title: Transcriptome analysis of Gibberellin-response gene in the fast-growing species moso Bamboo

city: fuzhou

first: Lianfeng

last: Gu

address: No.15 Shangxiadian Road, Cangshan District, Fuzhou City, Fujian Province, China

institute: Fujian Agriculture and Forestry University

summary: Moso bamboo is well known with its rapid growth rate. In order to shed light on the underlying mechanism of growth, we applied Gibberellin (GA) to mimic the fast development process in bamboo and found that exogenous GA can significantly increase the length of internode of moso bamboo. Subsequently, we sequenced the transcriptome by high-through sequencing and identified 5,148 different expressed genes (DEG) and find out 22 genes that take part in GA signaling pathway is significantly differently expressed, including GID1A, GID1B and GAI. From GO analysis, a group of genes related to response hormone stimulus are enriched in up-regulated DEGs and 178 GA-responded genes are involved in other plant hormone signaling pathway, of which genes MYB74 and NCED5 are belong to both two pathways. Besides, clusters of genes about photosynthesis are enriched in down-regulated DEGs. By looking into the content of chlorophyll, we find out that the concentrations of chlorophyll are obviously decreased which verify that photosynthesis do weakened after GA treatment. Through method of slicing by hand, it appears that an increased condensation of lignin after GA treatment. The results imply a functional role of GA in bamboo growth, and maybe major in cell wall formation, and photosynthesis. Differential AS alternative splicing (AS) events upons GA induce suggested that post-transcriptional regulation is involved in the GA response.

overall_design: triplicates

first: Hangxiao

last: Zhang

first: Huihui

last: Wang

first: Qiang

last: Zhu

first: Yubang

last: Gao

first: Huiyuan

first: Yongsheng

first: Liangzhen

last: Zhao

first: Chentao

last: Lin


title: Transcriptome change in response to patulin stress in Pichia caribbica

status: Public on Jun 21 2018

city: Zhenjiang

first: Xiangfeng

last: Zheng

state: Jiangsu

address: 301, Xuefu Road

department: Food school

country: China

institute: Jiangsu university

type: Expression profiling by high throughput sequencing

summary: The yeast Pichia caribbica shown the capability to degrade patulin by the intracellular enzymes. However, the enzymes which risponsible for the degradation process was unkonown. Transcriptome change in response to mycotoxin patulin was analyzed. The molecular mechanism of Pichia caribbica withstand patulin was revealed.

overall_design: each three samples were analyzed , the yeast Pichia caribbica amending with patulin and the control which was not amending with patulin

first: Hongyin


title: Circadian Clock Regulation of Hepatic Lipid Metabolism by Modulation of m6A mRNA Methylation [siMettl3]

city: Nanjing

first: Xiang

last: Zhong

address: No. 6, Tongwei Road, Xuanwu District

department: College of Animal Science and Technology

institute: Nanjing Agricultural University

summary: Circadian transcriptional rhythms are necessary for lipid metabolic homeostasis. Disruptions can lead to metabolic diseases. Whether epigenetic N6-methyladenosine (m6A) mRNA methylation impacts circadian regulation of lipid metabolism is unclear. Here, we show m6A mRNA methylation oscillations in murine liver depend upon a functional circadian clock. Hepatic deletion of Bmal1 increased m6A mRNA methylation, particularly of PPaRα. Inhibition of m6A methylation via knockdown of m6A methyltransferase METTL3 decreased PPaRα m6A abundance and increased PPaRα mRNA lifetime and expression, reducing lipid accumulation in cells in vitro. Our data suggest YTH domain family 2 (YTHDF2, a m6A binding protein) binds to PPaRα, prolonging its lifetime and mRNA expression. Reactive oxygen species accumulation increased PPaRα transcript m6A levels, revealing a possible mechanism for circadian clock disruption on m6A mRNA methylation. These data suggest m6A RNA methylation is important for circadian clock regulation of downstream genes and lipid metabolism that impacts metabolic outcome.

overall_design: Examination of  different m6A mRNA methylation  in sicontrol and siMettl3 sample from HepG2 cell.

first: Vanessa

last: Leone

first: Jiayao

last: Yu

first: Xiaocheng

last: Weng

first: Yu

last: Li

first: Candace

middle: M

last: Cham

first: Kyle

last: Dolan

first: Xiaorong

first: Nathaniel

last: Hubert

first: Yun

last: Tao

first: Fanfei

first: Kristina

last: Martinez

first: Yong

last: Huang

first: Tian

first: Jianzhao

last: Liu

first: Chuan

last: He

first: Eugene

middle: B

last: Chang


title: γδ T cells orchestrate the induction of protective type 2 immunity in neonatal influenza infection

status: Public on Jun 20 2018

city: Memphis

first: Jeremy

middle: Chase

last: Crawford

state: TN

address: MS 221, 262 Danny Thomas Place

department: Department of Host-Microbe Interactions

country: USA

institute: St. Jude Children's Research Hospital

summary: Influenza infection causes high rates of hospitalization and mortality in infants. γδ T cells are critical for immune responses against pathogens as regulators and effectors, especially in infants, and yet the roles of neonatal γδ T cells in influenza remain to be investigated. Here we report that γδ T cells were protective against mortality associated with neonatal influenza infection. Infection induced the accumulation and activation of γδ T cells, which transiently expressed IL-17a to enhance early IL-33 production by lung epithelial cells via STAT3 phosphorylation. Subsequently, this led to type 2 immune responses with elicited infiltration of ILC2s and Tregs resulting in increased amphiregulin secretion and tissue repair. Loss of γδ T cells did not alter viral clearance or IFN-γ production. Thus, our results identify a specific requirement for γδ T cells in influenza-infected neonates by initiating type 2 immune responses, mediating tissue homeostasis, and promoting lung integrity.

overall_design: RNA-Seq of total RNA from whole-lung homogenates of influenza-infected wild-type and TCRδ-/- neonatal mice at 8 days post infection.

first: Xizhi

last: Guo

middle: C

first: Paul

middle: G

last: Thomas


title: Gene expression of native Jurkat human leukemia cell line following 3h BET inhibition by MMQO or 3h HDAC inhibition by TSA

status: Public on Jun 22 2018

city: Barcelona

first: Albert

last: Jordan

address: Baldiri Reixac 4

department: Molecular Genomics

country: Spain

institute: IBMB-CSIC

summary: Basal Jurkat cell gene expression, MMQO or TSA treated Jurkat cell gene expression

overall_design: Jurkat cancer cells were grown in rich media, treated with either MMQO or TSA for 3 hours or left untreated. Total RNA was extracted to monitor basal gene expression

first: Jordan

last: Albert

first: Abner

last: Erik


title: DNA Topoisomerase I differentially modulates R loop across long genes and at human replication origins

status: Public on Jun 26 2018

city: Davis

first: Frederic

last: Chedin

state: CA

address: 1 Shields Avenue

department: MCB

institute: UC Davis

type: Genome binding/occupancy profiling by high throughput sequencing

summary: Co-transcriptional R-loops are abundant non-B DNA structures in mammalian genomes. DNA Topoisomerase I (Top1) is often thought to regulate R-loop formation owing to its ability to resolve both positive and negative supercoils. How Top1 regulates R-loop structures at a global level is unknown. Here, we performed high-resolution strand-specific R-loop mapping in human cells depleted for Top1 and found that Top1 depletion resulted in both R-loop gains and losses at thousands of transcribed loci, delineating two distinct gene classes. R-loop gains were characteristic for long, highly transcribed, genes located in gene-poor regions anchored to Lamin B1 domains and in proximity to H3K9me3-marked heterochromatic patches. R-loop losses, by contrast, occurred in gene-rich regions overlapping H3K27me3-marked active replication origins. Interestingly, Top1 depletion coincided with a block of the cell cycle in G0/G1 phase and a trend towards global replication delay. Our findings reveal new properties of Top1 in regulating R-loop homeostasis and suggest a potential role for Top1 in controlling replication origin via R-loop formation.

overall_design: DNA-RNA immunoprecipitation (DRIP-seq) and DNA-RNA immunoprecipitation strand-specific (DRIPc-seq) were performed on control, scramble, and two Top1 KD HEK293 cell lines. RNA Polymerase II ChIP-seq, and total RNA-seq were performed on two scramble and two Top1 KD HEK293 cell lines. All samples (control, scrambles, Top1 KD cells) are of different passages (i.e. control of DRIP did not come from the same population as DRIPc, et cetera.)

first: Stefano

last: Manzo

first: Stella

middle: R

last: Hartono

first: Lionel

middle: A

last: Sanz

first: Sara

last: De Biasi

first: Andrea

last: Cossarizza

first: Giovanni

last: Capranico


title: Ogye body map

city: Seoul

first: Jin-Wu

last: Nam

address: Seongdong-Gu Hangdang-dong

department: Department of Life Science

country: South Korea

institute: Hanyang University

type: Methylation profiling by high throughput sequencing

summary:
This SuperSeries is composed of 3 parts:
Ogye body map RNA-seq data: GSE104351, PRJNA412404 Ogye body map RRBS data: GSE104355, PRJNA412432 Ogye genome data: PRJNA412424

overall_design: Refer to individual Series


title: Capturing the onset of PRC2-mediated repressive domain formation [ChIP-Seq, 2]

city: New York

first: Danny

last: Reinberg

state: NY

address: 522 First Avenue

department: Biochemistry and Molecular Pharmacology

institute: NYU School of Medicine

summary: Our study defines nucleation and spreading regions for Polycomb repressive complex 2 (PRC2), demonstrating the principle of PRC2 domain formation in mammals. We elucidate the role of genome architecture in formation of these domains and identify JARID2 and MTF2 as being crucial for full recruitment of PRC2 to chromatin.

overall_design: In this experiment, we performed ChIP-seq with the indicated antibodies and genotpyes of mESCs.

first: Ozgur

last: Oksuz

first: Varun

last: Narendra

first: Chul-Hwan

last: Lee

first: Nicolas

last: Descostes

first: Gary

last: LeRoy

first: Ramya

last: Raviram

first: Lili

last: Blumenberg

first: Kelly

last: Karch

first: Pedro

middle: P

last: Rocha

first: Benjamin

last: Garcia

first: Jane

last: Skok


title: Transcriptional impact of MTHFD2 in Human Aortic Endothelial Cells

status: Public on Jun 19 2018

first: Jun

last: Zhu

address: 1 Gustave L. Levy Pl

department: Genetics and genomic sciences

institute: Icahn school of medicine at mount sinai

summary: We performed transcriptome analysis of Human Aortic Endothelial Cells after siRNA mediated knockdown of MTHFD2. We identified MTHFD2 as a key driver for a gene cluster which integrates mitochondrial one-carbon metabolism, serine synthesizing enzymes as well as common amino acid and ER stress response genes.

overall_design: Human Aortic Endothelial Cells were treated with three different siRNAs against MTHFD2 or scramble for 72 h

first: Juliane

last: Hitzel

first: Eunjee

first: Ralf

last: Brandes


title: Expression data from ovarian cells growing in three dimensional culture (Matrigel) with altered expression of miR-200s

status: Public on Jun 25 2018

city: Boston

first: pui wah

last: Choi

state: MA

address: 221 longwood Ave

department: OB/GYB

institute: Brigham and Women's Hospital

summary:
It is believed that incessant ovulation will cause formation of ovarian cysts which later lead to ovarian cancer maglinancy. miR-200s is highly expressed in ovarian cancer tissue when compared to ovarian normal tissue. To study wether miR-200s have a pathologenic role in ovarian cyst formation, normal ovarian cells with overexpression of miR-200s and two cancer cell lines with knockdown of miR-200s were grown in a 3D culture system and allowed to form cyst.
We used microarrays to detail the global programme of gene expression underlying ovarian cyst formation affected by expression of miR-200s and indentify distinct classes of up-regulated and down-regulated genes during this process.

