title: PerC manipulates metabolism and surface antigens in enteropathogenic Escherichia coli

city: Portland

first: Jay

last: Mellies

address: 3203 SE Woodstock Blvd

department: Biology

institute: Reed College

summary:
Purpose: This study aimed to identify the genes regulated by plasmid-encoded regulator C (PerC). Whole transcriptomes of WT typical enteropathogenic E. coli (tEPEC) strains E2348/69 and coisogenic null-perC mutant JPEP22 were analyzed to identify and quantify differentially expressed genes.
Methods: RNA was isolated from the WT and null-perC mutant strains and RNA integrity (RIN) was determined to be 10 out of possible 10 for all samples by Aligent Bioanalyzer. rRNA was depleted and resulting mRNA was reverse-transcribed into cDNA. Libraries were multiplexed for discrimination between libraries, barcoded for sequencing, and amplified with random hexamers for 15 PCR cycles. Transcripts were sequenced for 50 bases in single-end fashion within one lane of an Illumina Hiseq 2000 flow cell. This yielded roughly 30 million reads per sample.
Results: Differential gene expression (DGE) analysis showed that 157 genes were statistically significantly regulated using a false-discovery rate (FDR) of 10% (q ≤ 0.10). Of these genes, the perC-mutant strain had far greater transcripts for the fim operon genes, fewer transcripts of nitrate reductase genes and anaerobic metabolism genes, and fewer transcripts for Hfq-dependent ncRNAs compared to WT.
Conclusions: Differential transcript abundance between the perC-mutant and WT strains indicate PerC's negative regulation of the fim genes and positive regulation of anaerobic metabolism and ncRNA genes.

sample_organism:
Escherichia coli
Escherichia coli O127:H6 str. E2348/69

overall_design: Whole mRNA profiles of WT and coisogenic perC mutant EPEC strains were identified by isolation, mRNA enrichment, reverse-transcription, and Illumina sequencing

first: Jossef

last: Osborn


title: An intrinsic transcriptional program underlying synaptic scaling during activity suppression

status: Public on Feb 07 2017

city: Dallas

first: Gokhul

middle: Krishna

last: Kilaru

state: TEXAS

address: 6000 Harry Hines Boulevard

department: Department of Neuroscience

country: USA

institute: University of Texas Southwestern Medical Center

type: Expression profiling by high throughput sequencing

summary: Homeostatic scaling allows neurons to maintain stable activity patterns by globally altering their synaptic strength in response to changing activity levels. Suppression of activity by blocking action potentials increases synaptic strength through an upregulation of surface AMPA receptors. Although this synaptic up-scaling was shown to require transcription, the molecular nature of the intrinsic transcription program underlying this process and its functional significance have been unclear. Using RNA-seq, we identified 73 genes that were specifically upregulated in response to activity suppression. In particular, Neuronal pentraxin-1 (Nptx1) increased within 6 h of activity blockade, and knockdown of this gene blocked the increase in synaptic strength. Notably, Nptx1 induction is mediated by calcium influx through the T-type Voltage-Gated Calcium Channel, as well as two transcription factors, SRF and ELK1. Taken together, these results uncover a transcriptional program that specifically operates when neuronal activity is suppressed, to globally coordinate the increase in synaptic strength.

overall_design: mRNA profiles were generated from primary mouse cortical neurons at DIV12, comparing untreated neurons to neurons treated with Bicuculline or TTX for 30 m, 2 h, 4h, or 6 h, in duplicate

first: Katie

last: Schaukowitch

first: Austin

middle: L

last: Reese

first: Seung-Kyoon

last: Kim

first: Jae-Yeol

last: Joo

first: Ege

middle: T

last: Kavalali

first: Tae-Kyung


title: Mapping of H2A.Z nucleosomes in CD4/CD8 DP thymocytes

city: Freiburg

first: Pierre

middle: Daniel

last: Cauchy

state: Baden-Württemberg

address: Breisacher Str. 115

department: Zentrum für Translationale Zellforschung

country: Germany

institute: University Medical Center Freiburg

type: Genome binding/occupancy profiling by high throughput sequencing

summary: H2A.Z ChIP-Seq in CD4/CD8 DP thymocytes

overall_design: Examination of H2A.Z nucleosomes in CD4/CD8 DP thymocytes

first: Frederic

last: Koch

first: Jean-Christophe

last: Andrau


title: Dynamic DNA methylation landscape defines brown and white cell specificity during adipogenesis

city: Wenzhou

first: Chunming

last: Ding

address: Wenzhou Medical University, University Town, Chashan, Wenzhou, Zhejiang, P.R China

country: China

institute: Wenzhou Medical University

type: Methylation profiling by high throughput sequencing

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

overall_design: Refer to individual Series


title: Effect of SF3B1 suppression in cancer cells with different SF3B1 copy-number levels

city: Boston

first: Brenton

last: Paolella

state: Massachusetts

address: 450 Brookline Ave. Smith 1010

institute: Dana-Farber Cancer Institute

summary: Breast cancer cell lines containing stable dox inducible shRNAs targeting SF3B1 were profiled by RNA sequencing. We determined the effect of gene expression and splicing changes before and after knocking down SF3B1 in cell lines with normal copy number (SF3B1neutral) or partial copy loss (SF3B1loss) cell lines

overall_design: RNA profiles for SF3B1 suppression were generated from 8 breast cancer cell line pairs (-/+ dox) with no techincal replicates.

middle: R

first: William

middle: J

last: Gibson


title: The functions of m6A and Ythdf2 during zebrafish early development

city: Chicago

first: Boxuan

middle: Simen

last: Zhao

state: IL

address: 929 E. 57th. Street

department: Chemistry

institute: University of Chicago

summary: We report the m6A methylation maps of zebrafish embryos during early development, and transcriptome-wide changes occured in ythdf2 LOF mutant embryos. Our study reveals the m6A-dependent RNA decay as a previously unidentified maternal mode mechanism to regulate maternal mRNA clearance during zebrafish   MZT, highlighting the critical role of the m6A mRNA methylation in animal development.

overall_design: m6A-seq of mRNA from zebrafish embryos at 0, 2, 4, 6, 8 h.p.f.; mRNA-seq of wild-type and maternal ythdf2-null mutant embryos at 0, 2, 4, 6, 8 h.p.f.; mRNA-seq of embryos injected with control or ythdf2-MO at 4 h.p.f.; mRNA-seq of wild-type and maternal-zygotic ythdf2-null mutant embryos at 6, 8, 12, 24 h.p.f; and mRNA-seq of wild-type and maternal ythdf2-null mutant embryos injected with control or ythdf2-MO at 24, 36, 48 h.p.f. Replicate of each seq is also included.

middle: S

first: Chuan

last: He


title: Recurrent rearrangements of the Myb/SANT-like DNA-binding domain containing 3 gene (MSANTD3) in salivary gland acinic cell carcinoma

city: Stanford

first: Xue

last: Gong

state: CA

institute: Stanford University

summary: By transcriptome (RNAseq) analysis of 3 human acinic cell carcimoma (AcCC) cases, we discovered two novel gene fusions, and further validated recurrent rearrangement of the MSANTD3 gene. By RNAseq of engineered MSANTD3 overexpression in rat salivary epithelial cells (compared to vector control), we identifed elevated expression of genes involved in protein synthesis.

sample_organism:
Homo sapiens
Rattus norvegicus

platform_organism:
Homo sapiens
Rattus norvegicus

overall_design: Transcriptional profiling of human acinic cell carcinoma cases was done using FFPE specimens, by rRNA depletion, Illumina Truseq library preparation, and Illumina 75x2 sequencing.  RNAseq of rat salivary epithelial cells overexpressing MSANTD3 (vs. empty vector control) was done by Truseq mRNA library preparation and Illumina 50x1 sequencing.

first: Jonathan

last: Pollack


title: Multilineage communication regulates human liver bud self-organization from pluripotency I

status: Public on Feb 08 2017

city: Leipzig

first: Gray

last: Camp

address: Deutscher Pl. 6

department: Evolutionary Genetics

institute: Max Planck Institute for Evolutionary Anthropology

summary: Conventional 2-D differentiation from pluripotency fails to recapitulate cell interactions occurring during organogenesis. 3-D organoids generate complex organ-like tissues, however it is unclear how heterotypic interactions impact lineage identity. Here we use single-cell RNA-seq to reconstruct hepatocyte-like lineage progression from pluripotency in 2-D culture. We then derive 3-D liver bud (LB) organoids by reconstituting hepatic, stromal, and endothelial interactions, and deconstruct heterogeneity during LB self-organization. We find that LB hepatoblasts differentiate towards hepatocyte fate, and in addition express epithelial migration signatures characteristic of organ budding. We identify hypoxia and inflammation signatures in endothelial and mesenchymal cells, which we suggest induce LB vasculogenesis. We use network analysis to predict autocrine and paracrine signaling in LBs, and show that VEGF crosstalk potentiates endothelial network formation and hepatoblast differentiation. Our molecular dissection reveals inter-lineage communication that is required for self-organization, and illuminates previously inaccessible aspects of human organ development and regeneration.

overall_design: Single-cell transcriptomes from multiple time points during hepatocyte-like lineage progression from pluripotency in 2-D culture, and from 3-D liver bud (LB) organoids that self-organized after reconstituting hepatic, stromal, and endothelial interactions.

first: J

middle: G

first: Barbara

last: Treutlein


title: Dynamic DNA methylation landscape defines brown and white cell specificity during adipogenesis (RNA-Seq)

summary: We depicted a genome-wide integrative view of DNA methylome by reduced representation bisulfite sequencing (RRBS) and transcriptome by RNA-seq during brown and white adipocyte differentiation. Our analysis demonstrated that DNA methylation is a stable epigenetic signature for brown and white cell lineage before, during and after differentiation. When comparing white to brown adipocytes at all three time points of differentiation, we identified five members of the Hox family whose expression levels were anti-correlated with promoter methylation, suggesting a regulatory role of DNA methylation in transcription.

