title: RNA sequencing of macrophages derived from monocytes differentiated in presence of M-CSF, GM-CSF and heat killed mycobacteria M. obuense

city: Houston

first: Humam

last: Kadara

state: TX

address: 2130 W. Holcombe Blvd

institute: University of Texas MD Anderson Cancer Center

summary: Earlier work has shown that macrophages derived from differentiation of monocytes by heat killed (HK) mycobacteria (e.g. M. obuense) exhibit unique immunophenotypic and molecular properties. Yet, our knowledge of these properties is still limited. The goal of the study is to understand global gene expression programs that are differentially modulated in macrophages derived from monocytes that were differentiated through three different routes: in presence of M-CSF, GM-CSF and the heat killed mycobacterium M. obuense. We performed RNA sequencing (RNA-Seq) of monocyte-derived macrophages (MDM) that were acquired from four separate healthy donors and differentiated by incubation with M-CSF (M-MDM), GM-CSF (GM-MDM) and HK M. obuense (Mob-MDM) (n = 12 samples). We report that Mob-MDM exhibit unique gene expression programs that may explain its unique immunophenotypic properties and thus immunomodulatory capacity.

overall_design: We performed RNA-Seq of monocyte-derived macrophages (MDM) that were acquired from four phenotypically  healthy donors. Monocytes were differentiated by incubation with M-CSF (M-MDM), GM-CSF (GM-MDM) and HK M. obuense (Mob-MDM) (n = 12 samples).

first: Samer

last: Bazzi

first: Georges

last: Bahr


title: Enhancing the Potency of Mouse Embryonic Stem Cells [BS-Seq]

status: Public on Nov 01 2017

city: St Louis

first: Sabine

last: Dietmann

state: MO

address: 4565 McKinley Avenue

country: USA

institute: Washington University School of Medicine

type: Methylation profiling by high throughput sequencing

summary: Mouse naïve pluripotent stem cells (ESC) can contribute to all embryonic tissues and the germline, but rarely to the extra-embryonic tissues in chimeric embryos. Here we describe a novel advanced pluripotent stem cell (ASC) with higher potency, since a single ASC contributes very efficiently to the fetus, germline, yolk sac and the placental labyrinth in chimeras. ASCs were derived from blastocysts in two steps in a chemically defined medium with Activin A (ActA) and basic fibroblast growth factor (bFGF), followed by Wnt and BMP. Notably, ASCs exhibit a distinct transcriptome with the expression of both naïve pluripotent genes, as well as mesodermal somatic genes; Eomes, Eras, Tdgf1, Evx1, hand1, Wnt5a, and distinct repetitive elements. Established ESCs can also be readily and directly to ASCs. Importantly, ASCs exhibit a stable hypermethylated epigenome unlike the hypomethylated epiblast in blastocysts and naïve ESCs, indicating that ASCs might represent a state in between the naïve and primed states of pluripotency.

overall_design: Whole genome bisulfite sequencing of ASCs, ESCs and EpiSCs using the post bisulfite adaptor tagging method

first: Fuchou

last: Tang

first: Walfred

middle: W

first: Jingyun

last: Li

first: Lin


title: Differential Expression of MicroRNAs in Leprosy Skin Lesions

status: Public on Oct 31 2017

city: Belo Horizonte

first: Alex

middle: FIORINI

last: Carvalho

state: MG

address: Avenida Antonio Carlos 6627

department: DMVP

country: Brazil

institute: UFMG

summary:
In this study, a comprehensive assessment of human miRNA was performed on leprosy skin lesions using DNA chip microarrays, which included the entire spectrum of the disease along with its reactional states. Sixty-eight samples from leprotic lesions (10TT, 10BT, 10BB, 10BL, 4LL, 14R1, and 10R2) and nine skin biopsies from healthy
individuals were used as controls (CC) (ages ranged from 06 to 83 years, 48 were male and 29 female). The evaluation identified differentially expressed miRNAs [Fold Change (FC)≥2.0, p<0.05] in disease lesions versus healthy controls or between them. Some of these miRNAs were validated by RT-PCR.

overall_design: The sequence of events for this study followed the order below. Patients who were treated for leprosy were examined by leprologists and submitted to two biopsy procedures. One biopsy was processed for histopathological analysis and bacilloscopy, the other was immediately stored in RNAlater® solution (Ambion) for further RNA extraction. Sixty-eight samples from leprotic lesions (10TT, 10BT, 10BB, 10BL, 4LL, 14R1, and 10R2) were selected for analysis. In addition, nine skin biopsies from healthy individuals were usedas controls (CC). Differentially expressed miRNAs identified in the cDNA microarray assay were validated by quantitative RT-PCR.

first: Cleverson

middle: T

last: Soares

first: Ana

middle: P

last: Trombone

first: Luciana

middle: R

last: Fachin

first: Patricia

middle: S

last: Rosa

first: Cássio

middle: C

last: Ghidella

first: Rodrigo

middle: F

last: Ramalho

first: Mabel

middle: G

last: Pinilla

first: Dirce

middle: M

last: Carraro

first: Fernando

middle: A

first: Andrea

last: Belone


title: Submandibular lymph node, a key battleground for host-Yersinia pestis interaction: A transcriptomic study using non-human primate model

city: Silver Spring

first: Aarti

last: Gautam

state: MD

address: 503 Robert Grant Avenue

department: Medical Readiness Systems Biology

institute: WRAIR

summary: Initiation of treatment during the pre-symptomatic phase of infection with Yersinia pestis (Y. pestis) is particularly critical because the rapid proliferation of Y. pestis is coupled with the manifestation of common flu-like early symptoms that often delay the intervention. Our study used African Green Monkeys that didn’t exhibited clear clinical symptoms for nearly two days after intranasal challenge with Y. pestis and succumbed within a day after showing the first signs of clinical discomfort. Colonization of Y. pestis was detected in blood one day post-infection although blood transcripts were found to be altered immediately after the pathogenic assault. The organs of the respiratory tract and those adjacent, such as lungs and submandibular lymph nodes, accumulated significant Y. pestis colonization immediately after pathogenic challenge. Hence organ-specific molecular investigations are deemed to be the key in elucidation of the mechanisms of the initial host response.     Based on results from our previous investigation of the blood transcriptomic profile, we explored the early involvement of the ubiquitin-microtubule-mediated host defense mechanism in detail. Genes enriching the ubiquitin network were altered, indicating an early suppression of the network functions in the submandibular lymph nodes. In concert, the upstream toll-like receptor signaling and downstream IκB kinase/NFκB signaling were inhibited at the transcription level. The inflammatory response was suppressed in the lungs, submandibular lymph nodes and mediastinal lymph nodes. By dysregulating both ubiquitin and the microtubule networks, Yersinia pestis was able to impair host-mediated proteolysis activities and evade autophagosome capture. A synchronized suppression of the immune response may render the peripheral organs more vulnerable to the imminent pathogenic assault. Furthermore, a comprehensive early onset of apoptosis was found across these three organ types. This was possibly a parallel mechanism undertaken by Yersinia pestis to further weaken the host response and enable a permissive colonization of the host. Targeting these networks in an organ-specific and time-resolved fashion could be essential for development of the next generation therapeutics for pneumonic plague.

sample_organism:
Chlorocebus aethiops
Macaca fascicularis
Macaca mulatta

first: Nabarun

last: Chakraborty

first: Seid

last: Muhie

first: Stacy-Ann

last: Miller

first: Candace

last: Moyler

first: Marti

last: Jett

first: Rasha

last: Hammamieh


title: 5C analysis of the Epidermal Differentiation Complex locus reveals distinct chromatin interaction networks between gene-rich and gene-poor TADs in skin epithelial cells

city: Bradford

first: Natalia

middle: V.

last: Botchkareva

address: Richmond Road

country: United Kingdom

institute: University of Bradford

summary: Gene activity programmes in different cell types control development and homeostasis of multi-cellular organisms. Spatial genome organization controls gene activity by facilitating or restricting contacts between gene promoters and remote gene enhancers. Functionally related co-regulated genes are often located together in genomes loci. The spatial organization of very large co-regulated gene loci remains poorly understood. We analyse the spatial contact network in the Epidermal Differentiation Complex (EDC) locus that contains 61 co-regulated genes activated during epidermal differentiation in epidermal cells and thymocytes, where the locus is mostly inactive. Our analysis demonstrated that the gene-rich and gene-poor regions in the EDC are organized in separate Topologically Associating Domains (TADs). We further found that spatial contact in the EDC locus is mostly cell type specific. In keratinocytes such contacts connect gene promoters with gene enhancers both within and between gene-rich TADs. Chromatin architectural proteins CTCF and Rad21 together with chromatin remodeller Brg1 were often bound near the spatially contacting gene promoters and enhancers in keratinocytes. In contrast to gene-rich TADs, gene-poor TADs show preferential spatial contacts with each other, do not contain active enhancers and show decreased binding of CTCF, Rad21 and Brg1. These data illustrate how the chromatin networks required for lineage-specific transcription are organized in skin epithelial cells and demonstrate that spatial interactions involving gene promoters and enhancers at the EDC locus are not restricted by the TAD boundaries and involve, together with intra-TAD interactions, the extensive contacts between the different gene-rich TADs.

overall_design: Two independent 5C libraries were constructed for freshly plated epidermal keratinocytes and primary thymocytes. 5C probes were designed at HindIII restriction sites using the my5Csuite primer design tools http://my5C.umassmed.eduAn alternating scheme was pursued in which reverse and forward probes were designed against every other fragment. Probes were excluded if unique mapping could not be achieved for fragments spanning highly repetitive sequences. Probe setting were as follows: U-BLAST, 3; S-BLAST, 50; MER, 800; MIN, FRAGSIZE, 100; MAX FRAGSIZE, 50000; OPT_TM, 65: and OPT_PSIZE, 40. The universal T7 sequence was tethered to all forward primers (TAATACGACTCACTATAGCC) and the reverse complement to the universal T3 sequence was tethered to all reverse probes (TATTAACCCTCACTAAAGGGA). In total, 381 forward probes and 382 reverse probes were designed, spanning 5.3 Mb EDC containing locus.