overall_design: Normal ovarian surface epithelial cells (OSE7) with overexpression of miR-200s and ovarian cancer cells (MCAS and OVCA432) with knockdown of miR-200s growing in Matrigel for seven days were subjected to RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain the gene expression altered by miR-200s level after the cells encounted Matrigel environment for 7 days, when cysts are usually formed.  miR-200s consists of five members (miR-200a, miR-200b, miR-200c, miR-141 and miR-429). These five miRNAs form two clusters: cluster 1 of miR-200b, miR-200a and miR-429 maps to chromosome 1 (1p33.36), while the miR-200c and miR-141 cluster maps to chromosome 12 (12p13.31). Alternatively, the miR-200 family members can also be categorized in two functional groups based upon the similarities of their seed sequences. MiR-200b, miR-200c and miR-429 (Functional Group I) all share the same seed sequence (5’-AAUACUG-3’), while miR-200a and miR-141 (Functional Group II) both share the same seed sequence (5’-AACACUG-3’), with the two functional groups differing in the seed sequence only by one nucleotide. MiR-200s were over-expressed or knockdown in ovarian cells according to the dichotomous location rather than to their seed sequence because the qRT-PCR data from our previous work on miR-200 in ovarian cells showed an obvious dichotomous expression pattern of the miR-200 family members according to chromosome location. We used lentivrus system to overexpress or knockdown the genes. Scramble control were established with the lentiviral vector inserted with a random sequence for both normal and cancer cell lines.

first: Pui-wah

first: Shubai

last: Liu

first: Ng-Shu

last: Wing


title: Expression data from tibialis anterior muscle of rats fed different fatty acid enriched diets

city: Guelph

first: David

last: Mutch

state: Ontario

address: 50 Stone Road East

department: Human Health & Nutritional Sciences

country: Canada

institute: University of Guelph

summary:
Omega-3 and omega-6 polyunsaturated fatty acids (PUFA) have important signalling roles in the body. The goal of this study was to investigate the impact of linoleic acid (LA, omega-6) and alpha-linolenic (ALA, omega-3) on global skeletal muscle gene expression. We were also interested to study the impact of these fatty acids on myokine expression.
To differentiate the roles of essential dietary PUFA on skeletal muscle function, we fed male rats a control diet (AIN-93G) or diets containing 10% safflower oil or flaxseed oil. Skeletal muscle gene expression was investigated by microrray.

overall_design: Group comparison of tibialis anterior muscle from rats fed different fatty acid enriched diets.

first: Heather

last: Gibling


title: Manipulation of the gut microbiome as a strategy to treat the osteoarthritis of obesity

first: Jacquelyn

last: Myers

address: 262 Danny Thomas Pl

institute: St. Jude Children’s Research Hospital

summary: Obesity is a risk factor for Osteoarthritis (OA), the greatest cause of disability in the US.  The impact of obesity on OA is driven by systemic inflammation, now understood to be caused by an altered gut microbiome.  Oligofructose, a non-digestible prebiotic fiber, can correct the obese gut microbiome, suggesting a novel approach to treat the OA of obesity.  Here we report that in the obese murine gut, beneficial Bifidobacteria are lost while key proinflammatory species gain in abundance.  A downstream systemic inflammatory signature culminates with accelerated knee OA.  Oligofructose supplementation corrects the obese gut microbiome in part by supporting key commensal microflora, particularly Bifidobacterium pseudolongum.  This leads to reduced inflammation in the colon, circulation and knee, and protection from OA.  This novel recognition of a gut microbiome-OA connection sets the stage for discovery of new OA therapeutics targeting specific microbes inhabiting the intestinal space to inhibit disease pathology.

overall_design: mRNA-seq performed in quadruplicate for lean and obese colon samples with and without oligofructose treatment.

first: Michael

middle: J

last: Zuscik

first: Eric

last: Schott

last: Lillis


title: The DNA methylation landscape of glioblastoma disease progression shows extensive heterogeneity in time and space

city: Vienna

first: Christoph

last: Bock

address: Lazarettgasse 14

country: Austria

institute: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences

type: Genome variation profiling by high throughput sequencing

summary: Glioblastoma is characterized by widespread genetic and transcriptional heterogeneity, yet little is known about the role of the epigenome in glioblastoma disease progression. Here, we present genome-scale maps of DNA methylation in matched primary and recurring glioblastoma tumors, using data from a highly annotated clinical cohort that was selected through a national patient registry. We demonstrate the feasibility of DNA methylation mapping in a large set of routinely collected FFPE samples, and we validate bisulfite sequencing as a multipurpose assay that allowed us to infer a range of different genetic, epigenetic, and transcriptional characteristics of the profiled tumor samples. On the basis of these data, we identified subtle differences between primary and recurring tumors, links between DNA methylation and the tumor microenvironment, and an association of epigenetic tumor heterogeneity with patient survival. In summary, this study establishes an open resource for dissecting DNA methylation heterogeneity in a genetically diverse and heterogeneous cancer, and it demonstrates the feasibility of integrating epigenomics, radiology, and digital pathology for a national cohort, thereby leveraging existing samples and data collected as part of routine clinical practice.

overall_design:
Genome-wide profiling of DNA methylation levels by RRBS in 499 samples, derived from 217 glioblastoma (IDH wildtype) patients (112 progression cohort, 105 validation cohort), 14 IDH muated brain tumor patients, and 5 normal brain controls. For each patient of the progression cohort samples from at least two and up to six tumor resections are available. For 6 patients multiple regions of each tumor were sampled. For 37 samples matched RNA-seq was performed. For 43 samples matched low-coverage whole genome sequencing was performed.
*** Raw data requires controlled access and is deposited at EGAS00001002538 (EGA: https://www.ebi.ac.uk/ega/). Access to raw data can be requested from submitters ***

first: Johanna

last: Klughammer

first: Barbara

last: Kiesel

first: Thomas

last: Roetzer

first: Nikolaus

last: Fortelny

first: Amelie

last: Nemc

first: Paul

last: Datlinger

first: Nadine

last: Peter

first: Karl-Heinz

last: Nenning

first: Julia

last: Furtner

first: Martha

last: Nowosielski

first: Marco

last: Augustin

first: Mario

last: Mischkulnig

last: Ströbel

first: Patrizia

last: Moser

first: Christian

middle: F

last: Freyschlag

first: Johannes

last: Kerschbaumer

first: Claudius

last: Thomé

first: Astrid

middle: E

last: Grams

first: Günther

last: Stockhammer

first: Melitta

last: Kitzwoegerer

first: Stefan

last: Oberndorfer

first: Franz

last: Marhold

first: Serge

last: Weis

last: Trenkler

last: Buchroithner

first: Josef

last: Pichler

last: Haybaeck

first: Stefanie

last: Krassnig

first: Kariem

last: Ali

first: Gord

last: von Campe

last: Payer

first: Camillo

last: Sherif

first: Julius

last: Preiser

last: Hauser

first: Peter

last: Winkler

first: Waltraud

last: Kleindienst

last: Würtz

first: Tanisa

last: Brandner-Kokalj

first: Martin

last: Stultschnig

last: Schweiger

first: Karin

last: Dieckmann

first: Matthias

last: Preusser

first: Georg

last: Langs

first: Bernhard

last: Baumann

first: Engelbert

last: Knosp


title: Novel MYC-driven medulloblastoma models generated by CRISPR activation of endogenous Myc

first: David

last: Finkelstein

address: 332 N. Lauderdale St.

department: Computational Biology

institute: St Jude Children's Research Hospital

summary: Myc-driven Group 3 medulloblastoma (MB) is the most aggressive tumor among the four subgroups classified by transcriptome, genomic landscape and clinical outcomes. So far in all available mouse Group 3 models, the constitutive ectopic Myc expression was under control of LTR element or other exogenous promoters within the vectors, which were randomly inserted into the genome with multiple copies. Here we are deploying nuclease deficient CRISPR/dCas9-based transactivator that is targeted to promoter DNA sequences by specific guide RNA to force the transcriptional activation of endogenous Myc in p53-/-;cdkn2c-/- neurospheres cells. A combination of three sgRNAs together with dCas9-VP64 induced the highest expression of endogenous Myc. When the targeted cells were transplanted to the cortex of recipients, tumors arose fully recapitulate the Group 3 MB in human. This novel mouse model should significantly strengthen our understanding and treatment of the Myc-driven Group 3 medulloblastoma.

overall_design: We used microarrays to compare the  G3 MB Myc driven mouse tumors to GNP cells and other tumors

first: BaoHan

middle: T

last: Vo

first: Jin

last: Kwon

first: Shaela

last: Wright

first: Judith

last: Hyle

first: Beisi

last: Xu

first: Brent

last: Orr

first: Chunliang

last: Li

first: Charles

last: Sherr

first: Martine

last: Roussel


title: Expression profile of microRNAs in serum extracellular vesicles isolated from 6 healthy subjects

status: Public on Jun 16 2018

city: Kamakura

first: Satoshi

last: Kondo

state: Kanagawa

address: 10-1 tebiro 6-chome

country: Japan

institute: Toray Industries,Inc.

summary:
Sera were collected from 6 healthy subjects, and the expression profiles of microRNAs in serum extracellular vesicles were investigated by 3D-gene microarray.
The expression profile was used to investigate the correlation between immune responses to vaccines and microRNA expression levels.

overall_design: 5 ml of sera were collected from 6 healthy subjects. Extracellular vesicles were isolated using TRIZOL (Thermo). Total RNAs were isolated from extracellular vesicles and were subjected to microarray analysis using 3D-gene microarray chip.

first: Hiroyuki

last: Oshiumi

first: Masaaki

last: Okamoto


title: Multiorgan PIXUL-ChIP-seq analysis of genome-wide RNA polymerase II (Pol II)   binding in mouse heart, kidney, liver and lung

city: Seattle

first: Karol

last: Bomsztyk

state: WA

address: 850 Republican Street

department: Medicine

institute: University of Washington

summary: High throughput PIXUL-ChIP-seq genome-wide study allows to map simultaneously Pol II peaks in multiple organs harvested from the same mouse.

overall_design: Hearts, kidneys, livers and lungs harvested from two mice were simultaneously sheared  in a 96-well plate using  PIXUL, high throughput chromatin sonication instrument.  PIXUL-sheared heart, kidney, liver and lung chromatin was then used in  multiplex microplate ChIP platform (Matrix ChIP) to analyze in parallel genome-wide binding of Pol II  in these mouse organs.  Indexed libraries were constructed  from ChIP DNA using Tn5 transposase tagmentation. The eight libraries were pooled and clustered onto a flow cell lane.  Sequencing was performed using an Illumina HiSeq 2500 in Rapid Mode employing a paired-end read, 50-base read length (PE50) sequencing strategy.

first: Daniel

last: Mar


title: Evaluation of functional properties of current and novel protein sources using enteroids

city: Wageningen

first: Soumya

middle: Kanti

last: Kar

state: I am not in the U.S. or Canada

address: De Elst1

department: Animal Science Group

country: Netherlands

institute: WUR

summary:
This study was designed to address key questions concerning the use of alternative protein sources for animal feeds and addresses aspects such as their nutrient composition and impact on gut function. We used casein (CAS), spray dried porcine plasma (SDPP), soybean meal (SBM),  and yellow meal worm (YMW) as protein sources.
We have investigated the use of intestinal organoids as a model to test the effects of different protein sources on the intestinal epithelium. Mouse enteroids were exposed to different undigested protein sources (4% w/v, viz. soybean meal, SBM; casein, CAS; spray dried plasma protein, SDPP; and yellow meal worm, YMW) or DMEM as a control. Microarrays were used to detail the global gene expression.

