title: Whole-genome definitive haplotypes of SNPs and CNVs determined by genotyping duplicated haploid genomes

status: Public on Feb 13 2014

city: Fukuoka

first: Kenshi

last: Hayashi

address: Maidashi 3-1-1, Higashi-ku

department: Medical Institute of Bioregulation

institute: Kyushu University

type:
Genome variation profiling by SNP array
SNP genotyping by SNP array

summary: Copy number variations (CNVs) constitute the largest portion of the human genome variation. We determined a genome-wide high resolution SNP/CNV haplotype structure of Asians, by analyzing a collection of complete hydatidiform moles (CHMs) of Japanese, using high-density DNA arrays. CHMs are tissues carrying duplicated haploid genomes derived from single sperms, and are suitable material for the detection of CNVs, because they are expected to reveal greater signal to noise ratio in hybridization experiments. Also, the absence of heterozygosity ensures straightforward CNV interpretation without being bothered by overlapping CNV segments. We genotyped 100 CHM genomes using Affymetrix SNP 6.0 and Illumina 1M-duo, created a definitive haplotype map including 1.7 million SNPs and 2339 CNV region (CNVR) that is presented as D-HaploDB Phase 4.1.

overall_design: Illumina Human1M-Duov3 BeadChip analyses were performed according to the manufacturer's directions on DNA extracted from 97 complete hydatidiform moles (CHMs) tissues collected throughout Japan.

first: Tomoko

last: Tahira

first: Yoji

last: Kukita

first: Koji

last: Yahara

first: Miki

last: Sonoda

first: Ken

last: Yamamoto

first: Kiyoko

last: Kato

first: Norio

last: Wake


title: Deafness Gene Expression Patterns in the Mouse Cochlea Found by Microarray Analysis

status: Public on Jan 08 2014

city: Matsumoto

first: Shin-ya

last: Nishio

state: Nagano

address: 3-1-1 Asahi

department: Department of Otorhinolaryngology

country: Japan

institute: Shinshu University School of Medicine

summary: This study demonstrates the baseline data of gradient gene expression in the cochlea. Especially for genes whose mutations cause autosomal dominant non syndromic hearing loss (Pou4f3, Slc17a8, Tmc1, and Crym) as well as genes important for cochlear function (Emilin-2 and Tectb), gradual expression changes help to explain the various pathological conditions.

overall_design: Four C57BL/6 mice aged 6 weeks cochlea samples including the lateral wall, stria vascularis, spiral ligament, spiral prominence, and the organ of corti were dissected and separated into the apical, middle and basal turns to compare gene expression profiles of each cochlea turn.

first: Hidekane

last: Yoshimura

first: Yutaka

last: Takumi

first: Nobuyoshi

last: Suzuki

first: Yoh-ichiro

last: Iwasa

first: Shin-ichi

last: Usami


title: Transcriptomic profiles of beef marbling

status: Public on Feb 28 2014

city: Warsaw

first: Tomasz

last: Sadkowski

address: Nowoursynowska 159

department: Department of Physiological Sciences

country: Poland

institute: Warsaw University of Life Sciences - SGGW

summary: The goal was to identify beef marbling related genes

overall_design:
Comparisons of skeletal muscle of well-marbled beef (HER, H-F) vs. lean beef (LIM)

Sample 		Title
GSM1129882      Hereford (Cy5) vs. Limousin (Cy3) 1
GSM1129883      Hereford (Cy5) vs. Limousin (Cy3) 2
GSM1129884      Hereford (Cy5) vs. Limousin (Cy3) 3
GSM1129885      Hereford (Cy5) vs. Limousin (Cy3) 4

GSM1129886      Limousin (Cy5) vs. Holstein-Friesian (Cy3) 1
GSM1129887      Limousin (Cy5) vs. Holstein-Friesian (Cy3) 2
GSM1129888      Limousin (Cy5) vs. Holstein-Friesian (Cy3) 3
GSM1129889      Limousin (Cy5) vs. Holstein-Friesian (Cy3) 4

Samples GSM1129886, GSM1129887, GSM1129888, GSM1129889 were dye-swapped to make Limousin a control.

first: Anna

last: Ciecierska

first: Alicja

last: Majewska


title: Molecular Characterization of Basal-like and Non-Basal-like Triple-Negative Breast Cancers

status: Public on Jul 29 2014

city: Chapel Hill

first: Charles

middle: M.

last: Perou

state: NC

address: 12-044 Lineberger Comprehensive Cancer Center CB# 7295

department: Professor of Genetics, and Pathology & Laboratory Medicine; Lineberger Comprehensive Cancer Center

country: USA

institute: University of North Carolina at Chapel Hill

summary: Triple-negative (TN) and Basal-like (BL) breast cancer definitions have been used interchangeably to identify breast cancers that lack expression of the hormonal receptors (HR) and overexpression and/or amplification of HER2. However, both classifications when compared to each other, show substantial discordance rates. Here, we molecularly characterize TN tumors, and Basal-like tumors, and compare and contrast the results in terms of common patterns and distinct patterns for each.  In total, when testing 412 TN and 473 Basal-like tumors, 21.4% and 31.5% were identified as non-Basal-like and non-TN, respectively. TN tumors identified as Luminal or HER2-enriched showed undistinguishable overall gene expression profiles when compared versus Luminal or HER2-enriched tumors that were not TN. Similar findings were observed within Basal-like tumors regardless of the TN status. Interestingly, most TN tumors identified as HER2-enriched showed low HER2 expression and lack of HER2 amplification despite the similar overall gene expression profiles to HER2-E tumors that were not TN. Lastly, additional genomic classifications are examined within TN and Basal-like cancers, most of which are largely concordant with tumor intrinsic subtype. These results suggest that future clinical trials focused on TN disease should consider stratifying patients based on Basal-like versus non-Basal-like gene expression profiles as this appears to be the main biological difference seen within TN breast cancer patients.

overall_design: reference x sample

first: Aleix

last: Prat

middle: M


title: Hai1 Mediates Inflammation Through MMP9

status: Public on Jan 31 2014

city: Leiden

middle: Magdalena

last: Zakrzewska

address: Wassenaarseweg 64

department: IBL

country: Netherlands

institute: University of Leiden

summary:
Adults heterozygous for the hi2217 retroviral insertion within the HAI locus (Mathias et al 2007 JCS) were in-crossed for RNA from hi2217 mutants and corresponding WT siblings. Adults heterozygous for the hi1520 retroviral insertion within the Clint1 locus (Dodd et al, 2009) were in-crossed for RNA from hi1520 mutants and corresponding WT siblings.  Both hi2217 and hi1520 are mutants with epidermal defects and showing symptoms of chronic inflammation.
In this study we aimed to compare the RNA expression changes between Wild-type siblings (a non-inflammatory status) and homozygous mutants (a chronic inflammatory status) for each mutant background (hi2217 and hi1520).

overall_design: Pools of 30-50 zebrafish embryos of WT siblings and hi2217 or hi1520 mutants were collected for RNA isolation. RNA from the hi2217 mutant embryos or hi1520 mutant embryos (test samples)was labelled with Cy5 and hybridized against Cy3-labelled RNA from the corresponding WT sibling embryos (reference samples) . These experiments were performed in biological triplicate.

first: Julie

last: Green

first: Beth

last: Harvie

first: Ernest

last: Dodd

first: Annemarie

middle: H

last: Meijer

last: Huttenlocher


title: Vascular properties of breast cancer intrinsic subtypes

status: Public on Jan 01 2014

summary: Interactions of cancer cells with the vasculature are essential for tumor growth and likely promote metastatic progression. Endothelial cell content and lympho-vascular invasion are generally associated with tumor aggressiveness, however, these features are generally not employed in the clinic. We aimed to determine if endothelial cell gene expression signatures could be utilized to better characterize breast tumor biology, and to establish if vascular cell-derived signatures could provide information to predict tumors likely to metastasize. Here we report on the identification of a gene signature for vascular endothelial cells, and a second for cancer-activated vasculature. Both signatures independently identify subsets of aggressive breast cancers. Interestingly, the vascular content signature and a previously identified hypoxia signature both provide prognostic information beyond currently utilized clinical parameters and intrinsic subtype classifications. In these studies, we also examined the relationship that the breast cancer subtypes have with vascular gene expression profiles, and found that claudin-low tumors and cell lines express vascular gene expression profiles and displayed endothelial-like tube formation when grown in three-dimensions. These findings are directly applicable to clinical care and therapeutic treatment design as they identify highly aggressive subsets of tumors with genetic and morphologic vascular properties.