overall_design: Examination of DNA methylome in brown and white adipocytes

first: Yen

middle: C

last: Lim


title: Single Cell RNA-Sequencing Identifies Diverse Roles of Epithelial Cells in Idiopathic Pulmonary Fibrosis

status: Public on Feb 06 2017

city: Cincinnati

first: Yan

last: Xu

state: Ohio

address: 3333 Burnet Avenue

department: Pulmonary Biology

institute: Cicinnati children's Hospital Medical Center

summary: Idiopathic pulmonary fibrosis (IPF) is a lethal interstitial lung disease causing alveolar remodeling, inflammation, and fibrosis. We utilized single cell RNA-sequencing (scRNA-Seq) to identify epithelial cell types and associated biological processes involved in the pathogenesis of IPF. Transcriptomic analysis of epithelial cells from normal human lung defined gene expression patterns associated with highly differentiated alveolar type 2 (AT2) cells, indicated by enrichment of RNAs critical for surfactant homeostasis. In contrast, scRNA-seq of IPF cells identified three distinct subsets of epithelial cell types with characteristics of conducting airway basal and goblet cells and, an additional atypical "transitional" cell that contribute to pathological processes in IPF. Individual IPF cells frequently co-expressed alveolar AT1, AT2, and conducting airway selective markers, demonstrating "indeterminate" states of differentiation not seen in normal lung development. Pathway analysis predicted aberrant activation of canonical signaling via TGF-ß, HIPPO/YAP, P53, and AKT-PI3 Kinase. Immunofluorescence confocal microscopy identified the disruption of alveolar structure and loss of the normal proximal-peripheral differentiation of pulmonary epithelial cells. Single cell transcriptomic analyses of respiratory epithelial cells identified loss of normal epithelial cell identities and unique contributions of epithelial cells to the pathogenesis of IPF. Present scRNA-seq transcriptomic analysis of normal and IPF respiratory epithelial cells provides a rich data source to further explore lung health and disease.

overall_design: Dissociated single-cell preparations from peripheral lung of IPF patients (n = 3) and controls (n = 3) from cohort 2 were enriched for AT2 epithelial cells by FACS for CD326 (CD326) double positive, CD45 (hematopoietic) negative, CD31 (endothelial) negative cells, and HTII-280 after dissociation by proteases.

first: Y

last: Whitsett

first: BR

last: Stripp

first: T

last: Mizuno

last: Du


title: RNA-seq of N2 and lin-45(n2018) mutant C.elegans responses to osmotic stress

city: Cambridge

first: Nicholas

last: Burton

state: MA

address: 77 Massachusetts Ave.

institute: MIT

summary: We profiled how animals RNA expression changes in response to osmotic stress, how lin-45 mutants have an altered response to osmotic stress, and how maternal preconditioning at 300 mM NaCl modifies progeny response to 500 mM NaCl

overall_design: Examination of total RNAseq at 50 mM NaCl, 500 mM NaCl, and 500 mM NaCl from maternally preconditioned animals

first: Nick

first: H

last: Horvitz


title: Syringaresinol delays immunosenescence in aged mice: rejuvenating the immune system and reconstituting the gut microbiota

city: Seoul

first: Hang-Rae

last: Kim

address: 103 Daehak-ro, Jongno-gu

department: Anatomy and Cell Biology

country: South Korea

institute: Seoul National University College of Medicine

summary: Improving immune function during aging contributes to the extension of healthspan. However, little is known about interventions for overcoming immunosenescence. Here, we investigated whether syringaresinol (SYR), an activator of FOXO3, overcomes immunosenescence and the factors associated with this effect. To address this, we administered SYR to 42-week-old mice for 10 weeks and analyzed immunological parameters and the gut microbiota. Compared to control mice, SYR-treated mice exhibited reversal of the age-related changes in lymphocyte subsets—such as CD3+ T, CD19+ B and Foxp3+ regulatory T (Treg) cells—and T-cell function in vitro. SYR induced the expression of Bim as well as the activation of FOXO3 in Tregs, which probably regulated Treg homeostasis. Furthermore, SYR reduced the serum level of lipopolysaccharide-binding protein, an inflammatory marker, and enriched the gut microbiota with beneficial bacteria, Lactobacillus and Bifidobacterium, effects that were closely associated with the changes in lymphocyte subsets. Finally, SYR enhanced humoral immunity against influenza vaccination to the level of young control mice. Collectively, these findings indicate that SYR may rejuvenate immunosenescence by enhancing the immune response and modulating the gut microbiota, possibly affecting systemic inflammation, although the precise mechanism awaits further study, and suggest SYR to be a potent candidate for anti-immunosenescence intervention.

overall_design: Comparing the overall structural changes in the gut microbiota in young and old mice treated with vehicle, syringaresinol (SYR, 10 mg/kg or 50 mg/kg), or caloric restriction (CR) by bar-coded pyrosequencing of the V3 region of the 16S rRNA gene

first: Si-Young

last: Cho

first: Song-Seok

last: Shin


title: mRNA-seq comparison of L1 larvae experiencing osmotic and starvation-induced arrest

city: Eugene

first: Amy

middle: K

last: Webster

state: Oregon

address: Institute of Ecology and Evolution

institute: University of Oregon

summary: Wild-type (N2) C. elegans embryos were plated with or without E. coli OP50 as food and with 100mM or 500mM NaCl at 25C (4 conditions). They were allowed to develop for 24hr and collected as L1 larvae for RNA-seq.

overall_design: 3 biological replicates were sequenced for each of four conditions: 100mM NaCl & OP50, 100mM NaCl & no OP50, 500mM NaCl and OP50, 500mM NaCl and no OP50

first: A

first: R

last: Chitrakar

first: L

last: Baugh


title: Dnmt3a restrains mast cell inflammatory responses

city: Milan

first: Chiara

last: Balestrieri

address: Via Olgettina 58

department: Center for Omics Sciences

country: Italy

institute: IRCCS San Raffaele Scientific Institute

summary: DNA methylation and specifically the DNA methyltransferase enzyme DNMT3A are involved in the pathogenesis of a variety of hematological diseases and in regulating the function of immune cells. Although altered DNA methylation patterns and mutations in DNMT3A correlate with mast cell proliferative disorders in humans, the role of DNA methylation in mast cell biology is not understood. By utilizing mast cells lacking Dnmt3a, we found that this enzyme is involved in restraining mast cell responses to acute and chronic stimuli, both in vitro and in vivo. The exacerbated mast cell responses observed in absence of Dnmt3a were recapitulated or enhanced by treatment with the demethylating agent 5-aza-2'-deoxycytidine, as well as by down-modulation of Dnmt1 expression, further supporting the role of DNA methylation in regulating mast cell activation. Mechanistically, these effects were in part mediated by the dysregulated expression of the scaffold protein IQGAP2, which is characterized by the ability to regulate a wide variety of biological processes. Altogether, our data demonstrate that DNMT3A and DNA methylation are key modulators of mast cell responsiveness to acute and chronic stimulation.

overall_design: Murine bone marrow-derived mast cells were differentiated from DNMT3A-deleted animals (3 weeks old) and wild-type littermates age and sex-matched (females). Cells were cultured in vitro for 4 weeks in the presence of IL-3 prior to analysis.

first: Cristina

last: Leoni

first: Sara

last: Montagner

last: Polletti

first: Gioacchino

last: Natoli

first: Silvia

last: Monticelli


title: Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [ATAC-Seq]

city: Burlington

first: Seth

last: Frietze

state: VT

address: 149 Beaumont Avenue

department: Biomedical and Health Sciences

institute: University of Vermont

summary: Using patient-derived Ph+ pre-B ALL cells that harbor deletions of the IKZF1 DNA binding domain (Ik6), we performed ATAC-sequencing in cells that inducibly express wild-type Ikaros (Ik1) or an empty vector control.

overall_design: ATAC-Seq from human Ik6 BCR-ABL+ pre-B ALL cells following 24 h of DOX induction of IK1 or empty vector controls

first: Hilde

last: Schjerven


title: Genetic analysis of Ikaros target genes and tumor suppressor function in BCR-ABL1+ pre-B ALL [ChIP-seq]

summary: ChIP-seq was performed in patient-derived BCR-ABL1+ (Ph+) pre-B ALL cells that harbor heterozygote deletions of the IKZF1 DNA binding domain (Ik6), using cells that inducibly express wild-type Ikaros (Ik1) or an empty vector control.

overall_design: ChIP-Seq from human Ik6+ BCR-ABL1+ pre-B ALL cells following DOX induction of IK1 or empty vector control for the indicated time


title: A Molecular Census of Arcuate Hypothalamus and Median Eminence Cell Types

first: John

middle: N

last: Campbell

address: Center for Life Science, room 7-717

department: Medicine

institute: Beth Israel Deaconess Medical Center

summary: Drop-seq and single cell sequencing of mouse arcuate nucleus and median eminence

overall_design: Single-cell RNA-seq was performed on Cre-dependent AAV-GFP+ cells that were manually isolated from dissociated Arc-ME of two adult male RIP-Cre mice

first: Linus

last: Tsai


title: Global transcriptome profiling of the 889PF mouse pleural fluid disseminating tumour cell-derived cell line, with or without Cd109 knockdown

first: Jennifer

last: Brady

address: 269 Campus Drive

summary: In order to determine the role of Cd109 in regulating metastatic ability and identify Cd109-dependent transcriptonal targets in metastatic lung adenocarcinoma, we sequenced the mRNA from 3 mouse metastasis cell lines. Each of these cell lines (889PF-shGFP, 889PF-shCd109#1, and 889PF-shCd109#2) were derived from the same parental cell line 889PF. 889PF was derived from the pleural fluid of a Kras LSL G12D, p53 flox/flox 129S1/SvlmJ mouse model of metastatic lung adenocarcinoma. A comparison of shGFP and shCd109 cell lines reveals Cd109-dependent changes in the metastatic transcriptome.

