title: Two independent modes of chromosome organization are revealed by cohesin removal

status: Public on Jun 10 2017

city: Cambridge

first: Nezar

last: Abdennur

address: 77 Massachusetts Ave

institute: MIT

summary: The three-dimensional organization of chromosomes is tightly related to their biological function. Both imaging and chromosome conformation capture studies have revealed several layers of organization, including segregation into active and inactive compartments at the megabase scale, and partitioning into domains (TADs) and associated loops at the sub-megabase scale. Yet, it remains unclear how these layers of genome organization form, interact with one another, and contribute to or result from genome activities. TADs seem to have critical roles in regulating gene expression by promoting or preventing interactions between promoters and distant cis-acting regulatory elements, and different architectural proteins, including cohesin, have been proposed to play central roles in their formation. But so far, experimental depletions of these proteins have resulted in marginal changes in chromosome organization. Here, we show that deletion of the cohesin-loading factor, Nipbl, leads to loss of chromosome-associated cohesin and results in dramatic genome reorganization. TADs and associated loops vanish globally, even in the absence of transcriptional changes. In contrast, segregation into compartments is preserved and even reinforced. Strikingly, the disappearance of TADs unmasks a finer compartment structure that accurately reflects the underlying epigenetic landscape. These observations demonstrate that the 3D organization of the genome results from the independent action of two distinct mechanisms: 1) cohesin-independent segregation of the genome into fine-scale compartment regions, defined by the underlying chromatin state; and 2) cohesin-dependent formation of TADs possibly by the recently proposed loop extrusion mechanism, enabling long-range and target-specific activity of promiscuous enhancers. The interplay between these mechanisms creates an architecture that is more complex than a simple structural hierarchy and can be central to guiding normal development.

overall_design: This submission contains the following experiments on primary hepatocytes isolated from wildtype (WT), control (TAM) and Nipbl-/- (NIPBL) mice: 2 biological replicates of Hi-C (TCC) in WT, TAM and NIPBL cells, 1 replicate of H3K27ac ChIP-seq in WT and NIPBL cells, 1 replicate of H3K4me3 ChIP-seq in WT and NIPBL cells, 1 replicate of Rad21 ChIP-seq in TAM and NIPBL cells, 1 replicate of Smc3 ChIP-seq in TAM and NIPBL cells, 1 replicate of CTCF ChIP-seq in TAM and NIPBL cells, 4 replicates of RNA-seq in each of WT, TAM and NIPBL cells.

first: Wibke

last: Schwarzer

first: Anton

last: Goloborodko

first: Aleksandra

last: Pekowska

first: Geoffrey

last: Fudenberg

first: Yann

last: Loe-Mie

first: Nuno

last: Fonseca

first: Wolfgang

last: Huber

first: Christian

last: Haering

first: Leonid

last: Mirny

first: Francois

last: Spitz


title: Effect of in utero undernutrition on skeletal muscle gene expression

status: Public on Aug 01 2014

city: Ottawa

first: Alexandre

last: Blais

state: ON

address: 451 Smyth Road

country: Canada

institute: University of Ottawa

summary: In utero undernutrition is associated with obesity and insulin resistance, although its effect on skeletal muscle remains poorly defined. We report that, in mice, adult offspring from undernourished dams have decreased energy expenditure, decreased skeletal muscle mitochondrial content, and altered energetics in isolated mitochondria and permeabilized muscle fibers. Strikingly, when these mice are put on a 40% calorie restricted diet they lose half as much weight as calorie restricted controls.  Our results reveal for the first time that in utero undernutrition alters metabolic physiology having a profound effect on skeletal muscle energetics and response to calorie restriction in adulthood.

overall_design: We have used a mouse model of low birth weight generated through 50% food restriction of mouse dams during the third week of gestation. We have studied in utero food restricted offspring and control offspring that were not food restricted in utero in both the ad libitum and calorie restricted states. Gene expression profiling was performed on tibialis anterior muscle from 8 mice per group, pooled in pairs.