first: Chuck

last: Harrell


title: H3K79me3 (Abcam ab2621 lot 1).Kc.Affy 2

status: Public on Oct 31 2013

city: Toronto

first: DCC

last: modENCODE

state: Ontario

address: MaRS Centre, South Tower, 101 College Street, Suite 800

country: Canada

institute: Ontario Institute for Cancer Research

type: Genome binding/occupancy profiling by genome tiling array

summary:
modENCODE_submission_4947
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: Kc167; Tissue: embryo-derived cell-line; Developmental Stage: late embryonic stage; Genotype: se/e; Sex: Female;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line Kc167; Antibody H3K79me3 (Abcam ab2621 lot 1) (target is H3K79me3)

first: Gary

last: Karpen

first: Sarah

last: Elgin

first: Andrey

last: Gortchakov

first: Greg

last: Shanower

first: Michael

last: Tolstorukov

first: Peter

last: Kharchenko

first: Mitzi

last: Kuroda

first: Vincenzo

last: Pirrotta

last: Park

first: Aki

last: Minoda

first: Nicole

last: Riddle

first: Yuri

last: Schwartz

first: Art

last: Alekseyenko

first: Cameron

last: Kennedy


title: The Hox gene Abd-B controls stem cell niche function in the Drosophila testis

status: Public on Dec 30 2013

city: Heidelberg

first: nati

last: ha

address: Im Neuenheimer Feld, 267

country: Germany

institute: COS, University of Heidelberg

summary:
Stem cells reside in a specialized microenvironment, called niche, which provides essential signals controlling stem cell behavior. Proper niche architecture is a key for normal stem cell function, yet only few upstream regulators are known. Here we report that the Hox transcription factor Abd-B, active in pre-meiotic spermatocytes, affects niche positioning in the Drosophila testis by regulating integrin localization in differentiated somatic cyst cells. Loss of Abd-B results in cell non-autonomous effects within the niche including centrosome misorientation in germline stem cells (GSCs) and reduced GSC divisions in larval testis, leading to a dramatic reduction of pre-meiotic stages in adult testes. By identifying Abd-B binding regions throughout the genome, we find that Abd-B mediates its effects on niche function by directly controlling at multiple levels the localization and thus signaling activity of the Sevenless (Sev) ligand, Bride of Sevenless (Boss), via its direct targets src42A and sec63. In sum, our data show for the first time that Abd-B through local signaling provides positional cues for integrin localization, which is critical for niche localization and architecture, and ensures proper niche function and GSC activity.
DamID (DNA adenine methyltransferase identification) method was used to identify direct Abd-B target genes in the Drosophila 3rd instar larval testis

overall_design: Dam was fused to the N terminus of Abd-B and transgenic flies were generated. For identifying Abd-B targets in the Drosophila testis the fusion protein was expressed from the uninduced minimal Hsp70 promoter of the UAS vector pUAST (Brand and Perrimon, 1993). As a control for nonspecific Dam activity, transgenic flies expressing the Dam alone were used (Choksi et al., 2006). Subsequently, genomic DNA was extracted from 3rd instar larval testes, expressing either the Dam-Abd-B fusion protein or the Dam protein alone using a specific protocol (Tolhuis et al., 2011); and van Steensel personal communication). Two individual replicates, for Dam-AbdB and Dam alone, have been generated. Following a methylation-sensitive DNA digestion and PCR amplification, DNA fragments from Dam-Abd-B and control DNA were labeled and hybridized to genomic Affymetrix arrays in duplicates (Protocol available at “www.flychip.org.uk”).

first: Fani

last: Papagiannouli

first: Lisa

last: Schardt

first: Janin

last: Grajcarek

first: Nati

last: Ha

first: Ingrid

last: Lohmann


title: H3K27me1.Kc

first: DCC

last: modENCODE

summary:
modENCODE_submission_3942
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: Kc167; Tissue: embryo-derived cell-line; Developmental Stage: late embryonic stage; Genotype: se/e; Sex: Female;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line Kc167; Antibody H3K27me1 (target is H3K27me1)

first: Gary

last: Karpen

first: Sarah

last: Elgin

first: Andrey

last: Gortchakov

last: Shanower


title: Analysis of epigenetic changes in human colorectal cancer and matching mucosa tissues

status: Public on Dec 31 2013

city: Duarte

first: Xiwei

last: Wu

state: CA

address: 1500 E. Duarte Rd.

department: Computational and Quantitative Medicine

institute: City of Hope National Medical Center

type: Methylation profiling by genome tiling array

summary: We used NimbleGen human CpG/promoter microarrays for profiling epigenetic changes (DNA methylation, H3K27me3 and H3K4me3 marks) in colon tumors (Duke's stage II) and matching mucosa samples from patients.

overall_design: Analysis of DNA methylation was done by using the methylated CpG island recovery assay (MIRA) technique with further hybridization versus input on NimbleGen human CpG/promoter microarrays. For profiling of H3K27me3 and H3K4me3 marks, we performed chromatin immunoprecipitation with H3K27me3 (#07-449, Millipore) and H3K4me3 (#39159, Active Motif) antibodies and further hybridized versus input on NimbleGen human CpG/promoter microarrays. All experiments were performed simultaneously for matching tissue samples.

first: Maria

middle: A

last: Hahn

first: Arthur

middle: X

last: Li

first: Richard

last: Yang

first: Yong

last: Jiang

first: Raymond

middle: F

last: Schinazi

first: David

last: Drew

first: Daniel

middle: W

last: Rosenberg

first: Gerd

middle: P

last: Pfeifer


title: Mutant PI3K cooperates with HER2 to promote mammary tumor formation and induces trastuzumab resistance in vivo

status: Public on Sep 03 2013

first: Charles

last: Perou

summary: HER2 (ERBB2) gene amplification and PIK3CA mutations often co-occur in breast cancer, and aberrant activation of the PI3K pathway has been implicated in resistance to HER2-directed therapies. We have created a mouse model of HER2-overexpressing (HER2+), PIK3CAH1047R-mutant breast cancer. Mice expressing both human HER2 and mutant PIK3CA in their mammary glands developed tumors with a significantly shorter latency compared to mice expressing either oncogene alone. By microarray analysis, HER2-driven tumors clustered with the luminal subtype, whereas HER2+PIK3CA and PIK3CA-driven tumors were associated with the claudin-low breast cancer subtype. In accordance, PIK3CA and HER2+PIK3CA tumors expressed elevated levels of EMT and stem cell markers, and cells from HER2+PIK3CA tumors more efficiently formed mammospheres, providing further evidence that activated PIK3CA may enrich for cancer stem cells. Finally, HER2+PIK3CA tumors are resistant to the HER2 antibody trastuzumab; resistance is partially reversed by the addition of a PI3K inhibitor. Taken together, these studies suggest that the co-expression of HER2 and PI3KH1047R in the mouse mammary gland accelerates the formation of aggressive, trastuzumab-resistant tumors.

overall_design: referenceXsample

first: Ariella

middle: B

last: Hanker

first: Adam

last: Pfefferle

first: Carlos

middle: L

last: Arteaga


title: H3K4me3(ab8580 lot1).BG3.CTCF_RNAi

first: DCC

last: modENCODE

summary:
modENCODE_submission_3583
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The goal of these experiments are to validate and confirm the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. To do this, we are using RNAi to deplete individual non-histone chromosomal proteins in Drosophila BG3 and S2 tissue culture cells, and then using antibodies to perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. Comparison of a protein factor's binding profiles before and after depletion will increase the confidence of our predictions.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: ML-DmBG3-c2; Tissue: CNS-derived cell-line; Developmental Stage: third instar larval stage; Genotype: y v f mal; Sex: Unknown;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line ML-DmBG3-c2; Antibody H3K4me3 (ab8580 lot1) (target is H3K4me3); dsRNA (RNAi_reagent) CG8591_RNAi&oldid=38908

last: Karpen

first: Greg

first: Michael

last: Tolstorukov

first: Peter

last: Kharchenko

first: Mitzi

last: Kuroda

first: Vincenzo

last: Pirrotta

last: Park

first: Aki

last: Minoda

first: Nicole

last: Riddle

first: Yuri

last: Schwartz

first: Art

last: Alekseyenko

first: Cameron

last: Kennedy


title: Upper Palaeolithic Siberian genome reveals dual ancestry of Native Americans

status: Public on Nov 18 2013

city: Tartu

first: Mait

last: Metspalu

address: Riia 23

country: Estonia

institute: Estonian Biocentre

type:
SNP genotyping by SNP array
Genome variation profiling by SNP array

summary: Here we present genome-wide high-coverage genotyping data on a panel of 85 human samples from Eurasia that are used in addition to public data in studing the genomic context of  a 24 kya old DNA sample from Southern Siberia that was sequenced to the avwerage depth of 1X.