overall_design: This study includes 6 samples: 2 biological replicates of 889PF shGFP, 2 biological replicates of 889PF shCd109#1, and 2 biological replicates of 889PFshCd109#2. Poly-A RNA was isolated and prepared for sequencing using the Illumina TruSeq RNA kit (v2) to generate 100bp paired end reads. Reads were aligned to mm10.

first: Chen-Hua

last: Chuang

first: Monte

middle: M

last: Winslow


title: RNA sequencing of adult zebrafish spinal cord

city: Durham

first: Mayssa

last: Mokalled

state: NC

address: 307 Research Dr.

department: Cell Biology

institute: Duke University Medical Center

summary: The goal of this study is to determine gene expression changes in the adult zebrafish spinal cord at 2 weeks after complete transection.

overall_design: 2 samples were analyzed in duplicates:  sham injured spinal cord and transected spinal cord at 2 weeks post-injury

middle: H

first: Kenneth

middle: D

last: Poss


title: Gene expression profiling of metastatic lung adenocarcinoma across different stages of metastatic progression


title: Role of transcriptional coregulator GRIP1 in control of macrophage polarization and metabolic homeostasis

city: New york

first: Yurii

last: Chinenov

state: New York

address: 535 E 71 str, Hospital for Special Surgery

department: Research Division

institute: Hospital for special surgery

summary: Diet-induced obesity is characterized by macrophage (MΦ) infiltration and low-grade chronic inflammation in white adipose tissue (WAT) leading to insulin resistance. WAT MΦ are highly heterogeneous in their origin, patterns of gene expression and activities: unlike infiltrating monocyte-derived MΦ that promote inflammation and metabolic dysfunction, tissue-resident WAT MΦ originally described as ‘M2’ are phenotypically anti-inflammatory and counteract obesity and insulin resistance. Despite the critical role of the balance between these MΦ populations in metabolic homeostasis, the molecular mechanisms and key players that establish the resident MΦ transcription program are poorly understood. We recently reported that glucocorticoid receptor (GR)-interacting protein (GRIP)1 - a nuclear receptor coactivator - cooperates with GR to repress transcription of inflammatory genes. Here, using mice conditionally lacking GRIP1 in MΦ (cKO), we show that GRIP1 promotes MΦ polarization in response to IL4 (M2(IL4)) via a nuclear receptor-independent pathway by serving as a coactivator for Kruppel-like factor (KLF)4 – a critical driver of tissue MΦ differentiation. Interestingly, in vivo, GRIP1 cKO mice challenged with high-fat diet develop massive MΦ infiltration and chronic inflammation in WAT and liver, fatty livers, hyperglycemia, hyperinsulinemia and glucose intolerance consistent with metabolic syndrome phenotype. Together, our findings identify GRIP1 as a critical regulator of immunometabolism, which relies on distinct transcriptional mechanisms to coordinate the balance between MΦ populations in vivo thereby protecting mice from obesity-induced metabolic disease.

overall_design: 1. Examination of IL4 induced transcriptome in in vitro differentiated primary bone marrow-derived macrophages. 2. Examination of macrophage transcriptome in macrophages isolated from  the white adipose tissue of the WT and GRIP1(cKO) conditional KO animals

first: Maddalena

last: Coppo

first: Maria

middle: A

last: Sacta

first: Inez

last: Rogatsky


title: Loss of Ikaros tumor suppressor function in a mouse model of BCR-ABL1-induced B-ALL correlates with a developmental block at a highly proliferative stage

city: San Francisco

address: 513 Parnassus Ave

department: Laboratory Medicine

institute: UCSF

summary: Deletions within the human IKZF1 gene, which encodes Ikaros, a zinc finger transcription factor critical for lymphopoiesis, appear to be the most prominent recurring lesion in human BCR-ABL1+ (Ph+) B-ALL. Furthermore, IKZF1 mutations correlate with poor prognosis of progenitor B-ALL, further strengthening the notion that IKZF1 is a critical tumor suppressor gene in human B-lineage malignancies. To better understand the relationship between Ikzf1 mutations, BCR-ABL, and B-lineage leukemia, we examined the effect of two newly generated Ikzf1 germline mutation on BCR-ABL-induced proliferation and leukemogenesis in vitro and in vivo. We recently showed that deletion of either the exon encoding the first or the fourth DNA-binding zinc finger of Ikaros (IkZnF1-/- and IkZnF4-/-) led to distinct defects in lymphoid development and tumor suppression with de-regulation of distinct subsets of genes, providing a powerful tool for elucidation of Ikaros target genes and mechanism of function. Importantly, IkZnF4-/- had lost Ikaros tumor suppression function, while not abolishing B-cell development. Retroviral expression of BCR-ABL1 p185 in bone marrow cells from the two Ikzf1 mutant strains demonstrated that loss of ZnF4 resulted in expansion of progenitor B cells, with enhanced proliferation in vitro and a less mature cell surface B-cell phenotype in comparison to transduced wild-type bone marrow. Furthermore, in an in vivo model of BCR-ABL+ B-ALL, leukemias generated in the IkZnF4-/- background were more aggressive than those observed in a wild-type background, with cell phenotype corresponding to the in vitro cell cultures. Genome wide high throughput expression analysis (RNA-Seq) revealed a distinct subset of deregulated genes in the IkZnF4-/- BCR-ABL+ in vitro cell cultures, and molecular analysis demonstrated that this in vitro system is amendable for functional studies. These results establish a mouse model for studying the role of Ikzf1 mutations in B-ALL, and for understanding how BCR-ABL collaborates with Ikzf1 mutations to generate aggressive B-ALL.

overall_design: RNA-Seq from BCR-ABL+ transformed cells at day 14 of in vitro cell culture comparing wt, Ikaros-ZnF1-/- mutant and Ikaros-ZnF4-/- mutant (2 biological replicates).

first: Stephen

last: Smale


title: Genome wide mapping of IKAROS binding (ChIP-Seq) in human patient-derived BCR-ABL1+ (Ph+) pre-B ALL xenograft cells

summary: IKAROS is an important tumor suppressor in human pre-B ALL and is mutated or deleted in a high percentage of human BCR-ABL1+ (Ph+) pre-B ALL. We here report the genome-wide binding of IKAROS in two independent patient-derived BCR-ABL1+ (Ph+) pre-B ALL xenograft cells that express wild type full-length IKAROS.

overall_design: Two different patient-derived human BCR-ABL1+ (Ph+) pre-B ALL xenograft cells (ICN1 and LAX2), both expressing wild type full-length IKAROS, and no detectable level of dominant negative (DN) IKAROS isoform. Three IKAROS ChIP-Seq from each cell type: Two biological replicates with same Ab (H-100, Santa Cruz, sc-13039 X), and one sample with a separate Ab used for the ChIP (Ik-C, Smale lab, Hahm et al., 1998). One input control from each cell type (input-ICN1 and input-LAX2).

first: Markus

last: Muschen


title: Recruitment of the conserved protein Seb1 to chromatin during transcription drives transcription termination

status: Public on Feb 05 2017

city: Oxford

first: Sina

last: Wittmann

state: Oxfordshire

address: South Parks Road

department: Department of Biochemistry

country: United Kingdom

institute: University of Oxford

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

overall_design: Refer to individual Series


title: The effect of PPARG inhibition on human angiomyolipoma cells

status: Public on Feb 04 2017

city: Ramat-Gan

first: Tomer

last: Kalsiky

state: Israel

address: Ramat-Gan

country: Israel

institute: Bar-Ilan University

summary: Angiomyolipoma (AML), the most common benign renal tumor, can result in severe morbidity from hemorrhage and renal failure. While mTORC1 activation is involved in its growth, mTORC1 inhibitors fail to eradicate AML, highlighting the need for new therapies. Moreover, the identity of the AML cell of origin is obscure. AML research, however, is hampered by the lack of in-vivo models. Here, we establish a human AML-xenograft (Xn) model in mice, recapitulating AML at the histological and molecular levels. Microarray analysis demonstrated tumor growth in-vivo to involve robust PPARG-pathway activation. Similarly, immunostaining revealed strong PPARG expression in human AML specimens. Accordingly, we demonstrate that while PPARG agonism accelerates AML growth, PPARG antagonism is inhibitory, strongly suppressing AML proliferation and tumor-initiating capacity, via an anti-TGFb mechanism. Finally, we show striking similarity between AML cell lines and multipotent mesenchymal stromal cells (MSCs) in terms of antigen and gene expression and differentiation potential. Altogether, we establishment the first in-vivo human AML model, provide evidence that AML may originate in a PPARG-activated renal MSC lineage that is skewed towards adipocytes and smooth muscle and away from osteoblasts, and uncover PPARG as a regulator of AML growth, which could serve as an attractive therapeutic target.

overall_design: UMB (angiomyolipoma cell line derived from TSC-associated renal angiomyolipoma) and SV7 (angiomyolipoma cell line derived from sporadic renal angiomyolipoma) cell were treated for 12h or 24h with  50mM of the PPARG inhibitor GW9662 or vehicle (DMSO), and global gene expression changes were assessed in both cell lines at both time points, compated to control, vehicle-treated cells.

first: Oren

last: Pleniceanu

first: Dorit

last: Omer

first: Itamar

last: Kanter

last: Kalisky

first: Orit

last: Harari-Steinberg

first: Jack

last: Arbiser

first: Benjamin

last: Dekel


title: Comprehensive analysis of gene expression in human retina and supporting tissues

city: Phila

first: Dwight

last: Stambolian

state: Pa

address: 422 Curie Blvd

department: Ophthalmology

institute: University of Pennsylvania

summary:
Purpose: To identify the differences of gene expression between the macula and periphery of the eye.
Methods: RNA Seq was performed on 8 normal postmortem eyes.
Results: Significant differential expression was found between the layers of the posterior part of the eye and also between locations of a tissue layer.
Conclusions: These results potentially provide a path to more rapidly elucidate not only the genetic basis of eye disease but also the impact of gene expression on molecular networks that in turn induce variations in disease associated traits.

