title: Transcriptomic profiling of Lung adenocarcinoma brain metastasis

status: Public on Dec 10 2019

summary: Brain metastasis developed in nearly 40% of lung adenocarcinoma (LUAD) patients diagnosed with distant metastasis. There is lack of transcriptomic data of brain lesions from human lung adenocarcinoma patients. As part of the project to understanding the tumor microenvironment in brain metastasis of LUAD patients, we performed bulk RNA analysis on brain metastases from 6 LUAD patients. In order to understand the tumor intrinsic factors that potential shape the tumor microenvironment, we compared these data with bulk RNA sequencing data from 14 early stage and 11 late stage primary LUAD tumor from TCGA database. Pathway expression analysis showed a downregulation of pro-inflammatory signals in brain metastasis and upregulation of DNA synthesis and oxidative phosphorylation pathways related to rapid proliferation in brain lesions.

overall_design: Performed bulk RNA sequencing on surgical resected metastatic brain tissue from 6 human lung adenocarcinoma patients using  Illumina HiSeq X ten platform.

first: Wang

last: Liang

first: Dai

last: Jinxiang

first: Han

last: Runrun

first: Jin

last: Weilin


title: Dynamic allelic imbalance in early mouse embryo

status: Public on Nov 05 2019

city: Beijing

first: Wenjie

last: Shu

address: Taiping Road 27

country: China

institute: Beijing Institute of Radiation Medicine

type: Expression profiling by high throughput sequencing

summary: We used a reciprocal crosses model to assess the allelic imbalance in early mouse embryo

overall_design: We selected five stages of reciprocal crosses of early embryo. For each stage, two repeats are selected.

first: Qingqing

last: LI

first: Jingxiong

last: Han

first: Chao

last: Ren

first: Zhangyi

last: Ouyang

first: Xingxu

last: Huang

first: Fuchou

last: Tang


title: Distinct Roles of BET Family Members in ERα Enhancer Function and Gene Regulation in Breast Cancer Cells

status: Public on Sep 25 2019

city: Dallas

first: W. Lee

last: Kraus

state: TX

address: 5323 Harry Hines Blvd.

country: USA

institute: UT Southwestern Medical Center

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: Chromatin Remodeling and Immediate Early Gene Activation by SLFN11 in Response to Replication Stress

status: Public on Jan 17 2020

city: Tsuruoka

first: Junko

last: Murai

state: Yamagata

address: 246-2 Kakuganji Mizugami

country: Japan

institute: Keio University


title: Neuronal diversity and convergence in a visual system developmental atlas

status: Public on Jul 16 2020

city: Kansas City

first: Mehmet Neset

last: Ozel

state: MO

institute: Stowers Institute for Medical Research


title: RNA-seq analysis to identify Tricholoma matsutake mycorrhiza specific gene

status: Public on Sep 02 2019

city: Kitakami

first: Yuichi

last: Sakamoto

state: Iwate

department: Department of Bioresource

institute: Iwate Biotechnology Research Center

summary: Bioproject:PRJNA509493; Biosample:SAMN10583662; To identify T. matsutake mycorrhiza specific gene, transcriptomes were comapred among mycorrhiza (pine with T. matsutake), T. matsutake mycelia, T. matsutake fruiting body and pine root (without T. matsutake)

sample_organism:
Tricholoma matsutake
Pinus densiflora

platform_organism:
Tricholoma matsutake
Pinus densiflora

overall_design: Comparing mRNA profiles among mycorrhiza co-culturedwith pine root for 6 months/T. matsutake 6 months cultured mycelia on agar plate/fruiting body collected in wild, and mycorrhiza co-cultured with pine root for 6 months/pine root cultured 6 month without T. matsutake, in triplicate, using Illumina Next-seq

first: Shiho

last: Sato


title: Single-cell RNA-sequencing reveals profibrotic roles of distinct epithelial and mesenchymal lineages in pulmonary fibrosis

status: Public on Sep 05 2019

city: Phoenix

first: Nicholas

last: Banovich

state: AZ

address: 445 N. Fifth Street

department: Integrated Cancer genomics division

institute: Translational Genomics Research Institute

summary: Pulmonary fibrosis (PF) is a form of chronic lung disease characterized by progressive destruction of normal alveolar gas-exchange surfaces and accumulation of extracellular matrix (ECM). In order to comprehensively define the cell types, mechanisms and mediators driving ECM deposition and fibrotic remodeling in lungs with pulmonary fibrosis, we performed single-cell RNA-sequencing (scRNA-seq) of single-cell suspensions generated from non-fibrotic control and PF lungs. Analysis of over 114,000 cells from 20 PF and 10 control lungs identified 31 distinct cell types. We identified multiple distinct lineages directly contribute to ECM expansion, including a novel HAS1hi fibroblast subtype and a previously undescribed KRT5-/KRT17+, collagen and ECM-producing epithelial cell population that was highly enriched in PF lungs. Together these data provide high-resolution insights into the basic mechanisms of pulmonary fibrosis, and indicate a direct profibrotic role of the lung epithelium in PF pathogenesis.

overall_design: We performed single-cell RNA-sequencing (scRNA-seq) of single-cell suspensions generated from non-fibrotic control and pulmonary fibrosis (PF) lungs

first: Arun

middle: C

last: Habermann

first: Austin

middle: J

last: Gutierrez

first: Linh

middle: T

last: Bui

first: Nichelle

middle: I

last: Winters

first: Carla

middle: L

last: Calvi

first: Lance

last: Peter

first: Mei-I

last: Chung

first: Chase

last: Taylor

first: Stephanie

last: Yahn

first: Christopher

last: Jetter

first: Latha

last: Raju

first: Jamie

last: Roberson

first: Guixiao

last: Ding

first: Lori

last: Wood

first: Jennifer

middle: M

last: Sucre

first: Bradley

middle: W

last: Richmond

first: Ana

middle: P

last: Serezani

first: Wyatt

last: McDonnell

first: Simon

middle: B

last: Mallal

first: Matthew

last: Bacchetta

first: Ciara

last: Shaver

first: Lorraine

last: Ware

first: Ross

last: Bremner

first: Rajat

last: Walia

first: Timothy

middle: S

last: Blackwell

middle: E

first: Jonathan

middle: A

last: Kropski


title: IQGAP3 interacts with Rad17 to activate the MRN/ATM/Chk2 signaling and promote radioresistance in lung cancer

status: Public on Sep 21 2019

city: Wuhan

first: Qifan

last: Yang

state: Hubei

address: 13,Hangkong Road

department: Cancer Center

institute: Huazhong University of Science and Technology

summary: IQ motif containing GTPase activating protein 3 (IQGAP3) has been implicated in diverse cellular processes including neuronal morphogenesis, cell proliferation and motility as well as epithelial-mesenchymal transition. However, its roles in DNA damage and repair remain to be clarified. Here, we demonstrate that IQGAP3 is frequently overproduced and predicts poor prognosis in lung cancer patients. Functionally, we provide evidence that depletion of IQGAP3 impairs tumorigenesis and overcomes radioresistance in lung cancer in vitro and in vivo. Mechanistically, we uncover that IQGAP3 interacts with and controls the stability of Rad17 to activate the ATM/Chk2 signaling by recruiting Mre11-Rad50-Nbs1 (MRN) complex in response to DNA damage. Moreover, Rad17 is identified as the major downstream effector that mediates the functions of IQGAP3 in lung cancer. Clinically, IQGAP3 overexpression positively correlates with Rad17 protein levels in human lung cancer tissues. Collectively, these data support key roles for IQGAP3 in promoting tumorigenesis and radioresistance in lung cancer by stabilizing the Rad17 protein and suggest targeting IQGAP3 is a promising therapeutic strategy for lung cancer radiotherapy.

overall_design: Analysis of control and siIQGAP3 lung cell lines obtained from 3 independent samples each.

first: Li

last: Liu

first: Shuangbing

last: Xu

first: Yulan

last: Zeng


title: Lysophosphatidic acid treatment improves brush border maturation and apical SGLT1 activity in Myo5b deficient mice, a model of MVID

status: Public on Oct 24 2019

city: Nashville

first: Izumi

last: Kaji

state: TN

address: Rm 10465H, MRB IV

department: Surgery

institute: Vanderbilt University Medical Center

summary: Myosin Vb (Myo5b) is an essential trafficking protein for membrane recycling in gastrointestinal (GI) epithelial cells and its inactivating mutation causes the congenital diarrheal disease, microvillus inclusion disease (MVID). We previously reported that Myo5b deficiency in mice causes mislocalization of SGLT1 and NHE3, but retained apical function of CFTR, resulting in malabsorption and secretory diarrhea. Activation of lysophosphatidic acid (LPA) receptors can improve diarrhea, but the effects of LPA on MVID symptoms is unclear. We therefore tested whether LPA treatment can ameliorate the epithelial deficits in Myo5b knockout (KO) mice. Methods: Adult tamoxifen-induced, intestine-specific, Myo5b KO (VillinCreERT2;Myo5bflox/flox) and littermate control mice were treated with LPA, an LPAR2 agonist (GRI977143), or vehicle for 4 days after a single tamoxifen injection. Apical SGLT1 and CFTR activities were measured in Üssing chambers. The localization of membrane transporters was evaluated by immunostaining in mouse tissues and enteroids. RNA sequencing and enrichment analysis were performed with isolated jejunal epithelial cells. Results: Daily treatment with LPA decreased the frequency of multivesicular bodies and the expression of cathepsins, but did not affect the formation of microvillus inclusions in Myo5b KO mice. LPA partially restored the brush border height and the localization of SGLT1 and NHE3 in Myo5b KO small intestine and enteroids. SGLT1-dependent short-circuit current (Isc) was increased and abnormal CFTR activities were suppressed in LPA-treated jejunum compared to that of vehicle-treated Myo5b KO mice. Conclusions: Cell autonomous LPA signaling may modulate a Myo5b-independent trafficking mechanism and the brush border maturation, demonstrating a therapeutic potential for LPA in the treatment of MVID.