overall_design: 85 samples were analysed with the Illumina platforms Human610-Quad v1.0, HumanHap650Yv3 (HumanHap650Yv3_A) and Human660W-Quad v1.0 Genotyping BeadChips and are described herein.

first: Richard

last: Villems


title: H3K27me1.BG3

summary:
modENCODE_submission_3941
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: ML-DmBG3-c2; Tissue: CNS-derived cell-line; Developmental Stage: third instar larval stage; Genotype: y v f mal; Sex: Unknown;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line ML-DmBG3-c2; Antibody H3K27me1 (target is H3K27me1)

first: Gary

first: Sarah

last: Elgin

first: Andrey

last: Gortchakov

last: Shanower


title: Xenografting of advanced stage breast cancer preserves the genomic and clonal architecture and captures luminal tumors harboring mutations and gene rearrangements in ESR1

status: Public on Dec 22 2013

first: Charles

last: Perou

summary: End-stage breast cancers are clonally heterogeneous and harbor many poorly-understood treatment resistance mechanisms.  We therefore established multiple Patient-Derived-Xenograft (PDX) models to study genomic events driving advanced disease.  Comparative whole-genome sequencing of paired primary tumors and their PDX models demonstrated that PDX retain the vast majority of the structural variations and copy number aberrations seen within the originating tumor, and with high fidelity.  Variant allele fractions (VAF) were preserved, even for rare mutations.  Clonal representation is therefore a transplantable phenotype, indicating that genomic heterogeneity can be regulated in a tumor-autonomous mechanism, indifferent to host immune status.  Mutations and gene rearrangements were documented in the ESR1 gene in three of five sequenced luminal PDX/progenitor tumor pairs (amplification, point mutation and translocation), and were associated with clinical endocrine response phenotypes, differential PDX estradiol responsiveness and all induced estradiol-independent growth in standard cell lines.  PDX models are therefore a significant new tool for fundamental studies on the molecular basis for resistance to endocrine treatment in advanced breast cancer.

first: Aleix

last: Prat


title: SU(HW)-HB.Kc

first: DCC

last: modENCODE

summary:
modENCODE_submission_3801
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: Kc167; Tissue: embryo-derived cell-line; Developmental Stage: late embryonic stage; Genotype: se/e; Sex: Female;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line Kc167; Antibody SU(HW)-HB (target is SU(HW))

last: Karpen

first: Greg

last: Tolstorukov


title: Global modulation of gene expression in Paracoccidioides brasiliensis in response to thioridazine

city: Santo André

first: Luiz

middle: R.

last: Nunes

state: SP

address: Rua Santa Adélia 166

department: Centro de Ciências Naturais e Humanas

country: Brazil

institute: UFABC - Universidade Federal do ABC

summary: Phenothiazines are antipsychotic drugs used in the treatment of schizophrenia, which have been shown to present antimicrobial activity (in vitro and in vivo) against a great variety of pathogenic microorganisms, including bacteria, parasites (protozoa and helmints) and fungi. In this study, we used competitive microarray hybridization to evaluate the effects of increasing concentrations of the piperidinic phenothiazine derivative thioridazine (TR) on the transcriptome of Paracoccidioides brasiliensis, the causative agent of paracoccidioidomycosis (PCM) - the most common systemic mycosis in Latin America. These analyses showed that the presence of TR affected expression of more than 1,800 genes from this fungus, including genes related to cellular processes such as cell wall metabolism and drug resistance.

overall_design:
Microarray hybridizations were carried out with amplified RNA (aRNA), which was produced starting with total RNA extracted from cells treated with thioridazine (15, 20 or 25 µM) for 144 hours. The aRNA synthesized from cells unexposed to TR was taken as reference. Each treatment was analyzed with four independent hybridizations (two pairs of dye-swapped hybridizations), using RNA from two biological replicas.
The data has been filtered, normalized and adjusted as described in the "data processing" box for each individual sample. Dye swap consistency checking has been performed between equivalent experimental pairs with the aid of the software TIGR MIDAS v2.19 and inconsistent spots have been flagged and excluded from further analyses.
The values obtained from each dye swap pair have been averaged and consolidated into a single data file, generating a total of 8 hybridization files (four from each treatment concentration). These files have been loaded into the software TIGR Multi-Experiment Viewer, v.3.1 Experiments were then normalized and genes that displayed statistically significant modulation were identified by one-way ANOVA, considering p < 0.01 as a cutoff value.
A list of statisticaly significant, modulated genes was created, showing the average log ratio for each one of these genes, within each time point.

first: Ana

last: Claudia de Freitas Oliveira

first: Tiago

last: Rodrigues

first: Regina

last: Costa de Oliveira

last: Roberto Nunes


title: Specific Genomic and Transcriptomic Aberrations in Tumors Induced by Partial Hepatectomy of a Chronically Inflamed Murine Liver [aCGH]

status: Public on Apr 01 2015

city: Jerusalem

first: Daniel

last: Goldenberg

address: Ein Kerem

department: Gene therapy

country: Israel

institute: Hadassah medical center

summary: Background & Aims. Resection of hepatocellular carcinoma (HCC) tumors by partial hepatectomy (PHx) is associated with promoting hepatocarcinogenesis. We have previously reported that PHx promotes hepatocarcinogenesis in the Mdr2-knockout (Mdr2-KO) mouse, a model for inflammation-mediated HCC. Now, we explored the molecular mechanisms underlying the tumor-promoting effect of PHx in these mice. Methods. Using microarrays-based techniques, we compared genomic and transcriptomic profiles of HCC tumors developing in the Mdr2-KO mice either spontaneously or following PHx. Results. PHx accelerated HCC development in these mice by four months. PHx-induced tumors had only amplifications affecting multiple chromosomes and locating mainly near the acrocentric centromeres of murine chromosomes. Four different chromosomal regions were amplified each in at least three tumors. All tumors of untreated mice had chromosomal aberrations, including both deletions and amplifications. Comparison of gene expression profiles revealed a significantly enriched expression of oncogenes, chromosomal instability markers and E2F1 targets in the post-PHx compared to spontaneous tumors. Both tumor groups shared the same frequent amplification at chromosome 18. Here, we demonstrated that one of the regulatory genes encoded by this amplified region, Crem, was over-expressed in the nuclei of murine and human HCC cells in vivo, and that it stimulated proliferation of human HCC cells in vitro. Conclusions:  PHx of a chronically inflamed liver directed tumor development to a discrete pathway characterized by amplification of specific chromosomal regions and expression of specific tumor-promoting genes. Crem is a new candidate HCC oncogene frequently amplified in this model and frequently over-expressed in human HCC.

overall_design: To explore the mechanisms of the accelerated HCC development by PHx, we compared liver tumors and their matched non-tumor liver tissues between 9-month-old hepatectomized and 13-14-month-old untreated Mdr2-KO mice.

first: Ezra

last: Ella

first: Denise

last: Heim

first: Evgeniy

last: Stoyanov

first: Rona

last: Harari-Steinfeld

first: Israel

last: Steinfeld

first: Orit

last: Pappo

first: Temima

last: Schnitzer Perlman

first: Natalie

last: Nachmansson

first: Ludmila

last: Rivkin

first: Devorah

last: Olam

first: Rinat

last: Abramovitch

first: Henning

last: Wege

first: Eithan

last: Galun


title: Transcriptional profiling of Neurospora crassa Δmak-2 reveals that mitogen-activated protein kinase MAK-2 participates in the phosphate signaling pathway

status: Public on Jul 31 2013

city: Campinas

first: Gabriela

last: Persinoti

state: São Paulo

address: Rua Giuseppe Máximo Scalfaro, 10.000

department: Brazilian Biorenewables National Laboratory LNBR

institute: Brazilian Center for Research in Energy and Materials CNPEM

summary:
Transcriptional profiling of Neurospora crassa ∆mak-2 strain grown under phosphate-shortage were compared the transcription profile of the control strain grown in both low- and high-Pi cultures.
The filamentous fungus Neurospora crassa provides an excellent model system for the study of molecular responses to ambient signaling in eukaryotic microorganisms. Inorganic phosphate is an essential growth-limiting nutrient in nature and is crucial in genetic information. Numerous ambient signals activate the recruitment of mitogen-activated protein kinase (MAPK) cascades. Thus, in an attempt to identify genes involved in metabolic responses to exogenous phosphate sensing and in the functioning of a mitogen-activated protein kinase coding gene (mak-2) in N. crassa, we performed microarray experiments with the strain carrying the mak-2 gene knockout (Δmak-2) grown under phosphate-shortage by comparing the transcription profile to that of the control strain grown in both low- and high-phosphate cultures. Here we provide evidence that the mak-2 gene is an element of the adaptive response to extracellular Pi changes revealing novel aspects of phosphorus-sensing network in N. crassa.