first: Krzysztof

last: Poterlowicz


title: Transcriptome of specific cell types residing in human subcutaneous adipose tissue

city: Stockholm

first: Jurga

last: Laurencikiene

address: Hälsovägen 7

country: Sweden

institute: Karolinska Institutet

overall_design: White adipose tissue (WAT) from 3 lean and 3 overweight-obese patients was collagenase treated and adipocytes were separated from the stromal vascular fraction (SVF). SVF was then FACS sorted for the following fractions CD45-/CD34+/CD31- (progenitor), CD45+/CD14+/CD206+ (total macrophages), CD45+/CD14+/CD206+/CD11c+ (M1 macrophages), CD45+/CD14+/CD206+/CD11c- (M2 macrophages), CD45+/CD3+ (total T cells), CD45+/CD3+/CD4+/CD8- (Th T-cells), CD45+/CD3+/CD4-/CD8+ (Tc T-cells). RNA was isolated from all these fractions as well as from adipocytes and analyzed on the Affymetrix Human ClariomTMD microarray.

first: Juan

last: Acosta


title: Enhanced chromatin accessibility of the dosage compensated Drosophila male X chromosome requires the CLAMP zinc finger protein [START-SEQ]

city: Boston

first: Michael

last: Tolstorukov

state: MA

address: 185 Cambridge Street

department: Molecular Biology

institute: Massachusetts General Hospital

summary: The essential process of dosage compensation is required to equalize gene expression of X-chromosome genes between males (XY) and females (XX). In Drosophila, the conserved Male-specific lethal (MSL) histone acetyltransferase complex mediates dosage compensation by increasing transcript levels from genes on the single male X-chromosome approximately two-fold. Consistent with its increased levels of transcription, the male X-chromosome has enhanced chromatin accessibility, distinguishing it from the autosomes. Here, we demonstrate that the non-sex specific CLAMP (Chromatin-linked adaptor for MSL proteins) zinc finger protein that recognizes GA-rich sequences genome-wide promotes the specialized chromatin environment on the male X-chromosome. In contrast, MSL complex is not required for global male X-chromosome chromatin accessibility, and instead promotes chromatin accessibility just at its highest-occupancy sites. Overall, our results support a model where synergy between the global increases in accessibility promoted by CLAMP and the local effects of MSL complex create a specialized chromatin domain on the male X-chromosome.

overall_design: Drosophila S2 and Kc cells were evaluated using Start RNA sequencing (Start-seq) following a 6-day RNAi treatment of gfp (control) or clamp dsRNA. Three biologigal replicates were performed for each treatment.

first: Jennifer

last: Urban

first: Guray

last: Kuzu

first: Sarah

last: Bowman

first: Benjamin

last: Scruggs

first: Telmo

last: Henriques

first: Robert

last: Kingston

first: Karen

last: Adelman

first: Erica

last: Larschan


title: Sparus aurata transcriptomic data comparing long-term starvation and feeding with three diets differing in the macronutrient composition

city: Barcelona

first: Isidoro

last: Metón

state: Barcelona

address: Joan XIII 27-31

department: Bioquímica i Fisiologia

country: Spain

institute: Universitat de Barcelona

summary: Agilent custom-made 8x60k 60-mer oligonucleotide microarray slides were used, covering unique sequences (21,093 annotated sequences and 4,299 unannotated sequences) of Sparus aurata transcriptomic data obtained from assembling of reads deposited in the NCBI SRA database corresponding to BioProject ID PRJNA391557, together with controls (8 transcripts of Sparus aurata plus Agilent controls). Two probes per sequence were used (in sense orientation for annotated sequences).

overall_design: A double loop hybridisation with dye swap (Cy3/Cy5) experimental design was performed. For two tissues (liver and skeletal muscle), four conditions were analysed: long-term starvation and feeding with three diets differing in the macronutrient composition: HLL, MHL and LLH. For each condition, four samples were used (n = 4).

first: Jonás

middle: I

last: Silva-Marrero

first: Alberto

last: Sáez

first: Isabel

middle: V

last: Baanante


title: Landscape and evolution of tissue-specific alternative polyadenylation across Drosophila species

city: CANBERRA

first: Jiayu

last: Wen

state: ACT

address: 133 Garran Rd

department: Department of Genome Science

country: Australia

institute: John Curtin School of Medical Research, The Australian National University

type: Expression profiling by high throughput sequencing

summary: we generated developmental and tissue-specific 3'-seq libraries from D. yakuba and D. virilis  to study the role of alternative polyadenylation across Drosophila species

sample_organism:
Drosophila melanogaster
Drosophila virilis
Drosophila yakuba

overall_design:
Deep 3'-sequencing data from 23 developmental stages, tissues and cell lines of D. melanogaster,  D.yakuba, and D. virilis
Please note that 23 refer to # samples in Drosophila melanogaster.  D. yakuba and D. virillis samples were used to study species homology in the paper, which are from the same tissue type as D. melanogaster.

first: Piero

last: Sanfilippo

first: Eric

last: Lai


title: Cellular and molecular characterization of gametogenic progression in ex vivo culture of prepuberal mouse testis

city: Madrid

first: Jesus

last: del Mazo Martinez

address: C/ Ramiro de Maeztu 9

institute: Centro de Investigaciones Biologicas (CIB) - CSIC

type: Non-coding RNA profiling by high throughput sequencing

summary: Next Generation Sequencing (NGS) was performed by commercial agreement with Beijing Genomics Institute (BGI). We have evaluated the miRNA profiles of mouse testis during the spermatogenic progression after ex vivo culture. We have observed that as long as spermatogenesis progress, miRNA expression decreases. However, we have identified some miRNAs that did not follow this expression profile, like miR-34c-5p and miR-449a-5p, with a higher expression in samples where the spermatogenic process was more advanced, which suggest important roles at the last stages of spermatogenesis.

overall_design: For the analysis, we have isolated RNA from testis in 7 different situations: 6.5 days post-partum (dpp) testis, 10.5 dpp testis, 6.5 dpp testis cultured for 12 days with medium supplemented with KSR, 6.5 dpp testis cultured for 12 days with medium supplemented with AlbuMAX I, 10.5 dpp testis cultured for 12 days with medium supplemented with KSR, 10.5 dpp testis cultured for 12 days with medium supplemented with AlbuMAX I and adult testis.

first: Javier

last: Isoler-Alcaraz

first: Daniel

last: Fernandez-Perez

first: Eduardo

last: Larriba

first: Jesús

last: del Mazo


title: Using data from RNA sequencing, we investigated the transcriptional changes in a H2O2-evolved strain OE100 under 4˚С and 20 MPa

city: Shanghai

first: Zhe

last: Xie

address: 800 Dongchuan Road

country: China

institute: Shanghai Jiaotong University

summary: Purpose: The goal is to investigate how to enhance the adaptability of deep-sea bacterium Shewanella piezotolerans WP3 to low temperature and high pressure by experimental evolution with H2O2 stress

overall_design: Comparision of gene expression in evolved H2O2-stressed strain OE100 to ancestor WT strain at maximum growth yield under 4˚С and 20 MPa


title: Expression data from NRF3 knocked-down DLD-1 cells

city: Kyotanabe

first: Tsuyoshi

last: Waku

address: 1-3 Tatara Miyakodani

country: Japan

institute: Doshisha University

summary:
Accumulated evidences suggest physiological relevance between the transcription factor NRF3 (NFE2L3) and cancers. However NRF3 target genes in cancer cells remain poorly understood.
We used microarrays to identify to identify NRF3 taget genes which regulate cell proliferation.

overall_design: For RNA extraction and hybridization on Affymetrix microarrays, we prepated the DLD-1 cells transfected NRF3 or control siRNA in duplicate.

first: Akira

last: Kobayashi


title: Enhanced chromatin accessibility of the dosage compensated Drosophila male X chromosome requires the CLAMP zinc finger protein

first: Michael

last: Tolstorukov

type: Genome binding/occupancy profiling by high throughput sequencing

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

overall_design: Refer to individual Series


title: Hippocampal Gene Expression Profile of Mitogen Stress activated Kinase 1 (MSK1) null mice.

city: Columbus

first: Diego

middle: Fernando

last: Alzate Correa

state: OH

address: 333 W 10th Avenue

department: Neuroscience

institute: The Ohio State University

summary:
Analysis of alterations in the hippocampus transcriptome caused by deletion of Mitogen Stress activated Kinase 1 (MSK1).
MAPK signaling has been implicated in a wide range of neuronal processes,  including development, plasticity and viability. One of the principal  downstream targets of both the ERK/MAPK pathway and the p38 MAPK  pathway is Mitogen Stress activated Kinase 1 (MSK1). Here, we sought to  understand the role that MSK1 plays in neuroprotection against excitotoxic  stimulation in the hippocampus. To this end, we utilized a MSK1 null mouse  line, cell viability assays and array-based profiling approaches. Here we  show that MSK1 is broadly expressed within the major neuronal cell layers  of the hippocampus and that status epilepticus (SE) drives acute induction  of MSK1 activation. In response to the SE paradigm, MSK1 KO mice  exhibited a striking increase in vulnerability to pilocarpine-evoked cell  death within the CA1 and CA3 cell layers. Further, cultured MSK1 null  neurons exhibited a heighted level of NMDA-evoked excitotoxicity relative  to WT neurons, as assessed using the LDH assay. Given these findings, we  examined the hippocampal transcriptional profile of MSK1 null  mice. Affymetrix array profiling revealed that with MSK1 deletion a total of 115 genes showed  significant changes (> 1.25-fold) in expression. Notably, functional analysis indicated that a subset of these  genes contribute to neuroprotective signaling networks. Together, these  data provide important new insights into the mechanism by which the  MAPK/MSK1 signaling cassette confers neuroprotection against excitotoxic  insults. Approaches designed to upregulate or mimic the functional effects  of MSK1 may prove beneficial against an array of degenerative processes  resulting from excitotoxic insults.           MAPK signaling has been implicated in a wide range of neuronal processes,  including development, plasticity and viability. One of the principal  downstream targets of both the ERK/MAPK pathway and the p38 MAPK  pathway is Mitogen Stress activated Kinase 1 (MSK1). Here, we sought to  understand the role that MSK1 plays in neuroprotection against excitotoxic  stimulation in the hippocampus. To this end, we utilized a MSK1 null mouse  line, cell viability assays and array-based profiling approaches. Here we  show that MSK1 is broadly expressed within the major neuronal cell layers  of the hippocampus and that status epilepticus (SE) drives acute induction  of MSK1 activation. In response to the SE paradigm, MSK1 KO mice  exhibited a striking increase in vulnerability to pilocarpine-evoked cell  death within the CA1 and CA3 cell layers. Further, cultured MSK1 null  neurons exhibited a heighted level of NMDA-evoked excitotoxicity relative  to WT neurons, as assessed using the LDH assay. Given these findings, we  examined the hippocampal transcriptional profile of MSK1 null  mice. Affymetrix array profiling revealed that with MSK1 deletion a total of 115 genes showed  significant changes (> 1.25-fold) in expression. Notably, functional analysis indicated that a subset of these  genes contribute to neuroprotective signaling networks. Together, these  data provide important new insights into the mechanism by which the  MAPK/MSK1 signaling cassette confers neuroprotection against excitotoxic  insults. Approaches designed to upregulate or mimic the functional effects  of MSK1 may prove beneficial against an array of degenerative processes  resulting from excitotoxic insults.