overall_design: Retinal and RPE/choroid/sclera RNA profiles from macula and periphery of each eye were generated by deep sequencing on an Illumina Hi-Seq. 32 biological samples were analyzed.

first: Mingyao

last: Li

first: Christine

last: Curcio


title: Unbiased genomic analysis of multiple stages of lung cancer development

first: Jennifer

last: Brady

summary: To uncover the gene expression alterations that occur during lung cancer progression, we interrogated the gene expression state of neoplastic cells at different stages of malignant progression. We initiated tumors in KrasLSL-G12D/+;p53flox/flox;R26LSL-tdTomato  (KPT) mice with a pool of barcoded lentiviral-Cre vectors and purified Tomatopositive cancer cells away from the diverse and variable stromal cell populations. Five to nine months after tumor initiation, cancer cells were isolated from individual primary tumors and metastases using fluorescence-activated cell sorting. Sequencing of the barcode region of the integrated lentiviral vectors established primary tumor-metastasis and metastasis-metastasis relationships. Tumor barcoding allowed us to unequivocally distinguish non-metastatic primary tumors (TnonMet) from those primary tumors that had seeded metastases (TMet). We profiled 10 TnonMet samples as well as TMet and metastasis (Met) samples representing 12 metastatic events. To examine additional earlier stages of lung cancer development, we also analyzed premalignant cells from hyperplasias that develop in KPT mice shortly after tumor initiation (KPT-Early; KPT-E), as well as tumors from KrasG12D;R26LSL-tdTomato (KT) mice which rarely gain metastatic ability

overall_design: This study includes 52 samples: 3 KP late samples, 3KPT early samples,10 non-metastatic primary tumors, 9 metastatic primary tumors, and 27  metastasis in different organs. total RNA was isolated and prepared for sequencing using the Ovation® RNA-Seq system and Illumina TruSeq DNA kit (v2) to generate 100bp paired end reads. Reads were aligned to mm10.

first: Chen-Hua

last: Chuang

first: Monte

last: Winslow


title: Systematic Identification and Characterization of Long Non-coding RNAs in Mouse Mature Sperm

city: Nanchang

first: Xiaoning

last: Zhang

address: 999 Xuefu R.D., Nanchang

institute: Nanchang University

type: Non-coding RNA profiling by high throughput sequencing

summary: Increasingly, studies have shown that mature spermatozoa contain many transcripts including mRNAs and miRNAs. However, the expression profile of long noncoding RNAs (lncRNAs) in mammalian sperm has not been systematically investigated. Here, we used highly purified RNA to investigate lncRNA expression profiles in mouse mature sperm by stranded-specific RNA-seq. We identified 20907 known and 4088 novel lncRNAs transcripts, and the existence of intact lncRNAs was confirmed by RT-PCR and fluorescence in situ hybridization on two representative lncRNAs. Compared with testes, 2873 upregulated and 6629 downregulated lncRNAs and 1237 upregulated and 2513 downregulated mRNAs were identified in sperm. Based on the “Cis and Trans” RNA-RNA interaction principle, we found 1793 targeted coding genes of differently expressed lncRNAs. In terms of GO analysis, differentially expressed lncRNAs targeted genes mainly related to nucleic acid metabolic, protein modification, chromatin and histone modification, sperm function, and spermatogenesis. In contrast, differentially expressed transcripts of mRNAs were highly enriched for nucleic acid metabolic, spermatogenesis, sperm function, and chromatin organization. Furthermore, KEGG pathway analysis showed that the differentially expressed lncRNAs were involved in mRNA surveillance and AMPK signaling pathways. Besides these two pathways, RNA transport splicesome was another pathway incorporated with the differentially expressed mRNA. In summary, this study provides a preliminary database valuable for identifying lncRNAs critical in the late stage of spermatogenesis or important for sperm function regulation.

overall_design: LncRNA profiles of mice (3-5 months) were generated by stranded-specific RNA-seq, using Illumina HiSeqTM 4000 with PE100.

first: Xuhui

last: Zeng


title: The conserved protein Seb1 drives transcription termination by binding  RNA polymerase II and nascent RNA

last: Wittmann

summary: Termination of Pol II transcription is an important step in the transcription cycle and is responsible for dislodgement of polymerase from DNA which leads to the release of a functional transcript. Recent studies have identified key players important for termination and showed a conserved domain that interacts with the phosphorylated C-terminus of Pol II (CTD-Interacting-Domain, CID) to constitute a common feature of these proteins. However, the mechanism by which transcription termination is achieved, is not understood. Using genome-wide methods, we demonstrate that the fission yeast CID protein Seb1 is essential for termination of protein-coding and non-coding genes through interacting with S2-phosphorylated Pol II and nascent RNA. Furthermore, we present the crystal structures of the Seb1 CTD- and RNA-binding modules. Unexpectedly, the latter reveals a novel intertwined two-domain arrangement of a canonical RRM and a second domain. These results provide important insights into the mechanism underlying eukaryotic transcription termination.

overall_design: In this study, we studied binding of the S. pombe protein Seb1 directly to RNA by PAR-CLIP which was normalised to RNA expression levels (for which a RNA-Seq in WT cells was included). Point mutations were then introduced into Seb1 using a repressible system and RNA-Seq was performed for Seb1-WT and 5 different Seb1 point mutants that were all treated in the same way. Some samples were sequenced in duplicates and some (including the WT) in triplicates. Finally, binding was compared to another transcription factor, Pcf11, for which ChIP-Seq was performed. A control was done using an untagged strain. The binding profile was compared to phosphorylation levels of Ser2 on RNA-Pol II by doing ChIP-Seq for which an antibody against S2P was utilised. All ChIP-Seq experiments include an input sample.

first: Beth

last: Watts

first: Miles

last: Huseyin

first: Carlo

last: Baejen

first: Dong-Hyuk

last: Heo

first: Tea

last: Kecman

first: Patrick

last: Cramer

first: Lidia

last: Vasiljeva


title: A novel point mutation in RpoB improves osmotolerance and succinic acid production in Escherichia coli

city: Tianjin

first: feiyu

last: fan

state: Tianjin

address: 32 West 7th Avenue, Tianjin Airport Economic Area

department: Key Laboratory of Systems Microbial Biotechnology

institute: Tianjin Institute of Industrial Biotechnology, Chinese Academy of Sciences.

summary:
Purpose: To understand how D654Y mutated RpoB affect gene expression under either normal or osmotic stress conditions in Escherichia coli .
Methods: RNA-seq libraries were constructed for four samples, including (I) The parental strain Suc-T110 grown at normal condition (5%w/v glucose); (II)RpoB mutant RpoBD645Y [Suc-T110::rpoB (D654Y), RNA-seq library named NZ-502] grown at normal condition;(III) Suc-T110 grown at osmotic stress condition(12%w/v glucose);(IV) NZ-502 grown at osmotic stress condition. For preparation of RNA samples, Fresh colonies were picked from New NBS mineral salts plates containing 20 g liter-1 glucose, inoculated into 250 ml flasks containing 30 ml NBS mineral salts medium with 20 g liter-1 glucose, and grown at 37°C and 250 rpm for 12 h. Cultures were then transferred to a 500 ml fermentation vessel containing 250 ml NBS mineral salts medium with either 5%w/v or 12%w/v glucose. After 48 h, 1 ml culture was harvested by centrifugation, frozen in liquid nitrogen and sent to Beijing Genomics Institute (BGI, Shenzhen, China). The four 90-nt paired-end RNA-seq libraries were generated commercially at Beijing Genomics Institute by using the HiSeq™ 2000 platform. Sequencing data was handled essentially with Bowtie2, NOIseq. Expression levels are presented as Reads Per Kilobase of transcript per Million mapped reads (RPKM).
Results: we first comparative accessed expression levels of Suc-T110 and NZ-502 under normal condition. Among the 4200 predicted genes, 128 genes were found altered their expression in NZ502 compared with Suc-T110; with 38 targets specific up-regulated while 90 targets down-regulated. Genes engaged in biological function of amino acid metabolism (P-value=4.60E-05) were significantly enriched among in induced gene set. Under osmotic stress condition, 244 differential expressed genes were identified in NZ-502 when compared with Suc-T110, with 132 targets specific up-regulated while 112 targets down-regulated, Functional enrichment of 132 up regulated genes showed the most significantly enriched physiological function of NZ-502 upon hyperosmotic stress was associated with carbon source transportation (FunCat term: 20.01.03 C-compound and carbohydrate transport, P-value=9.51E-05), which containing a group of genes encoding diverse sugar transporters.
Conclusions: Transcriptome profiling suggested that derepression of sugar transporters might be the primary cause for NZ-502 to resist osmotic stress.

overall_design: mRNA profiles of Escherichia coli ATCC#8739 genetic engenerringed strain Suc-T110 and NZ-502  by deep sequencing, using Illumina HiSeq™ platform.

first: Mengyong

last: Xiao

first: Xinna

last: Zhu

first: Hongtao

last: Xu

first: Jinlei

last: Tang

first: Ru

last: Liu

first: Changhao

last: Bi

first: Feiyu*

last: Fan

first: Xueli*


title: Transcriptome analyses of rhesus monkey pre-implantation embryos reveal a reduced capacity for DNA double strand break (DSB) repair in primate oocytes and early embryos

city: Shanghai

first: Denghui

state: Shanghai

address: ShengLi Building, 320 Yueyang Road

institute: CAS-MPG Partner Institute for Computational Biology (PICB)

summary: Pre-implantation embryogenesis encompasses several critical events including genome reprogramming, zygotic genome activation (ZGA), and cell fate commitment, of which most remain mechanistically unclear in primate. Here we carried out time-series RNA-seq in 26 single and 8 pooled rhesus monkey oocytes and pre-implantation embryos encompassing representative developmental stages to explore these process.

overall_design: Transcriptome of 8 pooled and 26 single Rhesus Monkey oocytes and preimplantation embryos of stages from germinal vesicle-stage oocytes to blastocyst.