overall_design: Adult male VillinCreERT2;MYO5Bflox/flox mice were given a single dose of 2 mg of tamoxifen (KO, 7 mice) or corn oil (control, 3 mice) by ip injection. Induced KO mice were treated with LPA (3 mice) or vehicle (4 mice) by ip for 4 days. All mice were euthanized on day 4 and epithelial cells were mechanically isolated from jejunum by micro forceps in ice-cold PBS containing 10 mM EDTA and immersed in TRIzol Reagent (Invitrogen 15596018). RNA was extracted according to the manufacture instructions and RNA-seq was performed by Novogene Corporation Inc. (Sacramento, CA) on 3 or 4 independent preparations from each condition.

first: I

first: James

middle: R

last: Goldenring


title: LCM-Seq of niches and single-cell RNA-seq of mouse bone marrow

status: Public on Aug 08 2019

city: Barcelona

first: Lars

last: Velten

address: C. Dr. Aiguader 88, P05

department: Bioinformatics and Genomics

country: Spain

institute: CRG


title: Indexed single-cell RNA-seq of mensenchymal bone marrow cells

summary: This data set contains single-cell RNA-seq data from CD45-Ter119-Cd41-CD71-Vibrant Dye+VCAM1+ cells, indexed for the expression of these markers as well as CD51, CD61 and CD200

overall_design: One plate of CD45-Ter119-Cd41-CD71-Vibrant Dye+VCAM1+ cells, two plates of CD45-Ter119-Cd41-CD71-Vibrant Dye+VCAM1+CD61+ cells and two plates of CD45-Ter119-Cd41-CD71-Vibrant Dye+VCAM1+CD61- cells were sequenced.

first: Chiara

last: Baccin

first: Jude

last: Al-Sabah

first: Andreas

last: Trumpp

last: Steinmetz

middle: F

last: Haas


title: Effects of cordycepin on murine macrophage-like cells in the presence and absence of an inflammatory stimulus

status: Public on Feb 07 2019

city: London

first: Graeme

last: Thorn

address: Charterhouse Square

country: United Kingdom

institute: Barts Cancer institute, Queen Mary University of London

summary: To perform high-throughput, transcriptome-wide analysis on RAW 264.7 cells treated with cordycepin with and without bacterial lipopolysaccharide (LPS) to investigate cordycepin's anti-inflammatory properties and determine whether particular classes of RNAs were sensitive to cordycepin.

overall_design: RAW 264.7 cells were used with four conditions: cells were pre-treated for an hour with cordycepin or DMSO (vehicle), and then either did or did not have LPS added. Regardless of LPS treatment, cells were incubated for a further hour. Experiment was performed in biological quadruplicate, with each replicate collected on a different day.

first: Raj

middle: D

last: Gandhi

first: Victoria

last: Chapman

first: Cornelia

middle: H

last: de Moor


title: Single-cell RNA-seq of frequent and rare populations in mouse bone marrow

summary: This data set contains single-cell RNA sequencing data of mature immune cells, hematopoietic and immune progenitors, mesenchymal cells (CAR cells, fibroblasts, osteoblasts, chondrocytes, putative mesenchymal stem cells), endothelia, smooth muscle, and Schwann cells.

overall_design: The following fractions were subjected to single-cell RNA-sequencing using 10x genomics: Total live bone marrow; Lineage-negative CD45-negative bone marrow; Lineage-CD45-CD71- bone marrow (obtained by crushing or flushing of bones); Lineage-CD45-CD71- bone-associated fraction (obtained by digesting bone chips); Lineage-Kit+ bone marrow.

first: Simon


title: LCM-Seq of microscopically defined niches in mouse bone marrow

summary: This data set contains low-input RNA-seq data of 100-500 cells that were extracted from spatially defined locations in bone slices using laser capture microscopy.

overall_design: The following microscopically defined niches are included: Sca1+ Arteries; Emcn+ Sinusoids; Endosteum; Subendosteum; Areas low in Emcn+ sinusoids.


title: Analysis of HPV16 E2 host gene expression using TERT immortalized keratinocytes (NOKs) cell lines and RNA-sequencing

status: Public on Oct 23 2018

city: Richmond

first: Iain

last: Morgan

state: VA

address: School of Dentistry, W. Baxter Perkinson Bldg, 521 N 11th Street

institute: VIRGINIA COMMONWEALTH UNIVERSITY

summary: HPV must reprogram host gene expression to promote infection, and HPV proteins E6 and E7 contribute to this via targeting of cellular transcription factors including p53 and pRb respectively.  The HPV16 E2 protein regulated host gene expression in U2OS cells and in this study we extend these observations into NOKs that are capable of suporting late stages of the HPV16 life cycle.  We observed repression of innate immune genes by E2 that are also repressed by the intact HPV16 genome in NOKs.  There was a highly significant overlap of the E2 regulated genes with those regulated by the intact HPV16 genome in the same cell type.  siRNA targeting of E2 reversed repression of E2 targed genes.  The ability of E2 to repress innate immune genes was confirmed in an ano-genital immortalized keratinocyte cell line, N/Tert-1.

overall_design: In total, 8 samples are analyzed.  Two biological replicates of NOK controls, two biological replicates of NOKs containing HPV16 full genome, and two different NOKs cell lines overexpressing the HPV16 E2 protein.

first: Micael

last: Evans

first: Claire

last: James

first: Molly

last: Bristol

first: Tara

last: Nulton

first: Xu

last: Wang

first: Namsimar

last: Kaur

first: Elizabeth

last: White

first: Brad

last: Windle


title: Automated in situ profiling of chromatin modifications resolves cell types and gene regulatory programs

status: Public on Dec 22 2018

city: Grand Rapids

first: Derek

last: Janssens

state: MI

address: 333 Bostwick Ave. NE

department: Epigenetics

institute: Van Andel Institute

summary: Our understanding of eukaryotic gene regulation is limited by the complexity of protein-DNA interactions that comprise the chromatin landscape and inefficient methods for characterizing these interactions. We recently introduced CUT&RUN, an antibody-targeted method that profiles DNA-binding proteins, histones and chromatin modifying proteins with high sensitivity and resolution. Here we describe an automated CUT&RUN platform and apply it to profile the chromatin landscapes of human cell lines. We develop a metric to quantitatively compare chromatin features between cell types and identify their distinctive gene expression programs. Finally, we use this method to identify gene expression features of two different pediatric diffuse midline gliomas using frozen tissue from patient-derived xenografts. Our easy, cost-effective workflow makes automated CUT&RUN an attractive tool for high-throughput characterization of cell types and patient samples.

overall_design: We used Cleavage under targets and Release using nuclease (Cut-and-Run), a chromatin profiling strategy in which antibody-targeted controlled cleavage by micrococcal nuclease releases specific protein-DNA complexes into the supernatant for paired-end DNA sequencing.

first: Steven

last: Wu

first: Jay

last: Sarthy

first: Michael

last: Meers

first: Carrie

last: Myers

first: James

last: Olson

first: Kami

last: Ahmad

last: Henikoff


title: Tissue-specific transcriptomic and epigenomic profiles explain differential damage and repair of anti-cancer drug cisplatin induced DNA-adducts across mouse organs

status: Public on Jan 01 2019

city: Istanbul

first: Ogun

last: Adebali

address: Orta Mah. Universite Cad No 27

department: Faculty of Natural Sciences and Engineering

country: Turkey

institute: Sabanci University

summary: Platinum-based drug cisplatin is a widely used first-line therapy for several cancers.  Cisplatin interacts with DNA mainly in the form of Pt-d(GpG) di-adduct, which stalls cell proliferation and activates DNA damage response pathway.  Cisplatin DNA-adducts are primarily repaired by nucleotide excision repair system.  Despite cisplatin shows a broad spectrum of anticancer activity, it has limitation of use due to acquired drug resistance and toxicity to nontargeted tissues.    By integrating genome-wide high-throughput “damage-seq”, “XR-seq”, mRNA-seq approaches along with epigenomic data we studied the mechanism of action of cisplatin across the mouse genome in kidney, liver, lung and spleen.    Genome-wide damage-seq data reveal that kidney is highest cisplatin-damage accumulation site, while spleen is lowest.  Excision repair on transcribed strand (TS) and non-transcribed strand (NTS) in active genes is in positive correlation with gene transcription, and regarding to nucleotide excision repair efficiency, there is no significant difference across organs.  Lastly, in response to cisplatin treatment ATM signaling is upregulated in kidney, liver and lung, while PKA signaling is downregulated across all organs.  The methodology and data we presented here include four different mouse organs and three “omics” data, it unbiasedly constitutes a foundation for understanding the mechanism of cellular respond to cisplatin and by means of improving chemotherapy while reducing side effect to normal tissues.

overall_design:
Damage-seq XR-seq and RNA-seq samples from 4 mouse organs after cispaltin injection in two replicates and RNA-seq from 4 organs in two replicates as control are collected.