overall_design: Confluent 2D monolayers generated from mouse 3D enteroids derived of the duodenum were exposed to different undigested protein sources (4% w/v, viz. soybean meal, SBM; casein, CAS; spray dried plasma protein, SDPP; and yellow meal worm, YMW) or DMEM as a control and RNA isolated for genome-wide transcriptomics.

middle: K

first: Mark

last: Boekschoten


title: Gene expression kinetics in Murine Gut wall tissue: Reference (Total RNA Mixture of all samples) vs. Probiotics/Salmonella treated mice

status: Public on Jun 18 2018

city: Bhubaneswar

first: Biswaranjan

last: Pradhan

state: ODISHA

address: Jatni

department: Biological Sciences

country: India

institute: National Institute of Science Education and Research Bhubaneswar

summary: Transcriptional profiling of mouse gut wall tissue following infection with Salmonella or treatment with Probiotics to see the role of probiotics in preventing salmonella infection through gut mucosal route of mouse.

overall_design: Six-condition experiment with kinetics for 3 time points, Untreated mice (NT) vs. treatment with Salmonella(ST)/Lactobacillus acidophilus(LA)/Bacillus clausii(BC)/STLA/STBC. Biological replicates: 1 control (Pooled from 3 replicates), 1 transfected (pooled from 3 replicates).

first: Pradhan

last: Biswaranjan

first: Guha

last: Dipanjan

first: Aich

last: Palok


title: Ogye body map RNA-seq data

first: Jin-Wu

last: Nam

summary: The Yeonsan Ogye (Ogye) is the rare black chicken breed domesticated in Korean peninsula, which has been noted for entire black color upon its appearances including feather, skin, comb, eyes, shank, claws and internal organs. In this study, whole genome, transcriptome and epigenome sequencings of Ogye were performed using high-throughput NGS sequencing platforms. We have produced Illumina short-reads (Paired-End, Mate-Pair and FOSMID) and PacBio long-reads for whole genome sequencing (WGS), 1.4 billion reads for RNA-seq, and 123 million reads for RRBS (reduced representation bisulfite sequencing) data. Using WGS data, Ogye genome has been assembled, and coding/non-coding transcriptome maps were constructed on Ogye genome given largescale sequencing data. We have predicted 17,472 (3,550 newly annotated and 13,922 known) protein-coding transcripts, and 9,443 (6,689 novel and 2,754 known) long non-coding RNAs (lncRNAs).

overall_design:
Total RNAs were extracted from twenty respective tissues using Trizol reagent. The RNA concentration was checked by Quant-IT RiboGreen. To assess the integrity of the total RNA, samples were run on the TapeStation RNA screentape. Only RNA samples with a high quality (RIN≥7.0) were used for RNA-seq library construction. Each library was independently prepared with 300ng of total RNA by Illumina TruSeq Stranded Total RNA Sample Prep Kit. The rRNA in total RNA is depleted by Ribo-Zero kit. After the rRNA is depleted, the remaining RNA is purified, fragmented and primed for cDNA synthesis. The cleaved RNA fragments are copied into first strand cDNA using reverse transcriptase and random hexamers. This is followed by second strand cDNA synthesis using DNA Polymerase I, RNase H and dUTP. These cDNA fragments then go through an end repair process, the addition of a single ‘A’ base, and then ligation of the adapters. The products are then purified and enriched with PCR to create the final cDNA library. The libraries were quantified using qPCR according to the qPCR Quantification Protocol Guide (KAPA Library Quantificatoin kits for Illumina Sequecing platforms) and qualified using the TapeStation D1000 ScreenTape.

The affiliations for each contributor:
HS Hong 1, HH Chai 3,4, KW Nam 1, DJ Lim 3, KT Lee 3, YJ Do 3, CY Cho 5, JW Nam 1,2
1   Department of Life Science, College of Natural Sciences, Hanyang University, Seoul 133791, Republic of Korea; yohae25@gmail.com (H.H.); nkw0228@gmail.com (K.N.); jwnam@hanyang.ac.kr (J.N.)
2   Research Institute for Convergence of Basic Sciences, Hanyang University, Seoul 133791, Republic of Korea; jwnam@hanyang.ac.kr (J.N.)
3   Department of Animal Biotechnology & Environment of National Institute of Animal Science, RDA, Wanju 55365, Republic of Korea; hanha@korea.kr (H.C.); lim.dj@korea.kr (D.L.); leekt@korea.kr (K.L.); clonea@korea.kr (Y.D.);
4   College of Pharmacy, Chonnam National University, Kwangju 61186, Republic of Korea
5   Animal Genetic Resource Research Center of National Institute of Animal Science, RDA, Namwon 55717, Republic of Korea; bloodtype@korea.kr (C.C.);

first: J

middle: W

first: H

middle: S

last: Hong

first: K

first: D

last: Lim

last: Lee

first: Y

last: DO

first: C

middle: Y

last: Cho

middle: H

last: Chai


title: Next Generation Sequencing Analysis of WT and Hectd3–/– BMDMs during F. novicida infection

status: Public on Jun 15 2018

city: Kunm,ing

first: Xiaopeng

last: Qi

address: 32 East Jiaochang Rd

institute: Kunming Institute of Zoology, CAS

summary:
Purpose: The goals of this study are to compare NGS-derived WT and Hectd3–/– transcrip profiling (RNA-seq) in the absence and presence of F. novicida infection
Methods: Bone marrow derived macrophages (BMDMs) from WT and Hectd3–/– mice were infected with F .novicida for 8 and 12 hours.  mRNA profiles  were generated by deep sequencing using Illumina GAIIx.
Results: Using an optimized data analysis workflow, we mapped about 80 million sequence reads per sample (around 95% clean reads were successfully mapped) to the mouse genome and identified 22,589 transcripts in the WT and Hectd3–/– BMDMs with or without F. novicida infection.
Conclusions: Our study represents the first detailed analysis of HECTD3 deficiency regulated gene expression in response to F. novicida infection generated by RNA-seq technology. Our results demonstrated that the type I IFN signaling induced by F. novicida infection was impaired in the absence of HECTD3.

overall_design: mRNA profiles of  WT and Hectd3–/– BMDMs with or without F. novicida infection for 8 and 12 h were generated by deep sequencing,  using Illumina Hiseq platform.

first: Qi

last: Xiaopeng

first: Chen

last: Ceshi


title: Next-generation sequencing facilitates quantitative analysis of DNAM-1+ and DNAM-1- natural killer (NK) cells transcriptomes in mouse MLL-AF9 AML leukemia

status: Public on Jun 14 2018

city: Tianjin

first: Guo Guang

last: Zheng

state: Tianjin

address: Blood Hospital,288 Nanjing Road,Heping District

department: Institute of Hematology & Blood Hospital

institute: Chinese Academy of Medical Science& Peking Union  Medical College

summary: The goals of this study aim to reveal functional and phenotypic diversity of DNAM-1+ and DNAM-1- natural killer (NK) cells in response to the microenvironmental cues in mouse acute myeloid leukemia.

overall_design: Compare transcriptomes of DNAM-1+ and DNAM-1- natural killer (NK) cells in acute myeloid leukemia.

first: Feifei

last: Yang

first: Guo


title: Dynamic bimodal changes in CpG and non-CpG methylation genome-wide upon CGGBP1 loss-of-function

city: Gandhinagar

first: Umashankar

last: Singh

state: Gujarat

address: Acad Block 4 Room 317 IIT Gandhinagar Palaj

department: Biological Sciences and Engineering

institute: IIT Gandhinagar

summary: By depleting CGGBP1 in normal human fibroblasts 1064Sk using lentiviral shmiR (non-targeting or targeting CGGBP1) and by performing genome-wide sequencing (on bisulfite converted genomic DNA from both samples) we show that both gain and loss of cytosine methylation occurs upon CGGBP1 depletion. This gain and loss of methylation is clustered, spatially overlapping at major functional genomic regions and transcends all three cytosine sequence contexts. We demonstrate that CGGBP1 regulates cytosine methylation genome-wide through cis and trans-acting mechanisms. Library preparation for sequencing has been described in PMID 25981527.

overall_design: Control shmiR and CGGBP1 shmiR genomic DNA (both with bisulfite conversion) used for Illumina sequencing experiments.


title: Expression data from childhood obesity

city: Xi’an

first: Yuesheng

last: Liu

state: Shaanxi

address: 157 Xiwu Road

institute: The Second Affiliated Hospital of Xi’an Jiaotong University

type:
Non-coding RNA profiling by array
Expression profiling by array

summary:
In the past few decades, the prevalence of overweight and obesity has sharply increased in children and adolescents. Childhood obesity life are associated with increased risk of cardiovascular disease (CVD), diabetes mellitus, metabolic syndrome, sleep disturbances and certain cancers in adulthood. Childhood obesity has become a serious global public health challenge. Long noncoding RNAs (lncRNAs) have an important role in adipose tissue function and energy metabolism homeostasis, and abnormalities may lead to obesity.
We used microarrays to detail the differential expression profile of lncRNAs and mRNAs in obese children compared with non-obese children.

overall_design: Abdomen subcutaneous adipose tissue of children were selected for RNA extraction and hybridization on Affymetrix microarrays. To obtain the differential expression profile of lncRNAs and mRNAs expression profiles, we selected 4 obese children (sample number 32, 35, 37, 38) and 4 non-obese children (sample number 21, 22, 26, 27).

first: Yanfeng

last: Xiao


title: Gene expression analysis of c-Myc overexpressing human fibroblasts.

status: Public on Jun 13 2018

first: Jae whan

last: Song

address: Yonsei-ro 50

department: Department of Biochemistry

institute: College of Life Science and Biotechnology

summary: Analysis of gene expression change of normal cells, human fore skin fibroblast (HFFs) upon over-expression of c-Myc

overall_design: Total RNA obtained from HFFs with or without c-Myc over-expression and hybridized on Affymetrix microarrays.

first: Aram

last: Ko

first: Su

last: Han

first: Jaewhan


title: Expression data of miRNAs from PBMC of dogs infected with L. infantum

city: Araçatuba

first: Jaqueline

middle: Poleto

last: Bragato

state: SP

address: Clóvis Pestana, 793

department: Department of animal clinic, surgery and reproduction

country: Brazil

institute: Universidade Estadual Paulista Júlio de Mesquita Filho - UNESP

summary: Leishmania (L.) infantum is the etiologic agent of visceral leishmaniasis (VL). In Brazil represents a serious public health problem. Studies have shown that regulation of immune response appears to depend on miRNAs. In canine VL due to cell immune suppression being determinant of disease progression, knowledge of miRNAs may be important for the pattern of change in immune response. Here, we suggest that post-transcriptional regulation, mediated by miRNAs, may play a role in immune response of dogs with VL.

overall_design: Fifteen dogs were used to form two groups for the study: 5 healthy dogs in Control group and 10 dogs naturally Infected with L. infantum in Infected group. Peripheral blood mononuclear cells (PBMC) isolated from total blood using gradient Histopaque 1077 (Sigma-Aldrich, St. Louis, MO, USA). After isolation, total RNA was extracted and 250 ng of total RNA of RIN (RNA integrity number) over than 8 was used to evaluate the miRNA profile using a microarray strip containing 291 canine specific probes. Raw intensity values were background corrected, log2 transformed and then quantile normalized by the software Expression Console (Affymetrix) using the Robust Multi-array Average (RMA) algorithm. Next, statistical analysis was performed in the Transcriptome Analysis Console software (Affymetrix) by ANOVA (fold change ± 2, p <0.05).

first: Larissa

middle: M

last: Melo

first: Gabriela

middle: L

last: Venturin

last: Rebech

first: Leandro

last: Garcia

first: Flavia

last: Lopes

first: Valéria

last: Lima


title: Capturing the onset of PRC2-mediated repressive domain formation

first: Danny

last: Reinberg

address: 522 First Avenue

institute: NYU School of Medicine

summary:
Our study defines nucleation and spreading regions for Polycomb repressive complex 2 (PRC2), demonstrating the principle of PRC2 domain formation in mammals. We elucidate the role of genome architecture in formation of these domains and identify JARID2 and MTF2 as being crucial for full recruitment of PRC2 to chromatin.