first: Xinyi

last: Wang


title: Rhizophagus irregularis gene regulation in response to rice root exudates

city: Castanet-Tolosan

first: Christophe

last: Roux

address: Chemin de Borde Rouge

country: France

institute: University of Toulouse/CNRS

summary:
Purpose: The recent publication of the fungal mutualist R. irregularis genome facilitated transcriptomic studies. We here adress the gene regulation of R. irregularis in response to root exudates from rice wild-type and osnope1 (no perception candidate - mutant unable to host arbuscular mycorrhizal fungi)
Methods: Spores of R. irregularis were treated with root exudates and collected at 1 hour, 24 hours and 7 days after addition. To monitor fungal gene regulation, control conditions were also prepared at T0, 1h, 24h and 7d. mRNA were sequenced by HiSeq Illumina. Reads were mapped on the Rhizophagus irregularis genome assembly (Gloin1 - Tisserant et al., PNAS, 2013) using CLCworkbench suite.
Results:
-At 1h, a set of 92 fungal genes were found up-regulated in response to wt root exudates (92), not to osnope1 root exudates, many of them being involved in cell signaling.
-At 24h and 7d, numerous genes putatively involved in primary metabolism were up-regulated in response to wt root exudates, not in response to osnope1 root exudates
-Several vital genes involved in cell development are repressed in response to osnope1 RE compared to wt RE.
Conclusions:  these results argue for a high metabolic activity induced by wt root exudates, not by osnope1 root exudates.

overall_design: mRNA sequences from spores treated with root exudates were generated by Illumina Hiseq 2000 (triplicate).

first: Marina

last: Nadal

first: Uta

last: Paszkowski


title: Molecular role of the PAX5-ETV6 oncoprotein in promoting B cell acute lymphoblastic leukemia

city: Vienna

first: Maria

last: Fischer

address: Campus-Vienna-Biocenter 1

country: Austria

institute: Research Institute of Molecular Pathology

summary: PAX5 is a tumor suppressor in B-ALL, while the role of PAX5 fusion proteins in B-ALL development is largely unknown. Here we studied the function of PAX5-ETV6 and PAX5- FOXP1 in mice expressing these proteins from the Pax5 locus. Both proteins arrested Blymphopoiesis at the pro-B-to-pre-B cell transition and, contrary to their proposed dominantnegative role, did not interfere with the expression of most Pax5 target genes. Pax5-Etv6, but not Pax5-Foxp1, cooperated with loss of the Cdkna2a/b tumor suppressor in promoting B-ALL development. Regulated Pax5-Etv6 target genes identified in these B-ALLs encode proteins implicated in pre-BCR signaling and migration/adhesion, which could contribute to the proliferation, survival and tissue infiltration of leukemic B-cells. Together with similar observations made in human PAX5-ETV6+ B-ALLs, these data identified PAX5-ETV6 as a potent oncoprotein.

overall_design: 36 samples in total: A) 24 RNA-Seq samples in 5 cell types: pro-B (5 genotypes, 2-4 replicates) large pre-B (2 genotypes, 2 replicates each) small pre-B (1 genotype, 2 replicates) lymph node (1 genotype, 3 replicates) bone marrow (1 genotype, 2 replicates) B) 12 ChIP-Seq samples in 2 cell types: pro-B (H3K27me3, H3K9ac, H3K4me2, H3K4me3, H3K27ac, 1 replicate each; Pax5Etv6 ChIP, Prd ChIP, 2 replicates each; Pax5 ChIP 1 replicate) lymph node (1 genotype, 2 replicates).

first: Leonie

last: Smeenk

first: Sabine

last: Jurado

first: Markus

last: Jaritz

first: Anna

last: Azaryan

first: Barbara

last: Werner

first: Mareike

last: Roth

first: Johannes

last: Zuber

first: Martin

last: Stanulla

first: Monique

last: den Boer

first: Charles

last: Mullighan

last: Strehl

first: Meinrad

last: Busslinger


title: Gene expression data from the irradiated mouse hippocampus

status: Public on Feb 03 2017

city: Busan

first: BuHyun

last: Youn

address: Busandaehak-ro 63beon-gil, Geumjeong-gu

department: Biological Sciences

institute: Pusan National University

summary:
Although IR-induced depression may cause decreased life quality of brain cancer patients after radiotherapy, investigations of its molecular mechanism and therapeutic strategies are still insufficient.
We used microarrays to detail the global program of gene expression underlying development of radiation-induced depression and identified a variety of genes whose expression were changed during this process.

overall_design: To elucidate targets that might be regulated by cranial irradiation in the hippocampus, we isolated total RNA from mice hippocampuses treated or not-treated with 2 Gy of cranial radiation. RNA samples were then subjected to microarray analysis.

first: JiHoon

last: Kang

first: Wanyeon

last: Kim

first: HyunJeong

last: Seo

first: EunGi

first: Beomseok

last: Son

first: Sungmin

last: Lee

first: Gaeul

last: Park

first: Changjong

last: Moon

first: HyeSook


title: Both maternally and paternally imprinted genes regulate seed development in rice

city: Nanjing

first: Jingya

last: Yuan

address: 1 Weigang Road

institute: Nanjing Agricultural University

type: Genome variation profiling by high throughput sequencing

summary:
Genetic imprinting is an epigenetic phenomenon that describes unequal expression of paternal and maternal alleles of a gene in sexually reproducing organisms including mammals and flowering plants. The function of imprinted genes was rarely reported.
We report genome-wide analysis of gene expression, DNA methylation, and small RNAs in the rice endosperm and functional tests of five imprinted genes in seed development using CRISPR/Cas9 editing technology.
We identified 162 maternally expressed genes(MEGs) and 95 paternally expressed genes (PEGs) in the rice endosperm, which were associated with miniature inverted-repeat transposable elements, imprinted differentially methylated loci, and some 21-22-siRNAs and lncRNAs. Remarkably, one-third of MEGs and nearly half of PEGs were associated with grain-yield quantitative trait loci and enriched in the endosperm-expressed genes. Disrupting two MEGs increased the amount of small starch granules and reduced grain size, weight, and embryo size, while mutating three PEGs reduced starch content and seed fertility.
Our data support both MEGs and PEGs in rice are required for starch and nutrient accumulation, mediating offspring fitness and optimal seed size. This imprinting strategy provides potential means for improving grain yield of rice and other cereal crops.

overall_design: We have submitted 14 samples: two resequencing samples of rice cultivars (02428 and Longtefu); two BS-seq libraries of endosperm of reciprocal hybrids; two RNA-seq libraries of endosperm of reciprocal hybrids; 4 small RNA libraries of endosperm of reciprocal hybrids and parents; 4 small RNA libraries of seedling of reciprocal hybrids and parents.

first: Sushu

last: Chen

first: Wu

last: Jiao

first: Longfei

last: Wang

first: Limei

first: Wenxue

last: Ye

first: Jie

last: Lu

first: Delin

last: Hong

first: Siliang

last: You

first: Zhukuan

last: Cheng

first: Dong-Lei

last: Yang

first: Z


title: Interrogation of functional cell surface markers identifies CD151 dependency in high-grade serous ovarian cancer

city: Toronto

first: Mauricio

last: Medrano

state: ON

address: 101 College Street

country: Canada

institute: Princess Margaret Cancer Centre

summary: The high degree of genetic aberrations characteristic of high-grade serous ovarian cancer (HGSC) makes identification of the molecular features that drive tumor progression difficult. Here, we perform genome-wide RNAi screens and comprehensive expression analysis of cell surface markers in a panel of HGSC cell lines to identify genes that are critical to their survival. We report that the tetraspanin CD151 contributes to survival of a subset of HGSC cell lines associated with a ZEB transcriptional program and supports the growth of HGSC tumors. Moreover, we show that high CD151 expression is prognostic of poor clinical outcome. This study reveals cell-surface vulnerabilities associated with HGSC, provides a framework for identifying therapeutic targets, and reports a role for CD151 in HGSC.

overall_design: 40 epithelial ovarian cancer cell lines and one immortalized line derived from ovarian surface epithelium (OE-E6/E7)

first: Robert

last: Rottapel


title: polyA mRNA RNA-seq from K562 (ENCSR000BZV)

city: Stanford

first: ENCODE

last: DCC

address: 300 Pasteur Dr

institute: ENCODE DCC

summary:
RNA-seq on human K562 cytosol long polyadenalated RNA

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 MEL cell line (ENCSR000ADU)

summary:
Control ChIP-seq on mouse MEL treated with 2% DMSO produced by the Snyder lab

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: RNAseq analysis of GL261 GDC and mNS GSC transcriptome

city: Geneva

first: Natacha

last: Civic

address: Rue Michel-Servet 1

department: iGE3 Genomics Platform

country: Switzerland

institute: University of Geneva

summary: We compare the gene expression profile between GL261 glioma differentiated cells (GDC) and mNS Neurospheres glioma stem like cells (GSC).

overall_design: Methods: GL261 and mNS at different passage were havested for extraction. The libraries were prepared with 1 ug of total RNA as starting material and processed with the Illumina TruSeq stranded total RNA (Ribo-Zero Gold) kit according to the manufacturer instruction. Libraries were sequenced according to 100 single-read protocol on a HiSeq 2500 from Illumina. This experiments were performed at the iGE3 genomics platform of the University of Geneva (http://www.ige3.unige.ch/genomics-platform.php). Differential analysis was performed using the edgeR package (Robinson et al., 2010). Normalization factors were computed using the TMM technique, after which tagwise dispersions were calculated and subjected to an exact test. Resulting P values were subjected to Benjamini-Hochberg multiple testing correction to derive FDRs.

first: Esen

middle: Y

last: Bassoy

first: Atsuko

last: Kasahara

first: Valentina

last: Chiusolo

first: Guillaume

last: Jacquemin

first: Emma

last: Boydell

first: Sebastian

last: Zamorano

first: Cristina

last: Riccadonna

first: Serena

last: Pellegatta

first: Nicolas

last: Hulo

first: Valérie

last: Dutoit

first: Madiha

last: Derouazi

first: Pierre

last: Dietrich

first: Paul

last: Walker

first: Denis

last: Martinvalet


title: ChIP-seq from MEL cell line (ENCSR000AEA)

summary:
H3K4me3 Histone Modification by ChIP-seq on mouse MEL treated with 2% DMSO produced by the Snyder lab