UPDATE: [Feb-14-2025] The annotation of Samples GSM3272787-GSM3272794 was corrected: All Samples originally labeled as 'control' were changed to 'cisplatin' and vice versa.

first: Askar

last: Yimit

first: Aziz

last: Sancar

first: Yuchao

last: Jiang


title: Identification of Transcription Factor Relationships Associated with Androgen Deprivation Therapy Response and Metastatic Progression in Prostate Cancer

status: Public on Oct 11 2018

city: Atlanta

first: Carlos

middle: Sanchez

last: Moreno

state: GA

address: 101 Woodruff Circle NE, Room 2309

department: Pathology and Laboratory Medicine

institute: Emory University

summary: Background: Patients with locally advanced or recurrent prostate cancer typically undergo androgen deprivation therapy (ADT), but the benefits are often short-lived, and responses are variable. ADT failure results in castration-resistant prostate cancer (CRPC), that inevitably leads to metastasis. We hypothesized that differences in tumor transcriptional programs may reflect differential responses to ADT and subsequent metastasis.   Results: We performed whole transcriptome analysis of 20 patient-matched Pre-ADT biopsies and 20 Post-ADT prostatectomy specimens, and identified two subgroups of patients (high impact and low impact groups) that exhibited distinct transcriptional changes in response to ADT. We found that all patients lost AR-dependent subtype (PCS2) transcriptional signatures. The high impact group maintained the more aggressive subtype (PCS1) signal, while the low impact group more resembled an AR-suppressed (PCS3) subtype. Computational analyses identified transcription factor coordinated groups (TFCGs) enriched in the high impact group network. Leveraging a large public dataset of over 800 metastatic and primary samples, we identified 33 TFCGs in common between high impact group and metastatic lesions, including SOX4/FOXA2/GATA4, ERF/ETV5/ETV3/ELF4, and a TFCG containing JUN, JUNB, JUND, FOS, FOSB, and FOSL1. The majority of metastatic TFCGs were subsets of larger TFCGs in the high impact group network, suggesting refinement of critical TFCGs in prostate cancer progression.   Conclusions: We have identified TFCGs associated with pronounced initial transcriptional response to ADT, aggressive signatures, and metastasis. Our findings suggest multiple new hypotheses that could lead to novel combination therapies to prevent development of CRPC following ADT.

overall_design: Sequence alignment and gene level expression quantifications were obtained using the STAR read aligner. We obtained an average of 91,077,364 reads (sd: 41,923,139) with a mean transcriptome coverage of 64x (83% mapping to exons).

first: Nitya

last: Sharma


title: Canonical and non-canonical regulatory roles of androgen receptor variant 7 in prostate cancer

status: Public on Oct 02 2018

city: Durham

first: Greg

last: Wang

state: NC

address: 3 Genome Court

department: Duke Department of Pharmacology and Cancer Biology  and Duke Cancer Institute

institute: Duke University School of Medicine, and Department of Biochemistry and Biophysics, UNC at Chapel Hill (adjunct)

summary: The androgen receptor splice variant 7 (AR-V7) lacks the ligand-binding domain; is detected with increased frequency in advanced prostate cancer and is postulated to be one crucial mechanism for disease progression and therapeutic resistance to androgen deprivation in castration–resistant prostate cancer (CRPC). Targeting AR-V7 or unique downstream targets could provide novel therapeutic approaches for CRPC. Here, we report that, independent of ligand, AR-V7 binds not only to the androgen-responsive element (ARE) sites inducing canonical AR signaling but also to non-canonical target sites where ligand-stimulated full-length AR (AR-FL) does not bind. These AR-V7 “solo” binding sites are mainly found at gene promoters and are co-occupied by a zinc-finger transcription factor ZFX and the co-activator BRD4, both of which physically interact with AR-V7. Consequently, AR-V7 not only recapitulates AR-FL action without androgen but uniquely regulates transcripts correlating with AR-V7 expression in the TCGA prostate cancer cohort. Mechanistically, ZFX appears to function as a pioneer factor for AR-V7 at solo-binding sites and BRD4 inhibitors but not anti-androgens suppress AR-V7 action at solo-binding sites as well as AR-V7-dependent growth. Additionally, knockdown of ZFX, or two downstream targets uniquely co-activated by AR-V7 (ZNF32 and FZD6), also suppressed growth of AR-V7-dependent CRPC cells. AR-V7 directly activated genes differentiate tumor from normal prostate tissues and predict poor prognosis in patients. Thus AR-V7 has both canonical and non-canonical regulatory functions in CRPC, which may provide new therapeutic avenues.

overall_design:
mRNA profiles of knocking down AR-FL, AR-V7 or control vector in 22Rv1 cells were generated by deep-sequencing, in duplicate. mRNA profiles of knocking down ZFX or control vector in 22Rv1 cells were generated by deep-sequencing, in duplicate. mRNA profiles of 22Rv1 cells which were charcoal stripped for 3 days and then treated with vehicle, DHT, DHT plus MDV3100 or DHT plus JQ1 were generated by deep-sequencing, in duplicate.
Examination of the genome-wide binding of full-length androgen receptor (AR-FL), AR-V7, Brd4 and ZFX in an castration-resistant prostate cancer cell line in the presence of different drug treatments.

first: Ling

last: Cai

first: Joel

last: Parker

first: Shannon

last: Tsai

first: Deyou

last: Zheng

first: Shelley

last: Earp


title: Repressive mark H3K27me3 in PRMT6 KO NT2/D1 cells

status: Public on Sep 27 2018

city: Marburg

first: Uta

middle: Maria

last: Bauer

state: Hessen

address: Hans-Meerwein-Str. 2

department: Institute of Molecular Biology and Tumor Research

country: Germany

institute: Philipps University Marburg

summary: Protein arginine methyltransferase 6 (PRMT6) is an epigenetic regulator of fundamental cellular processes, such as gene expression and DNA repair. Asymmetric dimethylation of histone H3 at arginine 2 (H3R2me2a) is the major histone modification catalyzed by PRMT6. To identify the genome-wide deposition and transcriptional impact of H3R2me2a, we established PRMT6 deletion in a human cell model of neural differentiation. These knockout cells show severe neural differentiation defects. ChIP-seq profiling reveals that H3R2me2a is present at promoter as well as non-promoter sites in a PRMT6-dependent manner. Loss of H3R2me2a causes enhanced H3K4me3 deposition and target gene transcription supporting a genome-wide repressive nature of H3R2me2a. Intriguingly, the non-promoter H3R2me2a peaks co-localize with active enhancer marks, such as H3K4me1 and H3K27ac.

overall_design: Examining of PRMT6 influence on H3K27me3 deposition in CRISPR control and knockout PRMT6 with neighboring histone modification.

first: Peeyush

last: Sahu

first: Caroline

last: Bouchard

first: Uta-Maria


title: Distinct roles of BET Family Members in ERα Enhancer Function and Gene Regulation in Breast Cancer Cells [ChIP-seq]

first: W. Lee

last: Kraus

summary: Estrogen (E2)-dependent gene regulation mediated by estrogen receptor alpha (ERα) plays a mitogenic role in ER-positive breast cancer cells.  Although clinical applications of selective estrogen receptor modulators (SERMs), which directly interact with ERα to alter ERα activity, have been effective as a first line of treatment for breast cancer patients, a large subset of the patients will develop resistance after prolonged use of SERMs.  Thus, there is a great need to develop alternative therapeutic strategies for SERM-resistant breast cancers.  Here, we describe the potential use of the bromodomain family member protein (BRD) selective bromodomain inhibitor, JQ1, to alter E2-dependent gene expression program and inhibit E2-dependent growth of breast cancer cells.  We show that each family member has partially redundant roles as ERα coregulators that are required for ERα-mediated gene transcription.  Furthermore, we demonstrate the function of BRD3 as a molecular sensor of total BRD activity by the compensatory control of its protein levels.  In addition, BRD3 colocalizes with a subset of ERα binding sites (ERBSs) that are enriched for active enhancer features and associated with highly E2-induced genes.  Collectively, we illustrate a critical role of the BET family members in ERα dependent gene expression.

overall_design:
ChIP-seq datasets for BRD3 were generated using MCF-7 cells treated with 100 nM E2 for 3 hours to determine BRD3-enriched ERα enhancers.