overall_design: Neurospora crassa wild type strain St.L.74-OR23-1VA (FGSC #2489) cultivated in low and high Pi cultures and ∆mak-2 (FGSC #11482) mutant strain cultivated in low Pi cultures.

first: Diana

middle: E

last: Gras

first: Nalu

middle: T

last: Peres

first: Nilce

last: Martinez-Rossi

first: Ana

middle: C

last: Tahira

first: Eduardo

last: Reis

first: Antonio

last: Rossi

first: Rolf

last: Prade


title: Ubiquitinated histone H2A mapping in Drosophila ML-DmBG3 cells

status: Public on Aug 09 2013

city: Saint Louis

first: Dale

last: Dorsett

state: MO

address: 1100 South Grand Boulevard

department: Biochemistry and Molecular Biology

institute: Saint Louis University School of Medicine

summary: Monoubiquitinated histone H2A  produced by the Sce/Ring subunit of the Polycomb Repressive Complex 1 (PRC1) was mapped genome-wide in Drosophila ML-DmBG3 cells using chromatin immunoprecipitation followed by hybridization to Affymetrix tiling arrays.

overall_design: ML-DmBG3 chromatin immunoprecipitated with anti-histone H2AK119ub antibody and matching input chromatin were amplified, labeled and hybridized to Affymetrix tiling arrays to determine the locations of ubiquitinated H2A genome-wide.

first: Cheri

last: Schaaf

first: Ziva

last: Misulovin

first: Maria

last: Gause

first: Amanda

last: Koenig


title: SWI/SNF Chromatin-Remodeling Factor Smarcd3/Baf60c Controls Epithelial-Mesenchymal Transition by Inducing Wnt5a Signaling

status: Public on Aug 19 2013

first: Charles

last: Perou

summary: We previously identified a gene signature predicted to regulate the epithelial-mesenchymal transition (EMT) in both epithelial tissue stem cells and breast cancer cells. A phenotypic RNA interference (RNAi) screen identified the genes within this 140-gene signature that promoted the conversion of mesenchymal epithelial cell adhesion molecule-negative (EpCAM-) breast cancer cells to an epithelial EpCAM+/high phenotype. The screen identified 10 of the 140 genes whose individual knockdown was sufficient to promote EpCAM and E-cadherin expression. Among these 10 genes, RNAi silencing of the SWI/SNF chromatin-remodeling factor Smarcd3/Baf60c in EpCAM- breast cancer cells gave the most robust transition from the mesenchymal to epithelial phenotype. Conversely, expression of Smarcd3/Baf60c in immortalized human mammary epithelial cells induced an EMT. The mesenchymal-like phenotype promoted by Smarcd3/Baf60c expression resulted in gene expression changes in human mammary epithelial cells similar to that of claudin-low triple-negative breast cancer cells. These mammary epithelial cells expressing Smarcd3/Baf60c had upregulated Wnt5a expression. Inhibition of Wnt5a by either RNAi knockdown or blocking antibody reversed Smarcd3/Baf60c-induced EMT. Thus, Smarcd3/Baf60c epigenetically regulates EMT by activating WNT signaling pathways.

overall_design: sampleXreference

first: Nicole

middle: V

last: Jordan

first: Aleix

last: Prat

first: Gary

last: Johnson


title: Conditional loss of ErbB3 delays mammary gland hyperplasias induced by mutant PIK3CA but does not affect mammary tumor latency, gene expression or signaling

status: Public on Jun 20 2013

summary: Mutations in PIK3CA, the gene encoding the p110α subunit of PI3K, induce transformation of mammary epithelial cells (MEC). Studies suggest the transforming action of mutant PIK3CA requires binding to activated receptor tyrosine kinases or adaptors. We examined in transgenic mice if ErbB3, a powerful activator of PI3K, is required for mutant PIK3CA-mediated MEC transformation. ErbB3 loss delayed PIK3CAH1047R-dependent mammary gland hyperplasia, but tumor latency, gene expression and markers of PI3K signaling were unaffected. In ErbB3-deficient tumors, mutant PI3K remained associated with other tyrosine phosphorylated adaptors, potentially explaining the dispensability of ErbB3 for tumorigenicity and PI3K activity. Combined inhibition of ErbB RTKs and PI3K with lapatinib and the p110α inhibitor BYL719, respectively, reduced PIK3CAH1047R-dependent tumor growth and PI3K signaling more potently than the p110α inhibitor alone. In human breast cancer cells harboring PIK3CAH1047R, the combination with BYL719 and an ErbB3 inhibitor synergistically inhibited tumor growth and P-Akt. These data suggest that basal tumor growth and PI3K signaling do not depend on ErbB RTKs in PIK3CAH1047R-expressing tumors. However, upon inhibition of p110α, these receptors limit the action of PI3K inhibitors potentially explaining the more potent effect of the combination against PI3K-mutant cancers.

first: Christian

middle: D

last: Young

first: Adam

last: Pfefferle

first: Carlos

last: Arteaga


title: Characterization of Cell Lines Derived from Breast Cancers and Normal Mammary Tissues for the Study of the Intrinsic Molecular Subtypes

status: Public on Oct 29 2013

middle: M.

summary: Five molecular subtypes (Luminal A/B, HER2-enriched, Basal-like, and Claudin-low) with clinical implications have been identified. In this report, we evaluated molecular and phenotypic relationships of a large in vitro panel of human breast cancer cell lines (BCCLs), human mammary fibroblasts (HMFs) and human mammary epithelial cells (HMECs) with (1) breast tumors, (2) normal breast cell-enriched subpopulations and (3) human embryonic stem cells (hESCs) and bone marrow-derived mesenchymal stem cells (hMSC). First, by integrating genomic data of 337 breast samples with 93 cell lines we were able to identify all the intrinsic tumor subtypes in vitro, except for the Luminal A. Secondly, we observed that cell lines recapitulate the differentiation hierarchy observed in the mammary gland, with Claudin-low BCCLs and HMFs cells showing a stromal phenotype, HMECs showing a mammary stem cell/bipotent progenitor phenotype, Basal-like cells showing a luminal progenitor phenotype, and Luminal B cells showing a luminal phenotype. Thirdly, we identified Basal-like and highly migratory Claudin-low subpopulations of cells within a subset of triple-negative BCCLs (SUM149PT, HCC1143 and HCC38). Interestingly, both subpopulations within SUM149PT where found to have Tumor Initiating Cell (TIC) features, but the Basal-like subpopulation grew faster than the Claudin-low subpopulation. Finally, Claudin-low BCCLs were found to resemble the phenotype of hMSCs, whereas hESCs cells were found to have an epithelial phenotype without basal and luminal differentiation. The results presented here should help improve our understanding of the cell line model system through the appropriate pairing of cell lines with relevant in vivo tumor and normal cell counterparts.