overall_design: We profiled total RNA from bilateral hippocampal tissue obtained from 6 mice, corresponding to 3 animals per genotype (wild type and MSK1 null) using the GeneChip 430A 2.0 Mouse Genome Array. Raw data (.cel files) were processed using dChip software (http://www.hsph.harvard.edu/cli/complab/dchip/).

first: Yun-Sik

last: Choi

first: Kate

last: Karelina

first: Kari

last: Hoyt

first: Karl

last: Obrietan


title: A Comparative Analysis of Library Prep Approaches for Sequencing Low Input Translatome Samples

status: Public on Oct 30 2017

city: Baltimore

first: yang

last: song

address: HSF-3, 3rd Floor; 670 W Baltimore St.

department: Department: Institute for Genome Sciences

institute: University of Maryland in Baltimore

summary: We evaluated the performance of  5 library prep protocols  by using total mRNA and IP RNA of mouse liver,we found all the 5 library preparation kits detect more enrichment effects than depletion effect. The profiles being generated by SMARTer kit is different than all other kits.

overall_design: Cell-type specific RNA from livers of P30 mice was obtained using the RiboTag protocol. Briefly, liver tissue expressing HA-tagged ribosomes in specific cells was homogenized followed by immunoprecipitation of the tagged ribosomes using an HA antibody. The RNA was extracted from the immunoprecipitated ribosomes to obtain cell-type specific enriched transcripts (IP samples). An aliquot of the homogenized tissue before immunoprecipitation was used for total RNA extraction (input samples).

first: Beatrice

last: Milon

first: Ronna

last: Hertzano


title: Deciphering the combinatorial influence of diet and the microbiota on experimental colitis

city: New York

first: Jeremiah

last: Faith

state: NY

address: One Gustave L. Levy Place

institute: Icahn School of Medicine at Mount Sinai

summary: Background & Aims: The complex interactions between diet and the microbiota that influence mucosal inflammation and inflammatory bowel disease are poorly understood. Experimental colitis models provide the opportunity to control and systematically perturb diet and the microbiota in parallel to quantify the contributions between multiple dietary ingredients and the microbiota on host physiology and colitis.    Methods: To examine the interplay of diet and the gut microbiota on host health and colitis, we fed over 40 different diets with varied macronutrient sources and concentrations to specific pathogen free or germ free mice either in the context of healthy, unchallenged animals or dextran sodium sulfate colitis model.     Results: Diet influenced physiology in both health and colitis across all models, with the concentration of protein and psyllium fiber having the most profound effects. Increasing dietary protein elevated gut microbial density and worsened DSS colitis severity. Depleting gut microbial density by using germ-free animals or antibiotics negated the effect of a high protein diet. Psyllium fiber influenced host physiology and attenuated colitis severity through microbiota-dependent and microbiota-independent mechanisms. Combinatorial perturbations to dietary protein and psyllium fiber in parallel explain most variation in gut microbial density, intestinal permeability, and DSS colitis severity, and changes in one ingredient can be offset by changes in the other.     Conclusions: Our results demonstrate the importance of examining complex mixtures of nutrients to understand the role of diet in intestinal inflammation.    Keywords: IBD; Diet; Microbiota; Mouse Models; Systems Biology

overall_design: 18 samples were run with 3 mice from each diet. TD.09052/TD.09054 are controls of each other and should be compared and TD.130633 has a unique ingredient, psyllium, that can be compared to TD.09052/TD.09054. Animals with water only tests the effects of diets and Mice given DSS test the effects of diet and inflammation.

first: Sean

last: Llewellyn

middle: J


title: Global fibroblast activation in the left ventricle but localized fibrosis after myocardial infarction

city: Leuven

first: Chandan

last: Kadur Nagaraju

state: Leuven

address: UZ Herestraat 49 box 704

department: Cardiovascular Science

country: Belgium

institute: KU Leuven

summary: Copper coated stent were implanted into the LAD coronary artery of porcine animal weighing between 20-25 kg, which leads to a severe coronary stenosis and myocardial infarct (MI). After MI, Fb are activated throughout the LV, presumably through TGF-β1 in response to increased wall stress and/or inflammation. Additional regional specific signaling leads to interstitial fibrosis via collagen cross-linking in MIadjacent. Local LOX activity could be stimulated by higher mechanical load imposed by tethering to the infarct or signals could diffuse from the scar.Identifying specific signaling cues to maintain the mature state of MyoFb phenotype in the scar tissue may open new perspectives in targeting the MyoFb reversibility in interstitial fibrosis without damaging existing scar tissue.

overall_design: From each MI pig, Fb cells were isolated from these regions; MI-adjacent, MI-remote, MI-Scar. Total 4 pigs were use. So N=4(pig); n=12(per pig/3 regions/ total 4 pigs). Additionally, 3 pigs were used for SHAM.

middle: K

last: Nagaraju

first: Eef

last: Dries

first: Natasa

last: Popovic

first: Abhishek

last: Singh

first: Peter

last: Haemers

first: Llewelyn

middle: H

last: Roderick

first: Piet

last: Claus

first: Karin

last: Sipido

first: Ronald

middle: B

last: Driesen


title: Transcriptional analysis of freshwater bacterium Polynucleobacter asymbioticus strain QLW-P1DMWA-1T

city: Vienna

last: Srivastava

address: Althanstrasse 14

country: Austria

institute: University of Vienna

summary: Polynucleobacter asymbioticus strain QLW-P1DMWA-1T represents a group of highly successful heterotrophic planktonic bacteria, dwelling in freshwater systems (lakes, ponds, and streams) across all climatic zones and across all continents. This includes habitats characterised by strongly fluctuating environmental conditions. So the experiments were designed to mimick winter and summer scenarios with additional impact of UV irradiation. Comparative transcriptomic studies were conducted to analyse gene-expression levels in contrasting experimental conditions. Overall, molecular candidates were revealed that may contribute in rapid acclimatisation of this strain in their immediate environment.

overall_design: Bacterial cells were incubated in 500ml R2A liquid media, and samples were kept in sterile but UV permeable polyethylene bags. Samples were incubated at 26ºC (at constant rotation of 200 rpm). When the culture reached the O.D. of 0.1, the samples were transferred to their treatment incubators i.e. (a). 26ºC samples continued at the sample temperature; (b). second batch was transferred to 4ºC incubator; (c). third batch also continued incubation at 26ºC but with supplemented with 2x30 minutes of UV irradiation daily. Samples were harvested with RNAlaterTM solution. Agilent 60-mer Microarray was designed that contained strain QLW-P1DMWA-1T genome represented with 2123 genes.

first: Nadine

last: Genzel


title: BioProject PRJNA381064: Convergent origination of a Drosophila-like dosage compensation mechanism in a reptile lineage (Allelic Gene Expression in Anolis carolinensis, single-cell RNA-seq)

status: Public on Oct 27 2017

city: Lausanne

first: Diego

last: Cortez

address: Rue de Lausanne

country: Switzerland

institute: Univerity of Lausanne - CIG

type: Genome variation profiling by high throughput sequencing

summary: In order to rule out the presence of random X inactivation in A. carolinensis females we generated scRNA-Seq from liver cells and genome sequence data from liver.

overall_design: Call of heterozygous SNPs of exonic regions in genomic DNA (liver); call of expressed (allelic) SNPs from 6 liver cells of the same specimen.

first: Henrik

last: Kaessmann

first: Francesco

last: Lamanna


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

city: Indianapolis

first: Lyudmila

last: Sidorenko

state: Indiana

address: 9330 Zionsville Rd

institute: DOW AgroSciences

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

overall_design: Data for Arabidopsis small RNA and DNA methylation studies can be found under a separate GEO submission (GSE76406). Data for maize small RNA studies are in this submission. Maize small RNA data was generated using Illumina TruSeq sample preparation protocol.

first: Shreedharan

last: Sriram


title: STAT5-mediated chromatin interactions in superenhancers activate IL-2 highly inducible genes: Functional dissection of the Il2ra gene locus

city: Bethesda

first: Peng

last: Li

address: 9000 Rockville Pike

department: NHLBI

institute: NIH

summary: Cytokines critically control immune responses, but how regulatory programs are altered to allow T cells to differentially respond to distinct cytokine stimuli remains poorly understood. Here, we have globally analyzed enhancer elements bound by IL-2-activated STAT5 and IL-21-activated STAT3 in T cells and identified Il2ra as the top-ranked gene regulated by an IL-2-activated STAT5-bound superenhancer and one of the top genes regulated by STAT3-bound superenhancers. Moreover, we found that STAT5 binding was rapidly superenriched at genes highly induced by IL-2 and that IL-2-activated STAT5 binding induces new and augmented chromatin interactions within superenhancer-containing genes. Based on chromatin interaction analysis by paired-end tag (ChIA-PET) sequencing data, we used CRISPR-Cas9 gene editing to target three of the STAT5 binding sites within the Il2ra superenhancer in mice. Each mutation decreased STAT5 binding and altered IL-2-induced Il2ra gene expression, revealing that individual elements within the superenhancer were not functionally redundant and that all were required for normal gene expression. Thus, we demonstrate cooperative utilization of superenhancer elements to optimize gene expression and show that STAT5 mediates IL-2-induced chromatin looping at superenhancers to preferentially regulate highly inducible genes, thereby providing new insights into the mechanisms underlying cytokine-dependent superenhancer function.