first: Brittany

middle: L

last: Beauchamp

first: Sujoy

last: Ghosh

first: Alphonse

last: Chu

first: Mary-Ellen

last: Harper


title: High-throughput small molecule screen identifies inhibitors of aberrant chromatin accessibility

status: Public on Sep 24 2015

city: Chapel Hill

first: Ian

middle: Jonathan

last: Davis

state: NC

address: 450 West Drive

department: Genetics, Pediatrics

country: USA

institute: University of North Carolina

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Mutations in chromatin-modifying proteins and transcription factors are commonly associated with a wide variety of cancers. Through gain- or loss-of-function, these mutations may result in characteristic alterations of accessible chromatin, indicative of shifts in the landscape of regulatory elements genome-wide. The identification of compounds that reverse a specific chromatin signature could lead to chemical probes or potential therapies. To explore whether chromatin accessibility could serve as a platform for small molecule screening, we adapted formaldehyde-assisted isolation of regulatory elements (FAIRE), a chemical method to enrich for nucleosome-depleted genomic regions, as a high-throughput, automated assay. After demonstrating the validity and robustness of this approach, we applied this method to screen an epigenetically targeted small molecule library by evaluating regions of aberrant nucleosome depletion mediated by EWSR1-FLI1, the chimeric transcription factor critical for the bone and soft tissue tumor Ewing sarcoma. As a class, histone deacetylase inhibitors were greatly overrepresented among active compounds. These compounds resulted in diminished accessibility at targeted sites by disrupting transcription of EWSR1-FLI1. Capitalizing on precise differences in chromatin accessibility for drug discovery efforts offers significant advantages because it does not depend on the a priori selection of a single molecular target and may detect novel biologically relevant pathways.

overall_design: HT-FAIRE was performed on Human Umbilical Vein Endothelial Cells (HUVEC) in duplicate. No reference/control experiment is necessary.

first: Jeremy

middle: M

last: Simon

middle: J


title: Leucegene: AML sequencing (part 1)

status: Public on Nov 06 2013

city: Montreal

first: Guy

last: Sauvageau

state: QC

address: 2950, Chemin de Polytechnique

institute: Institute for Research in Immunology and Cancer

type: Expression profiling by high throughput sequencing

summary: RNA sequencing of human leukemia

overall_design: The goals of this project are to obtain a comprehensive study of mutations and gene expression in human acute myeloid leukemia (AML). Methods: AML cells were thawed. DNA and RNA (polyA) was extracted and sequences were obtained with an Illumina HiSeq 2000 sequencer.

first: Camille

first: Jalila

last: Chagraoui

first: Jana

last: Krosl

first: Patrick

last: Gendron

first: Brian

last: Wilhelm

first: Sébastien

last: Lemieux

first: Geneviève

last: Boucher

first: Pierre

last: Chagnon

first: Simon

last: Drouin

first: Raphaëlle

last: Lambert

first: Claude

last: Rondeau

first: Annie

last: Bilodeau

first: Sylvie

last: Lavallée

first: Martin

first: Josée

last: Hébert


title: Leucegene: AML sequencing (part 2)

status: Public on Feb 05 2014

summary: RNA sequencing of human leukemia

overall_design: The goals of this project are to obtain a comprehensive study of mutations and gene expression in human acute myeloid leukemia (AML). Methods: AML cells were thawed. DNA and RNA (polyA) was extracted and sequences were obtained with an illumina HiSeq 2000 sequencer. Results are pending.


title: H. salinarum NRC-1 vs VNG2099C knockout

status: Public on Mar 03 2014

city: Seattle

first: Elisabeth

last: Wurtmann

state: Washington

address: 401 Terry Ave N

institute: Institute for Systems Biology

type: Expression profiling by genome tiling array

summary: To investigate the contribution of ribonucleases to post-transcriptional regulation of mRNA levels, we examined the fitness consequences and gene expression changes of ribonuclease mutants in the extreme halophilic archaeon Halobacterium salinarum NRC-1. H. salinarum NRC-1 is known to use a large repertoire of environment-specific transcriptional regulatory programs, which may be complemented by post-transcriptional regulatory mechanisms. Homology searches identified putative RNase genes in H. salinarum NRC-1 that include likely orthologs for RNases found in prokaryotic and eukaryotic lineages. The VNG2099C protein sequence is significantly similar (e = 2 x 10^-34) to the sequence of the rat liver perchloric acid-soluble protein (L-PSP), which has been shown to have endoribonuclease activity in vitro (Morishita et al 1999). The VNG2099C protein, like the archaeal Sulfolobus tokodaii YjgF/L-PSP protein for which a crystal structure has been solved (Miyakawa et al 2006), shares conservation of residues proposed to constitute the active site of the rat protein. The purpose of this gene expression study was to investigate the role of the putative endoribonuclease VNG2099C on gene regulation.