Please note that each processed data was generated from both replicates (i.e *rep1 and *rep2 samples) and linked to the corresponding *rep1 sample records.

first: Shino

last: Murakami

first: Rui

last: Li

first: Anusha

last: Nagari

first: Minho

last: Chae

first: Cristel

middle: V

last: Camacho

first: Lee


title: Genomic location of PRMT6-dependent H3R2 methylation is decisive for the transcriptional outcome of associated genes [ChIP-seq]

overall_design: Examining of PRMT6 dependent H3R2me2a deposition in CRISPR control and knockout PRMT6 with neighboring histone modification.


title: Genomic occurrence analysis of PRMT6-dependent H3R2me2a

overall_design: Examining of PRMT6-dependent H3R2me2a deposition in CRISPR control and knockout PRMT6 with neighboring histone modification.

first: René

last: Nötzold


title: Transcriptome analysis of PRMT6 knock-out in NT2/D1 cells

summary: Whole transcriptome for PRMT6 knock-out and control NT2/D1 cells with and without ATRA (all-trans retinoic acid) was sequenced. These samples were compared to each other to find differentially regulated genes and PRMT6-dependent transcriptome in pluripotency and differentiating cells.

overall_design: Examining of PRMT6-dependent transcriptome in NT2/D1 cells using RNAseq.


title: Genomic location of PRMT6-dependent H3R2 methylation is decisive for the transcriptional outcome of associated genes

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

overall_design: Refer to individual Series


title: A comprehensive roadmap of spermatogenesis and testis niche from single-cell RNA-seq

status: Public on Aug 24 2018

city: Ann Arbor

first: Qianyi

last: Ma

address: 1141 E Catherine St

department: Human Genetics

institute: University of Michigan

summary: Continuous sperm production is not necessary for the survival of the organism, but is essential to maintain a species. The process of spermatogenesis is comprised of three phases: mitotic proliferation, meiosis, and spermiogenesis. To illuminate germline intrinsic and extrinsic programs, we performed single-cell RNA sequencing on ~35K cells from the adult mouse testis. This analysis provides a comprehensive molecular atlas of the testis, identifying both known and novel cell types. We demonstrate for the first time the continuous nature of germ cell differentiation, provide molecular signatures and subtype-specific molecular markers, and identify several novel candidate regulators of spermatogenesis. Finally, we demonstrate in vivo using spatial mapping that germ and somatic cell molecular subtypes correspond to previously defined histological cell types residing at different stages of seminiferous epithelial cycle. Taken together, our results unveil the complexity of the testis, and provide a global, unbiased roadmap of the in vivo gametogenesis program.

overall_design:
Drop-seq of whole mouse testis and enriched populations.

NOTE:
As the initial submission of raw data only included partial run (extracted mouse cells) for some samples, all raw data for the following samples have been replaced to include the complete/original run for each sample (Feb 2019):
GSM3069439, GSM3069440, GSM3069443-GSM3069448,GSM3069450, GSM3069451, GSM3069459-GSM3069463

All raw data for the 25 samples are paired-end, with 8 single-species samples + 17 mixed-species samples.
For mixed-species samples, the major species is mouse, and the spike-in can be either human or monkey. The spike-in species were only used to confirm cells are not doublets by two-species mixing experiments, but not analyzed in processed data under GSE112393.

first: Saher

last: Hammoud


title: Sexual stage-induced long noncoding RNAs in the filamentous fungus Fusarium graminearum [II]

status: Public on Aug 16 2018

city: East Lansing

first: Wonyong

last: Kim

state: Michigan

address: 612 Wilson Road, Room 166

department: Plant Biology

institute: Michigan State University

summary: Long noncoding RNA (lncRNA) plays important roles in morphological differentiation and development in eukaryotes. In filamentous fungi, however, little is known about lncRNAs and their roles in sexual development. Here we describe sexual stage-induced lncRNAs during the formation of perithecium, the sexual fruiting body of Fusarium graminearum. We identified 547 lncRNAs whose expression were developmental stage-specific; about 40% of them peaked during ascus development, when meiosis occurs. A large fraction of the lncRNAs were found to be antisense to mRNAs, forming 300 sense–antisense pairs. Although small RNAs were produced from these overlapped loci, most of the antisense lncRNAs appeared not to be involved in gene silencing pathways. Rather, the expression of antisense lncRNA and sense mRNA pairs tended to be induced in parallel as the perithecium matured. To identify regulatory components for lncRNA expression, we analyzed mutants defective in the nonsense-mediated decay (NMD) pathway. A subset of lncRNAs was specifically targeted by NMD, suggesting a suppressive role of NMD in lncRNA expression during vegetative growth. This study provides comprehensive resources for studying developmental lncRNA that may be important for laying out the multicellular fruiting body plan.

overall_design: Time-series mRNA profiles during the conidial germination for the Fusarium graminearum wild-type strain PH-1 were generated by deep sequencing, in triplicate, using the Illumina HiSeq 2500 system.

first: Cristina

last: Miguel-Rojas

first: Frances

last: Trail


title: Sexual stage-induced long noncoding RNAs in the filamentous fungus Fusarium graminearum


title: ROS production by PPARbeta-deficient fibroblasts reduces tumor load by triggering an epithelial antioxidant response

status: Public on Aug 05 2018

city: Singapore

first: Eddie

middle: Han Pin

last: Tan

address: 60 Nanyang Drive

department: School of Biological Sciences

country: Singapore

institute: Nanyang Technological University


title: RNA-seq identifies autophagy as the most prevalent upregulated pathway in dormant breast cancer cells

status: Public on Apr 19 2018

city: Bethesda

first: Maxwell

last: Lee

state: MD

address: Building 37, Room 5120

department: CCR

institute: National Cancer Institute, NIH

summary:
Purpose: The goal of this study is to evaluate the transcriptome profiling (RNA-seq) of dormant and proliferating breast cancer cells using an in vitro 3D model
Methods: mRNA profiles of D2.0R cells growing either on basal membrane extracts (BME) (dormant phase) or BME + Collagen (COL) (proliferative phase) at days 1 or 5 of culture were generated by deep sequencing in triplicate with Ilumina HiSeq2500 using Illumina TruSeq V4. Aligned reads (BAM files) were analysed using PartekFlow software for differential expression and gene enrichment analysis. Comparisons used Partek Gene Specific Analysis (GSA) algorithm and multiple comparisons were corrected using False Discovery Rate (FDR), which was set at 0.05
Results: Using an optimized data analysis workflow, we mapped about 118 – 133 million reads per sample to the mouse genome (build mm9). Total alignment with reference genome is between 81-90%. RNA-seq identified 5,524 transcripts showing differential expression between the D2.0R cells cultured on BME + COL vs D2.0R cells cultured on BME matrices at day 5, with a fold change ≥1.5 or ≤-1.5 and p value <0.05. On the other hand, only 1,097 were found to be differentially expressed between D2.0R cells growing on BME matrices at day 5 and day 1, with a fold change ≥1.5 or ≤-1.5 and p value <0.05. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to breast cancer dormancy and identifies autophagy as a top biological process activated in dormant D2.0R cells.
Conclusions: Our study represents a detailed analysis of the transcriptomes of dormant and proliferating D2.0R cells, with three biologic replicates, generated by RNA-seq technology. RNA-seq based transcriptome characterization identifies autophagy as the most prevalent upregulated pathway in dormant breast cancer cells.

overall_design: mRNA profiles of D2.0R cells after culture on BME or BME + COL matrices for 1 or 5 days were generated by deep sequencing in triplicate with Ilumina HiSeq2500 using Illumina TruSeq V4.

first: Laura

last: Vera-Ramirez

first: Suman

middle: K

last: Vodnala

first: Ryan

last: Nini

first: Kent

last: Hunter

first: Jeffrey

last: E Green


title: Efficient derivation of stable primed pluripotent embryonic stem cells from bovine blastocysts [RNA-seq]

status: Public on Feb 11 2018

city: Davis

first: Pablo

last: Ross

state: CA

address: 1 Shields Ave

institute: University of California, Davis

summary: Embryonic stem cells (ESCs) are derived from the inner cell mass of preimplantation blastocysts. From agricultural and biomedical perspectives, the derivation of stable ESCs from domestic ungulates is important for genomic testing and selection, genome engineering, and modeling human diseases. Cattle are one of the most important domestic ungulates that are commonly used for food and bioreactors. To date, however, it remains a challenge to produce stable pluripotent bovine ESC lines. Employing a culture system containing fibroblast growth factor 2 and an inhibitor of the canonical Wnt-signaling pathway, we derived pluripotent bovine ESCs (bESCs) with stable morphology, transcriptome, karyotype, population-doubling time, pluripotency marker gene expression, and epigenetic features. Under this condition bESC lines were efficiently derived (100% in optimal conditions), were established quickly (3–4 wk), and were simple to propagate (by trypsin treatment). When used as donors for nuclear transfer, bESCs produced normal blastocyst rates, thereby opening the possibility for genomic selection, genome editing, and production of cattle with high genetic value.

overall_design: RNAseq profiles from two CTFR-bESC lines (A and B) at passages number P10, P13, P23, P35, P45 and P10, P12, P24, P35, P46, respectively were produced. Pools of 10 whole blastocysts (2 replicates) and two lines of bovine fibroblasts (2 replicates) were used as controls.