overall_design: ChIP-Seq analyzes using pre-activated T cells from both WT and CRISPR mutant mice, with rabbit IgG, anti-STAT5B, anti-H3K4me3, anti-H3K27Ac. RNA-Seq analyses using total RNA from pre-activated CD4+ T cells from WT mice, without or with IL-2/IL-21 treatment for 0.5, 2, 4 and 24 hours.

first: Suman

last: Mitra

first: Rosanne

last: Spolski

first: Jangsuk

last: Oh

first: Wei

last: Liao

first: Zhonghui

last: Tang

first: Fei

last: Mo

first: Xingwang

first: Erin

middle: E

last: West

first: Daniel

last: Gromer

first: Jian-Xin

last: Lin

first: Chengyu

last: Liu

first: Yijun

last: Ruan

first: Warren

last: Leonard


sample_organism:
Arabidopsis thaliana
Zea mays

platform_organism:
Arabidopsis thaliana
Zea mays


title: Transfer RNA Genes Affect Chromosome Architecture and Function

city: Berkeley

first: Xavier

last: Darzacq

state: CA

address: 475D Li Ka Shing Center

department: Molecular and Cell Biology

institute: University of California, Berkeley

summary: Chromosomes are packaged and organized in the nucleus in an ordered, non-random manner. This organization influences many nuclear processes such as transcription, gene silencing and mitosis. While transfer RNA genes (tDNAs) are essential for the generation of tRNAs these gene loci are also binding sites for transcription factors and chromosomal architectural proteins.   In the yeast Saccharomyces cerevisiae, tDNAs are dispersed along all sixteen chromosomes. In this study, we investigated the role of tDNAs in genomic organization and nuclear function by editing a chromosome so that it lacks any tDNAs. Our analyses of this tDNA-less chromosome show that loss of tDNAs affect nucleosome positioning, binding of SMC proteins, centromere clustering, long-range chromosome folding and epigenetic gene silencing. We propose that these effects are primarily mediated via changes in local interactions between tDNAs and other regulatory sequences that then manifest as alterations in long-range chromosome architecture with effects on gene regulation over large distances.

overall_design: Chromatin is fragmented by MNase, subsequenct nucleosomal end repair, and a modified two-step method for purfiying ligation products. Using Illumina paired-end sequencing maps Micro-C library and generates nucleosome resolution contact maps.

first: Oliver

last: Rando

first: Tsung-Han

last: Hsieh


title: Gene expression profiling of murine skin transgenically generated to express HPV16 E7 oncoprotein

city: Brisbane

first: Zewen Kelvin

last: Tuong

state: QLD

address: 62 Graham Street, Centre for Children's Health Research (CCHR), South Brisbane, QLD, 4101

institute: The University of Queensland

summary: A validated animal model would assist with research on the immunological consequences of the chronic expression of HPV16 E7 oncoprotein expression. Here we performed RNA-seq analysis of normal C57BL/6 skin versus mouse transgenically generated to express HPV16 E7 oncogene under the keratin 14 promoter (K14E7). Mice present with epithelial hyperplasia and increased immune cell infiltrate associated with immune suppression.

overall_design:
Ear skin (n=6) 8-week old C57BL/6 and K14E7 mice
Grafted samples (n=18) of donor C57BL/6, K14E7 and CD1d-/-xK14E7 skin on C57BL6 recipients

first: Zewen

first: Ian

last: Frazer


title: Thyroid State Regulates Gene Expression in Human Whole Blood Cells

city: Rotterdam

first: Selmar

last: Leeuwenburgh

state: Zuid-Holland

address: Wytemaweg 80

department: Internal medicine

country: Netherlands

institute: Erasmus MC

summary: Context: Despite the well-recognized clinical features due to insufficient or excessive thyroid hormone (TH) levels in humans, it is largely unknown which genes are regulated by TH in human tissues. objective: To study the effect of TH on human gene expression profiles in whole blood, mainly consisting of TRα-expressing cells. Methods: We performed next-generation RNA sequencing on whole blood samples from 8 athyroid patients (4 females) on and after 4 weeks off levothyroxine replacement. Gene expression changes were analyzed through paired differential expression analysis and confirmed in a validation cohort. Weighted gene co-expression network analysis (WGCNA) was applied to identify thyroid state-related networks. Results: We detected 486 differentially expressed (DE) genes (fold-change above 1.5; multiple testing corrected P-value <0.05), of which 76 % were positively and 24 % were negatively regulated. Gene ontology (GO) enrichment analysis revealed that 3 biological processes were significantly overrepresented of which the process translational elongation showed the highest fold enrichment (7.3 fold, P=1.8 x 10-6). Comparative transcriptome analysis revealed significant overlap with DE-genes in muscle samples upon different thyroid state (1.7-fold enrichment; P=0.02). WGCNA analysis independently identified various gene clusters that correlated with thyroid state. Further GO-analysis suggested that thyroid state regulates platelet function. Conclusions: Changes in thyroid state regulate numerous genes in human whole blood, predominantly TRα-expressing leukocytes. In addition, TH may regulate gene expression in platelets. Whole blood samples might potentially be used as a proxy for other TRα-expressing tissues in humans.

overall_design: Transcriptome profiling (RNA-Seq) of 8 thyroidectomized human whole blood samples, sequenced first in hypothyroid state and after levothyroxine supplementation sequenced in a hypothyroid (mild thyreotoxic state) state on a Illumina HiSeq 2500 system.

first: Elske

middle: T

last: Massolt

first: Mirjam

last: van den Hout-van Vroonhoven

first: Robin

middle: P

last: Peeters

first: Theo

last: Visser

first: Marcel

last: Meima


title: Ethylene production in Synechocystis sp. PCC 6803 promotes phototactic movement

status: Public on Oct 26 2017

city: Freiburg

first: Stephan

last: Klähn

state: Baden-Würtemberg

address: Schänzlestrasse 1

department: Institute of Biology III

country: Germany

institute: University of Freiburg

summary: Ethylene is a gaseous signal sensed by plants and bacteria. Heterologous expression of the ethylene-forming enzyme (EFE) from Pseudomonas syringae in cyanobacteria leads to the production of ethylene under photoautotrophic conditions. The recent characterization of an ethylene responsive signaling pathway affecting phototaxis in the cyanobacterium Synechocystis sp. PCC 6803 implies that biotechnologically relevant ethylene synthesis may induce regulatory processes which are not related to changes in the metabolism. Here we provide data that endogenously produced ethylene accelerates movement of cells towards light. Microarray analysis demonstrates that ethylene deactivates transcription from the csiR1/lsiR promoter which is under control of the two-component system consisting of the ethylene and UV-A-sensing histidine kinase UirS and the DNA-binding response regulator UirR. Surprisingly, only very few other transcriptional changes were detected in the microarray analysis providing no direct hints to possible bottlenecks in phototrophic ethylene production.

overall_design: We performed whole-genome transcript profiling of an ethylene producing strain of Synechocystis sp. PCC 6803.

first: Ekaterina

last: Kuchmina

first: Annik

last: Jakob

first: Werner

last: Bigott

first: Ulf

last: Dühring

first: Annegret

last: Wilde


title: Nudt21 controls cell fate by connecting alternative polyadenylation to chromatin signaling

city: Houston

first: Bruno

last: Di Stefano

address: 1 Baylor Plaza

department: Molecular and Cellular Biology

institute: Baylor College of Medicine

summary: Cell fate transitions involve rapid changes of gene expression patterns and global chromatin remodeling, yet the underlying regulatory pathways remain incompletely understood. Here, we used transcription-factor induced reprogramming of somatic cells into pluripotent cells to screen for novel regulators of cell fate change. We identified the RNA processing factor Nudt21, a component of the pre-mRNA cleavage and polyadenylation complex, as a potent barrier to reprogramming. Importantly, suppression of Nudt21 not only enhanced the generation of induced pluripotent stem cells but also facilitated the conversion of fibroblasts into trophoblast stem cells and delayed the differentiation of myeloid precursor cells into macrophages, suggesting a broader role for Nudt21 in controlling cell fate change. Polyadenylation site sequencing (PAS-seq) revealed that Nudt21 directs differential polyadenylation of over 1,500 transcripts in cells acquiring pluripotency. While only a fraction of these transcripts changed expression at the protein level, this fraction was strongly enriched for chromatin regulators, including components of the PAF, Polycomb, and Trithorax complexes. Co-suppression analysis further suggests that these chromatin factors are potent mediators of reprogramming, providing a mechanistic basis for our observations. Collectively, our data uncover Nudt21 as a novel post-transcriptional regulator of mammalian cell fate and establish a direct, previously unappreciated link between alternative polyadenylation and chromatin signaling.

overall_design: Examination of the chromatin accessibility landscape by ATAC-seq during OSKM-mediated reprogramming of MEFs, transfected with siRNAs targeting Nudt21 or control siRNAs, into iPSCs at distinct time-points during the reprogramming process.

first: Justin

last: Brumbaugh

first: Konrad

last: Hochedlinger


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

city: Utrecht

first: Tuncay

last: Baubec

address: Padualaan 8

department: Department of Biology

institute: Utrecht University

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

overall_design: Biotin ChIP for DNMT3A proteins

first: Massimiliano

last: Manzo


title: Isoform-specific localization of DNMT3A regulates DNA methylation fidelity at bivalent CpG islands [5-hMeDIP]

overall_design: 5-hydoxylmethylcytosine IP (5-hMeDIP)