overall_design: The relative changes in transcript levels were determined for wild type (Dura3) and the VNG2099C knockout.

first: Min

last: Pan

first: Nitin

middle: S

last: Baliga


title: Suv39h-dependent H3K9me3 represses intact retrotransposons in mouse embryonic stem cells

status: Public on Jun 26 2014

city: Freiburg im Breisgau

first: Thomas

last: Manke

address: Stuebeweg 51

department: Bioinformatics and Deep-Sequencing Unit

country: Germany

institute: Max-Planck-Institute for Immunobiology and Epigenetics

summary: Heterochromatin is required to restrict aberrant expression of retrotransposons, but it remains poorly defined due to the underlying repeat-rich sequences. We dissected Suv39h-dependent histone H3 lysine 9 trimethylation (H3K9me3) by genome-wide ChIP-sequencing in mouse embryonic stem cells (ESCs). Refined bioinformatic analyses of repeat subfamilies indicated selective accumulation of Suv39h-dependent H3K9me3 at interspersed repetitive elements that cover ~ 5% of the ESC epigenome. The majority of the ~ 8,150 intact long interspersed nuclear elements (LINEs) and endogenous retroviruses (ERVs), but only a minor fraction of the > 1.8 million degenerate and truncated LINEs/ERVs, are enriched for Suv39h-dependent H3K9me3. Transcriptional repression of these intact LINEs and ERVs is differentially regulated by Suv39h and other chromatin modifiers in ESCs but governed by DNA methylation in committed cells. These data provide a novel function for Suv39h-dependent H3K9me3 chromatin to specifically repress intact retrotransposon elements in the ESC epigenome.

overall_design: ChIP-seq and RNA-seq in mouse ES cells, Neural precursors and MEFs wild type and Suv39h double KO. The input for ES cells is accessioned as GSM1251941.  A link to this sample can be found below.

first: Inti

middle: A

last: De La Rosa-Velazquez

first: Aydan

last: Bulut-Karslioglu

first: Fidel

last: Ramirez

first: Maxim

last: Barenboim

first: Sarah

last: Diehl

first: Monika

last: Lachner

last: Jenuwein


title: The Open Chromatin Landscape of Kaposi's Sarcoma-Associated Herpesvirus

status: Public on Sep 05 2013

first: Ian

last: Davis

summary: Kaposi’s sarcoma-associated herpesvirus (KSHV) is an oncogenic gammaherpesvirus which establishes latent infection in endothelial and B cells, as well as in primary effusion lymphoma (PEL). During latency, the viral genome exists as a circular DNA minichromosome (episome) and is packaged into chromatin analogous to human chromosomes. Only a small subset of promoters, those which drive latent RNAs, are active in latent episomes. In general, nucleosome depletion (“open chromatin”) is a hallmark of eukaryotic regulatory elements such as promoters and transcriptional enhancers or insulators. We applied formaldehyde-assisted isolation of regulatory elements (FAIRE) followed by next-generation sequencing to identify regulatory elements in the KSHV genome and integrated these data with previously identified locations of histone modifications, RNA polymerase II occupancy, and CTCF binding sites. We found that (i) regions of open chromatin were not restricted to the transcriptionally defined latent loci; (ii) open chromatin was adjacent to regions harboring activating histone modifications, even at transcriptionally inactive loci; and (iii) CTCF binding sites fell within regions of open chromatin with few exceptions, including the constitutive LANA promoter and the vIL6 promoter. FAIRE-identified nucleosome depletion was similar among B and endothelial cell lineages, suggesting a common viral genome architecture in all forms of latency.

overall_design: Ten total samples analyzed by FAIRE-seq from latent KSHV-infected cell lines.  Two replicates were performed for BC1, KSHV-BJAB, KSHV-HUVEC, and L1-TIVE cells using the Illumina HiSeq 2000 platform.  For BCBL1 cells, 1 FAIRE-seq sample and 1 non-cross-linked control BCBL1 sample was analyzed using the Illumina GAIIx

first: Isaac

middle: B

last: Hilton

first: Jeremy

last: Simon

first: Dirk

middle: P

last: Dittmer


title: au10-01_overexpressionoxi1-Transcriptomic analysis of the overexpression of Oxi1

status: Public on Jun 01 2012

city: evry

first: Soubigou-Taconnat

last: Ludivine

address: 2 rue gaston crémieux

department: URGV

country: France

institute: INRA

summary: au10-01_overexpressionoxi1 - au10-01_overexpressionoxi1 - Analysis of the overexpression of the Oxi1 - Comparision between the overexpression of oxi1 and wt.