title: HP1 wa191.S2

status: Public on Apr 04 2013

first: DCC

last: modENCODE

summary:
modENCODE_submission_6074
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: S2-DRSC; Tissue: embryo-derived cell-line; Developmental Stage: late embryonic stage; Sex: Male;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line S2-DRSC; Antibody HP1 wa191 (target is HP1a)

last: Karpen

first: Sarah

last: Elgin

first: Andrey

last: Gortchakov

first: Greg

last: Shanower

first: Michael

last: Tolstorukov

first: Peter

last: Kharchenko

first: Mitzi

last: Kuroda

first: Vincenzo

last: Pirrotta

last: Park

first: Aki

last: Minoda

last: Riddle

first: Yuri

last: Schwartz

first: Art

last: Alekseyenko

first: Cameron

last: Kennedy


title: S100P, a calcium-binding protein, is associated with polypoid tumour growth in colorectal carcinogenesis

status: Public on May 16 2013

city: TauYau

first: Yun-Shien

last: Lee

state: Taiwan

address: TauYau

department: Dept. Biotechnology

country: Taiwan

institute: Ming Chuan Univ

summary:
Colorectal cancer (CRC) is a genetically heterogeneous disease with several distinct morphological growth patterns. This study was aimed to investigate genes differentially expressed between ulcerative and polypoid colorectal CRC.  cDNA microarray was first employed to compare the gene expression profiling of ulcerative and polypoid CRC with paired normal mucosa.  Potential candidates identified by data filtering were further validated using quantitative real-time polymerase chain reaction, western blot and immunohistochemistry. Epigenetic regulation of gene expression was investigated using methylation-specific PCR (MSP).
cDNA microarray identified 11 up-regulated and 14 down-regulated genes differentially expressed in both types of tumor compared to matched normal mucosa.  Among them, S100P was the only upregulated gene preferentially associated with polypoid CRC (p = 0.032), whereas no genes demonstrated significantly differential association with ulcerative CRC.  S100P protein and mRNA expression level of polypoid CRC was significantly higher than that of ulcerative CRC (p < 0.05, respectively). Immunoreactivity of S100P protein was localized predominantly in the nuclei and to a less extent in the cytoplasm.  Overexpression of S100P occurred early in the adenoma stage.  80% (24/30) and 20% (6/30) polypoid CRC showed diffusely strong and moderate overexpression, respectively.  In contrast, S100P was diffusely and strongly expressed in 15% (6/40) ulcerative CRC, with 52.5% (21/40) and 32.5% (13/40) tumors having moderate and weak overexpression, respectively. S100P overexpression was preferentially associated with polypoid CRC (p < 0.001).  The relative methylation level determined by MSP was not statistically different between polypoid and ulcerative CRC (43.36% vs. 49.10%, p = 0.168), indicating that promoter hypomethylation was directly related to upregulation of S100P mRNA.

overall_design: The gene expression profiling of ulcerative and polypoid CRC with paired normal mucosa were compared. Dye swapping experiments with ulcerative CRC vs normal mucosa or polypoid CRC vs normal mucosa were performed and we averaged the log ratios of the duplicated spots on each slide.

first: Jy-Ming

last: Chiang

first: Jim-Ray

last: Chen


title: H3K9me2 antibody2.D.mel 3rd Instar Larvae Nuclei Sexed Female Jil mutant-heterozygous

last: modENCODE

summary:
modENCODE_submission_5621
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design:
EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Sexed Female Jil mutant-heterozygous(official name : JIL-1z2 genotype : Jil-1 z2/TM3 Ser-GFP outcross : 1 transgene : deletion tags : Transposon tag : none description : - The JIL-1 allele JIL-1z2 was isolated in a screen for imprecise excisions of the EP transposon (Rørth et al. description : 1998) in w; EP(3)3657/?2?3 Sb heterozygotes
Developmental Stage: 3rd Instar Larvae Sexed Female ; Genotype: Jil-1 z2/TM3 Ser-GFP; Sex: Female; Transgene: deletion;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Sexed Female Jil mutant-heterozygous(official name : JIL-1z2 genotype : Jil-1 z2/TM3 Ser-GFP outcross : 1 transgene : deletion tags : Transposon tag : none description : - The JIL-1 allele JIL-1z2 was isolated in a screen for imprecise excisions of the EP transposon (Rørth et al. description : 1998) in w; EP(3)3657/?2?3 Sb heterozygotes
Antibody H3K9me2 antibody2 (target is H3K9me2); Developmental Stage 3rd Instar Larvae Sexed Female

first: Gary

last: Karpen

first: Nicole


title: A Renewable Tissue Resource of Phenotypically Stable, Biologically and Ethnically Diverse, Patient-derived Human Breast Cancer Xenografts

status: Public on Jun 25 2013

first: Charles

last: Perou

summary: Translational breast cancer research is hampered by difficulties in obtaining and studying primary human breast tissue, and by the lack of in vivo preclinical models that reflect patient tumor biology accurately. In an effort to overcome these limitations, we propagated a cohort of human breast tumors grown in the mammary fat pad of SCID/Beige and NOD/SCID/IL2?-receptor null (NSG) two relatively new immunocompromised mouse models, under a series of transplant conditions.  Both models yielded stably transplantable xenografts relatively high rates compared with previously available immunocompromised mice. Xenograft lines were established directly from breast cancer patient samples, without intervening culture in vitro, using the epithelium-free mammary fat pad as the transplantation site. Of the conditions tested, xenograft take rate was highest in the presence of a low-dose estradiol pellet. Overall, 35 stably transplantable xenograft lines representing 27 patients were established, using pre-treatment, mid-treatment, and/or post-treatment samples.  Most patients yielding xenografts were “triple-negative” (ER-PR-HER2-) (n=21). However, we were able to establish lines from three ER-PR-HER2+ patients, one ER+PR-HER2-, one ER+PR+HER2- and one “triple-positive” (ER+PR+HER2+) patient. Serially passaged xenografts show biological consistency with the tumor of origin at the histopathology level, and remarkable stability across multiple transplant generations at the genomic, transcriptomic, and proteomic levels. Of the 27 patients represented, xenografts derived from 13 patients showed metastasis to the mouse lung. These models thus serve as a renewable, quality-controlled tissue resource, and should prove useful for preclinical evaluation of experimental therapeutics.

overall_design: reference x sample

first: Xiaomei

last: Zhang

first: Aleix

last: Prat

middle: M


title: HP4 Q4072.S2.HP4 RNAi

first: DCC

summary:
modENCODE_submission_5600
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The goal of these experiments are to a) validate/confirm the locations of 125 chromosomal proteins across the Drosophila melanogaster genome and b) evaluate their biological significance by assaying the impact of depletion on other proteins/marks. We are using RNAi to deplete individual non-histone chromosomal proteins in Drosophila BG3 and S2 tissue culture cells, followed by Chromatin ImmunoPrecipitation (ChIP) assayed on genomic tiling arrays. Comparison of a protein factor's binding profiles before and after depletion will increase the confidence of our predictions.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: S2-DRSC; Tissue: embryo-derived cell-line; Developmental Stage: late embryonic stage; Sex: Male;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line S2-DRSC; Antibody HP4 Q4072 (target is HP4); dsRNA (RNAi_reagent) CG8044_RNAi&oldid=70468

first: Sarah

last: Elgin

first: Andrey

last: Gortchakov

first: Greg

last: Shanower

last: Tolstorukov

last: Kharchenko


title: The transcription factor Mef2 links the Drosophila core clock to Fas2, neuronal morphology and circadian behavior

status: Public on May 03 2013

city: Waltham

first: Anna

last: Sivachenko

state: MA

address: 415 South St

institute: Brandeis University

summary: The transcription factor Mef2 regulates activity-dependent neuronal plasticity and morphology in mammals, and clock neurons are reported to experience activity-dependent circadian remodeling in Drosophila. We show here that Mef2 is required for this daily fasciculation-defasciculation cycle. Moreover, the master circadian transcription complex CLK/CYC directly regulates Mef2 transcription. ChIP-Chip analysis identified numerous Mef2 target genes implicated in neuronal plasticity, including the cell-adhesion gene Fas2.  Genetic epistasis experiments support this transcriptional regulatory hierarchy, CLK/CYC->Mef2-> Fas2, indicate that it influences the circadian fasciculation cycle within pacemaker neurons and suggest that this cycle also contributes to circadian behavior.  Mef2 therefore transmits clock information to machinery involved in neuronal remodeling, which contributes to locomotor activity rhythms.