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


title: Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells

city: Umeå

first: Marie-Louise

last: Hammarström

address: Peter Lestadius väg

department: Clinical Microbiology

institute: Umeå universitet


title: PCAN_TRAUMATEST

city: Göttingen

first: Victor

last: Chano

address: Buesgenweg 2

department: Forest Genetics and Forest Tree Breeding

institute: University of Göttingen

summary: Gene expression analysis in response to mechanical injuries in Pinus canariensis, known for a great healing ability. Traumatic xylem formed in the margins of the wounds were compared to control tissues, sampled from remote parts of the plant, in order to check transcriptomical variations in three dates during the response: H1, H2 and H3 for 7, 78 and 92 days after wounding.

overall_design: Two-color experiment comparing gene expression in response to wounding to regular growth, at three times during the healing process. Three biological replicates for each sampling date.

first: Víctor

first: Carmen

last: Collada

first: Álvaro

last: Soto


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

city: Montreal

first: Nada

last: Jabado

state: Québec

address: 1001 Décarie Boulevard

department: Department of Pediatrics

country: Canada

institute: McGill University

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Refer to individual Series


title: Gene expression profile of multiple myeloma cell lines treated with CB-5083

city: Burlingame

first: Daniel

last: Anderson

address: 866 Malcolm Rd #100

institute: Cleave Biosciences

summary:
The goal was to determine the gene expression differences between CB-5083 and Bortezomib treated multiple myeloma cell lines
Inhibition of the AAA ATPase, p97, was recently shown to be a novel method for targeting the ubiquitin proteasome system (UPS) and CB-5083, a first in class inhibitor of p97, has demonstrated broad antitumor activity in a range of both hematological and solid tumor models. Here, we show that CB-5083 has robust activity against multiple myeloma (MM) cell lines and a number of in vivo MM models. Treatment with CB-5083 is associated with accumulation of ubiquitinated proteins, induction of the unfolded protein response (UPR) and apoptosis. CB-5083 decreases viability in MM cell lines and patient derived MM cells, including those with background proteasome inhibitor (PI) resistance.  CB-5083 has a unique mechanism of action that combines well with PIs which is likely owing to the p97-dependent retro-translocation of the transcription factor, Nrf1, which transcribes proteasome subunit genes following exposure to a PI. In vivo studies using clinically relevant MM models demonstrate that single-agent CB-5083 inhibits tumor growth and combines well with MM standard of care agents. Our preclinical data demonstrate the efficacy of CB-5083 in several MM disease models and provide the rationale for clinical evaluation as monotherapy and in combination in MM.

overall_design: Cells were treated with compound or DMSO for 8hrs and then processed for RNAseq

first: S

middle: N

last: Djakovic

first: D


title: The Epstein-Barr virus B-ZIP protein Zta recognizes specific DNA sequences containing 5-methylcytosine and 5-hydroxymethylcytosine [Zta_5mC_5hmC]

first: Desiree

last: Tillo

address: 41 Center Dr, Room D310

institute: NIH/NCI

summary: The Epstein-Barr virus (EBV) B-ZIP transcription factor (TF) Zta binds to many DNA sequences containing methylated CG dinucleotides.  Using protein binding microarrays (PBMs), we analyzed the binding of Zta to four kinds of double-stranded DNA: 1) DNA containing cytosine on both strands, 2) DNA with 5-methylcytosine (5mC) on one strand and cytosine on the second strand, 3) DNA with 5-hydroxymethylcytosine (5hmC) on one strand and cytosine on the second strand, and 4) DNA where both cytosines in all CG dinucleotides contain 5mC. We compared the resulting data to PBM data for three other B-ZIP proteins (CREB1 and CEBPB homodimers, and cFos-cJun heterodimers).  With cytosine, Zta binds the TRE motif TGAC/GTCA as previously reported.  With CG dinucleotides containing 5mC on both strands, many TRE motif variants containing a methylated CG dinucleotide at two positions in the motif, such as MGAGTCA and TGAGMGA (where M=5mC) were preferentially bound.  5mC inhibits Zta binding to both TRE motif half sites GTCA and CTCA.  Like the CREB1 homodimer, the Zta homodimer and the cJun|cFos heterodimer bind the C/EBP half site tetranucleotide GCAA stronger when it contains 5mC.  Our results identify new DNA sequences that are well-bound by the viral B-ZIP protein Zta only when they contain 5mC or 5hmC, opening the potential for discovery of new viral and host regulatory programs controlled by EBV.

sample_organism:
Mus musculus
human gammaherpesvirus 4

overall_design: Protein binding microarray (PBM) experiments were performed for a set of B-ZIP transcription factors:  Zta and CEBPB homodimers, and cJun|cFos heterodimers. Briefly, the PBMs involved binding GST-tagged DNA-binding proteins to double-stranded 44K Agilent microarrays (Berger et al., Nature Biotechnology 2006) in order to determine their binding preferences to sequences containing modified cytosines.  We modified the double stranding step of the PBM protocol in which the nucleotide mixture contained 5-methylcytosine or 5-hydroxymethylcytosine.  Details of the modified cytosine PBM protocol are described in Khund-Sayeed S et al., Integrative Biology, 2016.


title: The Epstein-Barr virus B-ZIP protein Zta recognizes specific DNA sequences containing 5-methylcytosine and 5-hydroxymethylcytosine [Zta_5mCG]

overall_design: Protein binding microarray (PBM) experiments were performed for a set 3 B-ZIP homodimers from Epstein Barr Virus (Zta) and mouse (CREB1 and CEBPB). Briefly, the PBMs involved binding GST-tagged DNA-binding proteins to double-stranded and methylated or unmethylated 44K Agilent microarrays, containing a DeBruijn sequence design, in order to determine their sequence preferences. Details of the methylated PBM protocol are described in Mann et al., Genome Research, 2013


city: Irvine

first: Elmira

last: Forouzmand

address: B228 Medical Science I

department: Department of Microbiology and Molecular Genetics

institute: University of California Irvine

summary: Cell fate transitions involve rapid changes of gene expression patterns and global chromatin remodeling, yet the underlying regulatory pathways remain incompletely understood. Here, we used transcription-factor induced reprogramming of somatic cells into pluripotent cells to screen for novel regulators of cell fate change. We identified the RNA processing factor Nudt21, a component of the pre-mRNA cleavage and polyadenylation complex, as a potent barrier to reprogramming. Importantly, suppression of Nudt21 not only enhanced the generation of induced pluripotent stem cells but also facilitated the conversion of fibroblasts into trophoblast stem cells and delayed the differentiation of myeloid precursor cells into macrophages, suggesting a broader role for Nudt21 in restricting cell fate change. Polyadenylation site sequencing (PAS-seq) revealed that Nudt21 directs differential polyadenylation of over 1,500 transcripts in cells acquiring pluripotency. While only a fraction of these transcripts changed expression at the protein level, this fraction was strongly enriched for chromatin regulators, including components of the PAF, polycomb, and trithorax complexes. Co-suppression analysis further suggests that these chromatin factors are largely responsible for Nudt21’s effect on reprogramming, providing a mechanistic basis for our observations. Collectively, our data uncover Nudt21 as a novel post-transcriptional regulator of mammalian cell fate and establish a direct, previously unappreciated link between alternative polyadenylation and chromatin signaling.

overall_design: PAS-Seq


title: Molecular Mechanism of Directional CTCF Recognition of a Diverse Range of Genomic Sites

city: Shang Hai

first: Zhang

last: Mo

address: Dong Chuan Road 800

institute: SJTU

summary: CTCF, a conserved 3D genome architecture protein, determines proper genome-wide chromatin looping interactions through directional binding to specific sequence elements of four modules within numerous CTCF-binding sites (CBSs) by its 11 zinc fingers (ZFs). Here, we report the crystal structures of four human CTCF-CBS complexes of the protocadherin (Pcdh) clusters, and show that directional CTCF binding to cognate CBSs of the Pcdh enhancers and promoters is achieved through inserting its ZF3, ZFs 4-7, and ZFs 9-11 into the major groove along CBSs, resulting  in a sequence-specific recognition of module 4, modules 2-3, and module 1, respectively, with ZF8 as a spacer element for variable distances between modules 1 and 2. In addition, the base-contact with the asymmetric “A” in the central position of modules 2-3, is essential for directional recognition of the CBSs with symmetric core sequences and lack of module 1. Furthermore, CTCF tolerates base changes at specific positions within the degenerated CBS sequences, permitting genome-wide CTCF binding to a diverse range of CBSs. Together, these complex structures provide important insights into the molecular mechanisms for the directionality, diversity, flexibility, dynamics, and conservation of multivalent CTCF binding to its cognate sites across the entire human genome

overall_design: Examination of CTCF binding sites  in 293T cell.

first: Mo

last: Zhang

first: Qiang

last: Wu


title: Differential Gene Expression Analysis with Altered Local CRH Signaling in the Mouse Olfactory Bulb

first: Benjamin

middle: R

last: Arenkiel

state: Texas

address: 1250 Moursund St, 11th floor, Ste 1150.01

department: Molecular and Human Genetics

summary: We report genome-wide gene expression changes in olfactory bulb cells, in the context of low, wild-type or high levels of local CRH signaling by local interneurons onto adult-born CRHR1+ granule neurons. To test the gene expression changes associated with altered local CRH signaling, we utilize the following animal models: CRHR1-/- mice whose bulbs were infected with a control AAV-flex-EGFP virus = low local CRH signaling, CRHR1-Cre mice whose bulbs were infected with AAV-flex-EGFP = pseudo-wild-type local CRH signaling, and CRHR1-Cre mice whose bulbs were infected with AAV-flex-(CA)CRHR1, which is a constitutively active variant of CRHR1 = high local CRH signaling. We find that, in response to changes in local CRH signaling in the bulb, the largest ontological category of transcription changes in the bulb that occurs reciprocally between low and high levels of CRH signaling are gene regulatory factors. To test the contributions of one of these factors, POU6f1, we perform loss- and gain-of-function analysis. We show that CRHR1 activation results in transcriptional activation of POU6f1 and that POU6f1 in turn influences synaptogenesis and dendritic patterning of adult-born neurons and olfactory circuit behavior.