overall_design: 2 dye-swap - normal vs transgenic comparison

first: Heribert

last: Hirt

first: Sandrine

last: Balzergue

first: Marie-Laure

last: Martin-Magniette


title: Chromosome-wide profiling of X-inactivation status and epigenetic regulation in opossum fetal brain and placenta

status: Public on Sep 23 2013

city: Ithaca

first: Andrew

last: Clark

address: 227 Biotech Building

institute: Cornell University

summary: Evidence from a few genes of diverse species suggests that marsupial X-chromosome inactivation (XCI) is characterized by exclusive, but leaky, inactivation of the paternally derived X chromosome. To comprehensively study the mechanism of marsupial XCI, we profiled parent-of-origin-specific-allele expression, DNA methylation, and histone modifications in opossum fetal brain and extra-embryonic membranes. The majority (152/176) of X-linked genes exhibited paternally imprinted expression with nearly 100% maternal allele expression, whereas 24 loci (14%) escaped inactivation showing varying levels of biallelic expression. In addition to regulation by the non-coding RSX transcript, strong depletion of H3K27me3 at escaper gene loci indicates that histone states also influence opossum XCI. Notably, the opossum does not show an association between X-linked gene expression and promoter DNA methylation. Our study provides the first comprehensive catalogue of parent-of-origin expression status for X-linked genes in a marsupial and sheds light on the regulation and evolution of imprinted XCI in mammals.

overall_design: Profiling of expression level and allele-specific expression ratios in embryonic day 13 opossum (Monodelphis domestica) fetal brain and extra-embyonic membranes by Illumina RNA-seq

middle: G

first: Paul

last: Samollow

first: Xu

last: Wang


title: Transcriptional Differences between Normal and Glioma-Derived Glial Progenitor Cells Identify a Core Set of Dysregulated Genes.

status: Public on May 16 2013

city: Rochester

first: Steven

last: Goldman

state: NY

address: 601 Elmwood Ave

department: Center for Translational Neuromedicine

institute: University of Rochester

summary:
Glial progenitor cells (GPCs) of the adult human white matter, which express gangliosides recognized by monoclonal antibody A2B5, are a potential source of glial tumors of the brain. We used A2B5-based sorting to extract progenitor-like cells from a range of human glial tumors, that included low-grade glioma, oligodendroglioma, oligo-astrocytomas, anaplastic astrocytoma, and glioblastoma multiforme. The A2B5+ tumor cells proved tumorigenic upon orthotopic xenograft, and the tumors generated reflected the phenotypes of those from which they derived.
Expression profiling revealed that A2B5+ tumor progenitors expressed a cohort of genes by which they could be distinguished from A2B5+ GPCs isolated from normal adult white matter. Most of the genes differentially expressed by glioma-derived A2B5+ cells varied as a function of tumor stage; however, a small number were invariably expressed at all stages of gliomagenesis.
These glioma progenitor-associated genes included CD24, SIX1 and EYA1, which were up-regulated at all stages of gliomagenesis, and MTUS1 and SPOCK3, which were down-regulated at all stages of tumor progression. qPCR and immunolabeling confirmed the differential expression of these genes in primary gliomas, while pathway analysis permitted their segregation into differentially active signaling pathways.
By comparing the expression patterns of glial tumor progenitors to their identically-isolated normal homologues, we have identified a discrete set of oncogenic pathways by which glial tumorigenesis may be both better understood, and more efficiently targeted.

overall_design: Samples originating from patients with matched disease and/or pathology were considered as replicates either on the basis of exact tumor phenotype, tumor grade, or tumor vs. normal tissue samples.