first: Yanina

last: Bogliotti

middle: J


title: Efficient derivation of stable primed pluripotent embryonic stem cells from bovine blastocysts


title: High-Resolution temporal profiling of developing pancreas uncovers the mechanisms of endocrine cell fate determination

status: Public on Jun 05 2018

city: Houston

first: Malgorzata

last: Borowiak

address: 1 Baylor Plaza

institute: Baylor College of Medicine


title: Expression data from dissected caudal area of urogenital ridges of Sox11 knockout and wildtype E10.75 mouse embryos

status: Public on Dec 31 2017

city: Nice

first: Yasmine

last: Neirijnck

address: Parc Valrose

department: iBV

country: France

institute: University of Nice

summary: The transcription factor Sox11 is a crucial regulator of kidney development. It is expressed in both mesenchymal and epithelial components of the early kidney anlagen. Deletion of Sox11 in mice causes an extension of the domain expressing Gdnf within rostral regions of the nephrogenic cord and results in duplex kidney formation. To gain insight into potential targets we performed microarray analysis on RNA isolated from the caudal region of E10.75 wildtype and mutant nephrogenic cords. 281 probe sets presented statistically significant changes (76 up, 205 down; FDR<0.1)

overall_design: Total RNA from dissected caudal area of urogenital ridges of Sox11 knockout and wildtype E10.75 embryos was extracted in 4 independent replicates for each genotype

first: Andreas

last: Schedl

first: Antoine

last: Reginensi

first: Herbert

last: Schulz


title: Ovarian tumors associated with Yo-PCD

status: Public on Feb 01 2018

city: LYON

first: Daniel

last: PISSALOUX

address: 28 rue Laënnec

department: Biopathology

institute: Centre Léon Bérard

type: Genome binding/occupancy profiling by genome tiling array

summary: Intra-tumor immune attack associated with genetic alterations of onconeural antigens characterize ovary tumors of patients with Yo paraneoplastic cerebellar degeneration

overall_design: 17 genomic profiles corresponding to 17 ovarian tumors from 17 distinct Yo-PCD patients, using commercial reference DNA (Male)

first: Mathilde

last: Small

first: Virginie

last: Desestret

first: Jérôme

last: Honnorat

last: Pissaloux

first: Sandrine

last: Paindavoine

first: Isabelle

last: Treilleux


title: High-Resolution temporal profiling of developing pancreas uncovers the mechanisms of endocrine cell fate determination [Drop-seq]

summary: Drop-sequencing of the whole e14.5 and e16.5 mouse pancreas

overall_design: Three litters and 39 mouse embryonic day 14.5 pancreata was dissociated to single cells. 15,228 single cells were sequenced using Drop-seq. For e16.5, three litters and 31 embryos were used and 2,006 transcriptomes were recovered by Drop-seq.

first: Matthew

last: Hill

first: Marissa

last: Scavuzzo

first: James

last: Martin


title: High-Resolution temporal profiling of developing pancreas uncovers the mechanisms of endocrine cell fate determination [MATQ-seq]

summary: MATQ-sequencing of single isolated endocrine progenitors (EPs) from the e14.5 and e16.5 mouse pancreas

overall_design: MATQ-seq from two litters of Ngn3-eGFP e14.5 and two litters of e16.5 mice, with 15 cells from e14.5 and 12 cells from e16.5. sequenced in two batches of library prep and sequencing

first: Kuanwei

last: Sheng

first: Diane

last: Yang

first: Jessica

last: Teaw

first: Chenghong

last: Zong


title: High-Resolution temporal profiling of developing pancreas uncovers the mechanisms of endocrine cell fate determination [ATAC-Seq]

first: Malgorzata

last: Borowiak

summary: Chromatin accessibility of endocrine progenitor cells from the e14.5 and e16.5 mouse pancreas

overall_design: fast ATAC-seq of 3 replicates of e14.5 and 3 replicates of e16.5 Ngn3-eGFP+ cells.


title: Epigenetic Landscapes in Breast Cancer Cells

status: Public on Dec 15 2017

first: Yuanxin

last: Xi

address: 1400 Pressler St

department: Bioinformatics and Computational Biology

institute: The University of Texas MD Anderson Cancer Center

summary: Chromatin architecture is essential to transcriptional regulation. Cancer cells undergo critical chromatin remodeling processes that interact with the activation or silencing of oncogenes or tumor suppressor genes. These processes, together with other alterations of the functional status of chromatins, are characterized by epigenetic marks such as covalent histone modifications, DNA methylations and etc. The epigenetic landscapes defined by these marks are key to understand their regulatory mechanisms as well as the contributions to cancer onset and progression. In this study, we focus on defining the epigenetics landscapes across different breast cancer subtypes. Here we present a collection of 11 key histone modifications across 13 distinct breast cancer cell lines, representing 5 major breast cancer subtypes, including two ER positive subtypes: Lumina-A and Lumina-B, HER2 positive subtype and triple-negative subtypes TNBC-Basal and TNBC-ClaudinLow, as well as normal-like immortal breast cells. Using combinatorial patterns of multiple histone modifications, we defined the whole genome chromatin state maps and identified specific signatures in breast cancer subtypes.

overall_design: H3K4me1, H3K4me3, H3K27me3, H3K36me3, H3K9me3, H3K9ac, H3K79me2, H3K27ac, H2BK120ub1, H3K23ac, and H4K8ac ChIP-seq, and input in 76NF2V, MCF10A, MCF7, ZR751, MB361, UACC812, SKBR3, AU565, HCC1954, MB231, MB436, MB468, and HCC1937 cells.

first: Xiaobing

last: Shi

first: Wenqian

last: Li

first: Kendra

last: Allton


title: Zinc transporter ZIP8 (SLC39A8) overexpression effect on primary mouse articular chondrocytes

status: Public on Oct 10 2017

city: Gwangju

first: Yoonkyung

last: Won

address: 123 Cheomdangwagiro

country: South Korea

institute: Gwangju Institute of Science and Technology

summary:
Gene expression profiling of primary mouse articular chondrocyte infected with recombinant adenovirus expressing the zinc transporter ZIP8 (SLC39A8) protein.
In this study, we have attempted to explore the effects of ZIP8 overexpression on mouse transcriptome and have identified numerous genes which are involved in osteoarthritis pathogenesis.

overall_design: Primary mouse articular chondrocytes were isolated from mouse femoral condyles and tibial plateaus cartilage tissue (WT ICR 5-day-old mice) and were infected with null(control) or recombinant adenovirus expressing zinc transporter ZIP8 for 24 hours. At 24 hours post-infection, total RNA was extracted from infected with null(control) adenovirus (4 biological replicates) or infected with recombinant adenovirus expressing the zinc transporter ZIP8 (4 biological replicates) on primary mouse articular chondrocytes and subjected to microarray analysis.

first: Jang-Soo

last: Chun


title: RNA-sequencing

status: Public on Oct 30 2017

city: Shanghai

first: Meng-Meng

last: Ji

address: Ruijin No.2 Road

institute: Shanghai Ruijin Hospital

summary: RNA-sequencing for 4 samples

overall_design: Examing 4 conditions


title: Translational profiling of B cells infected with the Epstein-Barr virus reveals 5’ leader ribosome recruitment through upstream open reading frames

status: Public on Dec 29 2017

city: Heidelberg

first: Henri-Jacques

last: Delecluse

address: Im Neuenheimer Feld 280

department: Pathogenesis of Virus Associated Tumors

institute: DKFZ

summary: The Epstein-Barr virus (EBV) genome encodes several hundred transcripts. Using total RNA sequencing and ribosome profiling, we have characterized the transcriptional and translational scope of B cells infected with EBV. We could show that viral transcripts are translated at variable efficiency and that several viral genes show ribosome recruitment to the 5’ leader region of mRNAs. We used two different virus strains with differing in vitro characteristics to study EBV translation and could show that in cells infected with the weakly replicating EBV strain some lytic genes showed evidence of monosomal ribosome recruitment mainly in the 5’ leader region and on start codons in the absence of protein production. Finally, we could identify 25 novel upstream open reading frames that potentially regulate the translation efficiency of some viral genes.

overall_design:
Sample 1 experimental set-up: B cells were infected with either the B95-8 or M81 Epstein-Barr virus (EBV) strain. These cells were then treated with cycloheximide for 10 min and ribosome profiles were generated that were then converted into a cDNA library for sequencing. In parallel, these cells were also treated for 2 minutes with harringtonine and again ribosome profiles were generated that were subsequently sequenced. Additionally, the total RNA was sequenced from cells infected with the B95-8 or M81 strain.
Sample 2 experimental set-up: B cells were infected with either the B95-8 or M81 EBV strain. These cells were treated for 2 or 5 minutes with harringtonine and ribosome profiles were generated that were subsequently sequenced. Additionally, the total RNA from cells infected with the B95-8 or M81 strain was sequenced.
HEK293 cells carrying a stably transfected B95-8 BACMID were  induced into lytic replication by transfecting a lytic cycle transactivator and these cells were then treated for 2 minutes with harringtonine. Ribosome profiling was also performed with this sample and it was subsequently sequenced.

first: Maja

last: Bencun

first: Olaf

last: Klinke

first: Agnes

last: Hotz-Wagenblatt

first: Severina

last: Klaus

first: Ming-Han

last: Tsai

first: Remy

last: Poirey


title: Interleukin-1β effect on primary mouse articular chondrocytes

summary:
Gene expression profiling of primary mouse articular chondrocyte treated with interleukin-1β.
In this study, we have attempted to explore the effects of interleukin-1β on mouse transcriptome and have identified numerous genes which are involved in osteoarthritis pathogenesis.