overall_design: Mef2 ChIP-chip samples collected at 6 timepoints,  input and IP samples

first: Michael

last: Rosbash


title: Physiological change under OsHV-1 contamination in Pacific oyster Crassostrea gigas through massive mortality events on fields

status: Public on Jun 28 2013

city: CAEN

first: christophe

last: lelong

address: Esplanade de la Paix

country: France

institute: UNICAEN

summary: Massive mortalities have been observed in France since 2008 on spat and juvenile Pacific oysters, Crassostrea gigas. A herpes virus called OsHV-1, easily detectable by PCR, has been implicated in the mortalities as demonstrated by the results of numerous field studies linking mortality with OsHV-1 prevalence. Moreover, experimental infections using viral particles have documented the pathogenicity of OsHV-1.  The physiological responses of host to pathogen are not well known. In this study, a number of genes involved in the response to viral challenge have been identified and can be considered as confirmation of the role of the virus in the observed mortality. The aim of this study was to understand mechanisms brought into play against the virus during infection in the field. A microarray assay has been developed for a major part of the oyster genome and used for studying the host transcriptome.  Spat with and without detectable OsHV-1 infection were compared by microarray during mortality episodes. The result allowed establishment of a hypothetic scheme of the host cell’s infection by, and response to, the pathogen. This response seems to be different to “sensu stricto” innate immunity through genic regulation of the virus life cycle. . Some regulatory response against the virus may explain that some oysters are able to survive infection by regulation of the viral genes associated with the OsHV-1 life cycle.

overall_design: Gene expression was measured from four individual animals of three sites, an oyster production area where mortalities on spat was observed in Spring (BL: Blainville sur mer) and two sanctuary sites (CRIC, Cricqueville en Bessin without production and CAB, an offshore storage structure)

first: Aude

last: Jouaux

first: Maxime

last: Lafont

first: Jean-Louis

last: Blin

first: Maryline

last: Houssin

first: Michel

last: Mathieu

first: Christophe

last: Lelong


title: H4K20me (2nd lot).2-4 hr OR embryo

status: Public on Mar 27 2013

last: modENCODE

summary:
modENCODE_submission_5261
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Developmental Stage: Embryo 2-4hr OR; Genotype: wild type;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Antibody H4K20me1 (2nd lot) (target is H4K20me); Developmental Stage Embryo 2-4hr OR

first: Gary

last: Karpen

first: Peter

first: Mitzi

last: Kuroda

first: Vincenzo

last: Pirrotta

last: Park

first: Aki

last: Minoda

first: Nicole

last: Riddle

first: Yuri

last: Schwartz

first: Art

last: Alekseyenko

first: Cameron

last: Kennedy


title: SU(HW)-HB.S2.SuHw_RNAi

first: DCC

summary:
modENCODE_submission_5147
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: The goal of these experiments are to a) validate/confirm the locations of 125 chromosomal proteins across the Drosophila melanogaster genome and b) evaluate their biological significance by assaying the impact of depletion on other proteins/marks. We are using RNAi to deplete individual non-histone chromosomal proteins in Drosophila BG3 and S2 tissue culture cells, followed by Chromatin ImmunoPrecipitation (ChIP) assayed on genomic tiling arrays. Comparison of a protein factor's binding profiles before and after depletion will increase the confidence of our predictions.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: S2-DRSC; Tissue: embryo-derived cell-line; Developmental Stage: late embryonic stage; Sex: Male;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line S2-DRSC; Antibody SU(HW)-HB (target is SU(HW)); dsRNA (RNAi_reagent) CG8573_RNAi&oldid=39665

first: Sarah

last: Elgin

first: Andrey

last: Gortchakov

first: Greg

last: Shanower

first: Michael

last: Tolstorukov

last: Kharchenko


title: H3K9me2 antibody2.OR Head Nuclei

summary:
modENCODE_submission_5059
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Developmental Stage: Mixed Adult; Genotype: wild type;  NUMBER OF REPLICATES: 6;  EXPERIMENTAL FACTORS: Strain Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); tissue (organism part) ; Antibody H3K9me2 antibody2 (target is H3K9me2); Developmental Stage Mixed Adult


title: RPD3-Q3451.D.mel 3rd Instar Larvae Nuclei

summary:
modENCODE_submission_4189
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Developmental Stage: 3rd Instar Larvae; Genotype: wild type;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Antibody RPD3-Q3451 (target is RPD3); Developmental Stage 3rd Instar Larvae


title: Cohesin and Polycomb proteins functionally interact to control transcription at silenced, restrained, and active genes [tiling array data]

status: Public on Apr 25 2013

city: St Louis

first: Cheri

last: Schaaf

address: 1100 South Grand Ave

department: Biochemistry & Molecular Biology

summary: Cohesin is crucial for proper chromosome segregation, but also regulates gene transcription and organism development by poorly understood mechanisms. We find that in Drosophila, cohesin functionally interacts with Polycomb group (PcG) silencing proteins at both silenced and active genes. Cohesin unexpectedly facilitates binding of Polycomb Repressive Complex 1 (PRC1) to many active genes. In contrast, cohesin and PRC1 binding are mutually antagonistic at silenced genes. PRC1 depletion decreases phosphorylated RNA polymerase and mRNA at many active genes, but increases them at silenced genes. Cohesin also facilitates long-range interactions between Polycomb Response Elements in the invected-engrailed gene complex where it represses transcription. These multiple distinct cohesin-PcG interactions reveal a previously unrecognized role for PRC1 in facilitating productive gene transcription, and provide new insights into how cohesin and PRC1 control development.

overall_design: ChIP-chip of cohesin, Polycomb group proteins, and RNA Polymerase II was performed in whole wing imaginal discs in developing wing imaginal disc, revealing that cohesin and Polycomb Repressive Complex 1 (PRC1) components co-bind with cohesin proteins at active genes. We then measured cohesin, Pc, and H3K27me3 separately in anterior and posterior wing imaginal discs and compared their binding at the invected-engrailed complex, which is silenced in the anterior disc, and expressed in its posterior.  This  confirmed that cohesin and PRC1 (Pc) co-bind at inv-en in its active state, and H3K27me3 and PRC1 (Pc) co-target inv-en in its silenced state. Comparison of binding between Pc-RJ and Pc-VP was performed, and revealed that Pc-VP is subject to epitope masking specifically at active genes. Finally, we measured cohesin and Pc binding in Drosophila ML-DmBG3-c2 cells, and found that they co-bind active genes in this cell line in as well as in wing imaginal discs. ChIP-chip of cohesin subunit Rad21 after PRC1 component Ph depletion, and ChIP-chip of PRC1 subunit Pc after Rad21 RNAi depletion, revealed that these two complexes affect one another's binding.  Finally, ChIP-chip of Rpb3 (representing total Pol II) and Ser2P-Pol II (representing elongating Pol II) after PRC1 component Ph depletion revealed that PRC1 restrains entry of non-phosphorylated Pol II into gene bodies.

first: Dale

last: Dorsett


title: GAF.2-4 hr OR embryo

last: modENCODE

summary:
modENCODE_submission_6387
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Developmental Stage: Embryo 2-4hr OR; Genotype: wild type;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Antibody GAF (target is GAF); Developmental Stage Embryo 2-4hr OR


title: Genome-wide control of RNA polymerase II activity by cohesin (tiling)

status: Public on Apr 24 2013

summary: Cohesin is a well-known mediator of sister chromatid cohesion, but it also influences gene expression and development. These non-canonical roles of cohesin are not well understood, but are vital: gene expression and development are altered by modest changes in cohesin function that do not disrupt chromatid cohesion. To clarify cohesin’s roles in transcription, we measured how cohesin controls RNA polymerase II (Pol II) activity by genome-wide chromatin immunoprecipitation and precision global run-on sequencing. On average, cohesin-binding genes have more transcriptionally active Pol II and promoter-proximal Pol II pausing than non-binding genes, and are more efficient,  producing higher steady state levels of mRNA per transcribing Pol II complex. Cohesin depletion frequently increases pausing at cohesin-binding genes, indicating that cohesin  often facilitates transition of paused Pol II to elongation. In many cases this likely reflects a role for cohesin in transcriptional enhancer function. Strikingly, more than 95% of predicted extragenic enhancers bind cohesin, and cohesin depletion can reduce their association with Pol II, indicating that cohesin facilitates enhancer-promoter contact. Cohesin directly promotes transcription of the myc gene, and cohesin depletion reduces Pol II activity at most Myc target genes. The multiple transcriptional roles of cohesin revealed by these studies likely underlie the growth and developmental deficits caused by minor changes in cohesin activity.

overall_design: We performed ChIP-chip of Rpb3 (representing total Pol II), Ser2P-Pol II (representing elongating Pol II), and Cdk12 and CycT Pol II kinase components in Mock RNAi-treated and cohesin subunit Rad21 RNAi-treated ML-DmBG3-c2 cells, which revealed that cohesin depletion has a variety of effects on Pol II occupancy and modification, as well as on occupancy of Pol II kinases.