This SuperSeries is composed of the SubSeries listed below.

overall_design: Refer to individual Series


title: Single-cell RNA sequencing of Drosophila melanogaster optic lobe cells

city: Paris

first: NIKOLAOS

last: KONSTANTINIDES

address: 15 rue Helene Brion

country: France

institute: Institut Jacques Monod

summary: Transcription factors regulate the molecular, morphological, and physiological characters of neurons and generate their impressive cell type diversity. To gain insight into general principles that govern how transcription factors regulate cell type diversity, we used large-scale single-cell mRNA sequencing to characterize the extensive cellular diversity in the Drosophila optic lobes. We sequenced 57,000 single optic lobe neurons and glia and assigned them to 52 clusters of transcriptionally distinct single cells. We validated the clustering and annotated many of the clusters using RNA sequencing of characterized FACS-sorted single cell types, as well as marker genes specific to given clusters. To identify transcription factors responsible for inducing specific terminal differentiation features, we used machine-learning to generate a ‘random forest’ model. The predictive power of the model was confirmed by showing that two transcription factors expressed specifically in cholinergic (apterous) and glutamatergic (traffic-jam) neurons are necessary for the expression of ChAT and VGlut in many, but not all, cholinergic or glutamatergic neurons, respectively. Therefore, the same terminal characters can be regulated by different transcription factors in different cell types, arguing for extensive phenotypic convergence. Our data provide a deep understanding of the developmental and functional specification of a complex brain structure.

overall_design: We sequenced 120,000 single cells using Dropseq. Of these, ~55,000 were used for downstream analyses.

first: Nikos

last: Konstantinides

first: Katarina

last: Kapuralin

first: Claude

last: Desplan


title: Integrated transcriptomics network analysis of miRNA and mRNA in human myometrium in term and preterm labor.

city: Columbus

first: William

middle: Edward

last: Ackerman IV

state: Ohio

address: N521 Doan Hall, 410 West 10th Avenue

department: Obstetrics and Gynecology

institute: The Ohio State University

type: Non-coding RNA profiling by high throughput sequencing

summary: Myometrial biopsies were collected from 20 women undergoing primary cesarean sections in well-characterized clinical scenarios: 1) term labor of spontaneous onset (TL, n=5); 2) term non-labor (TNL, n=5); 3) spontaneous PTB in the setting of chorioamnionitis (PTB-HCA) and 4) indicated preterm birth (PTB) non-labor (PTB-NL, n=5).  RNAs were profiled using 2nd-generation RNA sequencing.

overall_design:
We applied integrated RNA-sequencing of long RNAs and miRNAs along with various computational algorithms to uncover novel molecular signals that could be responsible for the transition of the human myometrium from a quiescent to the contractile laboring state
Raw data for this series are not available because consent forms do not allow for public access to raw data.

last: Ackerman

first: Irina

last: Buhimschi

first: Catalin


title: Genome-wide H3K4me3 and H3K27me3 in HL-60 cells.

city: shanghai

first: wang

last: yujie

state: Shanghai

address: Chi Feng road No:65

institute: Shanghai JiaYin Biological technology co., LTD

summary: To characterize genome-wide H3K4me3 and H3K27me3 chromatin-state of HL-60 cells.

overall_design: Examination of H3K4me3 and H3K27me3 in parental and JMJD3 knockout HL-60 cells.

first: Shan-he

last: Yu

first: Jiang

last: Zhu


title: Genome-wide C/ebpβ and Jmjd3 traget genes in 32D cells.

summary: To characterize genome-wide  C/ebpβ and Jmjd3 traget genes in 32D cells by ChIP-seq.

overall_design: Examination of C/ebpβ and Jmjd3 traget genes in 32D cells


title: Integration of genomic driver events and gene expression profiles in cutaneous squamous cell carcinoma

city: London

first: Ai

last: Nagano

state: --- Select a state ---

address: John Vane Science Centre, Charterhouse Square

department: Centre for Molecular Oncology

country: United Kingdom

institute: Barts Cancer Institute

summary: Analysis of cutaneous squamous cell carcinoma cell lines at genomic and transciptomic level. The molecular landscape of patient derived cell lines reflects that of primary tumours.

overall_design: The cell lines were derived from cutateous squamous cell carcinoma and normal human keratinocyte. The gene experssion profile was bioinformatically analysed.

first: Gareth

last: Inman

first: Jun

last: Wang


title: Investigation of potential tumour suppressor or tumour promoter roles in cutaneous squamous cell carcinoma progression

summary: Analysis of the combined dataset of normal skin, actinic keratosis and cutaneous squamous cell carcinoma (cSCC) previously submitted in (GSE45216) at genomic/transciptomic level. We identified potential cSCC driver genes significantly mutated and upregulated in cSCC relative to normal skin.

overall_design: RNA was extracted by laser capture microdissection from actinic keratosis (AK), normal Sun exposed skin (SE) and normal non-Sun exposed skin (NSE), for analysis using the Affymetrix HG U133 Plus 2.0 microarrays.


title: Genome-wide C/EBPβ traget genes in C/EBPβ-overexpressed HL-60 cells.

summary: To characterize genome-wide C/EBPβ traget genes in C/EBPβ-overexpressed HL-60 cells by ChIP-seq.

overall_design: Examination of C/EBPβ traget genes in C/EBPβ-overexpressed HL-60 cells.


title: Arabidopsis NAP-related proteins (NRPs) contribute to the coordination of plant growth, developmental rate, and age-related pathogen resistance under short days

first: Balazs

last: Balint

state: Csongrad

address: Vallalkozok street

country: Hungary

institute: Seqomics Ltd

summary: Plant nucleosome assembly protein-related proteins (NRPs) are histone chaperons involved in nucleosome turnover. Despite this basic cellular function, the Arabidopsis nrp1-1 nrp2-1 knock out mutant has been reported to exhibit only relatively mild seedling root phenotypes and to significantly affect the expression of only few hundred genes (Zhu et al., 2006). Here we report that NRP loss-of-function as well as the ectopic overexpression of At NRP1 significantly affected the growth, development, and the pathogen response of Arabidopsis plants under short day conditions. The nrp1-1 nrp2-1 mutant grew faster and flowered weeks earlier than the wild type and the overexpressor. The latter developed slower and flowered at a lower number of leaves than the mutant and the wild type. Moreover, the mutant was more sensitive, the overexpressor was more tolerant to pathogen infection correlating with their more adult and juvenile character, respectively. Transcriptomic comparison of mature non-bolting plants agreed with the phenotypes. The presented and published data indicate that although NRPs might not be absolutely required for plant growth and development, they contribute to the epigenetic coordination of metabolic, growth, defence and developmental processes during adaptation.

overall_design: Three groups of Arabidopsis thaliana samples (nrp1-1 nrp2-1 double mutant, wild-type, NRP1 overexpressor), each containing two biological replicates were included in the study

first: Balázs

last: Barna

first: Katalin

last: Gémes

first: Mónika

last: Domoki

first: Dóra

last: Bernula

first: Györgyi

last: Ferenc

last: Bálint

first: István

last: Nagy

first: Attila

last: Fehér


title: mRNA profiling of soybean seed regions and tissues at five developmental stages

city: Davis

first: John

last: Harada

address: One Shields Avenue

department: Plant Biology

institute: University of California

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


title: Cellular stress alters 3’UTR landscape through alternative polyadenylation and isoform-specific degradation

city: Newark

first: Bin

last: Tian

state: NJ

address: 205 South Orange Ave.

department: Department of Microbiology, Biochemistry and Molecular Genetics

institute: Rutgers New Jersey Medical School

summary: Most eukaryotic genes express alternative polyadenylation (APA) isoforms with different lengths of 3’ untranslated region (3’UTR). Here we show arsenic stress elicits global shortening of 3’UTRs through two mechanisms. First, stress leads to immediate shortening of 3’UTR due to preferential usage of proximal cleavage and polyadenylation sites (PASs), as revealed by 3’ end sequencing of newly made RNAs that are metabolically labeled with 4-thiouridine. Second, long 3’UTR isoforms are more rapidly degraded during recovery from stress as compared to short 3’UTR isoforms, further shortening 3’UTR lengths in the cell. Using ribonucleoprotein immunoprecipitation coupled with 3’ end sequencing (3’READS+RIP), we show that the RNA-binding protein T cell-restricted intracellular antigen-1 (Tia1) preferentially interacts with long 3’UTR isoforms via U-rich elements in alternative 3’UTR sequences, and the interaction correlates with stress granule (SG) association during stress and with mRNA decay during recovery from stress, indicating SG-mediated RNA clearance mechanism post stress. Importantly, genes whose 3’UTRs are shortened by APA during stress can evade stress-induced 3’UTR size-based mRNA degradation, leading to higher transcript abundance post stress. Moreover, proliferating and differentiated cells display different extents of 3’UTR shortening after stress, indicating cell type-specific of impact of stress on the 3’UTR landscape. Together, our data indicate that 3’UTR length plays important roles in gene expression in stressed cells, and APA functions as an adaptive stress response mechanism to preserve mRNAs.

overall_design: 4 RNA-seq libraries from NIH3T3 cells for gene expression analysis;  4 3'READS libraries for analysis of APA using total RNA from NIH3T3 cells treated with sodium arsenite for 1h; 6 3'READS libraries for analysis of APA time course using total RNA from NIH3T3 cells treated with sodium arsenite for 1h and recovered for different amount of time;  8 3'READS libraries for analysis of APA isoform stability using 4sU metabolic labeling in NIH3T3 cells; 8 3'READS libraries for analysis of stress response of proliferating and differented C2C12 cells using cytoplasmic RNA; 4 3'READS libraries for the analysis of APA during C2C12 cell differentiation.

first: Dinghai

last: Zheng

first: Ruijia

first: Tianying

first: Bingning

last: Xie

first: Qingbao

last: Ding

first: Zhaohua

last: Zhong


title: Chemotherapy and terminal skeletal muscle differentiation in WT1 mutant Wilms tumors

status: Public on Jun 17 2018

city: Duesseldorf

first: Brigitte

last: Royer-Pokora

address: Universitätsstr. 1

country: Germany

institute: Institute of Human Genetics and Anthropology, Heinrich-Heine-University Duesseldorf

summary: Gene expression profiling of six chemotherapy and two untreated WT1 mutant tumors; see also GSE63616

overall_design: Array expression experiment of direct Wilms tumor

first: Manfred

last: Beier

first: Artur

last: Brandt

first: Constanze

last: Duhme

first: Maike

last: Busch

first: Carmen

last: Torres

first: Jaume

last: Mora

first: Hans-Dieter

last: Royer


title: Activity-Induced Regulation of Synaptic Strength through the Chromatin Reader L3mbtl1

status: Public on Jun 12 2018

city: Worcester

first: Kensuke

last: Futai

address: 364 Plantation St

department: Neurobiology

institute: University of Massachusetts Medical School

summary: Homeostatic synaptic downscaling reduces neuronal excitability by modulating the number of postsynaptic receptors. Histone modifications and the subsequent chromatin remodeling play critical roles in activity-dependent gene expression. Histone modification codes are recognized by chromatin readers that affect gene expression by altering chromatin structure. We show that L3mbtl1 (lethal 3 malignant brain tumor-like 1), a polycomb chromatin reader, is downregulated by neuronal activity and is essential for synaptic response and downscaling. Genome-scale mapping of L3mbtl1 occupancies identified Ctnnb1 as a key gene downstream of L3mbtl1. Importantly, the occupancy of L3mbtl1 on the Ctnnb1 gene was regulated by neuronal activity. L3mbtl1 knockout neurons exhibited reduced Ctnnb1 expression. Partial knockdown of Ctnnb1 in wild-type neurons reduced excitatory synaptic transmission and abolished homeostatic downscaling, and transfecting Ctnnb1 in L3mbtl1 knockout neurons enhanced synaptic transmission and restored homeostatic downscaling. These results highlight a role for L3mbtl1 in regulating homeostasis of synaptic efficacy.

