural, Neural Crest, Placode and Non-Neural Progenitor Identity in Vertebrates.

city: Orsay

first: Anne-Helene

last: Monsoro-Burq

address: Bat 110

department: Université Paris Sud

country: France

institute: Institut Curie

summary: During vertebrate neurulation, the embryonic ectoderm is patterned into lineage progenitors for neural plate, neural crest, placodes and epidermis. Here, we use Xenopus laevis embryos to analyze the spatial and temporal transcriptome of distinct ectodermal domains in the course of neurulation, during the establishment of cell lineages. In order to define the transcriptome of small groups of cells from a single germ layer, and to retain spatial information, dorsal and ventral ectoderm was subdivided along the anterior-posterior and medial-lateral axes by microdissections. Principal Component Analysis on the transcriptomes of these ectoderm fragments primarily identifies embryonic axes and temporal dynamics. This provides a genetic code to define positional information of any ectoderm sample along the anterior-posterior and dorsal-ventral axes, directly from its transcriptome. In parallel, we use Non-Negative Matrix Factorization to predict enhanced gene expression maps onto early and mid-neurula embryos, and specific signatures for each ectoderm area. The clustering of spatial and temporal datasets allowed detection of multiple biologically relevant groups (e.g. Wnt signaling, neural crest development, sensory placode specification, ciliogenesis, germ layer specification). We provide an interactive network interface, EctoMap, for exploring synexpression relationships among genes expressed in the neurula, and suggest several strategies to use this comprehensive dataset to address questions in developmental biology as well as stem cell or cancer research.

overall_design: Xenopus laevis ectodermal sample were dissected at embryonic stages 12.5, 14, and 17 and mRNA profiles were generated by deep sequencing using an Illumina HiSeq 2000

first: Jean-Louis

last: Plouhinec

first: Sofía

last: Medina-Ruiz

first: Caroline

last: Borday

first: Elsa

last: Bernard

first: Jean-Philippe

last: Vert

first: Michael

last: Eisen

first: Richard

last: Harland

first: Anne


title: ChIP-seq from HepG2 (ENCSR872EVQ)

summary:
PCBP1 ChIP-seq in HepG2

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Reversing SKI–SMAD4-mediated suppression is essential for TH17 cell differentiation

city: Chapel Hill

first: Yisong

last: Wan

state: NC

address: 125 Mason Farm Road

department: Lineberger Comprehensive Cancer Center

institute: University of North Carolina-Chapel Hill

summary: Disruption of Ski/Smad4 license Th17 differentiation. TGF-b-Ski-Smad4-RORgt-Th17 axis

overall_design: Examination of transcriptome under two different conditions (WT vs.Smad4 KO), two different treatment (Th0 and IL6) and three time point( 0hr, 3hr and 12hr)

first: Song

last: Zhang

first: Xiaojiang

last: Xu


title: High throughput single-cell whole transcriptome analysis of induced cardiomyocytes during direct cardiac reprogramming [Bulk-seq]

city: WAUWATOSA

first: ZIQING

last: LIU

address: 8701 W Watertown Plank Rd, BSB 5320

institute: Medical College of Wisconsin

summary: Direct lineage conversion offers a new strategy for tissue regeneration and disease modeling. Despite recent success in directly reprogramming fibroblasts into a wide spectrum of cell types, the precise changes that fibroblasts undergo as they progress to target cell fates remain unclear. The inherent heterogeneity and asynchronous nature of the reprogramming process make it difficult to study using bulk genomic techniques. Therefore, a fundamental and detailed understanding of global transcriptome changes at the single cell level is necessary to better optimize reprogramming for therapeutic purposes and to advance the understanding of cell plasticity and cell identity acquisition. Here, we applied single-cell RNA-seq to analyze global transcriptome changes at early stages of induced cardiomyocyte (iCM) reprogramming. Using unsupervised dimensionality reduction and clustering algorithms, we identified molecularly distinct subpopulations of cells along the reprogramming process from fibroblasts to iCMs, including a novel intermediate state that exhibited molecular signatures of both fibroblast and cardiomyocyte. In summary, our single cell transcriptomics approaches enabled us to construct a reprogramming trajectory and uncover the intermediate cell populations, regulatory pathways and genes putatively involved in iCM induction.

overall_design: To control for single cell experiments and to analyze Ptbp1 depletion induced splicing pattern changes, we performed bulk RNAseq of freshly isolated neonatal cardiac fibroblast, cardiomyocytes and cells undergoing reprogramming with or without Ptbp1 silencing.

first: Ziqing

last: Liu

first: Li

last: Wang

last: Qian


title: ChIP-seq from liver (ENCSR893QWP)

city: Stanford

first: ENCODE

last: DCC

summary:
Chip-Seq on REST-human

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from HEK293 (ENCSR781EQJ)

summary:
eGFP-ZBTB48 ChIP-seq on human HEK293 cells.