title: H3K9me2-Ab2 (new lot).ovary

summary:
modENCODE_submission_3946
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Developmental Stage: Adult Female; Genotype: wild type; Sex: Female;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: tissue (organism part) Tissue:Ovary:GK:1&oldid=100182; Developmental Stage Adult Female; Antibody H3K9me2-Ab2 (new lot) (target is H3K9me2); Strain Oregon-R(official name : Oregon-R-modENCODE genotype : wild type )

last: Karpen


title: HP1 wa191.ovary

summary:
modENCODE_submission_3947
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Developmental Stage: Adult Female; Genotype: wild type; Sex: Female;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: tissue (organism part) Tissue:Ovary:GK:1&oldid=100182; Developmental Stage Adult Female; Antibody HP1 wa191 (target is HP1a); Strain Oregon-R(official name : Oregon-R-modENCODE genotype : wild type )

last: Kuroda


title: H3K4me2_JBC 1360331.ovary

summary:
modENCODE_submission_4125
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Developmental Stage: Adult Female; Genotype: wild type; Sex: Female;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: tissue (organism part) Tissue:Ovary:GK:1&oldid=100182; Developmental Stage Adult Female; Antibody H3K4me2 JBC 1360331 (target is H3K4me2); Strain Oregon-R(official name : Oregon-R-modENCODE genotype : wild type )

last: Pirrotta


title: H3K9ac.2-4 hr OR embryo

status: Public on Mar 13 2013

summary:
modENCODE_submission_6072
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Developmental Stage: Embryo 2-4hr OR; Genotype: wild type;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Antibody H3K9ac (target is H3K9ac); Developmental Stage Embryo 2-4hr OR

last: Park


title: H4K16ac(M).D.mel 3rd Instar Larvae Nuclei Sexed Male Jil mutant

summary:
modENCODE_submission_5620
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design:
EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Sexed male Jil mutant(official name : Jil-1 z2 genotype : Jil-1 z2/Jil-1z2 outcross : 1 transgene : deletion tags : Transposon tag : none description : - The JIL-1 allele JIL-1z2 was isolated in a screen for imprecise excisions of the EP transposon (Rørth et al. description : 1998) in w; EP(3)3657/?2?3 Sb heterozygotes
Developmental Stage: 3rd Instar Larvae Sexed Male; Genotype: Jil-1 z2/Jil-1z2; Sex: Male; Transgene: deletion;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Sexed male Jil mutant(official name : Jil-1 z2 genotype : Jil-1 z2/Jil-1z2 outcross : 1 transgene : deletion tags : Transposon tag : none description : - The JIL-1 allele JIL-1z2 was isolated in a screen for imprecise excisions of the EP transposon (Rørth et al. description : 1998) in w; EP(3)3657/?2?3 Sb heterozygotes
Antibody H4K16ac(M) (target is H4K16ac); Developmental Stage 3rd Instar Larvae Sexed Male

last: Minoda


title: H2AV_9751.BG3

summary:
modENCODE_submission_6073
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: ML-DmBG3-c2; Tissue: CNS-derived cell-line; Developmental Stage: third instar larval stage; Genotype: y v f mal; Sex: Unknown;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line ML-DmBG3-c2; Antibody H2AV 9751 (target is H2AV)

last: Riddle


title: RNA Pol II (abcam).D.mel 3rd Instar Larvae Nuclei G9a mutant.Affy 2

summary:
modENCODE_submission_5614
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design:
EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: G9a mutant (official name : G9a mutant genotype : G9a[RG5]/G9a[RG5] outcross : 3 transgene : n/a tags : homologous recombination tag : none description : Mutation generated by end-out homologous recombination at the G9a locus. The entire open reading frame of G9a has been removed.
Developmental Stage: 3rd Instar Larvae; Genotype: G9a[RG5]/G9a[RG5]; Transgene: n/a;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain G9a mutant (official name : G9a mutant genotype : G9a[RG5]/G9a[RG5] outcross : 3 transgene : n/a tags : homologous recombination tag : none description : Mutation generated by end-out homologous recombination at the G9a locus. The entire open reading frame of G9a has been removed.
Antibody RNA Pol II (abcam) (target is PolII); Developmental Stage 3rd Instar Larvae

last: Schwartz


title: RNA Pol II (abcam).D.mel 3rd Instar Larvae Nuclei HP1b mutant

summary:
modENCODE_submission_5616
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: HP1b mutant(official name : Hp1b^16 genotype : Hp1b^16/Hp1b^16 outcross : n/a transgene : n/a tags : Transposon tag : GFP description : Allele of HP1b generated by imprecise excision of CB02849.  The 539bp deletion removes the Start codon and a large part of the Hp1b coding region. made_by : Nicole Riddle ); Developmental Stage: 3rd Instar Larvae; Genotype: Hp1b^16/Hp1b^16; Transgene: n/a;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain HP1b mutant(official name : Hp1b^16 genotype : Hp1b^16/Hp1b^16 outcross : n/a transgene : n/a tags : Transposon tag : GFP description : Allele of HP1b generated by imprecise excision of CB02849.  The 539bp deletion removes the Start codon and a large part of the Hp1b coding region. made_by : Nicole Riddle ); Antibody RNA Pol II (abcam) (target is PolII); Developmental Stage 3rd Instar Larvae

last: Alekseyenko


title: H3K9me2-Ab2 (new lot 3).D.mel 3rd Instar Larvae Nuclei G9a mutant.Affy 2

summary:
modENCODE_submission_5618
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design:
EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: G9a mutant (official name : G9a mutant genotype : G9a[RG5]/G9a[RG5] outcross : 3 transgene : n/a tags : homologous recombination tag : none description : Mutation generated by end-out homologous recombination at the G9a locus. The entire open reading frame of G9a has been removed.
Developmental Stage: 3rd Instar Larvae; Genotype: G9a[RG5]/G9a[RG5]; Transgene: n/a;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain G9a mutant (official name : G9a mutant genotype : G9a[RG5]/G9a[RG5] outcross : 3 transgene : n/a tags : homologous recombination tag : none description : Mutation generated by end-out homologous recombination at the G9a locus. The entire open reading frame of G9a has been removed.
Antibody H3K9me2-Ab2 (new lot 3) (target is H3K9me2); Developmental Stage 3rd Instar Larvae

last: Kennedy


title: H4K16ac(M).D.mel 3rd Instar Larvae Nuclei Sexed Female Jil mutant

summary:
modENCODE_submission_5619
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design:
EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Sexed Female Jil mutant(official name : Jil-1 z2 genotype : Jil-1 z2/ Jil-1 z2 outcross : 1 transgene : deletion tags : Transposon tag : none description : - The JIL-1 allele JIL-1z2 was isolated in a screen for imprecise excisions of the EP transposon (Rørth et al. description : 1998) in w; EP(3)3657/?2?3 Sb heterozygotes
Developmental Stage: 3rd Instar Larvae Sexed Female ; Genotype: Jil-1 z2/ Jil-1 z2; Sex: Female; Transgene: deletion;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Sexed Female Jil mutant(official name : Jil-1 z2 genotype : Jil-1 z2/ Jil-1 z2 outcross : 1 transgene : deletion tags : Transposon tag : none description : - The JIL-1 allele JIL-1z2 was isolated in a screen for imprecise excisions of the EP transposon (Rørth et al. description : 1998) in w; EP(3)3657/?2?3 Sb heterozygotes
Antibody H4K16ac(M) (target is H4K16ac); Developmental Stage 3rd Instar Larvae Sexed Female

last: Elgin


title: H4K16ac(M).D.mel 3rd Instar Larvae Nuclei Sexed male Jil mutant-heterozygous

summary:
modENCODE_submission_5622
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design:
EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Sexed male Jil mutant-heterozygous(official name : JIL-1z2 genotype : Jil-1 z2/TM3 Ser-GFP outcross : 1 transgene : deletion tags : Transposon tag : none description : - The JIL-1 allele JIL-1z2 was isolated in a screen for imprecise excisions of the EP transposon (Rørth et al. description : 1998) in w; EP(3)3657/?2?3 Sb heterozygotes
Developmental Stage: 3rd Instar Larvae Sexed Male; Genotype: Jil-1 z2/TM3 Ser-GFP; Sex: Male; Transgene: deletion;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Sexed male Jil mutant-heterozygous(official name : JIL-1z2 genotype : Jil-1 z2/TM3 Ser-GFP outcross : 1 transgene : deletion tags : Transposon tag : none description : - The JIL-1 allele JIL-1z2 was isolated in a screen for imprecise excisions of the EP transposon (Rørth et al. description : 1998) in w; EP(3)3657/?2?3 Sb heterozygotes
Antibody H4K16ac(M) (target is H4K16ac); Developmental Stage 3rd Instar Larvae Sexed Male