overall_design: RNA-seq from four biological replicates of picrotoxin-treated or control primary cultures from wildtype mouse hippocampus; ChIP-seq using antibody against endogenous L3mbtl1 protein from three biological replicates of hippocampal tissue from postnatal day 7 wildtype or L3mbtl1-/- mice.

first: Wenjie

last: Mao

first: Anna

middle: C

last: Salzberg

first: Motokazu

last: Uchigashima

first: Yuto

last: Hasegawa

first: Hanno

last: Hock

first: Masahiko

last: Watanabe

first: Schahram

last: Akbarian

first: Yuka Imamura

last: Kawasawa


title: Sequencing-based analyses characterize a tumor suppressive role of mir-1271 repressed by DNA hypermethylation in gastric cancer

city: Daejeon

first: Jong Hwan

last: Kim

address: 125 Gwahak-ro, Yuseong-gu

department: Genome structure research center

institute: Korea Research Institute of Bioscience and Biotechnology

summary: To identify tumor suppressive microRNAs repressed by DNA hypermethylation in gastric cancer (GC), we analyzed methylome and miRNome of EpCAM+/CD44+ GC cells. Among a set of microRNAs hypermethylated and downregulated in GC, mir-1271 was uncovered as a microRNA repressed by DNA hypermethylation in GC. Forced expression of mir-1271 significantly suppressed growth, migration, and invasion of GC cells both in vitro and in vivo. To identify target genes and cancer signaling pathways regulated by mir-1271, we examined differentially-expressed genes responsive to mir-1271 by performing RNA-sequencing.

overall_design: 2 paired normal and GC cancer cells miRNA-seq, 3 GC cell lines MBD-seq, miR-1271 mimic treated GC cells and control cells RNA-seq

first: Byungho

last: Lim

first: Su-Jin

last: Baek

first: Jong-Hwan

first: Seon-Young

first: Yong

first: Mirang


title: Novel MYC-driven medulloblastoma models generated by CRISPR activation of endogenous Myc

city: Memphis

first: Beisi

last: Xu

state: Tennessee

address: 262 Danny Thomas Pl

department: Center for Applied Bioinformatics

institute: St Jude Children's Research Hosipital

summary: Myc-driven Group 3 (G3) medulloblastoma (MB) is the most aggressive tumor among the four subgroups classified by transcriptome, genomic landscape and clinical outcomes.  Several successful mouse models have been developed to recapitulate G3 MB tumor development; however, all models currently used facilitate tumorigenesis by constitutive ectopic expression of exogenously regulated Myc randomly integrated in multiple events into the genome.  To overcome limitations of ectopically expressed Myc models, we used nuclease deficient CRISPR/dCas9-based transactivators in combination with specific single guide RNA (sgRNA) to force the transcriptional activation of endogenous Myc in Trp53-null neurosphere cells followed by orthotopic transplantations. Combination of three sgRNAs with dCas9-VP64 induced endogenous Myc expression and formed large cell anaplastic MBs which recapitulated the molecular characteristics of other mouse G3 MBs. This novel model more closely mimics human Myc-driven G3 MB disease development, and will be a valuable tool for future pre-clinical and therapeutic studies.

overall_design: Examination of off-target effect by dCas9 binding sites using ChIPSEQ for 3 different guide RNA(gRNA), gRNA M5 have two replicates

first: BaoHan

last: Vo

first: Jin

middle: A

last: Kwon

first: Shaela

last: Wright

first: Judith

last: Hyle

first: David

last: Finkelstein

first: Brent

last: Orr

first: Charles

last: Sherr

first: Chunliang

last: Li

first: Martine

last: Roussel


title: JMJD3 facilitates C/EBPβ-centered transcriptional program to exert oncorepressor activity in AML

first: wang

last: yujie

summary:
JMJD3, a stress-inducible H3K27 demethylase, plays a critical regulatory role in the initiation and progression of malignant hematopoiesis. However, how this histone modifier effects in a cell type-dependent manner remains unclear. Here, we show that in contrast to its oncogenic effect in preleukemia state and lymphoid malignancies, JMJD3 relieves the differentiation-arrest of certain subtypes (such as M2 and M3) of acute myeloid leukemia (AML) cells. RNA-sequencing and ChIP-PCR analyses revealed that JMJD3 exerts anti-AML effect by directly modulating H3K4 and H3K27 methylation levels to activate the expression of a number of key myelopoietic regulatory genes. Mechanistic exploration identified a physical and functional association of JMJD3 with C/EBPβ that presides the regulatory network of JMJD3. Thus, the leukemia regulatory role of JMJD3 varies in a disease phase- and lineage-dependent manner, and acts as a potential oncorepressor in certain subsets of AML largely by coupling to C/EBPβ-centered myelopoietic program.

This SuperSeries is composed of the SubSeries listed below.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus


title: Transcriptional repression by FACT is linked to regulation of chromatin accessibility at the promoter of ES cells

city: Cologne

first: Peter

last: Tessarz

state: Nordrhein-Westfalen

address: Joseph-Stelzman-Str 9b

institute: Max Planck Institute

summary: The conserved and essential histone chaperone FACT (Facilitates Chromatin Transcription) reorganizes nucleosomes during DNA transcription, replication and repair and ensures both, efficient elongation of RNA Pol II and nucleosome integrity. In mammalian cells, FACT is a heterodimer, consisting of SSRP1 and SUPT16. Here, we show that in contrast to yeast, FACT accumulates at the transcription start site of genes reminiscent of RNA Polymerase II profile. Depletion of FACT in mouse embryonic stem cells leads to de-regulation of developmental and pro-proliferative genes concomitant with hyper-proliferation of mES cells. Using MNase-, ATAC-, and Nascent Elongating Transcript Sequencing (NET-seq) we show that up-regulation of genes coincides with loss of nucleosomes upstream of the TSS and concomitant increase in antisense transcription, indicating that FACT impacts the promoter architecture to regulate expression of these genes. Finally, we demonstrate a role for FACT in cell fate determination and show that FACT depletion primes ES cells for the neuronal lineage.

overall_design: ChIP-seq for FACT and RNA-seq, MNase-seq, ATAC-seq, and NET-seq profiles following knock-down of FACT were generated

first: Constantine

last: Mylonas


title: APP levels mediate beta-amyloid but not tau-related aspects of Alzheimer’s disease in a Down syndrome model of cortical neurogenesis.

city: St. Lucia

first: Othmar

last: Korn

state: Queensland

address: University of Queensland

country: Australia

institute: Australian Institute for Bioengineering and Nanotechnology

summary: Early-onset Alzheimer’s disease-like pathology in Down syndrome (DS, trisomy 21) is commonly attributed to an increased dosage of the amyloid precursor protein (APP) gene.  To test this central tenet of the amyloid-cascade hypothesis we deleted the supernumerary copy of the APP gene in trisomic DS iPSC, or upregulated APP expression in euploid human pluripotent stem cell lines with dCas9-VP64, and subjected these lines to prolonged cortical neural differentiation. Our data reveal that increased APP gene dosage and expression is necessary and sufficient for increased beta-amyloid production and pyroglutamate(E3)-containing plaque deposition, but is neither sufficient nor required for tau hyperphosphorylation, neurofibrillary tangle formation, or increased oxidative stress-induced apoptosis in neurons. Transcriptome comparisons of the isogenic neurons demonstrates that the supernumerary APP gene copy has profound temporally-modulated genome-wide effects on gene expression during differentiation and maturation of DS neuronal cultures that link APP function to regulation of genes involved in neuronal synaptic function and outgrowth of neuronal processes. Collectively, our data reveal that APP plays an important role in the amyloidogenic aspects of Alzheimer’s disease, but challenge the hypothesis that increased APP levels are solely responsible for hyperphosphorylation of tau or enhanced oxidative stress-induced neuronal cell death in Down syndrome associated AD-pathogenesis.

overall_design: 34 samples

first: Dmitry

last: Ovchinnikov

first: Isaac

last: Virshup

first: Christine

last: Wells

first: Ernst

last: Wolvetang


title: The genomic landscape of cutaneous squamous cell carcinoma

first: Ai

last: Nagano


title: Enhancer profiling in metastatic cancer

city: Helsinki

first: Sakari

last: Vanharanta

address: Haartmaninkatu 8

department: Translational Cancer Medicine Program

country: Finland

institute: University of Helsinki


title: Characterization of regulators of G protein signaling, rgsD and rax1 of Aspergillus fumigatus

first: Kwang-Soo

last: Shin

department: Life Science

institute: Daejeon University

summary: RgsD functioned in asexual development and melanin synthesis. Rax1 involved in the protection against oxidative stresses.

overall_design: Examination the transcriptomes of the rgsD and rax1 deletion mutants compared with wild type.

first: Yong

last: Kim

first: Jae-Hyuk

last: Yu


title: SMAD3 and SOX4 binding profiling in human breast cell lines

status: Public on Jun 11 2018

city: Utrecht

first: Ana

last: Lourenço

address: Uppsalalaan 8

institute: UMC Utrecht

summary: In order to identify genes co-bound by SOX4 and SMAD3 in the context of breast cancer, different breast cell lines (HMLEs, MDA-MB-231 or HCC-1954) were used. Due to low endogenous expression levels for SOX4 in HMLEs in untreated conditions, doxycycline-dependent SOX4 overexpression was obtained by transducing HMLE cells with pIINDUCER21-SOX4 vector..Cells were plated and SOX4 and SMAD3 chromatine-immunoprecipitation was performed in untreated conditions, TGF-beta (2.5ng/ml), doxycycline (0.5ug/ml) or both as indicated. Genome-wide binding sites for SOX4 and SMAD3 was identified in HMLEs, MAD-MB-231 and HCC-1954 cells.

overall_design: SOX4 and SMAD3 ChIP-sequencing of different human mammary cells in the presence and absence of TGF-β

first: S

last: Vervoort

first: A

middle: R

first: P

last: Coffer


title: The interplay between SOX4 and SMAD3 in the context of breast cancer

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

The experiments are described in 2 papers:
PMID 30137431 and PMID 30507376

overall_design: Refer to individual Series


title: Methylome Changes During the Progression of Colitis-accelerated Colon Cancer in Mouse and the Blockage by Curcumin

city: Piscataway

first: Renyi

last: Wu

address: 160 Frelinghuysen road

department: Pharmacy School

institute: Rutgers University

summary: Inflammation is highly associated with colon carcinogenesis. Epigenetic mechanisms play an important role in the initiation and progression of colon cancer. Curcumin is a dietary cancer preventive phytochemical with promising effect in suppressing colitis-associated colon cancer (CAC) in azoxymethane (AOM) and dextran sulfate sodium (DSS) mouse model. In the present study, we confirmed the effect of curcumin in suppressing colon cancer. Using Agilent SureSelect Methyl-seq and RNA-seq, we obtained single-base methylation profile and transcriptome analyses of epithelial cells from control group, AOM and DSS induced group (AOM+DSS), and AOM and DSS induced plus curcumin treated group (AOM+DSS+Curcumin) in a 18 weeks long-term colon cancer mouse model. The average DNA methylation levels of the three groups are significantly different also. Based on differential methylation patterns of three groups, several pathways of genes were identified including IL-8 signaling, LPS-stimulated MAPK signaling and colorectal cancer metastasis signaling. Among these methylated pathways and genes, Tnf, an inflammatory gene stood out with decreased DNA CpG methylation in the AOM-DSS as compared to the control group and interestingly curcumin reversed the CpG methylation (validated by pyrosequencing). The functional role of DNA methylation of Tnf was confirmed by in vitro luciferase transcriptional activity assay. In addition, we found that a group of genes associated with the inflammatory responses and their methylation level was decreased in AOM+DSS group but restored in the curcumin treated group. Taken together, in this study, aberrant DNA CpG methylation of the inflammatory response was found in colitis-associated colon cancer and curcumin restored their CpG methlyation, which could potentially explain the inflammatory and cancer protective effects of curcumin. (Note this GEO/dataset is the DNA methyl-seq part of the study.)