overall_design: Primary mouse articular chondrocytes were isolated from mouse femoral condyles and tibial plateaus cartilage tissue (WT ICR 5-day-old mice) and incubated with interleukin-1β for 24 hours. Total RNA was extracted from untreated primary mouse articular chondrocytes (3 biological replicates) or primary mouse articular chondrocytes cultured with IL-1β for 24 hours (3 biological replicates) and subjected to microarray analysis.


title: Transcriptomic analysis of Arabidopsis thaliana seedlings in response to impaired mitochondrial translation

status: Public on Nov 02 2017

city: Lausanne

first: Xu

last: Wang

address: EPFL SV IBI-SV NCEM AI 1148 (Bâtiment AI) Station 15

department: School of Life Sciences

country: Switzerland

institute: École polytechnique fédérale de Lausanne

summary: The goal of this study is to establish the global gene expression profiles of seedlings under doxycycline treatment or genetic silencing of MRPL1 (AT2G42710).

overall_design: RNA-seq was performed using Arabidopsis wild type (Col-0) and mrpl1-1  mutant seedlings under normal condition, as well as wild type seedlings exposed to doxycycline (Dox). Three biological replicates were conducted for each condition.

first: Johan

last: Auwerx


title: Sexual stage-induced long noncoding RNAs in the filamentous fungus Fusarium graminearum [I]

first: Wonyong

last: Kim

overall_design: Time-series mRNA profiles during the perithecial development for the Fusarium graminearum wild-type strain PH-1 were generated by deep sequencing, in triplicate, using the Illumina HiSeq 2500 system. Also, sexual_stage0 and sexual_stage4 data for xrn1-deletion mutant (∆xrn1) were generated using the Illumina HiSeq 4000 system.

first: Frances

last: Trail


title: Genomic Analysis of Nasopharyngeal Carcinoma Reveals TME-based Subtypes

status: Public on Aug 09 2017

city: Boston

first: Kenzie

last: MacIsaac

state: MA

address: 33 Avenue Louis Pasteur

department: Genetics and Pharmacogenomics

institute: Merck Research Labs

summary: We performed an integrated genomic analysis of NPC using a large clinical cohort of treatment-naïve tumor specimens which identified three gene expression-based subtypes differing in their pattern of immune and stromal gene expression.

overall_design: mRNA-sequencing to quantify genome-wide transcript levels in 113 fresh, treatment-naive undifferentiated nasopharyngeal carcinoma tumors.

first: Yao

last: Yao


title: Hypoxia inducible factor-2 alpha (HIF-2α) overexpression effect on primary mouse articular chondrocytes

summary:
Gene expression profiling of primary mouse articular chondrocyte infected with recombinant adenovirus expressing the hypoxia inducible factor-2 alpha (HIF-2α) protein.
In this study, we have attempted to explore the effects of HIF-2α overexpression on mouse transcriptome and have identified numerous genes which are involved in osteoarthritis pathogenesis.

overall_design: Primary mouse articular chondrocytes were isolated from mouse femoral condyles and tibial plateaus cartilage tissue (WT ICR 5-day-old mice) and were infected with null (control) or recombinant adenovirus expressing hypoxia inducible factor-2 alpha (HIF-2α, Ad-Epas1) for 24 hours. At 24 hours post-infection, total RNA was extracted from infected with null (control) adenovirus (4 biological replicates) or infected with recombinant adenovirus expressing the hypoxia inducible factor-2 alpha (4 biological replicates) on primary mouse articular chondrocytes and subjected to microarray analysis.


title: Human genome wide repair map of DNA damage caused by the cigarette smoke carcinogen benzo[a]pyrene

status: Public on Jun 12 2017

city: Athens

first: Wentao

last: Li

address: 500 D. W Brooks Drive

department: Environmental Health Science

institute: University of Georgia

summary: Benzo[a]pyrene (BaP), a  polycyclic aromatic hydrocarbon, is the major cause of lung cancer. It forms covalent DNA adducts after metabolic activation and induces mutations. We have developed a method capturing oligonucleotides carrying bulky base adducts, including UV-induced cyclobutane pyrimidine dimers (CPDs) and BaP diol epoxide-deoxyguanosine (BPDE-dG), which are removed from the genome by nucleotide excision repair. The isolated oligonucleotides are ligated to adaptors and after damage-specific immunoprecipitation the adaptor-ligated oligonucleotides are converted to dsDNA with an appropriate translesion DNA synthesis (TLS) polymerase followed by PCR amplification and next-generation sequencing (NGS) to generate genome-wide repair maps. We have named this method as translesion eXcision Repair-sequencing (tXR-seq). In contrast to our previously described XR-seq method, the tXR-seq does not depend on repair/removal of the damage in the excised oligonucleotides and hence it is applicable to essentially all DNA damages processed by nucleotide excision repair. Here, we present the excision repair maps for CPDs and BPDE-dG adducts generated by tXR-Seq for the human genome. Additionally, we observe novel sequence specificity of BPDE-dG excision repair by using tXR-seq.

overall_design: We performed tXR-seq for UV-induced CPD and BPDE-dG repair in GM12878 cell line. We also compared our tXR-seq data with our published dataset from XR-seq for CPD and (6-4)PP (GEO accession: GSE67941).

first: Jinchuan

last: Hu

first: Ogun

last: Adebal

first: Sheera

last: Adar

first: Yanyan

last: Yang

first: Yi-Ying

last: Chiou

first: Aziz

last: Sancar


title: RNA-Seq of mESCs based on sex chromosome complement

status: Public on Sep 15 2017

city: Camden

first: Jozef

last: Madzo

state: NJ

address: 403 Haddon Avenue

department: Bioinformatics

institute: Coriell Institute

summary: RNA-Seq was performed on mESCs generated from F1 hybrids from reciprocal crosses of C57BL/6J and CAST/EiJ, denoted B and C hereafter; cell lines are designated as BC or CB, with the maternal line symbolized first

overall_design: 3 XX and 3 XY lines were used from each cross as well as two XO lines for a total of 14 samples.

first: Rachael

last: Werner

first: Bryant

last: Schultz

first: Jaroslav

last: Jelinek

first: Jean-Pierre

last: Issa

first: Nora

last: Engel


title: Identification of Resistance Genes to BRAF Inhibitor in Melanoma by piggyBac Transposon Activation Mutagenesis Screen

status: Public on Jul 01 2016

city: Charlestown

first: Cyril

middle: H.

last: Benes

address: 149 Thirteenth St

department: Cancer Center

institute: Massachusetts General Hospital/Harvard Medical School

summary: Genotype directed anti-cancer therapies such BRAF inhibitor in BRAF mutant melanoma can show remarkable clinical efficacy but resistance limits their benefit. We show that a transposon activation screen efficiently identifies resistance genes to BRAF and captures a number of previously uncharacterized resistance mechanisms, including an E3 ubiquitin ligase NEDD4L and the Hippo pathway effector WWTR1 (TAZ). Resistance can be reversed by combining BRAF inhibition with tyrosine kinase inhibitors as observed previously for other resistance genes. Moreover, an integrative analysis of several gain- and loss-of-function genetic screens performed in the same context reveals smaller functional diversity of resistance mechanisms to MAPK inhibition than suggested by the broad range of resistance genes identified, implying common therapeutic strategies.

overall_design: A375 cells with lentiviral vector controls or WWTR1 cDNA plasmid.

first: Li

last: Chen


title: Effects of NAFLD/NASH on hepatic gene expression.

status: Public on Jan 03 2014

city: Chapel Hill

first: Robert

last: Schuck

state: North Carolina

address: 301 Pharmacy Lane

institute: UNC Chapel Hill

summary: To characterize gene expression changes in arachidonic acid metabolism pathway genes in the presense of non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) mice administered were administered an atherogenic diet for a period of four weeks. Administration of the atherogenic diet resulted in significant enrichment of the arachidonic acid metabolism pathway by gene set enrichment analysis (GSEA). The core enrichment subset of genes was down-regulated in mice administered the atherogenic diet and the majority of the genes that were down-regulated were cytochrome P450s.

overall_design: A total of 4 wild-type mice were administered a standard diet (STD; control group) and 4 wild-type mice were administered a HFHC diet (HFHC).

first: Craig

last: Lee


title: Biobank of Karolinska Endarterectomy (BiKE)

status: Public on Mar 28 2012

city: Copenhagen

first: Lasse

last: Folkersen

address: Artellerivej

country: Denmark

institute: National Genome Center

summary: A biobank collection of carotid plaque samples taken from patients undergoing endarterectomy operations.

overall_design: Samples from carotid plaques and peripheral blood mononuclear cells in a setup with clinical registry data collection. See PMID 22371308 for further details.