last: Gortchakov


title: HP1b Q4114.D.mel 3rd Instar Larvae Nuclei HP1b mutant

summary:
modENCODE_submission_5604
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: HP1b mutant(official name : Hp1b^16 genotype : Hp1b^16/Hp1b^16 outcross : n/a transgene : n/a tags : Transposon tag : GFP description : Allele of HP1b generated by imprecise excision of CB02849.  The 539bp deletion removes the Start codon and a large part of the Hp1b coding region. made_by : Nicole Riddle ); Developmental Stage: 3rd Instar Larvae; Genotype: Hp1b^16/Hp1b^16; Transgene: n/a;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain HP1b mutant(official name : Hp1b^16 genotype : Hp1b^16/Hp1b^16 outcross : n/a transgene : n/a tags : Transposon tag : GFP description : Allele of HP1b generated by imprecise excision of CB02849.  The 539bp deletion removes the Start codon and a large part of the Hp1b coding region. made_by : Nicole Riddle ); Antibody HP1b Q4114 (target is HP1b); Developmental Stage 3rd Instar Larvae

last: Shanower


title: HP1b Q4113.D.mel 3rd Instar Larvae Nuclei HP1b mutant.Affy 2

summary:
modENCODE_submission_5573
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: HP1b mutant(official name : Hp1b^16 genotype : Hp1b^16/Hp1b^16 outcross : n/a transgene : n/a tags : Transposon tag : GFP description : Allele of HP1b generated by imprecise excision of CB02849.  The 539bp deletion removes the Start codon and a large part of the Hp1b coding region. made_by : Nicole Riddle ); Developmental Stage: 3rd Instar Larvae; Genotype: Hp1b^16/Hp1b^16; Transgene: n/a;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain HP1b mutant(official name : Hp1b^16 genotype : Hp1b^16/Hp1b^16 outcross : n/a transgene : n/a tags : Transposon tag : GFP description : Allele of HP1b generated by imprecise excision of CB02849.  The 539bp deletion removes the Start codon and a large part of the Hp1b coding region. made_by : Nicole Riddle ); Antibody HP1b Q4113 (target is HP1b); Developmental Stage 3rd Instar Larvae

last: Tolstorukov


title: dSFMBT Q2642.2-4 hr OR embryo

summary:
modENCODE_submission_5256
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Developmental Stage: Embryo 2-4hr OR; Genotype: wild type;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Antibody dSFMBT Q2642 (target is dSFMBT); Developmental Stage Embryo 2-4hr OR

last: Kharchenko


title: dRING Q3200.2-4 hr OR embryo.Affy 2

summary:
modENCODE_submission_5255
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Developmental Stage: Embryo 2-4hr OR; Genotype: wild type;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Antibody dRING Q3200 (target is dRING); Developmental Stage Embryo 2-4hr OR


title: WDS_Q2691.BG3

summary:
modENCODE_submission_5148
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: ML-DmBG3-c2; Tissue: CNS-derived cell-line; Developmental Stage: third instar larval stage; Genotype: y v f mal; Sex: Unknown;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line ML-DmBG3-c2; Antibody WDS Q2691 (target is WDS)


title: HP1 wa191.D.mel 3rd Instar Larvae Nuclei AGO2_414 mutant

summary:
modENCODE_submission_5263
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design:
EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Ago2 414(official name : Ago2[414] genotype : w;;ago2[414] outcross : 0 description : Ago2 null mutant description : described in
Developmental Stage: 3rd Instar Larvae; Genotype: w;;ago2[414];  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Ago2 414(official name : Ago2[414] genotype : w;;ago2[414] outcross : 0 description : Ago2 null mutant description : described in
Antibody HP1 wa191 (target is HP1a); Developmental Stage 3rd Instar Larvae


title: ZW5.2-4 hr OR embryo

summary:
modENCODE_submission_5265
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Developmental Stage: Embryo 2-4hr OR; Genotype: wild type;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Oregon-R(official name : Oregon-R-modENCODE genotype : wild type ); Antibody ZW5 (target is ZW5); Developmental Stage Embryo 2-4hr OR


title: H3K9me2 antibody2.D.mel 3rd Instar Larvae Nuclei Sexed male Jil mutant-heterozygous

summary:
modENCODE_submission_5602
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design:
EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: Sexed male Jil mutant-heterozygous(official name : JIL-1z2 genotype : Jil-1 z2/TM3 Ser-GFP outcross : 1 transgene : deletion tags : Transposon tag : none description : - The JIL-1 allele JIL-1z2 was isolated in a screen for imprecise excisions of the EP transposon (Rørth et al. description : 1998) in w; EP(3)3657/?2?3 Sb heterozygotes
Developmental Stage: 3rd Instar Larvae Sexed Male; Genotype: Jil-1 z2/TM3 Ser-GFP; Sex: Male; Transgene: deletion;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain Sexed male Jil mutant-heterozygous(official name : JIL-1z2 genotype : Jil-1 z2/TM3 Ser-GFP outcross : 1 transgene : deletion tags : Transposon tag : none description : - The JIL-1 allele JIL-1z2 was isolated in a screen for imprecise excisions of the EP transposon (Rørth et al. description : 1998) in w; EP(3)3657/?2?3 Sb heterozygotes
Antibody H3K9me2 antibody2 (target is H3K9me2); Developmental Stage 3rd Instar Larvae Sexed Male


title: H3K9me3 abcam.D.mel 3rd Instar Larvae Nuclei G9a mutant.Affy 2

summary:
modENCODE_submission_5611
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design:
EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: G9a mutant (official name : G9a mutant genotype : G9a[RG5]/G9a[RG5] outcross : 3 transgene : n/a tags : homologous recombination tag : none description : Mutation generated by end-out homologous recombination at the G9a locus. The entire open reading frame of G9a has been removed.
Developmental Stage: 3rd Instar Larvae; Genotype: G9a[RG5]/G9a[RG5]; Transgene: n/a;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Strain G9a mutant (official name : G9a mutant genotype : G9a[RG5]/G9a[RG5] outcross : 3 transgene : n/a tags : homologous recombination tag : none description : Mutation generated by end-out homologous recombination at the G9a locus. The entire open reading frame of G9a has been removed.
Antibody H3K9me3 abcam (target is H3K9me3); Developmental Stage 3rd Instar Larvae


title: JHDM1_Q2634.BG3.Affy 2

summary:
modENCODE_submission_5145
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: ML-DmBG3-c2; Tissue: CNS-derived cell-line; Developmental Stage: third instar larval stage; Genotype: y v f mal; Sex: Unknown;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line ML-DmBG3-c2; Antibody JHDM1 Q2634 (target is JHDM1)


title: H4K12ac.S2

summary:
modENCODE_submission_5144
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of the major histone modifications across the Drosophila melanogaster genome. The modifications under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages.
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: S2-DRSC; Tissue: embryo-derived cell-line; Developmental Stage: late embryonic stage; Sex: Male;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line S2-DRSC; Antibody H4K12ac (target is H4K12ac)


title: SPT16(Cosmo).S2

summary:
modENCODE_submission_5146
This submission comes from a modENCODE project of Gary Karpen. For full list of modENCODE projects, see http://www.genome.gov/26524648
Project Goal: We aim to determine the locations of 125 chromosomal proteins across the Drosophila melanogaster genome. The proteins under study are involved in basic chromosomal functions such as DNA replication, gene expression, gene silencing, and inheritance. We will perform Chromatin ImmunoPrecipitation (ChIP) using genomic tiling arrays. We will initially assay localizations using chromatin from three cell lines and two embryonic stages, and will then extend the analysis of a subset of proteins to four additional animal tissues/stages
For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf

overall_design: EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Cell Line: S2-DRSC; Tissue: embryo-derived cell-line; Developmental Stage: late embryonic stage; Sex: Male;  NUMBER OF REPLICATES: 4;  EXPERIMENTAL FACTORS: Cell Line S2-DRSC; Antibody SPT16(Cosmo) (target is SPT16)