first: Cynthia

last: McClard

first: Mikhail

middle: Y

last: Kochukov

first: Zhandong

last: Liu

first: Isabella

last: Herman

last: Colchado

first: Sugi

last: Panneerselvam

first: Aiden

last: Eblimit

first: Yalda

last: Moayedi

first: Joshua

last: Ortiz-Guzman


title: Differences of gene expression profiling of breast cancer cells with stable SREBP1 knockdown and the control cells

status: Public on Oct 25 2017

city: Jinan

first: Qifeng

last: Yang

state: Shandong

address: Wenhua West Road No.44

department: Department of Breast Surgery

institute: Qilu Hospital

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


title: BioProject PRJNA381064: Convergent origination of a Drosophila-like dosage compensation mechanism in a reptile lineage (Gene expression profiling in several tetrapod species, bulk tissue RNA-seq)

first: Diego

last: Cortez

address: Rue de Lausanne

institute: Univerity of Lausanne - CIG

summary: In order to study the green anole dosage compensation mechanism we generated strand-specific RNA-seq libraries for a total of 186 samples from the green anole and other representative amniotes (human, mouse, opossum, platypus, chicken and xenopus). Moreover, in order to understand the dosage compensation mechanism of A. carolinensis, we generated ChIP-Seq data for the histone modification H4K16ac and compared levels of acetylation between males and females. Moreover, we reconstructed 7 Y-linked transcripts of Anolis carolinensis based on a male/female subtraction approach and validate these Y sequences using re-sequenced genomes.

sample_organism:
Xenopus tropicalis
Gallus gallus
Ornithorhynchus anatinus
Homo sapiens
Mus musculus
Monodelphis domestica
Anolis carolinensis

overall_design: We generated strand-specific RNA-seq libraries using the Illumina TruSeq Stranded mRNA Library protocol. Sample size (minimum one male and one female for each species) was established to have a wide spectrum across amniotes and to capture general male/female sex-specific patterns. Each source RNA was of high quality, as assessed using a Fragment Analyzer machine from Advanced Analytical (RIN median = 9, RQN median = 8). Each library was sequenced on Illumina HiSeq 2500 platforms at the Lausanne Genomic Technologies Facility (https://www.unil.ch/gtf/en/home.html). At least 17 million sequencing reads (100 nt, single-end) were produced for each library (median: 34 million reads). Examination of H4K16ac enrichment between males and females in liver and brain. Two biological replicates, four genomic DNA input libraries. Y-linked transcripts of Anolis carolinensis were obtained using a male/female subtraction approach. The sequences were validated using re-sequenced male and female genomes.

first: Henrik

last: Kaessmann

first: Francesco

last: Lamanna

first: Madapura

last: Pradeepa


title: Whole transcriptome analysis of induced cardiomyocytes during direct cardiac reprogramming [expression]

city: WAUWATOSA

first: ZIQING

last: LIU

state: WI

address: 8701 W Watertown Plank Rd, BSB 5320

department: Biology

institute: Medical College of Wisconsin

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

overall_design: To compare with single-cell RNAseq of induced cardiomyocytes (iCM), we also performed whole-genome gene expression profiling with reprogramming cells collected at different time points (D0, D3, D5, D7, D10, and D14 post MGT transduction). Microarray was performed on Agilent mouse 8x60K GE 1color platform.

first: Yang

last: Zhou

first: Li

last: Wang

first: Ziqing

first: Sahar

last: Alimohamadi

first: Chaoying

last: Yin

first: Jiandong

last: Qian


title: Detailed transcriptome analysis of the plant growth promoting Paenibacillus riograndensis SBR5 using RNAseq technology

city: Bielefeld

first: Volker

last: F. Wendisch

state: NRW

address: Universitätsstr. 25

department: Genetics of Prokaryotes

institute: Bielefeld University

summary:
Background- The plant growth promoting rhizobacterium Paenibacillus riograndensis SBR5 is a promising candidate to serve as crop inoculant. Despite its potential regarding environmental and economic benefits, the species P. riograndensis is poorly characterized. Here, we performed for the first time a detailed transcriptome analysis of P. riograndensis SBR5 using RNAseq technology.
Results- Sequence analysis of the library enriched in 5’-ends of the primary transcripts was used to identify 1,082 TSS belonging to novel transcripts and allowed us to determine a promoter consensus sequence and regulatory sequences in 5’ untranslated regions including riboswitches
Conclusions- Our RNAseq analysis provides insight into the P. riograndensis SBR5 transcriptome at the systems level and will be a valuable basis for differential RNAseq analysis of this bacterium.

overall_design: P. riograndensis SBR5 was cultivated under 16 different growth conditions and RNA was isolated from samples collected during growth experiment and combined together in order to analyze an RNA pool representing a large set of expressed genes. The resultant total RNA was used to generate two different libraries, one enriched in 5’-ends of the primary transcripts and the other representing the whole transcriptome. Both libraries were sequenced and analyzed to identify the conserved sequences of ribosome biding sites and translation start motifs, and to elucidate operon structures present in the transcriptome of P. riograndensis.

first: Luciana

last: Fernandes de Brito

first: Marta

last: Irla

middle: F

last: Wendisch


title: Defining the location of promoter-associated R-loops at near-nucleotide resolution using bisDRIP-seq

city: New York City

first: Jason

middle: Gardiner

last: Dumelie

address: 1300 York Ave

department: Phamacology

institute: Weill Cornell Medicine

summary: R-loops are features of chromatin consisting of a strand of DNA hybridized to RNA, as well as the expelled complementary DNA strand.  R-loops are enriched at promoters where they have recently been shown to have important roles in modifying gene expression.  However, the location of promoter-associated R-loops and the genomic domains they perturb to modify gene expression remain unclear.  To resolve this issue, we developed a bisulfite-based approach, bisDRIP-seq, to map R-loops across the genome at near-nucleotide resolution in MCF-7 cells.  We found the location of promoter-associated R-loops is dependent on the presence of introns.  In intron-containing genes, R-loops are bounded between the transcription start site and the first exon-intron junction.  In intronless genes, the 3' boundary displays gene-specific heterogeneity.  Moreover, intronless genes are often associated with promoter-associated R-loop formation.  Together, these studies provide a high-resolution map of R-loops and identify gene structure as a critical determinant of R-loop formation.

overall_design:
Mapping R-loop structures using bisDRIP-seq. Standard bisDRIP-seq was performed in thirteen control-treated samples. Two samples were generated from cells treated with the transcription inhibitor triptolide.

The R-loop signal from bisDRIP-seq experiment was shown to be RNase H-sensitive using RNase H and matched-control bisDRIP-seq experiments.

For each sample, reads on the "CTOB" strand are in the positive orientation and reads on the "CTOT" strand are in the negative orientation.

middle: G

first: Samie

last: Jaffrey


title: Reversing SKI–SMAD4-mediated suppression is essential for TH17 cell differentiation [ChIP-seq]

city: Chapel Hill

first: Yisong

last: Wan

state: NC

address: 125 Mason Farm Road

department: Lineberger Comprehensive Cancer Center

institute: University of North Carolina-Chapel Hill

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

overall_design: Examination of Smad4 ChIP-seq in two different cells (WT vs.Smad4 KO) under IL6+TGFbR inhibitor condition

first: Song

last: Zhang

first: Xiaojiang

last: Xu


title: The Epstein-Barr virus B-ZIP protein Zta recognizes specific DNA sequences containing 5-methylcytosine and 5-hydroxymethylcytosine

city: Bethesda

first: Desiree

last: Tillo

state: MD


title: Oncolytic reactivation of KSHV as a therapeutic approach for primary effusion lymphoma: high-resolution mapping of BRD4 binding sites in the KSHV genome

status: Public on Oct 24 2017

city: Sacramento

first: Clifford

middle: G.

last: Tepper

address: 4645 2nd Avenue, Room 2300A

department: Biochemistry and Molecular Medicine

institute: UC Davis School of Medicine

summary: Primary effusion lymphoma (PEL) is an aggressive subtype of non-Hodgkin lymphoma caused by Kaposi's sarcoma-associated herpesvirus (KSHV) infection. Currently, treatment options for patients with PEL are limited. Oncolytic viruses have been engineered as anticancer agents and have recently shown increased therapeutic promise. Similarly, lytic activation of endogenous viruses from latently infected tumor cells can also be applied as a cancer therapy. In theory, such a therapeutic strategy would induce oncolysis by viral replication, while simultaneously stimulating an immune response to viral lytic cycle antigens. We examined the combination of the FDA-approved drug ingenol-3-angelate (PEP005) with epigenetic drugs as a rational therapeutic approach for KSHV-mediated malignancies. JQ1, a bromodomain and extra terminal (BET) protein inhibitor, in combination with PEP005, not only robustly induced KSHV lytic replication, but also inhibited IL6 production from PEL cells. Using the dosages of these agents that was found to be effective in reactivating HIV (as a means to clear latent virus with highly active antiretroviral therapy), we were able to inhibit PEL growth in vitro and delay tumor growth in a PEL xenograft tumor model. KSHV reactivation was mediated by activation of NF-kB pathway by PEP005, which led to increased occupancy of RNA polymerase II onto the KSHV 33  genome. RNA-sequencing analysis further revealed cellular targets of PEP005, JQ1, and the synergistic effects of both. Thus, combination of PEP005 with a BET inhibitor may be considered as a rational therapeutic approach for the treatment of PEL.