overall_design: DNA methylation profiles of colon epithelial cells from 18 weeks old C57BL6 mice of 3 groups (1, Contro; 2, AOM and DSS induced; 3, AOM and DSS induced,and curcumin treated.

first: Yue

last: Guo

first: John

last: Gaspar

first: Davit

last: Sargsyan

first: Zheng-Yuan

last: Su

first: Chengyue

last: Zhang

first: Linbo

last: Gao

first: Wenji

last: Li

first: Chao

last: Wang

first: Ran

last: Yin

first: Mingzhu

last: Fang

first: Ronald

middle: P

last: Hart

first: Michael

last: Verzi

first: Ah-Ng

last: Kong


title: Transcriptome Changes During the Progression of Colitis-accelerated Colon Cancer in Mouse and the Blockage by Curcumin

summary: Inflammation is highly associated with colon carcinogenesis. Epigenetic mechanisms play an important role in the initiation and progression of colon cancer. Curcumin is a dietary cancer preventive phytochemical with promising effect in suppressing colitis-associated colon cancer (CAC) in azoxymethane (AOM) and dextran sulfate sodium (DSS) mouse model. In the present study, we confirmed the effect of curcumin in suppressing colon cancer. Using Agilent SureSelect Methyl-seq and RNA-seq, we obtained single-base methylation profile and transcriptome analyses of epithelial cells from control group, AOM and DSS induced group (AOM+DSS), and AOM and DSS induced plus curcumin treated group (AOM+DSS+Curcumin) in a 18 weeks long-term colon cancer mouse model. We observed differentially expressed genes in pair-wise comparison and identified several pathways of small set of genes involved in the potential preventive effect of curcumin. These pathways include LPS/IL-1 mediated inhibition of RXR function, NRF2-mediated oxidative stress response, aldosterone signaling in epithelial cells, production of NO and ROS in macrophages, and IL-6 signaling. The average DNA methylation levels of the three groups are significantly different also. Based on differential methylation patterns of three groups, several pathways of genes were identified including IL-8 signaling, LPS-stimulated MAPK signaling and colorectal cancer metastasis signaling. Among these methylated pathways and genes, Tnf, an inflammatory gene stood out with decreased DNA CpG methylation in the AOM-DSS as compared to the control group and interestingly curcumin reversed the CpG methylation (validated by pyrosequencing).  These observations correlated with decreased, and increased with curcumin, Tnf expression in RNA-seq (validated by qPCR), respectively. The functional role of DNA methylation of Tnf was confirmed by in vitro luciferase transcriptional activity assay. In addition, we found that a group of genes associated with the inflammatory responses and their methylation level was decreased in AOM+DSS group but restored in the curcumin treated group. Taken together, in this study, aberrant DNA CpG methylation of the inflammatory response was found in colitis-associated colon cancer and curcumin restored their CpG methlyation, which could potentially explain the inflammatory and cancer protective effects of curcumin. (Note this GEO/dataset is the RNA-seq part of the study.)

overall_design: mRNA profiles of colon epithelial cells from 18 weeks old C57BL6 mice of 3 groups (1, Contro; 2, AOM and DSS induced; 3, AOM and DSS induced,and curcumin treated.


title: Gene expression changes in white adipose tissue from Ing1- and Gadd45a- single- or double-knockout mice

city: Mainz

first: Emil

last: Karaulanov

address: Ackermannweg 4

institute: Institute of Molecular Biology

summary: ING1b and GADD45a are nuclear proteins involved in the regulation of cell growth, apoptosis and DNA repair. We previously found that ING1b is essential to target GADD45a-mediated active DNA-demethylation via TET1 to specific loci. Hence, GADD45a and ING1 play a crucial role in epigenetic gene regulation. In order to study the physiological role of ING1-GADD45a on gene expression regulation, we compared the expression profiles of white adipose tissue (WAT) from wildtype, Ing1-/-, Gadd45-/- and double-knockout (DKO) mice.

overall_design: WAT gene expression profiling in all 4 genotypes with triplicates consisting of pooled RNA from 3 male mice each.

first: Andrea

last: Schäfer

first: Bernadette

last: Mekker

first: Medhavi

last: Mallick

first: Viviana

last: Vastolo

first: Dominik

last: Sebastian

first: Carina

last: von der Lippen

first: Bernd

last: Epe

first: Damien

middle: J

last: Downes

first: Carola

last: Scholz

first: Christof

last: Niehrs


title: NG Capture-C analysis of GADD45a-bound adipogenic super-enhancers

summary: ING1b and GADD45a are nuclear proteins involved in the regulation of cell growth, apoptosis and DNA repair. We previously found that ING1b is essential to target GADD45a-mediated active DNA-demethylation via TET1 to specific loci. In order to study the physical interaction of distant GADD45a and ING1 bound regions, we performed multiplexed NG Capture-C chromatin conformation capture assay in wildtype and knockout mouse embryonic fibroblasts.

overall_design: NG Capture-C analysis of multiple GADD45a-bound adipogenic super-enhancers in wildtype, Gadd45a knockout, Ing1 knockout and Gadd45a/Ing1 double-knockout (DKO) mouse embryonic fibroblasts.


title: Gene expression changes in Ing1- and Gadd45a- single- or double-knockout mouse embryonic fibroblasts during adipogenesis

summary: ING1b and GADD45a are nuclear proteins involved in the regulation of cell growth, apoptosis and DNA repair. We previously found that ING1b is required to target GADD45a-mediated active DNA-demethylation via TET1 to specific loci. In order to study the  impact of ING1-GADD45a on MEF-to-adipocyte differentiation, we compared the gene expression profile of wildtype mouse embryonic fibroblasts (MEFs) with Ing1- and Gadd45a- single- or double-knockout (DKO) MEFs at day 6 of adipogenic differentiation via RNA-sequencing.

overall_design: Gene expression profiling in all 4 genotypes in triplicates after 6 days of MEF-to-adipocyte differentiation.


title: ING1 ChIP-Seq in mouse embryonic fibroblasts

summary: ING1b is a nuclear protein involved in the regulation of cell growth, apoptosis and DNA repair. Importantly, we previously found that ING1 is implicated in epigenetic gene regulation and required for targeting GADD45a-mediated active DNA demethylation via TET1. In this study, we identified  ING1 bound genomic regions in mouse embryonic fibroblasts (MEFs) via ChIP-Sequencing.

overall_design: ChIP-Seq of ectopic HA-tagged ING1 in wildtype MEFs in duplicates


title: Transcriptome and Methylome Changes During the Progression of Colitis-accelerated Colon Cancer in Mouse and the Blockage by Curcumin

first: Renyi

last: Wu

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


title: Effect of Pre- and Postnatal Exposure to urban PM2.5 on the Transcriptome of the Developing and Early-Life Mouse Lung

status: Public on Jun 08 2018

city: Großhansdorf

first: Espen

middle: E

last: Groth

address: Wöhrendamm 80

department: Department of Pulmonology

institute: LungenClinic Grosshansdorf

summary: Over the last years, evidence has grown that exposure to air pollution, in addition to impairing lung function and health in individuals of all age, can be linked to negative effects in newborn when present during pregnancy. Data suggests that intrauterine exposure of fetuses (exposure of the mother to air pollution during pregnancy) in fact exerts a negative impact on lung development. However, the means by which exposure during pregnancy affects lung development, have not been studied in depth yet. In this study, we investigated alterations of the transcriptome of the developing lung in a mouse model of gestational and early-life postnatal exposure to urban PM2.5 (from Sao Paulo, Brazil).

overall_design: Pregnant BALB/c mouse dams were randomly assigned to two study groups: one group exposed to a PM2.5 dose equivalent to 600µg/m3 for 1h daily (exposed group), the other group kept in filtered air during the whole study period (control group). Exposure to PM2.5 was started on embryonic day 5.5 (E5.5, time of placental implantation), dams from both groups were sacrificed and fetus lungs submitted to transcriptomic analysis at E14.5 (pseudoglandular stage of lung development, n=4 per group) and E18.5 (saccular stage, n=4 per group). The offspring of mice that carried out the whole pregnancy was furthermore exposed (and kept in filtered air, repectively) after birth until being sacrificed on the 40th day of life (P40, state of finished lung alveolarization, n=5 per group). This study included no cross-over, i.e. the offspring of PM2.5-expsosed dams was exposed until P40 alike and vice-versa.

first: Tatiane

last: Furuya

first: Thais

last: de Barros Mendes Lopes

first: Roger

last: Chammas

last: Mauad


title: Whole genome bisulfite sequencing of Ing1/Gadd45a double knockout and wildtype mouse embryonic fibroblasts

last: Karaulanov

summary: ING1b and GADD45a are nuclear proteins involved in the regulation of cell growth, apoptosis and DNA repair. We previously found that ING1b is essential to target GADD45a-mediated active DNA-demethylation via TET1 to specific loci. In order to study the physiological impact of ING1-GADD45a on DNA methylation in base-resolution genome-wide, we compared the methylation levels of wildtype mouse embryonic fibroblasts (MEFs) with Ing1/Gadd45a double-knockout MEFs via whole genome bisulfite sequencing.

overall_design: The DNA methylation level of Ing1/Gadd45a double knockout (DKO) MEFs was analysed in comparison to wild-type (WT) MEFs via whole genome bisulfite sequencing (WGBS).


title: GADD45a ChIP-Seq in mouse embryonic fibroblasts

summary: GADD45a is a nuclear protein involved in the regulation of cell growth, apoptosis and DNA repair. We previously found that GADD45a physically and functionally interacts with TET1 to mediate active DNA demethylation and is recruited by ING1 to its target sites. In this study, we identified GADD45a bound genomic loci in mouse embryonic fibroblasts (MEFs)  via ChIP-Sequencing.

overall_design: ChIP-Seq of ectopic HA-tagged GADD45a in wildtype MEFs in duplicates

last: Schäfer


title: Enhancer profiling in metastatic cancer [ChIP-Seq]

first: Sakari

last: Vanharanta

summary: Metastases cause the majority of cancer-related deaths. Yet, the origins of metastatic cancer phenotypes remain poorly understood. Few metastasis-specific driver mutations have been identified [1-3], raising the possibility that metastatic transcriptional programmes may emerge from perturbations in the oncogenic signalling cascades that support the development of primary tumours. Here, using genome-wide histone modification profiling, high-throughput chromatin conformation capture by Hi-C and functional analysis in human-derived metastasis models of renal and breast cancers, we identify transcriptional enhancers that drive metastatic cancer progression. We demonstrate that specific enhancers and enhancer clusters are activated in metastatic cancer cell populations. The activation status of these enhancers is associated with gene expression patterns predictive of poor patient outcome in clinical samples. CRISPRi-mediated inhibition of enhancer activity and genetic ablation of enhancer sequences demonstrated the requirement of metastasis-associated regulatory elements for metastatic colonization in vivo. We further show that metastatic cancer clones co-opt evolutionarily conserved enhancers that converge on shared metastasis driver genes, such as CXCR4. Thus, we provide functional evidence for the requirement of specific enhancers for metastatic colonization and show that metastatic traits can arise through tissue-specific commissioning of distal gene regulatory elements.