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 MEL cell line (ENCSR000ADR)

summary:
H3K4me3 Histone Modification by ChIP-seq on mouse MEL produced by the Snyder lab

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: Subinhibitory concentrations of ciprofloxacin enhance antimicrobial resistance and pathogenicity of Enterococcus faecium

city: Rennes

first: Vincent

last: Cattoir

address: 2 rue Henri Le Guilloux

institute: CHU de Rennes

summary: Enterococcus faecium has emerged as a major opportunistic pathogen for two decades, with the spread of hospital-adapted multidrug-resistant clones. Members of the intestinal microbiota, they are subjected to numerous bacterial stresses, including antibiotics at subinhibitory concentrations (SICs). Since fluoroquinolones are extensively prescribed, SICs are very likely to occur in vivo with potential effects on bacterial metabolism with subsequent modulation of opportunistic traits. The aim of the study was to evaluate globally the impact of subinhibitory concentrations (SICs) of ciprofloxacin on antimicrobial resistance and pathogenicity of E. faecium. Transcriptomic analysis was performed by RNA-seq (HiSeq 2500, Illumina) using the vanB-positive reference strain E. faecium Aus0004 in the absence or presence of ciprofloxacin SIC (0.38 mg/L, i.e. MIC 1/8). Several genetic and phenotypic tests were used for validation. In the presence of ciprofloxacin SIC, 196 genes were significantly induced whereas 286 were significantly repressed, meaning that 16.8% of the E. faecium genome was altered. Amongst upregulated genes, EFAU004_02294 (fold change of 14.3) encoded a protein (EfmQnr) homologue of Qnr proteins involved in quinolone resistance in Gram-negative bacilli. Its implication in intrinsic and adaptive FQ resistance in E. faecium was experimentally ascertained. Moreover, EFAU004_02292 coding for the collagen adhesin Acm was also induced by SIC of ciprofloxacin (fold change of 8.2), and higher adhesion capabilities were demonstrated phenotypically. Both Efmqnr and Acm determinants may play an important role in the transition from a commensal to a pathogenic state of E. faecium that resides in the gut of patients receiving a fluoroquinolone therapy.

overall_design: Transcriptome analysis by RNA-seq to monitor the levels of all transcripts in bacterial cells grown in the absence or the presence of a subinhibitory concentration (0.38 mg/L) of ciprofloxacin

first: Clara

last: Sinel


title: ChIP-seq from MEL cell line (ENCSR000ADP)

first: ENCODE

last: DCC

summary:
H3K27me3 Histone Modification by ChIP-seq on mouse MEL produced by the Snyder lab

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 dendritic cell (ENCSR986ZZK)

summary:
ChIP-seq

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: total RNA-seq from dendritic cell (ENCSR975YGW)

summary:
Ovation Human FFPE RNA-Seq Multiplex System

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: ATAC-seq from dendritic cell (ENCSR939XWM)

summary:
ATAC-seq

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 dendritic cell (ENCSR945BBR)


title: total RNA-seq from dendritic cell (ENCSR945SYV)

summary:
RNA-Seq

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: ATAC-seq from dendritic cell (ENCSR940QJU)


title: ATAC-seq from dendritic cell (ENCSR926TFY)


title: ATAC-seq from dendritic cell (ENCSR926GDT)


title: total RNA-seq from dendritic cell (ENCSR916YUR)


title: ATAC-seq from dendritic cell (ENCSR901IEQ)


title: ATAC-seq from dendritic cell (ENCSR904UKR)


title: total RNA-seq from dendritic cell (ENCSR892ZUK)


title: total RNA-seq from dendritic cell (ENCSR870DRE)


title: total RNA-seq from dendritic cell (ENCSR867RTO)


title: ATAC-seq from dendritic cell (ENCSR780HBP)


title: total RNA-seq from dendritic cell (ENCSR760INS)

summary: 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 dendritic cell (ENCSR740ROX)


title: ATAC-seq from dendritic cell (ENCSR984HFU)


title: ATAC-seq from dendritic cell (ENCSR679NRJ)


title: total RNA-seq from dendritic cell (ENCSR670MXT)


title: total RNA-seq from dendritic cell (ENCSR707JVU)


title: ChIP-seq from MEL cell line (ENCSR000ADN)

summary:
Control ChIP-seq on mouse MEL produced by the Snyder lab

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: total RNA-seq from dendritic cell (ENCSR652RSO)


title: total RNA-seq from dendritic cell (ENCSR682CFV)


title: ChIP-seq from dendritic cell (ENCSR650OZF)


title: ATAC-seq from dendritic cell (ENCSR648JJT)


title: total RNA-seq from dendritic cell (ENCSR602ODY)


title: ATAC-seq from dendritic cell (ENCSR605EGR)


title: ATAC-seq from dendritic cell (ENCSR628SXX)


title: ATAC-seq from dendritic cell (ENCSR566LZT)


title: ATAC-seq from dendritic cell (ENCSR544YXV)


title: total RNA-seq from dendritic cell (ENCSR571IUZ)


title: total RNA-seq from dendritic cell (ENCSR536GUD)


title: ATAC-seq from dendritic cell (ENCSR535NOD)


title: ChIP-seq from dendritic cell (ENCSR482UTI)


title: RNA-seq analysis of Drosophila clock and non-clock neurons reveals neuron-specific cycling and novel candidate neuropeptides

city: Waltham

first: Katharine

last: Abruzzi

address: 415 South St.

department: Biology

institute: HHMI; Brandeis University

summary: LNd, LNv, DN1 and TH neurons were manually sorted from dissociated Drosophila brains.  RNA was extracted and transcriptomes analyzed via RNA-seq.

overall_design: LNd, LNv, DN1 and TH neurons at various timepoints.

first: Michael

last: Rosbash


title: ATAC-seq from dendritic cell (ENCSR787YJK)


title: total RNA-seq from dendritic cell (ENCSR476TKU)


title: total RNA-seq from dendritic cell (ENCSR519NFO)


title: Dynamic DNA methylation landscape defines brown and white cell specificity during adipogenesis (RRBS)

city: Wenzhou

first: Chunming

last: Ding

address: Wenzhou Medical University, University Town, Chashan, Wenzhou, Zhejiang, P.R China

institute: Wenzhou Medical University

summary: We depicted a genome-wide integrative view of DNA methylome by reduced representation bisulfite sequencing (RRBS) and transcriptome by RNA-seq during brown and white adipocyte differentiation. Our analysis demonstrated that DNA methylation is a stable epigenetic signature for brown and white cell lineage before, during and after differentiation. When comparing white to brown adipocytes at all three time points of differentiation, we identified five members of the Hox family whose expression levels were anti-correlated with promoter methylation, suggesting a regulatory role of DNA methylation in transcription.

overall_design: Examination of DNA methylome in brown and white adipocytes

first: Yen

last: Lim


title: total RNA-seq from dendritic cell (ENCSR475TVN)


title: ChIP-seq from dendritic cell (ENCSR450JZC)


title: ChIP-seq from dendritic cell (ENCSR427BKJ)


title: ChIP-seq from dendritic cell (ENCSR403BAT)


title: ATAC-seq from dendritic cell (ENCSR347RZI)


title: total RNA-seq from dendritic cell (ENCSR332SRS)


title: ATAC-seq from dendritic cell (ENCSR290AUK)


title: ATAC-seq from dendritic cell (ENCSR589ROM)


title: ATAC-seq from dendritic cell (ENCSR237VSF)


title: ATAC-seq from dendritic cell (ENCSR329XFZ)


title: ChIP-seq from dendritic cell (ENCSR399QWL)


title: ChIP-seq from dendritic cell (ENCSR531MLI)


title: ATAC-seq from dendritic cell (ENCSR370QWN)


title: ATAC-seq from dendritic cell (ENCSR204FCV)


title: ATAC-seq from dendritic cell (ENCSR208NBF)


title: total RNA-seq from dendritic cell (ENCSR227MWL)


title: ATAC-seq from dendritic cell (ENCSR222SCA)


title: total RNA-seq from dendritic cell (ENCSR198JTV)


title: ATAC-seq from dendritic cell (ENCSR116SPR)


title: total RNA-seq from dendritic cell (ENCSR146PLL)


title: total RNA-seq from dendritic cell (ENCSR085TSA)


title: ATAC-seq from dendritic cell (ENCSR459AYS)


title: total RNA-seq from dendritic cell (ENCSR084JIA)


title: ChIP-seq from dendritic cell (ENCSR075AVX)


title: total RNA-seq from dendritic cell (ENCSR022BYE)


title: polyA mRNA RNA-seq from spleen (ENCSR966JPL)

summary:
RNA-seq of mouse spleen tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from lung (ENCSR870AQU)

summary:
RNA-seq of mouse lung tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from testis (ENCSR693GGB)

summary:
RNA-seq of human testis tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from adrenal gland (ENCSR680AAZ)

summary:
RNA-seq of human adrenal gland. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from heart (ENCSR635GTY)

summary:
RNA-seq of human heart tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from small intestine (ENCSR612HYR)

summary:
RNA-seq of human small intestine tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from brain (ENCSR554PHF)

summary:
RNA-seq of mouse brain tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from ovary (ENCSR516UNF)

summary:
RNA-seq in mouse ovary.