first: Romane

last: Auvergne

first: Fraser

last: Sim

first: Su

first: Devin

last: Chandler-Militello

first: Jaclyn

last: Burch

first: Xiaojie

last: Li

first: Nimish

last: Mohile

first: Kevin

last: Walter

first: Mahlon

last: Johnson

first: Pragathi

last: Achanta

first: Alfredo

last: Quinones-  Hinojosa

first: Sridaran

last: Natesan


title: Tumor-specific retargeting of an oncogenic transcription factor chimera results in dysregulation of chromatin and transcription

status: Public on Nov 09 2011

first: Ian

last: Davis

summary: Using EWS-FLI and its parental transcription factor, FLI1, we created a unique experimental system to address questions regarding the genomic mechanisms by which chimeric transcription factors cause cancer. We found that in tumor cells, EWS-FLI targets regions of the genome distinct from FLI1, despite identical DNA-binding domains. In primary endothelial cells, however, EWS-FLI and FLI1 demonstrate similar targeting.  To understand this mistargeting, we examined chromatin organization. Regions targeted by EWS-FLI are normally repressed and nucleosomal in primary endothelial cells. In tumor cells, however, bound regions are nucleosome-depleted and harbor the chromatin signature of enhancers. We next demonstrated that through chimerism, EWS-FLI acquired the ability to alter chromatin. Expression of EWS-FLI results in nucleosome depletion at targeted sites, whereas silencing of EWS-FLI in tumor cells restored nucleosome occupancy. Thus, the EWS-FLI chimera acquired chromatin-altering activity, leading to mistargeting, chromatin disruption, and ultimately transcriptional dysregulation.

overall_design: Examination of two transcription factors in two different cell types, as well as three histone methylation marks and FAIRE

first: Mukund

middle: K

last: Patel

first: Jeremy

last: Simon

first: Jason

middle: D

last: Lieb


title: MAQC-II Project: Hamner data set

status: Public on Sep 10 2010

city: Shanghai

first: Leming

last: Shi

address: 2005 Songhu Road

department: School of Life Sciences

country: China

institute: Fudan University

summary: The Hamner data set (endpoint A) was provided by The Hamner Institutes for Health Sciences (Research Triangle Park, NC, USA). The study objective was to apply microarray gene expression data from the lung of female B6C3F1 mice exposed to a 13-week treatment of chemicals to predict increased lung tumor incidence in the 2-year rodent cancer bioassays of the National Toxicology Program. If successful, the results may form the basis of a more efficient and economical approach for evaluating the carcinogenic activity of chemicals. Microarray analysis was performed using Affymetrix Mouse Genome 430 2.0 arrays on three to four mice per treatment group, and a total of 70 mice were analyzed and used as the MAQC-II's training set (GEO Series GSE6116). Additional data from another set of 88 mice were collected later and provided as the MAQC-II's external validation set (this Series). The training dataset had already been deposited in GEO by its provider and its accession number is GSE6116.

overall_design: 88 Samples


title: RNA-seq transcriptome analysis of epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- T cells from healthy human skin

status: Public on Feb 14 2017

city: Stockholm

first: Liv

last: Eidsmo

address: L8:02 Karolinska Univeristy Hospital

country: Sweden

institute: Karolinska Insitutet

summary: We report the transcriptome analysis of epidermal CD8 tissue resident memory T (TRM) cells from healthy human skin. Specifically, epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- TRM cells from healthy human skin were sorted by FACS. Differential gene expression analysis revealed functional dichotomy of epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- TRM cells.

overall_design: Analysis of differentially expressed genes between epidermal CD8+CD103+CD49a+ and CD8+CD103+CD49- T cells from healthy human skin, biological replicates (n=7) (healthy skin donors).

first: Stanley

last: Cheuk

first: Yenan

middle: T

last: Bryceson


title: Genome-wide Expression of Trabecular Meshwork in POAG

status: Public on Aug 31 2013

city: Augusta

first: Yutao

last: Liu

state: GA

address: 1120 15th Street

department: Cellular Biology and Anatomy

institute: Augusta University

summary: This study compared genome-wide expression profiles of individuals with and without Primary Open-Angle Glaucoma (POAG). One POAG case (case #6 with two replicates #10 and #11) carried a Q368X myocilin mutation.

overall_design: This study compared the genome-wide expression in human trabecular meshwork tissue between 13 controls and 15 POAG cases. Six controls and one POAG cases had the expression performed from both left and right eyes. One technical replicate was done between two cases. The average from the biological replicates for each inidividual was used for analysis.