overall_design: The goal of these studies was to perform genome-wide mapping of BRD4 binding sites across the KSHV genome during viral reactivation using ChIP-Sequencing (ChIP-Seq). This was performed in the context of the BCBL-1 cell line model, which is derived from a KSHV-infected human primary effusion lymphoma (PEL) and contains latent KSHV genomes. For these studies, we utilized an engineered subline, referred to as TREx-K-Rta BCBL-1, which contains a Tetracycline/Doxycycline (Dox)-inducible Flagx3- and HAx3-tagged K-Rta expression cassette. Viral reactivation is then stimulated by inducing K-Rta expression in individual TREx-K-Rta BCBL-1 cultures by treatment with Dox for 24 hours. Following treatment, the cells were then processed for ChIP-Seq analyses by formaldehyde cross-linking, chromatin solubilization, and chromatin immunoprecipitation (ChIP) with anti-BRD4 antibody. Subsequently, DNA was isolated from the ChIP and total chromatin (Input) samples, and followed by library preparation and next-generation sequencing (NGS).

first: Yoshihiro

last: Izumiya

first: Feng


title: Generation of induced progenitor-like cells from mature epithelial cells using interrupted reprogramming

city: Toronto

first: Li

last: Guo

address: 101 College Street

institute: University Health Network

summary:
A suitable source of progenitor cells is required to attenuate disease or affect cure. We present a novel interrupted reprogramming strategy to generate induced Progenitor-Like (iPL) cells using carefully timed -expression of induced Pluripotent Stem  cell reprogramming factors (Oct4, Sox2, Klf4 and c-Myc; OSKM) from non-proliferative Club cells. Interrupted reprogramming allowed controlled expansion yet preservation of lineage commitment. Under clonogenic conditions, iPL cells expanded and functioned as a bronchiolar progenitor-like population to generate mature Club cells, mucin-producing goblet cells, and CFTR-expressing ciliated epithelium. In vivo, iPL cells can repopulate CFTR-deficient epithelium. This interrupted reprogramming process could be metronomically applied, to achieve controlled progenitor-like proliferation. By carefully controlling the duration of -expression of OSKM, iPL cells don't become pluripotent and maintain their memory of origin and retain their ability to efficiently return to their original phenotype. A generic technique to produce highly specified populations may have significant implications for regenerative medicine.
Microarray analysis of genome-wide transcriptional changes showed Club-iPL cells have minimal expression of ES cell-related genes (e.g. Nanog, Utf1, Dapp4) and maintained significant overlapping expression of Club cell-related genes. Further analysis showed that the expression of large numbers of genes temporally changed during Dox-driven expansion of Club cells but returned upon withdrawal of the factors.

overall_design: Day0 freshly isolated Club cells,3w+Dox (Club-iPL cells), Club-iPL cells with subsequent 2-week culture in Dox-free media (3w+Dox+2w-Dox), and Club-iPS cells were collected for RNA extraction and hybridization on Affymetrix microarrays.

first: Tom

last: Waddell


title: MBD2 Ablation Impairs Lymphopoiesis and Impedes Progression and Maintenance of T-cell Acute Lymphoblastic Leukemia

status: Public on Oct 23 2017

city: Wuhan

first: Mi

last: Zhou

address: Jiefang Ave

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

summary:
Little is known about the roles of methyl-CpG-binding domain protein 2 (MBD2), a “reader” of DNA methylation, in T-cell acute lymphoblastic leukemia (T-ALL). Here, we investigated the role of MBD2 in T-ALL by using an Mbd2 knockout mouse model. We found that MBD2 ablation impeded the progression and maintenance of Notch1-driven T-ALL.Our data reveals essential roles for MBD2 in lymphopoiesis and T-ALL and support an intriguing potential of MBD2 as a therapeutic target for T-ALL.
To explore potential mechanisms underlying the anti-ALL effects of MBD2 ablation, leukemic cells were harvested from mice transplanted with WT or Mbd2-/- T-ALL cells, and their global gene expression profiles (GEP) were compared. Double positive (DP) thymocytes were isolated and used as a normal control.

overall_design: To understand the critical molecular events caused by MBD2 ablation in Notch1-driven T-ALL,the GFP+ leukemic mice BM cells were sorted from the recipients of MBD2-/- (TALL_M1,TALL_M2,TALL_M3) or MBD2+/+ (TALL_C1,TALL_C2,TALL_C3), and subjected to microarray analysis on Affymetrix microarrays.Furthermore, the normal DP (double positive) cells from steady-state mice thymus were chosen for examination as the other control groups.The DP cells were sorted from thymus of MBD2-/- (DP_M1,DP_M2,DP_M3) or MBD2+/+ (DP_C1,DP_C2,DP_C3) mice, and subjected to microarray analysis on Affymetrix microarrays.

first: Jianfeng


title: Expression profiles of TIS21/BTG2/PC3 gene knockout in liver of C57BL/6J mice in response to starvation

city: Suwon-si

first: In Kyoung

last: Lim

state: Gyeonggi Do

address: Song-Jae Gwan, rm309,  Ajou univ.,  Woncheon-dong, Yeongtong-gu

department: Biochemistry and Molecular Biology

country: South Korea

institute: Ajou University School of Medicine

summary: TIS21/BTG2/PC3 has been known as one of the primary response genes regulated by p53-dependent and p53-independent manners. In our study, TIS21 reveals various functions as a tumor suppressor in human and mouse tumors. Recently, it has been reported that expression of TIS21 can be induced during starvation in liver, muscle and white adipose tissues. However, there was no report on the role of TIS21 in response to starvation. To investigate any role of TIS21 gene in the metabolic stimulation, we fasted C57BL/6J mice for overnight (20 hour), and then transcriptional profiles of the TIS21-knockout and TIS21-wild type mice were compared. Along with this trial, we also analyzed transcriptional profiles of fetal livers of the 13.5 day-old embryos derived from the TIS21-wild type and knockout mice.

overall_design:
TIS21-KO vs. TIS21-WT from the livers of the 10 week-old male mice starved for 20 hour (from 5:00pm to next day 1:00 pm), and the fetal livers of the 13.5 days old embryos. The mRNAs isolated from fetal livers were pooled (n>3).
Biological samples: mRNAs isolated from livers of the TIS21-KO adult mice  (KO-Ad)  vs. livers of the TIS21 wild-type adult mice (WT-Ad);  pooled mRNAs from livers of TIS21-KO embryos (KO-Fetal) vs. pooled mRNAs from livers of wild-type fetal embryos (WT-Fetal);  Per each sample, the transcriptional profile was measured in technical duplication.

first: Min Sook

last: Ryu

first: Seung

last: Kim

first: Allen

last: Hong


title: The phosphatidylinositol 3-kinase pathway as a potential therapeutic target in bladder cancer

summary: Activation of the phosphatidylinositol 3-kinase (PI3K) pathway occurs in over 40% of bladder urothelial cancers. The aim of this study is to determine the therapeutic potential, the underlying action and resistant mechanisms of drugs targeting the PI3K pathway. Urothelial cancer cell lines and patient-derived xenografts (PDXs) were analyzed for alterations of the PI3K pathway and for their sensitivity to the small molecule inhibitor pictilisib alone and in combination with cisplatin and/or gemcitabine. Potential predictive biomarkers for pictilisib were evaluated and RNA-sequencing was performed to explore drug resistance mechanisms. The bladder cancer cell line TCCSUP, which harbors a PIK3CA E545K mutation, was sensitive to pictilisib compared to cell lines with wild type PIK3CA. Pictilisib exhibited stronger anti-tumor activity in bladder cancer PDX models with PI3KCA H1047R mutation or amplification than a model with wild-type. Pictilisib synergized with cisplatin and/or gemcitabine in vitro, significantly delayed tumor growth and prolonged survival compared with single drug targeted treatment in the PDX models. The phosphorylation of ribosomal protein S6 correlated with response to pictilisib both in vitro and in vivo, and could potentially serve as biomarker to predict response to pictilisib. The inhibitor activated the compensatory MEK/ERK pathway that likely contributed to pictilisib resistance, which was reversed by co-treatment with the RAF inhibitor sorafenib. RNA-sequencing of tumors resistant to treatment suggested that LSP1 down-regulation might play a role in inducing drug resistance. These preclinical results provide new insight into the therapeutic potential of targeting the PI3K pathway for the treatment of bladder cancer.

overall_design: A total of 9 samples were analyzed by transcriptome sequencing (RNA-seq) in this study. The study included BL0269 bladder cancer patient-derived xenograft (PDX) tumors derived from subcutaneous injection of tumor pieces into 10 mice. Mice were randomized into 5 treatment groups: control (untreated), cisplatin, pictilisib (GDC-0941), combination (cisplatin+pictilisib), and sequential (cisplatin -> pictilisib) treatments. Each treatment group had biological duplicate tumors from two separate mice.

first: Chong-xian

last: Pan


title: Analysis of induced cardiomyocytes during direct cardiac reprogramming

first: ZIQING

last: LIU


title: Pilot screen for human PRC1 targeting elements (PTEs)

first: Yuri

last: Schwartz

address: Byggnad 6L, NUS

institute: Umeå University

summary: PcG proteins are critical epigenetic regulators of development. Here we compared genomic distributions of MEL18 and SUZ12 in NTERA-2 cells to search for sites with unusually high presence of PRC1 compared to that of PRC2 and H3K27me3.

overall_design: ChIPs of MEL18 and SUZ12 proteins coupled to next-generation sequencing from chromatin of human NTERA-2 cultured cells. Done in single replicate.