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: total RNA-seq from dendritic cell (ENCSR178SNP)


title: polyA mRNA RNA-seq from sigmoid colon (ENCSR518GDK)

summary:
RNA-seq of mouse sigmoid colon tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from spleen (ENCSR448VSW)

summary:
RNA-seq of human spleen tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: ATAC-seq from dendritic cell (ENCSR156FDX)


title: polyA mRNA RNA-seq from brain (ENCSR274JRR)

summary:
RNA-seq of human brain tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: ATAC-seq from dendritic cell (ENCSR059IHA)

summary:
ATAC-seq

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: polyA mRNA RNA-seq from kidney (ENCSR394YLM)

summary:
RNA-seq of mouse kidney tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: ATAC-seq from dendritic cell (ENCSR131CHJ)


title: polyA mRNA RNA-seq from testis (ENCSR266ESZ)

summary:
RNA-seq of mouse testis tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from adipose tissue (ENCSR288TLO)

summary:
RNA-seq of mouse adipose tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from sigmoid colon (ENCSR270OKS)

summary:
RNA-seq of human sigmoid colon tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from pancreas (ENCSR248XKS)

summary:
RNA-seq of mouse pancreas tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from liver (ENCSR216KLZ)

summary:
RNA-seq of mouse liver tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from small intestine (ENCSR170SVO)

summary:
RNA-seq of mouse small intestine tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from liver (ENCSR085HNI)

summary:
RNA-seq of human liver tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from kidney (ENCSR071ZMO)

summary:
RNA-seq of human kidney tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from heart (ENCSR164BAZ)

summary:
RNA-seq of mouse heart tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from adrenal gland (ENCSR713OCQ)

summary:
RNA-seq of mouse adrenal gland tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from adipose tissue (ENCSR236OON)

summary:
RNA-seq of human adipose tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from pancreas (ENCSR001UXR)

summary:
RNA-seq of human pancreas tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from ovary (ENCSR046XHI)

summary:
RNA-seq in human ovary.

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: polyA mRNA RNA-seq from G1E-ER4 (ENCSR000CIH)

summary:
RNA-seq on mouse G1E-ER4 (single end) differentiated for 24 hours

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: polyA mRNA RNA-seq from MEL cell line (ENCSR000CIE)

summary:
RNA-seq on mouse erythroleukemia cells treated with dimethylsulfoxide 2.0% (single end)

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: polyA mRNA RNA-seq from MEL cell line (ENCSR000CID)

summary:
RNA-seq on mouse erythroleukemia cells cell (single end)

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: polyA mRNA RNA-seq from brown adipose tissue (ENCSR000CHN)

summary:
RNA-seq on 24 week adult mouse brown 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: polyA mRNA RNA-seq from bone marrow macrophage (ENCSR000CHO)

summary:
RNA-seq on 8 week adult mouse bone marrow derived macrophage

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: polyA mRNA RNA-seq from limb (ENCSR000CHJ)

summary:
RNA-seq on 14.5 day embryonic mouse limb

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: polyA mRNA RNA-seq from lung (ENCSR129KCJ)

summary:
RNA-seq of human lung tissue tissue. The second technical replicate was performed in May 2015 and was not part of the original Lin et al. 2014 publication (PMID:25413365).

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: polyA mRNA RNA-seq from testis (ENCSR000CHH)

summary:
RNA-seq on 8 week adult mouse testis

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: polyA mRNA RNA-seq from brain (ENCSR000CHG)

summary:
RNA-seq on 14.5 day embryonic mouse whole brain

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: polyA mRNA RNA-seq from olfactory bulb (ENCSR000CHL)

summary:
RNA-seq on 8 week adult mouse olfactory bulb

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: polyA mRNA RNA-seq from cortical plate (ENCSR000CGY)

summary:
RNA-seq on 8 week adult mouse cortex

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: polyA mRNA RNA-seq from MEL cell line (ENCSR000CHM)

summary:
RNA-seq on mouse MEL cell line

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: polyA mRNA RNA-seq from heart (ENCSR000CGZ)

summary:
RNA-seq on 8 week adult mouse heart

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: polyA mRNA RNA-seq from kidney (ENCSR000CHA)

summary:
RNA-seq on 8 week adult mouse kidney

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: polyA mRNA RNA-seq from thymus (ENCSR000CHK)

summary:
RNA-seq on 8 week adult mouse thymus

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: polyA mRNA RNA-seq from small intestine (ENCSR000CHI)

summary:
RNA-seq on 8 week adult mouse small intestine

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: polyA mRNA RNA-seq from embryonic fibroblast (ENCSR000CGV)

summary:
RNA-seq on mouse embryonic fibroblast (MEF)

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: polyA mRNA RNA-seq from lung (ENCSR000CHC)

summary:
RNA-seq on 8 week adult mouse 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: polyA mRNA RNA-seq from bone marrow (ENCSR000CGT)

summary:
RNA-seq on 8 week adult mouse bone marrow

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: polyA mRNA RNA-seq from Panc1 (ENCSR000BYM)

summary:
RNA-seq on Panc-1 greater than 200bp polyA+

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: polyA mRNA RNA-seq from SK-N-SH (ENCSR000BYL)

summary:
RNA-seq on SK-N-SH greater than 200bp polyA+

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: polyA mRNA RNA-seq from cerebellum (ENCSR000CGX)

summary:
RNA-seq on 8 week adult mouse cerebellum

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: polyA mRNA RNA-seq from liver (ENCSR000CHE)

summary:
RNA-seq on 14.5 day embryonic mouse 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: polyA mRNA RNA-seq from placenta (ENCSR000CHD)

summary:
RNA-seq on 8 week adult mouse placenta

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: polyA mRNA RNA-seq from CH12.LX (ENCSR000CHR)

summary:
RNA-seq on mouse CH12 (single end)

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: polyA mRNA RNA-seq from spleen (ENCSR000CGW)

summary:
RNA-seq on 8 week adult mouse 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: polyA mRNA RNA-seq from heart (ENCSR000CHF)

summary:
RNA-seq on 14.5 day embryonic mouse heart

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: polyA mRNA RNA-seq from PFSK-1 (ENCSR000BYN)

summary:
RNA-seq on PFSK-1 greater than 200bp polyA+

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: polyA mRNA RNA-seq from A549 (ENCSR000BYI)

summary:
RNA-seq on A549 greater than 200bp polyA+ treated with dexamethasone at 500pM

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: polyA mRNA RNA-seq from A549 (ENCSR000BYJ)

summary:
RNA-seq on A549 greater than 200bp polyA+ treated with dexamethasone at 5nM

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: polyA mRNA RNA-seq from BE2C (ENCSR000BYK)

summary:
RNA-seq on BEC-C greater than 200bp polyA+

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: polyA mRNA RNA-seq from A549 (ENCSR000BYH)

summary:
RNA-seq on A549 greater than 200bp polyA+ treated with dexamethasone at 1nM

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: polyA mRNA RNA-seq from T47D (ENCSR000BYE)

summary:
RNA-seq on T-47D greater than 200bp polyA+ treated with dimethylsulfoxide for 4 hours

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: polyA mRNA RNA-seq from ES-Bruce4 (ENCSR000CGU)

summary:
RNA-seq on embryonic mouse stem cell line Bruce4

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: polyA mRNA RNA-seq from T47D (ENCSR000BYF)

summary:
RNA-seq on T-47D greater than 200bp polyA+ treated with estradiol at 10nM for 4 hours

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: polyA mRNA RNA-seq from T47D (ENCSR000BYD)

summary:
RNA-seq on T-47D greater than 200bp polyA+ treated with bisphenol A at 100nM for 4 hours

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: polyA mRNA RNA-seq from Ishikawa (ENCSR000BYA)

summary:
RNA-seq on ECC-1 greater than 200bp polyA+ treated with dimethylsulfoxide for 4 hours. Note- This experiment previously referred to its biosample as ECC-1, however it has been found that all currently available ECC-1 are actually Ishikawa 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: polyA mRNA RNA-seq from Ishikawa (ENCSR000BYB)

summary:
RNA-seq on ECC-1 greater than 200bp polyA+ treated with estradiol at 10nM for 4 hours. Note- This experiment previously referred to its biosample as ECC-1, however it has been found that all currently available ECC-1 are actually Ishikawa 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: polyA mRNA RNA-seq from Ishikawa (ENCSR000BXZ)

summary:
RNA-seq on ECC-1 greater than 200bp polyA+ treated with bisphenol A at 100nM for 4 hours. Note- This experiment previously referred to its biosample as ECC-1, however it has been found that all currently available ECC-1 are actually Ishikawa 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: polyA mRNA RNA-seq from A549 (ENCSR000BXY)

summary:
RNA-seq on A549 greater than 200bp polyA+ treated with dexamethasone at 100pM

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: Immune Escape via A Transient Gene Expression Program Enables Productive Replication of A Latent Pathogen

city: New York

first: Mariko

last: Kobayashi

state: NY

address: 1230 York Avenue

department: Molecular Neuro-Oncology

institute: Rockefeller University

summary: How type I / II interferons (IFNs) prevent periodic re-emergence of latent pathogens in tissues of diverse cell-types remains unknown. Using homogenous neuron cultures latently-infected with herpes simplex virus (HSV), we show that extrinsic type I or II IFN act directly on neurons to induce unique gene expression signatures and inhibit the reactivation-specific burst of viral genome-wide transcription called Phase I. Surprisingly, IFNs suppressed reactivation only during a limited period early in Phase I preceding productive virus growth. Sensitivity to type II IFN was selectively lost if viral ICP0, which normally accumulates later in Phase I, was expressed prior to reactivation. Thus, IFNs suppress reactivation by preventing initial expression of latent genomes but are ineffective once Phase I viral proteins accumulate and limit IFN action. This demonstrates that inducible reactivation from latency is only transiently sensitive to IFNs. Moreover, it illustrates how latent pathogens escape host immune control to periodically replicate by rapidly deploying an interferon-resistant state.

overall_design: Superior cervical ganglia (SCG) neuron cultures harboring reactivating HSV-1 treated with IFNb or IFNg.  Neurons were harvested for RNA 20h after reactivation (in the presence or absence of IFN) for RNA-seq.  Libraries were generated following Illumina Truseq Ribo-Zero protocol.

first: Ian

last: Mohr

first: Robert

middle: B

last: Darnell


title: Expression Analysis of 2D, 3D Quiescent, and 3D Activated Pancreatic Stellate Cells

city: Cold Spring Harbor

first: David

middle: A.