first: Jonas

last: Persson

first: Johan

last: Ekstrand

first: Hanna

last: Agardh

first: Göran

last: Hansson

first: Anders

last: Gabrielsen

first: Ulf

last: Hedin

first: Gabrielle

last: Paulsson-Berne


title: Fine mapping of genome activation in bovine embryos by RNA sequencing

status: Public on Feb 09 2014

city: Munich

first: Alexander

last: Graf

address: Feodor-Lynen-Str. 25

department: Gene Center Munich

institute: Ludwig-Maximilians-Universität München

summary: During maternal-to-embryonic transition control of embryonic development gradually switches from maternal RNAs and proteins stored in the oocyte to gene products generated after embryonic genome activation (EGA). Detailed insight into the onset of embryonic transcription is obscured by the presence of maternal transcripts. Using the bovine model system, we established by RNA sequencing a comprehensive catalogue of transcripts in germinal vesicle and metaphase II oocytes, and in embryos at the 4-cell, 8-cell, 16-cell and blastocyst stages. These were produced by in vitro fertilization of Bos t. taurus oocytes with sperm from a Bos t. indicus bull to facilitate parent-specific transcriptome analysis. Transcripts from 12.4 to 13.7 × 10^3 different genes were detected in the various developmental stages. EGA was analyzed by i) detection of embryonic transcripts which are not present in oocytes; ii) detection of transcripts from the paternal allele; and iii) detection of primary transcripts with intronic sequences. These strategies revealed (i) 220, (ii) 937, and (iii) 6,848 genes to be activated from the 4-cell to the blastocyst stage. The largest proportion of gene activation, i.e. (i) 59%, (ii) 42%, and (iii) 58%, was found in 8-cell embryos, indicating major EGA at this stage. Gene ontology analysis of genes activated at the 4-cell stage identified categories related to translation, RNA processing and transport, consistent with preparation for major EGA. Our study provides the largest transcriptome data set of bovine oocyte maturation and early embryonic development and new insight into the timing of embryonic activation of specific genes.

overall_design: RNA-Seq profiles from pools of 10 ooytes/embryos from bovine Bos t. taurus GV and MII oocytes and a cross-breed of Bos t. taurus x Bos t. indicus from 4-cell, 8-cell, 16-cell and blastocysts generated using Illumina GAIIx

first: Stefan

last: Krebs

first: Valeri

last: Zakhartchenko

first: Björn

last: Schwalb

first: Helmut

last: Blum

first: Eckhard

last: Wolf


title: Microarray analysis of Merkel cell carcinoma (MCC) tumors, small cell lung cancer (SCLC) tumors, and MCC cell lines

status: Public on Dec 23 2014

first: Isaac

last: Brownell

address: 10 Center Drive

department: Dermatology Branch

institute: National Cancer Institute

summary: When using cell lines to study cancer, phenotypic similarity to the original tumor is paramount. Yet, little has been done to characterize how closely Merkel cell carcinoma (MCC) cell lines model native tumors. To determine their similarity to MCC tumor samples, we characterized MCC cell lines via gene expression microarrays. Using whole transcriptome gene expression signatures and a computational bioinformatic approach, we identified significant differences between variant cell lines (UISO, MCC13, and MCC26) and fresh frozen MCC tumors. Conversely, the classic WaGa and Mkl-1 cell lines more closely represented the global transcriptome of MCC tumors. When compared to publicly available cancer lines, WaGa and Mkl-1 cells were similar to other neuroendocrine tumors, but the variant cell lines were not. WaGa and Mkl-1 cells grown as xenografts in mice had histological and immunophenotypical features consistent with MCC, while UISO xenograft tumors were atypical for MCC. Spectral karyotyping and short tandem repeat analysis of the UISO cells matched the original cell line's description, ruling out contamination. Our results validate the use of transcriptome analysis to assess the cancer cell line representativeness and indicate that UISO, MCC13, and MCC26 cell lines are not representative of MCC tumors, whereas WaGa and Mkl-1 more closely model MCC.

overall_design: RNA was extracted from MCC cell lines and MCC and SCLC tumor samples and hybridized to Affymetrix microarrays for transcriptome profiling.

first: Kenneth

last: Daily


title: Enhancer identification and activity evaluation in the red flour beetle, Tribolium castaneum

status: Public on Oct 03 2017

city: Oxford

first: Yoshinori

last: Tomoyasu

state: Ohio

address: 700E High St

department: Biology

institute: Miami University

summary: Evolution of cis-properties (such as enhancers) often plays an important role in the production of diverse morphology. However, a mechanistic understanding is often limited by the absence of methods to study enhancers in species outside of established model systems. Here, we sought to establish methods to identify and test enhancer activity in the red flour beetle, Tribolium castaneum. To identify possible enhancer regions, we first obtained genome-wide chromatin profiles from various tissues and stages of Tribolium via FAIRE (Formaldehyde Assisted Isolation of Regulatory Elements)-sequencing. Comparison of these profiles revealed a distinct set of open chromatin regions in each tissue and stage. Second, we established the first reporter assay system that works in both Drosophila and Tribolium, using nubbin in the wing and hunchback in the embryo as case studies. Together, these advances will be useful to study the evolution of cis-language and morphological diversity in Tribolium and other insects.

overall_design: Open chromatin profiling by FAIRE-seq during Tribolium development: 3 stages of embryogenesis (2-replicates each); larval CNS(2-replicates); larval second and third thoracic segments (3-replicates each); Genomic DNA Inputs. Sequencing performed on Illumina HiSeq 2000.

first: Yi-Ting

last: Lai

first: Kevin

last: Deem

first: Ferran

last: Borras-Castells

first: Nagraj

last: Sambrani

first: Heike

last: Rudolf

first: Kushal

last: Suryamohan

first: Ezzat

last: El-Sherif

first: Marc

last: Halfon

first: Daniel

last: McKay


title: Gene expression data of human hepatocellular carcinoma (HCC)

status: Public on Dec 01 2010

city: Bethesda

first: Xin

middle: Wei

last: Wang

address: 37 Convent Drive

department: Laboratory of Human Carcinogenesis

summary: We used Affymetrix microarray profiling to analyze gene expression patterns in healthy donor liver as well as tumor and paired non-tumor tissue of HCC patients.

overall_design:
For gene expression profiling, tumors and paired non-tumor tissues were profiled separately using a single channel array platform. Tumor and paired non-tumor samples of 22 patients of cohort1 and the normal liver pool were carried out on Affymetrix GeneChip HG-U133A 2.0 arrays (Affymetrix, Santa Clara, CA) according to the manufacturer's protocol. The fluorescent intensities were determined with an Affymetrix GeneChip Scanner 3000, controlled by GCOS Affymetrix software. All samples of cohort2 and 42 tumor and paired non-tumor samples of cohort2 were processed on the 96 HT HG-U133A microarray platform. The fluorescent intensities were determined with an Affymetrix GeneChip HT Array Plate Scanner, controlled by GCOS Affymetrix software.

Cohort 1 Training Group:
LCS-005A, LCS-019A, LCS-029A, LCS-039A, LCS-039B, LCS-254A, LCS-254B, LCS-068A, LCS-068B, LCS-076A, LCS-076B, LCS-004A, LCS-004B, LCS-007A, LCS-007B, LCS-024B, LCS-042B, LCS-062B, LCS-023A, LCS-023B, LCS-067A, LCS-065A, LCS-073A, LCS-067B, LCS-065B, LCS-073B, LCS-024A, LCS-042A, LCS-062A, LCS-015A, LCS-069A, LCS-015B, LCS-069B, LCS-033A, LCS-061A, LCS-020A, LCS-045A, LCS-033B, LCS-020B, LCS-045B, LCS-057A, LCS-009A, LCS-057B, LCS-009B, LCS-049A, LCS-049B, LCS-061B, LCS-047A, LCS-047B, LCS-075A, LCS-075B, LCS-034A, LCS-034B, LCS-041A, LCS-041B, LCS-044A, LCS-044B, LCS-071A, LCS-071B, LCS-036A, LCS-064A, LCS-064B, LCS-038A, LCS-038B, LCS-002A, LCS-028B, LCS-016B, LCS-054A, LCS-063A, LCS-022A, LCS-054B, LCS-063B, LCS-022B, LCS-036B, LCS-025A, LCS-066A, LCS-027A, LCS-048A, LCS-012A, LCS-025B, LCS-066B, LCS-027B, LCS-048B, LCS-012B, LCS-051A, LCS-056A, LCS-051B, LCS-056B, LCS-028A, LCS-016A, LCS-196A, LCS-196B, LCS-072A, LCS-072B, LCS-333A, LCS-333B, LCS-339A, LCS-339B, LCS-341A, LCS-341B, LCS-343A, LCS-343B, LCS-344A, LCS-344B, LCS-346A, LCS-346B, LCS-347A, LCS-347B, LCS-393A, LCS-393B, LCS-400A, LCS-400B, LCS-401A, LCS-401B, LCS-403A, LCS-403B, LCS-406A, LCS-406B, LCS-415A, LCS-415B, LCS-424A, LCS-424B, LCS-426A, LCS-426B