first: Y

first: T

last: Kahn


title: ChIP-seq from K562 (ENCSR594BNR)

city: Stanford

first: ENCODE

last: DCC

address: 300 Pasteur Dr

institute: ENCODE DCC

summary:
HNRNPL ChIP-seq in K562

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


title: ChIP-seq from VCaP (ENCSR597ULV)

summary:
H3K27ac ChIP-seq on human VCaP

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: Denaturing CLIP (dCLIP) pipeline identifies discrete RNA footprints on chromatin-associated proteins and reveals that CBX7 targets 3’UTRs to regulate mRNA expression

city: Boston

first: Michael

last: Rosenberg

state: MA - Massachusetts

address: 185 Cambridge street

department: Molecular Biology

institute: Massachusetts General Hospital, Harvard Medical School

summary: Interaction networks between chromatin complexes and long noncoding RNAs have become a recurrent theme in epigenetic regulation. However, technical limitations have precluded identification of RNA binding motifs for chromatin-associated proteins. Here we add a denaturation step to UV-crosslink RNA immunoprecipitation (dCLIP), and apply dCLIP to mouse and human chromobox homolog 7 (CBX7), an RNA-binding subunit of Polycomb repressive complex 1 (PRC1). In both species, CBX7 predominantly binds 3’ untranslated regions (UTRs) of messenger RNAs. CBX7 binds with a median RNA “footprint” of 171-183 nucleotides, the small size of which facilitates motif identification by bioinformatics. We find four families of consensus RNA motifs in mouse, and independent analysis of human CBX7 dCLIP data identifies similar motifs. Their mutation abolishes CBX7 binding in vitro. Pharmacological intervention with antisense oligonucleotides paradoxically increases CBX7 binding and enhances gene expression. These data support the utility of dCLIP and reveal an unexpected functional interaction between CBX7 and the 3’UTRs of mRNA.interacts with a range of transcripts, it predominantly binds 3’ untranslated regions (UTRs) of messenger RNAs. CBX7 has a median RNA “footprint” of 171 nucleotides, enabling identification of four families of motifs that tend to co-cluster in the 3’UTR. Manipulating the CBX7-3’UTR interactions and motifs with antisense oligonucleotides results in upregulation of mRNA and protein expression, thereby validating the dCLIP method and revealing functional interactions between CBX7 and mRNA.

overall_design: CBX7 RNA interactome was identified by UV-crosslinking and immunoprecipitation followed by high-throughput sequencing (CLIP-seq), and was compared to CBX7 epigenomic landscape as obtained by chromatin immunoprecipitation (ChIP-seq).

first: Roy

last: Blum

first: Barry

middle: A

last: Kesner

first: Verena

last: Maier

first: Attila

last: Szanto

first: Jeannie

last: Lee


title: microRNA-seq from midbrain (ENCSR591SJC)

summary:
miRNA-seq on embryonic 12.5 day mouse midbrain

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 ovary (ENCSR594DIR)

summary:
Chip-Seq on -human (fragmentation date:Thu Nov 03 2016 23:00:00 GMT-0600 (CST)

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


title: Pseudomonas aeruginosa response to potable (tap) water and freshwater from a pond

city: Burlington

first: Matthew

last: Wargo

state: VT

address: 95 Carrigan Dr

institute: University of Vermont

summary: Pseudomonas aeruginosa is a common bacterium in the terminal plumbing system of buildings and it is from this niche that a substantial fraction of infections are acquired. To better understand P. aeruginosa biology in this environment, we examined the transcriptomes in tap water and pond water.

overall_design: Pseudomonas aeruginosa transcriptomes from four conditions were compared using dilute R2B (1/2R2B) as the control condition. Three conditions were in duplicate and the tap water condition was in triplicate.

first: Graham

last: Willsey


title: ChIP-seq from HepG2 (ENCSR590QQP)

summary:
FUS ChIP-seq in HepG2

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


title: ChIP-seq from K562 (ENCSR598TIR)

summary:
eGFP-ZNF507 ChIP-seq on human K562

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


title: ChIP-seq from C4-2B (ENCSR585FQO)

summary:
ChIP-seq on human C4-2B

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


title: ChIP-seq from HEK293 (ENCSR586BRJ)

summary:
eGFP-ZNF433 ChIP-seq on human HEK293 cells.

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


title: ChIP-seq from Peyer's patch (ENCSR584RZY)

summary:
ChIP-seq on human Peyer's patch

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


title: ChIP-seq from prostate gland (ENCSR499JBP)

summary:
ChIP-seq on human prostate gland

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


title: ChIP-seq from Peyer's patch (ENCSR576PII)

summary:
POLR2A ChIP-seq on human Peyer's patch

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


title: ChIP-seq from Peyer's patch (ENCSR588APY)


title: ChIP-seq from lower leg skin (ENCSR582MTM)

summary:
CTCF ChIP-seq on human lower leg skin

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


title: ChIP-seq from esophagus squamous epithelium (ENCSR581RPO)

summary:
ChIP-seq on human esophagus squamous epithelium

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


title: ChIP-seq from testis (ENCSR494TNM)

summary:
CTCF ChIP-seq on human 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: ChIP-seq from stomach (ENCSR493PYN)

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

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


title: ChIP-seq from ovary (ENCSR493APD)

summary:
CTCF ChIP-seq on 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: ChIP-seq from tibial nerve (ENCSR580XUK)

summary:
Chip-Seq on tibial nerve

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


title: ChIP-seq from HEK293 (ENCSR497IAS)

summary:
eGFP-ZNF747 ChIP-seq on human HEK293 cells.

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


title: ChIP-seq from subcutaneous adipose tissue (ENCSR496OMO)

summary:
ChIP-seq on human adipose tissue

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


title: ChIP-seq from stomach (ENCSR573WYW)

summary:
Chip-Seq on stomach

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


title: ChIP-seq from K562 (ENCSR580IAO)

summary:
eGFP-ZNF197 ChIP-seq on human K562

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


title: ChIP-seq from MCF-7 (ENCSR582ZOA)

summary:
NFIB ChIP-seq on human MCF-7

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


title: ChIP-seq from upper lobe of left lung (ENCSR492GDK)

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

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


title: ChIP-seq from transverse colon (ENCSR567EKU)

summary:
ChIP-seq on human transverse colon

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


title: ChIP-seq from A549 (ENCSR496AXR)

summary:
Control ChIP-seq on human A549 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 K562 (ENCSR491EBY)

summary:
ARID2 ChIP-seq on human K562

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


title: ChIP-seq from K562 (ENCSR492LTS)

summary:
BCLAF1 ChIP-seq on human K562

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


title: Hi-C from NCI-H460 (ENCSR489OCU)

summary:
HiC experiment done on NCI-H460

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 thyroid gland (ENCSR492ZIW)

summary:
CTCF ChIP-seq on human thyroid gland

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


title: ChIP-seq from lower leg skin (ENCSR570HXV)

summary:
ChIP-seq on human lower leg skin

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


title: ChIP-seq from MCF-7 (ENCSR573OJP)

summary:
NCOA3 ChIP-seq on human MCF-7

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


title: ChIP-seq from MCF-7 (ENCSR569XNP)

summary:
FOS ChIP-seq on human MCF-7

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


title: ChIP-seq from MCF-7 (ENCSR487ASM)

summary:
SMARCA5 ChIP-seq on human MCF-7

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


title: ChIP-seq from HEK293 (ENCSR567XAM)

summary:
eGFP-ZNF473 ChIP-seq on human HEK293 cells.

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


title: ChIP-seq from tibial nerve (ENCSR569SZK)

summary:
Chip-Seq on tibial nerve

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


title: ChIP-seq from vagina (ENCSR558QYH)

summary:
ChIP-seq on human vagina

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


title: ChIP-seq from HEK293 (ENCSR564YYW)

summary:
eGFP-ZNF157 ChIP-seq on human HEK293 cells.

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


title: ChIP-seq from heart left ventricle (ENCSR699ZGH)

summary:
POLR2A ChIP-seq on human heart left ventricle

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


title: ChIP-seq from K562 (ENCSR699PVC)

summary:
CBFA2T2 ChIP-seq on human K562

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


title: ChIP-seq from A549 (ENCSR563FBT)

summary:
USF2 ChIP-seq on human A549

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


title: ChIP-seq from K562 (ENCSR563LLO)

summary:
E2F1 ChIP-seq on human K562

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


title: ChIP-seq from K562 (ENCSR490LWA)

summary:
eGFP-CEBPG ChIP-seq on human K562

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


title: ChIP-seq from HEK293 (ENCSR483VJQ)

summary:
eGFP-ZNF662 ChIP-seq on human HEK293 cells.

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


title: ChIP-seq from HEK293 (ENCSR550ZZK)

summary:
eGFP-ZNF493 ChIP-seq on human HEK293 cells.

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


title: ChIP-seq from stomach (ENCSR488BXS)

summary:
ChIP-seq on human stomach

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


title: ChIP-seq from spleen (ENCSR485ITK)

summary:
ChIP-seq on human spleen

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


title: ChIP-seq from ovary (ENCSR696LQU)

summary:
Chip-Seq on female gonad

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 thyroid gland (ENCSR485BEB)

summary:
POLR2A ChIP-seq on human thyroid gland

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


title: ChIP-seq from esophagus muscularis mucosa (ENCSR559KAB)

summary:
CTCF ChIP-seq on human esophagus muscularis mucosa

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


title: ChIP-seq from K562 (ENCSR697YLJ)

summary:
CBFA2T3 ChIP-seq on human K562

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


title: ChIP-seq from transverse colon (ENCSR558HTE)

summary:
CTCF ChIP-seq on human transverse colon

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


title: ChIP-seq from body of pancreas (ENCSR484DDO)

summary:
CTCF ChIP-seq on human body of pancreas

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 gastroesophageal sphincter (ENCSR551MLB)

summary:
Chip-Seq on esophagogastric junction

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


title: ChIP-seq from K562 (ENCSR556FBD)

summary:
Input control ChIP-seq on human eGFP-TFDP1 tagged K562 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: ChIP-seq from gastroesophageal sphincter (ENCSR483GTS)

summary:
ChIP-seq on human gastroesophageal sphincter

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


title: Hi-C from endometrial microvascular endothelial cells (ENCSR551IPY)

summary:
HiC experiment done on endometrial microvascular endothelial cells

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


title: ChIP-seq from ovary (ENCSR548DDS)

summary:
CTCF ChIP-seq on 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: microRNA-seq from embryonic facial prominence (ENCSR549EOE)

summary:
miRNA-seq on embryonic 10.5 day mouse embryonic facial prominence

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


title: ChIP-seq from tibial artery (ENCSR699BEK)

summary:
CTCF ChIP-seq on human tibial artery

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


title: ChIP-seq from spleen (ENCSR692ILH)

summary:
CTCF ChIP-seq on human spleen

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


title: ChIP-seq from breast epithelium (ENCSR697YIN)

summary:
CTCF ChIP-seq on human breast epithelium

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


title: Hi-C from T47D (ENCSR549MGQ)

summary:
HiC experiment done on T47D

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