overall_design: Examination of 2 different histone modifications and transcription factors in experimental model systems of metastasis.

first: Paulo

last: Rodrigues


title: Enhancer profiling in metastatic cancer [HiC-seq]

overall_design: Examination of chromatin conformation by HiC in experimental model systems of metastasis.

first: Louise

last: Harewood

first: Ioana

last: Olan

first: Shamith

last: Samarajiwa


title: Impaired DNA demethylation of C/EBP sites causes premature aging

first: Emil

summary:
Changes in DNA methylation are among the best-documented epigenetic alterations accompanying organismal aging. However, whether and how altered DNA methylation is causally involved in aging have remained elusive. GADD45α (growth arrest and DNA damage protein 45A) and ING1 (inhibitor of growth family member 1) are adapter proteins for site-specific demethylation by TET (ten-eleven translocation) methylcytosine dioxygenases. Here we show that Gadd45a/Ing1 double-knockout mice display segmental progeria and phenocopy impaired energy homeostasis and lipodystrophy characteristic of Cebp (CCAAT/enhancer-binding protein) mutants. Correspondingly, GADD45α occupies C/EBPβ/δ-dependent superenhancers and, cooperatively with ING1, promotes local DNA demethylation via long-range chromatin loops to permit C/EBPβ recruitment. The results indicate that enhancer methylation can affect aging and imply that C/EBP proteins play an unexpected role in this process. Our study suggests a causal nexus between DNA demethylation, metabolism, and organismal aging.

This SuperSeries is composed of the SubSeries listed below.


title: Master retinal transcription factors define a subgroup-specific photoreceptor program and implicate novel dependencies in medulloblastoma

city: Paris

first: Wilfrid

last: Richer

address: 26 rue d'Ulm

institute: Institut Curie

summary: We used microarrays to compare gene expression between shRNA targeting NRL and control replicates in D458Med cell line.

overall_design: 3 samples with shRNA targeting NRL (D458Med cell line), 3 control replicates (D458Med cell line).

first: Celio

last: Pouponnot

first: Garancher

last: Alexandra


title: Polycomb-Dependent Chromatin Looping Contributes to Gene Silencing during Drosophila Development

city: Taipei

first: Jia-Ming

last: Chang

address: NO.64, Sec. 2, ZhiNan Rd., Wenshan District

department: Department of Computer Science

country: Taiwan

institute: National Chengchi University

summary: Interphase chromatin is organized into topologically associating domains (TADs). Within TADs, chromatin looping interactions are formed between DNA regulatory elements, but their functional importance for the establishment of the 3D genome organization and gene regulation during development is unclear. Using high-resolution Hi-C experiments, we analyze higher order 3D chromatin organization during Drosophila embryogenesis and identify active and repressive chromatin loops that are established with different kinetics and depend on distinct factors: Zelda-dependent active loops are formed before the midblastula transition between transcribed genes over long distances. Repressive loops within polycomb domains are formed after the midblastula transition between polycomb response elements by the action of GAGA factor and polycomb proteins. Perturbation of PRE function by CRISPR/Cas9 genome engineering affects polycomb domain formation and destabilizes polycomb-mediated silencing. Preventing loop formation without removal of polycomb components also decreases silencing efficiency, suggesting that chromatin architecture can play instructive roles in gene regulation during development.

overall_design:
HiC experiment in drosophila embryos

**Please note that the processed data was generated from both replicates (*rep1 and *rep2) and linked to 'rep 1' sample records for each sample.

first: Yuki

last: Ogiyama

first: Bernd

last: Schuettengruber

first: Giorgio

last: Papadopoulos

first: Giacomo

last: Cavalli


title: Aberrant expression of histone homocysteinylation: Implications for neural tube defects

city: Beijing

first: Qin

last: Zhang

address: 2 YaBao Road，Chao Yang Distinct

country: China

institute: Capital Institute of Pediatrics


title: Aberrant expression of histone homocysteinylation: Implications for neural tube defects (ChIP-seq)

summary: Neural tube defects (NTDs) are serious congenital malformations. Excessive maternal homocysteine (Hcy) increases the risk of NTDs, while its mechanism remains elusive. In this study, we evaluated the role of histone homocysteinylation in neural tube closure (NTC). A total of 39 histone homocysteinylation sites were identified in samples from human embryonic brain tissue using mass spectrometry. Elevated levels of histone KHcy and H3K79Hcy were detected at increased cellular Hcy levels in human fetal brains. Using ChIP-seq and RNA-seq assays, we demonstrated that increase in H3K79Hcy level downregulated the expression of selected NTC-related genes including Cecr2, Smarca4, and Dnmt3b. In human NTD brain tissues, decrease in expression of Cecr2, Smarca4, and Dnmt3b was also detected along with high levels of Hcy and H3K79Hcy. Our results suggest that higher levels of Hcy contribute to the onset of NTDs through upregulation of histone H3K79Hcy, leading to abnormal expression of selected NTC-related genes.

overall_design: Examination of 3 different histone modifications in 1 cell types.


title: Transcription profiles of WT or MST1/2-KO total, CD8+ and CD8- DCs in vivo

first: Jiyang

last: Yu

state: TN

address: 262 Danny Thomas Place, MS 1135

department: Computational Biology

country: USA

institute: St. Jude Children's Research Hospital

summary:
CD8+ DCs play key role in CD8+ T cell priming, however, the underlying signaling mechansim is unclear. We used a data-driven network-based systems biology approach and identified Hippo signaling kinases as key selective modualtors in CD8+ DCs. We focused on Mst1/Stk4 to further investigate the novel function of Hippo signaling in CD8+ DCs. All transcriptional profies were evalated by microarray.
1) We used microarrays of total DCs in previous (GSE98481) and current studies to reverse engineer a DC-specific signaling interactome (DCI). 2) We integrated DCI with profiles of sorted CD8+ with CD8- DCs to identify signaling drivers of CD8+ DCs. 3) We profiled and compared Mst1/2-KO with WT cells from total, CD8+ and CD8- DCs to understand the mechanism of Mst1 in CD8+ DCs.

overall_design: Previous microaarays (GSE98481) and 4 more total DC samples were used for network reconstruction.  Four replicates for sorted WT CD8+ and CD8- DCs. Three replicates for Mst1/2-KO total DCs, four replicates for Mst1/2-KO CD8+ and CD8- DCs.

first: Xingrong

last: Du

first: Geoffrey

last: Neale

first: Hongbo

last: Chi


title: Analysis of differential gene expression in Mus spretus mice exposed to p,p’-DDE

status: Public on Jun 05 2018

city: Cordoba

first: Nieves

last: Abril

state: Not Applicable

address: Campus Rabanales, edificio C6, 2ª planta

country: Spain

institute: University of Córdoba

summary: The complexity of environmental systems requires the use of holistic methodologies to conduct studies of contamination effects over individuals who inhabit specific polluted areas. Microarrays are an appropriate tool since they allow the simultaneous expression analysis of thousand genes. As an omic and unbiased technology, it allows for the identification of novel biological responses within certain environmental conditions. A commercial microarray based on probes of the Mus musculus entire genome has been used in order to study transcriptional changes in M. spretus mice exposed to p,p’-DDE, a metabolic by-product of the organochlorine pesticide DDT, whose use is nowadays limited due to the hazardous environmental impact it causes. The success of this approach lies in the high phylogenetic closeness between M. spretus, a species of large environmental interest, whose genome is not sequenced, and the laboratory mouse M. musculus. The results obtained with these heterologous microarrays, verified by qRT-PCR, indicate that the exposed mice to this compound present alterations in their gene expression profiles relative to control animals. Based on the data obtained herein, it can be inferred that mice exposed to p,p’-DDE show alterations in lipids and carbohydrates metabolism, in the immune response, cell cycle control and signaling and molecular transport processes.

overall_design: Four seven-week Mus spretus (inbred SPRET/EiJ strain) were fed for 30 days with Harlan diet supplemented with p,p'-DDE (450 mg/kg) dissolved in corn oil. Control group (four mice) was fed only with Harlan diet and corn oil.

first: Noelia

last: Morales-Prieto


title: Transcriptome-pathology correlations predict CSNK1E-mediated TDP-43 phosphorylation in sporadic amyotrophic lateral sclerosis

status: Public on Jun 06 2018

city: La Jolla

first: Gene

last: Yeo

state: CA

address: 2880 Torrey Pines Scenic Dr. Room 3805/Yeo Lab

institute: UCSD

summary: Sporadic amyotrophic lateral sclerosis (sALS) is the most common (~90%) form of ALS. There are no animal models of sALS and exact molecular mechanisms remain elusive. Here, we elucidate gene-expression profiles in laser capture microdissected enriched surviving motor neurons (MNs) from sALS lumbar spinal cords in patients who had rostral onset and caudal progression. A strong signature was detected and immunological signals were computationally filtered. The filtered dataset showed clustering groups that were significantly explained by levels of phosphorylated TDP-43 (pTDP-43). Transcriptome-pathology correlations and enhanced crosslinking and immunoprecipitation combined with sequencing (eCLIP-seq) identified that Casein kinase 1ε (CSNK1E) had the highest correlation with pTDP-43 status and TDP-43 binding in its 3’UTR. Furthermore, CSNK1E interacted with TDP-43 on protein level and its overexpression lead to increased cytoplasmic pTDP-43 accumulations in iPSC-MNs, suggesting CSNK1E directly mediates TDP-43 phosphorylation. Therefore, we report an essential framework for molecular disease classification and transcriptome – pathology correlation in sALS to identify candidate genes for elucidating disease mechanisms and potential therapeutic interventions.

overall_design: eCLIP-seq was performed in for TDP-43 in two controls and three sALS patients. Each sample has a size-matched input control for analysis

first: Florian

last: Krach

first: Ranjan

last: Batra

first: Anthony

middle: Q

last: Vu

first: Emily

last: Wheeler

first: Kasey

last: Hutt

first: Stuart

last: Rabin

first: Michael

last: Baughn

first: Ryan

middle: T

last: Libby

first: Sandra

last: Diaz-Garcia

first: Jennifer

last: Stauffer

first: Elaine

last: Pirie

first: Shahram

last: Saberi

first: Ruth

last: Wang

first: Zacharias

last: Kohl

first: Beate

last: Winner

first: John

last: Ravits


title: Persistence of stem cell metabolism in cancers as a failure of differentiation

city: boston

first: qiong

last: xu

address: CLS Building 3 Blackfan Circle

institute: dana farber cancer institute

summary: Tumor glucose uptake was measured by FDG-PET in 859 patients with histologically diverse cancers. We used normal mixture modeling to explore FDG-PET standardized uptake values (SUV) distributions and tested for association between glucose uptake and histological differentiation, risk of lymph node metastasis, and survival. Using RNA-seq data, we performed pathway and transcription factor analyses to compare tumors with high and low levels of glucose uptake. We found that well-differentiated tumors had low FDG uptake, while moderately and poorly differentiated tumors had higher uptake. The distribution of SUV for each histology was bimodal with a low peak at SUV 2-4 and a high peak at SUV 8-11. The cancers in the two modes were clinically distinct in terms of the risk of nodal metastases and of death. Carbohydrate metabolism and the pentose related pathway were elevated in the poorly differentiated/high SUV clusters. Embryonic stem cell-related signatures were activated in poorly differentiated/ high SUV clusters.