last: Tuveson

address: 1 Bungtown Rd.

department: Cancer Center

institute: Cold Spring Harbor Laboratory

summary: This study used Illumina single-end RNA-sequencing to examine gene expression differences between 2 mouse-derived pancreatic stellate cell lines (PSC4, PSC5) grown either in 2D monolayers, as 3D quiescent cultures, or as 3D activated transwell cocultures with 2 mouse tumor-derived pancreatic ductal organoid lines (T4, T5). Mouse pancreatic stellate cell (PSC) lines were derived from the pancreata of wild-type C57Bl/6J mice. Mouse tumor organoid lines were derived from mouse pancreata containing pancreatic ductal adenocarcinoma (PDAC) from the KrasLSL-G12D; Trp53LSL-R162H; Pdx1-Cre mouse model. We measured genes differentially expressed among 2D, quiescent, and 3D activated PSCs that may reflect the expression changes of heterogeneous CAF population in pancreatic tumors.

overall_design: Gene expression comparison of 2 murine pancreatic stellate cell lines grown either in 2D monolayers, 3D quiescent cultures, or 3D activated transwell cocultures with 2 murine pancreatic ductal adenocarcinoma-derived pancreatic ductal organoid lines.

first: Lindsey

last: Baker

first: Abram

last: Handly-Santana


title: 5C with wild type mESC, wild type NPC and mESC with various PcG components knocked-out

city: Boston

first: Sharmistha

last: Kundu

address: 185 Cambridge St

institute: Massachusetts General Hospital

summary: Master regulatory genes require stable silencing by the Polycomb-Group (PcG) to prevent improper expression during differentiation and development. Some PcG proteins covalently modify histones, which contributes to heritable repression. The role for other effects on chromatin structure is less understood. We characterized the organization of PcG target genes in mouse ES cells and neural progenitors using high-resolution 5C technology and super-resolution microscopy. The genomic loci of repressed PcG target genes formed discrete, small domains of tight interaction that corresponded to locations bound by canonical Polycomb Repressive Complex 1 (PRC1). These domains changed during differentiation as PRC1 binding changed. Their formation depended upon the Polyhomeotic component of canonical PRC1, and occurred independently of PRC1-catalyzed ubiquitylation. PRC1 domains differ from topologically associating domains in numerous aspects . These domains have the potential to play a key role in transmitting epigenetic silencing of PcG targets by linking PRC1 to formation of a repressive higher order structure.

overall_design: 5C performed to compare 3D chromatin interactions of in vitro derived NPC and various PcG mutant mESC with wild type ESC. Experiments were performed in dupicates. 100bp paired end sequencing was performed on Illumina HiSeq2500. Reference genome is mm9.

middle: E

last: Kingston


title: RNA-Seq with wild type mESC, wild type NPC and Phc1 knock-out ESC

overall_design: RNA-Seq was performed to compare gene expression of in vitro derived NPC and Phc1 knock-out mESC with wild type ESC. Experiments were performed in dupicates. 50base single end sequencing was performed on Illumina HiSeq2000. Reference genome is mm9.


title: ChIP-Seq with wild type mESC and NPC

summary: Master regulatory genes require stable silencing by the Polycomb-Group (PcG) to prevent improper expression during differentiation and development. Some PcG proteins covalently modify histones, which contributes to heritable repression. The role for other effects on chromatin structure is less understood. We characterized the organization of PcG target genes in mouse ES cells and neural progenitors using high-resolution 5C technology and super-resolution microscopy. The genomic loci of repressed PcG target genes formed discrete, small domains of tight interaction that corresponded to locations bound by canonical Polycomb Repressive Complex 1 (PRC1). These domains changed during differentiation as PRC1 binding changed. Their formation depended upon the Polyhomeotic component of canonical PRC1, and occurred independently of PRC1-catalyzed ubiquitylation. PRC1 domains differ from topologically associating domains in numerous aspectsá. These domains have the potential to play a key role in transmitting epigenetic silencing of PcG targets by linking PRC1 to formation of a repressive higher order structure.

overall_design: ChIP-Seq was performed to compare PRC1 ans PRC2 occupancy between wild type ESC and in vitro derived NPC. 50 base single end sequencing was performed on Illumina HiSeq2500. Reference genome is mm9.


title: Distinct roles for motif affinity, chromatin state, and co-regulatory motifs in PPARγ binding and enhancer activity

city: Cambridge

first: Sharon

last: Grossman

address: 415 Main Street

institute: Broad Institute

summary: Sequence-specific transcription factors (TFs) regulate gene expression by binding to cognate motifs in promoters and enhancers. However, predicting genomic TF binding events and their quantitative contribution to expression remains a major challenge. In principle, the binding and enhancer activity of specific sites in vivo might depend on: (i) latent properties of the motif instance, (ii) cooperative interactions with other TFs that bind in the immediate vicinity, and (iii) the chromatin state of the sites in the genome. Here, we used massively parallel reporter assays (MPRA) involving 32,115 natural and synthetic enhancers, together with high-throughput in vivo assays, to systematically dissect the contributions of motif affinity, cooperative interactions, and chromatin accessibility to the binding and regulatory activity of genomic sequences that contain motifs for PPARγ, a TF that serves as a key regulator of adipogenesis. We show that PPARγ binding and enhancer activity are governed by distinct features. Genomic PPARγ binding to motif sites is largely governed by on larger-scale features, such as chromatin accessibility, whereas the degree to which a PPARγ motif site enhances transcriptional activity depends on the sequence immediately surround the motif. We detect and functionally validate a network of TFs comprised of multiple functional classes that collaborate with PPARγ to drive transcription. We extensively perturb this network, revealing functional cooperativity among classes of TFs that does not depend on precise positioning. Together, these results present a clear picture of how chromatin and TFs from distinct functional classes interact with PPARγ to determine binding and enhancer activity, and provide a paradigm for studying any TF.

sample_organism:
Mus musculus
synthetic construct

platform_organism:
Mus musculus
synthetic construct

overall_design: The study consisted of 7 MPRA experiments and 2 ChIP-seq experiments. Raw data for MPRA experiments are provided as Illumina reads of the 16 bp barcode from the RNA extracted 16 hours post transfection as well as from the plasmid library used for transfection. Raw data for ChIP-seq experiments are provided as paired-end Illumina reads for PPARg ChIP DNA fragments extracted 16 hours post transfection as well as input DNA fragments. For pools 4-7, we have provided barcode/oligo combinations as paired-end Illumina reads covering the barcode and enhancer sequence. Processed count files are counts corresponding to each barcode (Pools 1-3) or counts summed across all barcodes for each oligo (Pools 4-7).


title: Polycomb-mediated chromatin compaction during cell differentiation

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

overall_design: Refer to individual Series


title: Bacillus subtilis SMC complexes juxtapose chromosome arms as they travel  from origin to terminus

city: Bloomington

first: Xindan

last: Wang

state: IN

address: 1001 E 3rd St

institute: Indiana University at Bloomington

summary: Structural maintenance of chromosomes (SMC) complexes play critical roles in chromosome dynamics in virtually all organisms but how they function remains poorly understood. In Bacillus subtilis, SMC condensin complexes are topologically loaded at centromeric sites adjacent to the replication origin. Here we provide evidence that these ring-shaped assemblies tether the left and right chromosome arms together while traveling from the origin to the terminus (>2 Mb) at rates >50kb/min. Condensin movement scales linearly with time arguing for an active transport mechanism. These data support a model in which SMC complexes function by processively enlarging DNA loops. Loop formation followed by processive enlargement provides a mechanism for how condensin complexes compact and resolve sister chromatids in mitosis and how cohesin generates topologically associating domains (TADs) during interphase.

overall_design: Hi-C experiments were performed on wild type and mutant cells of Bacillus subtilis PY79 growing in rich media. ChIP-seq experiments were performed on cells growing in the same condition as in Hi-C experiments.

middle: Z

last: Rudner


title: polyA mRNA RNA-seq from T47D (ENCSR000BYG)

summary:
RNA-seq on T-47D greater than 200bp polyA+ treated with genistein at 100nM for 4 hours

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: Oncogenic ZEB2 activation drives sensitivity towards LSD1 inhibition in T-cell acute lymphoblastic leukemia

city: Gent

first: Sofie

last: Peirs

address: De Pintelaan 185

country: Belgium

institute: Ghent University

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus


title: Single cell transcriptome sequencing of mammary stem cells in the pubertal mammary gland

city: Utrecht

first: Mauro

last: Muraro

state: Utrecht

address: Uppsalalaan, 8

country: Netherlands

institute: Single Cell Discoveries

summary: The mammary gland is a highly dynamic organ that mainly develops during puberty. Based on morphology and proliferation analysis, mammary stem cells (MaSCs) are thought to be close to or reside in the terminal end buds (TEBs) during pubertal development. However, exclusive stem cell markers are lacking, and therefore the true identity of MaSCs, including their location, multiplicity, dynamics and fate during branching morphogenesis, has yet to be defined. To gain more insights into the molecular identity and heterogeneity of the MaSC pool, we performed single cell transcriptome sequencing of mammary epithelial cells micro-dissected from ducts and TEBs during puberty. These data show that the behaviour of MaSCs cannot be directly linked to a single expression profile. Instead, morphogenesis of the mammary epithelium relies upon a heterogeneous population of MaSCs that functions long-term as a single equipotent pool of stem cells.

overall_design: Ducts and terminal end buds were micro-dissected from the 4th and the 5th murine mammary gland at 5 weeks-of-age, dissociated into single cells, and FACS sorted. Single-cell transcriptomics was performed on live cells using an automated version of CEL-seq2 on live, FACS sorted cells. The StemID algorithm was used to identify clusters of cells corresponding to basal and luminal cells types derived from ducts and terminal end buds.

first: Colinda

last: Scheele

first: Jacco

last: van Rheenen

first: Alexander

last: van Oudenaarden