first: Michael

last: Hauser


title: Six1 and Six4 function in myoblast differentiation

status: Public on Jul 05 2010

first: Alexandre

last: Blais

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

overall_design: Refer to individual Series


title: Genomic mapping of Six1 binding sites during skeletal myoblast differentiation

type: Genome binding/occupancy profiling by genome tiling array

summary: In this study, the C2C12 cell line, a model used to study myogenesis and regeneration, was allowed to differentiate from myoblast precursor cells to myotubes. Cells were harvested at 3 different timepoints to perform ChIP-on-Chip of Six1, which is a key muscle regulator. We identified global loci bound by Six1 during skeletal myoblast differentiation.

overall_design: C2C12 Myoblasts were allowed to differentiate into myotubes. Cells at three timepoints were harvested for ChIP-on-Chip, including myoblasts stage,  24h after differentiation and myotubes (96h after differentiation). Myotubes were detached from the undifferentiated myoblast reserve cells using diluted trypsin. 3 independent biological replicates were used for each time point experiment. A microarray set counts 3 arrays (Custom Arrays A, B and C) for a total of approximately 2.9 million probes.

first: Yubing


title: Gene Expression Profiling of C2C12 Myoblast Differentiation

summary: In this study, the C2C12 cell line, a model used to study myogenesis and regeneration, was allowed to differentiate from myoblast precursor cells to myotubes. Cells were harvested at 4 different timepoints to perform gene expression profiling. We identified genes that were up-regulated and down-regulated during the differentiation process.

overall_design: C2C12 Myoblasts were allowed to differentiate into myotubes. Cells at different timepoints were harvested for gene expression profiling. Cells from the myoblasts stage, the start of differentiation, 24h after the start of differentiation and myotubes (96h after start of differentiation) were harvested. Myotubes were detatched from the undifferentiated myoblast reserve cells using diluted trypsin. 3 independent biological replicates per timepoint were submitted to gene expression profiling.

first: Alphonse

last: Chu


title: Leucegene

first: Guy

last: Sauvageau


title: Gene Expression Profiling of siRNA Knock-Down of Six1, Six4 and Myogenin in C2C12

summary: Six1, Six4 and Myogenin are transcription factors that are known to be required for skeletal myogenesis. Currently, very little is known about the genes targeted by Six1 and Six4. Gene expression profiling when one or both transcription factors were knock-down by siRNA was performed to identify genes affected by their absence. We also hypothesized that Six1 and Six4 can work in cooperation with the myogenic regulatory factor (MRFs) family of transcription factors, such as Myogenin. Therefore, we performed the same type of experiment where the myogenin was knocked-down by siRNA to identify genes that are possibly regulated by the Six1 or Six4 in conjunction with Myogenin.

overall_design: C2C12 Myoblasts were transfected with siRNA against Six1, Six4, Six1 with Six4, Myogenin, or control 24h before start of differentiation. The cells were allowed to differentiate in differentiation medium for 24h and were harvested for gene expression profiling. Four replicates per siRNA were performed.


title: DSBCapture: in situ capture and direct sequencing of dsDNA breaks

status: Public on Jul 18 2016

first: Giovanni

last: Marsico

address: Robinson Way

country: United Kingdom

institute: CRUK Cambridge Institute

summary: Double-strand DNA breaks (DSBs) continuously arise and are a source of mutations and chromosomal rearrangements. Here, we present DSBCapture, a sequencing-based method that captures DSBs in situ and directly maps these at single nucleotide resolution enabling the study of DSB origin. DSBCapture shows substantially increased sensitivity and data yield compared to other methods. Employing DSBCapture, we uncovered a striking relationship between DSBs and elevated transcription within nucleosome-depleted chromatin.

overall_design: 6 library samples, 75 base pairs (50 bp for the EcoRV library) custom protocol (DSBCapture or BLESS) sequenced as paired-end reads on Illumina NextSeq 500 (MiSeq for EcoRV library): 1 replicate for the EcoRV library, 1 replicate for the library coming from the U2OS AID-DlvA cell line with AsiSI restriction enzyme, 2 replicates for the BREAk-seq NHEK libraries and 2 replicates for the BLESS NHEK libraries. 4 RNA-Seq library samples from HEK Gibco cells, single-end sequencing on the Illumina NextSeq 500, 75 base pairs.

first: Stefanie

last: Lensing

first: Robert

last: Hansel-Hertsch

first: David

last: Tannahill

first: Shanakr

last: Balasubramanian