Cohort 2 Testing Group:
LCS-079A, LCS-092A, LCS-101A, LCS-079B, LCS-092B, LCS-101B, LCS-083A, LCS-095A, LCS-102A, LCS-083B, LCS-095B, LCS-102B, LCS-085A, LCS-096A, LCS-103A, LCS-085B, LCS-096B, LCS-103B, LCS-091A, LCS-099A, LCS-105A, LCS-091B, LCS-099B, LCS-105B, LCS-122A, LCS-130A, LCS-123A, LCS-135A, LCS-123B, LCS-135B, LCS-125A, LCS-127A, LCS-136A, LCS-125B, LCS-127B, LCS-136B, LCS-122B, LCS-130B, LCS-212B, LCS-180B, LCS-183B, LCS-153B, LCS-018B, LCS-188A, LCS-185A, LCS-154A, LCS-120A, LCS-286A, LCS-086A, LCS-177A, LCS-140A, LCS-035A, LCS-188B, LCS-185B, LCS-154B, LCS-120B, LCS-286B, LCS-238B, LCS-086B, LCS-177B, LCS-035B, LCS-275B, LCS-132A, LCS-205A, LCS-274A, LCS-159A, LCS-150A, LCS-014A, LCS-227A, LCS-283A, LCS-162A, LCS-104A, LCS-272A, LCS-132B, LCS-205B, LCS-274B, LCS-159B, LCS-227B, LCS-046B, LCS-283B, LCS-272B, LCS-237A, LCS-152A, LCS-209A, LCS-211A, LCS-230A, LCS-262A, LCS-144A, LCS-158B, LCS-237B, LCS-152B, LCS-209B, LCS-211B, LCS-230B, LCS-262B, LCS-144B, LCS-212A, LCS-180A, LCS-183A, LCS-153A, LCS-018A, LCS-275A, LCS-118A, LCS-234A, LCS-210A, LCS-265A, LCS-149A, LCS-040A, LCS-169A, LCS-256A, LCS-190B, LCS-118B, LCS-234B, LCS-210B, LCS-265B, LCS-149B, LCS-040B, LCS-169B, LCS-213A, LCS-164A, LCS-223A, LCS-245A, LCS-281B, LCS-191A, LCS-171A, LCS-249A, LCS-213B, LCS-164B, LCS-245B, LCS-094B, LCS-094A, LCS-191B, LCS-171B, LCS-249B, LCS-131A, LCS-241A, LCS-074A, LCS-160A, LCS-179A, LCS-134A, LCS-224A, LCS-078A, LCS-131B, LCS-201B, LCS-074B, LCS-160B, LCS-179B, LCS-134B, LCS-147B, LCS-224B, LCS-078B, LCS-093A, LCS-253A, LCS-279A, LCS-008A, LCS-291A, LCS-281A, LCS-156A, LCS-282A, LCS-090A, LCS-151A, LCS-253B, LCS-279B, LCS-008B, LCS-172B, LCS-291B, LCS-156B, LCS-282B, LCS-090B, LCS-151B, LCS-259A, LCS-010A, LCS-264A, LCS-264B, LCS-163A, LCS-163B, LCS-089A, LCS-089B, LCS-143A, LCS-143B, LCS-199A, LCS-199B, LCS-278A, LCS-278B, LCS-119A, LCS-119B, LCS-184A, LCS-184B, LCS-203A, LCS-203B, LCS-178A, LCS-178B, LCS-284A, LCS-284B, LCS-108A, LCS-261B, LCS-043A, LCS-043B, LCS-174A, LCS-174B, LCS-166A, LCS-193A, LCS-193B, LCS-215A, LCS-215B, LCS-021A, LCS-021B, LCS-129A, LCS-129B, LCS-198A, LCS-198B, LCS-084A, LCS-084B, LCS-250A, LCS-011A, LCS-108B, LCS-011B, LCS-219A, LCS-219B, LCS-194A, LCS-194B, LCS-170A, LCS-170B, LCS-204A, LCS-204B, LCS-261A, LCS-195A, LCS-195B, LCS-200B, LCS-206A, LCS-206B, LCS-161B, LCS-145A, LCS-145B, LCS-236A, LCS-236B, LCS-270A, LCS-270B, LCS-182A, LCS-182B, LCS-197B, LCS-173B, LCS-240B, LCS-266B, LCS-167B, LCS-032B, LCS-050B, LCS-285B, LCS-031B, LCS-189A, LCS-277A, LCS-117A, LCS-267A, LCS-100A, LCS-228A, LCS-268A, LCS-222A, LCS-192A, LCS-175A, LCS-277B, LCS-117B, LCS-267B, LCS-100B, LCS-228B, LCS-268B, LCS-222B, LCS-192B, LCS-248A, LCS-121A, LCS-157A, LCS-148A, LCS-126A, LCS-260A, LCS-223B, LCS-121B, LCS-157B, LCS-148B, LCS-260B, LCS-247A, LCS-088A, LCS-243A, LCS-165A, LCS-208A, LCS-110A, LCS-146A, LCS-247B, LCS-243B, LCS-165B, LCS-208B, LCS-110B, LCS-146B, LCS-147A, LCS-173A, LCS-240A, LCS-266A, LCS-167A, LCS-032A, LCS-050A, LCS-285A, LCS-031A, LCS-106A, LCS-106B, LCS-107A, LCS-107B, LCS-109A, LCS-109B, LCS-116A, LCS-137A, LCS-137B, LCS-138A, LCS-138B, LCS-139A, LCS-139B, LCS-142A, LCS-142B, LCS-207A, LCS-231A, LCS-231B, LCS-251A, LCS-263A, LCS-263B, LCS-269A, LCS-269B, LCS-273A, LCS-273B, LCS-289A, LCS-289B, LCS-290A, LCS-290B, LCS-093B, LCS-097A, LCS-097B, LCS-104B, LCS-140B, LCS-150B, LCS-158A, LCS-161A, LCS-162B, LCS-014B, LCS-166B, LCS-172A, LCS-197A, LCS-200A, LCS-201A, LCS-216A, LCS-216B, LCS-238A, LCS-241B, LCS-046A, LCS-248B, LCS-259B, Normal1, Normal2, LCS-003B, LCS-006B, LCS-026B, LCS-128B, LCS-168B, LCS-181B, LCS-190A, X02-342A, X02-342B, X02-362A, X02-362B


title: Natural Selection has Shaped Coding and Non-coding Transcription in Primate CD4+ T-cells

status: Public on Dec 29 2016

city: Ithaca

first: Charles

middle: G

last: Danko

state: NY

address: Hungerford Hill Rd

department: Baker Institute

institute: Cornell University

summary: Transcriptional regulatory changes have been shown to contribute to phenotypic differences between species, but many questions remain about how gene expression evolves.  Here we report the first comparative study of nascent transcription in primates.  We used PRO-seq to map actively transcribing RNA polymerases in resting and activated CD4+ T-cells in multiple human, chimpanzee, and rhesus macaque individuals, with rodents as outgroups.  This approach allowed us to directly measure active transcription separately from post-transcriptional processes.  We observed general conservation in coding and non-coding transcription, punctuated by numerous differences between species, particularly at distal enhancers and non-coding RNAs.  Transcription factor binding sites are a primary determinant of transcriptional differences between species.  We found evidence for stabilizing selection on gene expression levels and adaptive substitutions associated with lineage-specific transcription.  Finally, rates of evolutionary change are strongly correlated with long-range chromatin interactions.  These observations clarify the role of primary transcription in regulatory evolution.

sample_organism:
Macaca mulatta
Pan troglodytes
Homo sapiens
Mus musculus
Rattus norvegicus

overall_design: We analyzed collected PRO-seq data from CD4+ T-cells isolated from five mammalian species in two conditions.


title: TNFα Signaling Exposes Latent Estrogen Receptor Binding Sites in Breast Cancer Cells [ChIP-seq]

status: Public on Mar 05 2015

city: Dallas

first: W. Lee

last: Kraus

state: TX

address: 5323 Harry Hines Blvd.

institute: UT Southwestern Medical Center

summary: The interplay between mitogenic and proinflammatory signaling pathways play key roles in determining the phenotypes and clinical outcomes of breast cancers.  We have used global nuclear run-on coupled with deep sequencing to characterize the immediate transcriptional responses of MCF-7 breast cancer cells treated with estradiol, TNF?, or both.  In addition, we have integrated these data with chromatin immunoprecipitation coupled with deep sequencing for estrogen receptor alpha (ER?), the pioneer factor FoxA1 and the p65 subunit of the NF-?B transcription factor. Our results indicate extensive transcriptional interplay between these two signaling pathways, which is observed for a number of classical mitogenic and proinflammatory protein-coding genes.  In addition, GRO-seq has allowed us to capture the transcriptional crosstalk at the genomic locations encoding for long non-coding RNAs, a poorly characterized class of RNAs which have been shown to play important roles in cancer outcomes.  The synergistic and antagonistic interplay between estrogen and TNF? signaling at the gene level is also evident in the patterns of ER? and NF-?B binding, which relocalize to new binding sites that are not occupied by either treatment alone.  Interestingly, the chromatin accessibility of classical ER? binding sites is predetermined prior to estrogen treatment, whereas ER? binding sites gained upon co-treatment with TNF? require NF-?B and FoxA1 to promote chromatin accessibility de novo.  Our data suggest that TNF? signaling recruits FoxA1 and NF-?B to latent ER? enhancer locations and directly impact ER? enhancer accessibility. Binding of ER? to latent enhancers upon co-treatment, results in increased enhancer transcription, target gene expression and altered cellular response.  This provides a mechanistic framework for understanding the molecular basis for integration of mitogenic and proinflammatory signaling in breast cancer.

overall_design: Using GRO-seq and ChIP-seq (ER, FoxA1 and p65) to assay the molecular crosstalk of MCF-7 cells treated with E2, TNFa or both E2+TNFa.

first: Hector

middle: L

last: Franco

first: Anusha

last: Nagari

first: Lee

middle: W