overall_design: Comparison of gene expression pattern in cancer with high and low SUV.

first: Markus

last: Riester

first: Qiong

last: Xu

first: Franziska

last: Michor

first: Robert

last: Downey


title: SPINK7 transcriptome

status: Public on Jun 04 2018

city: Cincinnati

first: Nurit

middle: Pereg

last: Azouz

state: Oh

address: 240 Albert Sabin Way

department: Allergy and Immunology

institute: Cincinnati Childrens Hospital Medical center

summary:
RNA sequencing  data of SPINK7 gene silencing (SPINK7) as compared to Non silencing control (NSC) treatment in EPC2 cells differentiated in ALI culture for 14 days and RNA sequencing  data of NSC cells before differentiation.
We show that a serine protease inhibitor SPINK7, is part of the differentiation program of human esophageal squamous epithelium and that SPINK7 depletion occurs in a human allergic, inflammatory, esophageal condition termed eosinophilic esophagitis (EoE). Herein, we employed experimental manipulation strategies designed to reduce SPINK7 in vitro in order to assess the transcriptional changes that are associates with the loss of SPINK7. A whole-transcriptome sequencing analysis of EPC2 cells after ALI differentiation revealed 270 genes that were differentially expressed in the SPINK7-deficient cells compared to NSC-treated cells (p < 0.05, fold change >2, RPKM >1). The modified genes were enriched for those involved in epidermal differentiation, inflammation and skin physiology including known differentiation markers such as FLG, FLG2, LOR, and keratins. These data suggest that loss of SPINK7 promote an un-differentiated phenotype. We further analyzed the transcription profile of differentiated cells as compared to un-differentiated cells. This analysis revealed 3225 differentially expressed genes (p < 0.05, fold change >2, RPKM >1). The majority of the genes modified by SPINK7 deficiency (77%) were also modulated during epithelial cell differentiation. Importantly, the genes that were most overexpressed during differentiation were downregulated after SPINK7 silencing, indicating that loss of SPINK7 promotes transcriptional changes that result in an undifferentiated epithelial phenotype.
We propose that loss of SPINK7 is a key checkpoint in regulating mucosal differentiation, barrier function, and inflammatory esophageal responses.
mRNA profile of SPINK7 silenced cells and control cells before and after differentiation in the ALI differentiation

overall_design: RNA sequencing  data of SPINK7 gene silencing (SPINK7) bas compared to non-silencing control (NSC) treatment in EPC2 cells differentiated in ALI culture for 14 days

first: Marc

last: Rothenberg


title: ChIP-Seq of H4K5acK8ac, H3K27ac, H3K4me1, H3K4me3, H3K36me3, H3K9me3, H3K27me3 and BRD2 in H23 NSCLC cell line

city: TSURUMI WARD YOKOHAMA

first: Aki

last: Minoda

state: KANAGAWA

address: 230-0045, 1 CHOME-7-22 SUEHIROCHO

department: IMS

institute: RIKEN YOKOHAMA

summary: The bromodomain and extra-terminal domain (BET) proteins are known as drug targets in diseases. However, the BET protein association profile to histone H4 hyperacetylation is not well understood and BET inhibition effects have been studied more in the context of BRD4 than BRD2. Here, by integrating chromatin and transcriptome analyses of ChIP-seq and Cap Analysis Gene Expression (CAGE) datasets, we show that di-acetylation at K5 and K8 of histone H4 (H4K5acK8ac) co-localizes with H3K27ac and BRD2 in the majority of active enhancers and promoters, where BRD2 has a stronger association with H4K5acK8ac than H3K27ac. Interestingly, although BET inhibition by JQ1 led to complete reduction of BRD2 binding, only local changes of H4K5acK8ac were observed and surprisingly a remarkable number of BRD2-bound genes including MYC and its target genes were upregulated. Using BRD2-enriched sites and transcriptional activity analysis, we identified candidate transcription factors (TFs) potentially involved in the JQ1 response in BRD2-dependent and independent manner.

first: Takashi

last: Umehara


title: A Cdk9-PP1 switch regulates the elongation-termination transition of RNA polymerase II

status: Public on Jun 07 2018

city: Bronx

first: PABITRA

middle: K

last: PARUA

state: NY

address: 1300 Morris Park Avenue, Forchheimer 236, Molecular Pharmacology

department: Molecular Pharmacology

institute: Albert Einstein College of Medicine

summary: The end of the RNA polymerase II (Pol II) transcription cycle is strictly regulated to ensure proper mRNA maturation and prevent interference between neighboring genes. Pol II slowing downstream of the cleavage and polyadenylation signal (CPS) leads to recruitment of cleavage and polyadenylation factors and termination, but how this chain of events is initiated remains unclear. In a chemical-genetic screen we identified protein phosphatase 1 (PP1) isoforms as substrates of human positive transcription elongation factor b (P-TEFb), the cyclin-dependent kinase 9 (Cdk9)-cyclin T1 complex. Here we show that Cdk9 and PP1 govern phosphorylation of the conserved transcription factor Spt5 in the fission yeast Schizosaccharomyces pombe. Cdk9 phosphorylates both Spt5 and a negative regulatory site on the PP1 isoform Dis2. Sites phosphorylated by Cdk9 in the Spt5 carboxy-terminal domain (CTD) are dephosphorylated by Dis2 in vitro, and Cdk9 inhibition in vivo leads to rapid Spt5 dephosphorylation that is retarded by concurrent Dis2 inactivation. Chromatin immunoprecipitation and sequencing (ChIP-seq) analysis indicates that Spt5 is dephosphorylated as transcription complexes traverse the CPS, prior to or concomitant with Pol II pausing. A Dis2-inactivating mutation stabilizes Spt5 phosphorylation (pSpt5) on chromatin, promotes transcription beyond the normal termination zone detected by precision run-on transcription and sequencing (PRO-seq), and is suppressed by ablation of Cdk9 target sites in Spt5. These results support a model whereby the transition of Pol II from elongation to termination is regulated by opposing activities of Cdk9 and Dis2 towards their common substrate Spt5—a bistable switch analogous to a Cdk1-PP1 module that controls exit from mitosis.

overall_design:
PRO-seq: Data represent 20 different treatments of various S. pombe strains performed in biological replicates. There are processed files for both replicates and combined replicate data for each experiment.
ChIP-seq: Data represent 6 different ChIP-seq experiments in S. pombe, performed in biological replicates. There are raw and processed files for all biological replicates.
ChIP-seq: Data represent 16 different ChIP-seq experiments in S. pombe, performed in biological replicates. There are raw and processed files for all biological replicates.
PRO-seq: Experiment was done in five different S. pombe strains as biological duplicates. There are processed files for both replicates and combined replicate data for each sample.

first: Pabitra

last: Parua

first: Gregory

last: Booth

first: Miriam

last: Sanso

first: Jason

last: Tanny


title: ChIP-Seq and CAGE profiling of cell lines

overall_design: Refer to individual Series


title: Global gene repression by Dicer-independent tRNA fragments

city: Charlottesville,

first: Anindya

last: Dutta

email: ad8q@virginia.edu, pk7z@virginia.edu

state: VA

address: Room no. 1232, Jordan Hall

department: MD-BIOC BC/Mole Genetics~School of medicine

institute: University of Virginia

summary: We have performed RNA sequencing after tRNA/tRF overexpression

overall_design: Examination of gene expression changes upon two different tRNA/tRF overexpression in two replicates

first: Canan

last: Kuscu

first: Pankaj

last: Kumar


title: Salmonella activation of STAT3 signaling by SarA effector promotes intracellular replication and production of IL-10

status: Public on Jun 01 2018

city: Durham

first: Liuyang

last: Wang

state: NC

address: 0049 CARL Building

institute: Duke University

summary: Salmonella enterica is an important foodborne pathogen that utilizes secreted effector proteins to manipulate host pathways to facilitate survival and dissemination. Different S. enterica serovars cause disease syndromes ranging from self-limited gastroenteritis to typhoid fever and vary in their repertoire of effectors. We leveraged this natural diversity to identify stm2585, here designated sarA (Salmonella anti-inflammatory response activator), as a Salmonella effector secreted primary by the SPI-2 type III secretion system. SarA is necessary and sufficient to induce STAT3 phosphorylation and IL-10 production, contributing to intracellular replication in vitro and bacterial load at systemic sites in mice. These results demonstrate that Salmonella has evolved effector mechanisms for regulating a host anti-inflammatory signaling pathway important in infection, autoimmunity, and cancer.

overall_design: Two human LCLs' mRNA profiles from WT, Salmonella Typhimurium and ΔsarA S. Typhimurium mutant infections were generated by deep sequencing, in triplicate, using Illumina HiSeq 2500 platform.

first: Sarah

last: Jaslow

first: Kyle

middle: D

last: Gibbs

first: W

middle: F

last: Fricke

first: Kelly

last: Pittman

first: Mark

last: Mammel

first: Joshua

last: Thaden

first: Vance

middle: G

last: Fowler Jr

first: Gianna

last: Hammer

first: Johanna

last: Elfenbein

first: Dennis

last: Ko


title: An integrated global regulatory network of hematopoietic precursor cell self-renewal and differentiation

city: Monterrey

first: Raquel

last: Cuevas Diaz Duran

address: Av Morones Prieto No. 3000, Colonia Los Doctores

department: Escuela de Medicina y Ciencias de la Salud

country: Mexico

institute: Tecnologico de Monterrey

summary: The mammalian blood system is a hierarchically structured tissue. Hematopoietic stem cells (HSC) reside at the top of this hierarchy and the HSC-derived progenitor cells (HPC) have capacities for both differentiation and self-renewal. Systematic study of the regulatory mechanisms of HSC self-renewal and differentiation is fundamentally important for understanding hematopoiesis and for manipulating HSCs for therapeutic purposes. Herein, the mechanisms regulating HSC biology were studied on a genome-wide scale by integrating epigenomic, transcriptomic, proteomic, and protein-protein interaction data. Previously, we have characterized gene expression and identified important transcription factors (TFs) regulating the switch between self-renewal and differentiation in a multipotent hematopoietic progenitor cell line, EML (Erythroid, Myeloid, and Lymphoid). In the present study, we report binding maps for three additional TFs (SOX4, STAT3, and GABP) that were developed by chromatin immunoprecipitation (ChIP)-Sequencing. Assay for Transposase Accessible Chromatin (ATAC)-Sequencing was applied to globally identify the open chromatin regions associated with TF binding in the self-renewing subpopulation lin-CD34+.Mass spectrometry (MS) was also used to identify proteins and assess differences in their relative abundances. We found that MAPK (Mitogen-activated protein kinase) pathway and JAK-STAT (Janus kinase-signal transducer and activator of transcription) pathway components were highly enriched among the binding targets of these TFs in CD34+ cells, and that the TGF-β/SMAD signaling pathway comprised a sub-network of molecules that were differentially expressed between the lin-CD34+ and partially differentiated lin-CD34- cellular states. The present study integrates regulatory information at multiple levels to paint for the first time a more comprehensive picture of the mechanisms underlying the decision between HPC self-renewal and differentiation. We anticipate that this work will provide valuable clues for understanding the molecular switch that controls cell fate decisions between self-renewal or differentiation and blood formation.

overall_design: In vivo binding targets of transcription factors STAT3, SOX4, and GABPa were found through ChIP-sequencing in lin-CD34+ and lin-CD34- cells. Additionally, open chromatin regions were studied through ATAC-seq sequencing in lin-CD34+ cells. Epigenetic, transcriptomic, and proteomic data were integrated into a regulatory network.

first: Yanan

last: You

last: Cuevas-Diaz

first: Shan

last: Zong

first: Lihua

last: Jiang

first: Michael

last: Snyder

first: Jiaqian

last: Wu