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Differential gene expression of mouse liver samples after poly I:C treatment

city: La Jolla

first: Jin

last: Lee

address: 9500 Gilman Drive BRF II

department: Pathology Department

institute: University California, San Diego

summary: To understand differential gene expression globally with/without poly I:C treatment on liver cancer mouse model, RNA-seq analysis were examined using diethlynitrosamine-induced Shp2∆H (Shp2F/F:Alb-cre) and Pten∆H (PtenF/F:Alb-cre) mice.

overall_design: Total RNA extracts from liver on 1 week and 2 weeks after poly I:C treatment of Shp2 and Pten mice. Group 1: diethlynitrosamine (DEN)-treated Shp2 mice (n=3); Group 2: poly I:C + DEN-treated Shp2 mice (n=3); Group 3: Pten mice (n=3); Group 4: poly I:C + Pten mice (n=3).

first: Gen

last: Feng


title: Fibroblast-specific genetic dissection of TGFβ-Smad2/3 signaling in cardiac fibrosis

city: Cincinnati

first: Vikram

last: Prasad

state: OH

address: 240, Albert Sabin Way

department: Molecular Cardiovascular Biology

institute: Cincinnati Children's Hospital Medical Center

summary: Overall goal: To elucidate fibroblast-specific role of TGFβ-Smad2/3 signaling in fibroblast activation and their differentiation to myofibroblasts. Purpose of analysis: To generate transcriptional profile of Smad2/3 and TGFβreceptors1/2-deficient fibroblasts in the context of pathological cardiac fibrosis.

overall_design: Experimental structure: Transcriptional profile generated using RNAseq and differential gene expression analyses of fibroblasts lacking either Smad2/3 or TGFbreceptors1/2 fibroblasts isolated from stressed/diseased hearts.

first: Jeffery

last: Molkentin

first: Hadi

last: Khalil


title: ChIP-seq from K562 (ENCSR786OQY)

summary:
ZBTB5 ChIP-seq on human K562

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Read-write integration by the IRF4 gene regulatory module dynamically controls T helper cell fate

city: Chicago

first: Mark

last: Maienschein-Cline

state: IL

address: 900 S Ashland Ave, Rm 1058, M/C 937

department: Research Resources Center

institute: University of Illinois at Chicago

summary: Transcriptional regulation of cell fate decisions in the immune system endows cells with specialized function; an iterative process that adapts to the changing landscape of infections. As coordinators of the immune system, T helper cells of the CD4+ lineage possess the ability to differentiate into an array of functional cell states in order to guide the response towards antibody production via the formation of T follicular helper (Tfh) cells or inflammation by the generation of T effector (Teff) cells. Tfh–Teff cell fate choice is mediated by the BCL6–Blimp-1 counter-antagonistic gene regulatory module, polarizing Tfh and Teff cells, respectively. A key question is how T helper cells establish and negotiate BCL6–Blimp-1 counter antagonism to control the output of Tfh and Teff cells. We show that the T cell receptor (TCR)-signal induced transcription factor, IRF4, is necessary for the generation of both BCL6-expressing Tfh cells and Blimp-1-expressing Teff cells. Importantly, we show that increasing TCR signal strength augments the amounts of IRF4 expressed as well as Teff cell fate trajectories that occur at the expense of Tfh cells. Using an orthogonal genetic system, based on a tet-inducible allele of Irf4, we demonstrate that increasing IRF4 expression during priming redirected Tfh cell fate choices towards those of Teff. Importantly, promotion of Teff cell fate trajectories by increased IRF4 expression occurred independently of IL-2 signals. At the molecular level, we link greater IRF4 abundance with its recruitment to low affinity DNA binding sites embedded within regulatory elements affiliated with the Teff gene program, including Blimp-1. Together, these results demonstrate that the Irf4 locus functions as the “reader” of TCR signal strength, in turn, the concentration dependent activity of the IRF4 transcription factor “writes” T helper cell fate choice.

overall_design: 14 ATAC-seq, 15 RNA-seq samples

first: Veena

last: Krishnamoorthy

first: Sunil

last: Kannanganat

first: Neil

last: Bahroos

first: Sarah

last: Cook

first: Jianjun

last: Chen

first: Emily

last: Corse

first: Anita

last: Chong

first: Roger

last: Sciammas


title: ChIP-seq from esophagus squamous epithelium (ENCSR783XDX)

summary:
ChIP-seq on human esophagus squamous epithelium

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Comparison of gene expression by RNA-seq in canine gonads from embryos at risk of XX Disorder of Sex Development (XX), male (XY) littermate controls, and age-matched female (XX) and male (XY) controls.

city: Ithaca

first: Jennifer

last: Grenier

state: NY

address: 526 Campus Rd

department: Biomedical Sciences

institute: Cornell University

summary: In a rare subtype of XX Disorder of Sex Development (DSD), individuals are negative for SRY, the testis determining factor on the Y chromosome, yet develop testes or ovotestes, and both of these phenotypes occur in the same family. This is a naturally occurring disorder in humans (Homo sapiens) and dogs (C. familiaris), and phenotypes in the canine XX DSD model are strikingly similar to those in this type of human XX DSD. The purposes of this study were to identify 1) a variant associated with XX DSD in the canine model and 2) gene expression alterations in canine embryonic gonads that could be informative to causation. Using a genome wide association study (GWAS) and whole genome sequencing (WGS), we identified a variant on C. familiaris autosome 9 (CFA9) that is significantly associated with XX DSD in the canine model and in affected purebred dogs. This is the first marker and candidate causative variant identified for inherited canine XX DSD. It lies within the canine ortholog for the human disorder (OMIM 278850), which resides on 17q24, upstream of SOX9. Gene expression studies (RNA-seq and PRO-seq) in embryonic gonads at risk of XX DSD from the canine model identified significant RSPO1 downregulation in comparison to XX controls, without significant upregulation of SOX9 or other known testis pathway genes. A novel mechanism is proposed in which the canine XX DSD variant acts upstream of RSPO1 to induce epigenomic gonadal mosaicism.

overall_design: Total of 55 samples analyzed from several gestational ages: 1) One sample (XX d34 control female) was total RNA from pooled gonad pairs of 6 female canine embryos (breed: Beagle/Labrador retriever mix, A1056, A1057, A1060, A1063, A1067, A1068). 2) One sample (XY d34 control male) was total RNA from pooled gonad pairs of 7 male canine embryos (breed: Beagle/Labrador retriever mix, A1055, A1058, A1059, A1061, A1064, A1065, A1066). 3) For the remaining 53 samples (d35-44), a barcoded cDNA library was prepared from total RNA of a gonad pair from one embryo. Barcoded libraries were pooled for sequencing according to group [XX DSD at risk (C# XX DSD), XY littermate control (C# XY), XX age-matched control (XX A#), XY age-matched control (XY A#)]. Sequence output was sorted by barcode to generate one transcriptome per gonad pair.

first: Vicki

middle: N

last: Meyers-Wallen


title: ChIP-seq from breast epithelium (ENCSR869JUM)

status: Public on Oct 24 2017

first: ENCODE

last: DCC

summary:
Chip-Seq on -human (fragmentation date:Fri Nov 11 2016 00:00:00 GMT-0600 (CST)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from GM12878 (ENCSR778UBR)

summary:
ARID3A ChIP-seq on human GM12878

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from HEK293T (ENCSR778QLY)

summary:
ELF4 ChIP-seq on human HEK293T

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from adrenal gland (ENCSR867NUH)

summary:
ChIP-seq on human adrenal gland

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from 22Rv1 (ENCSR777CQW)

summary:
H3K27ac ChIP-seq on human 22Rv1

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from liver (ENCSR867WPH)


title: ChIP-seq from omental fat pad (ENCSR779NON)

summary:
Chip-Seq on adipose tissue of omentum

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from stomach (ENCSR864PNP)

summary:
Chip-Seq on -human (fragmentation date:Tue Aug 30 2016 00:00:00 GMT-0500 (CDT)

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: ChIP-seq from K562 (ENCSR869IUD)

summary:
ATF2 ChIP-seq on human K562

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf


title: Hi-C from RPMI-7951 (ENCSR862OGI)

summary:
HiC experiment done on RPMI-7951

For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf