title: DNase-seq from A549 (ENCSR347CEH)

summary:
DNase-seq on A549 cell line treated with 100 nM dexamethasone for 7 hours.

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


title: ChIP-seq from A549 (ENCSR350EFV)

status: Public on Jan 10 2017

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

country: USA

institute: ENCODE DCC

type: Genome binding/occupancy profiling by high throughput sequencing

summary:
H3K27ac ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 3 hours.

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


title: ChIP-seq from A549 (ENCSR299MNA)

summary:
H3K9me3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 5 hours.

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


title: ChIP-seq from A549 (ENCSR287FWE)

summary:
NR3C1 (GR) ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 12 hours.

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


title: ChIP-seq from A549 (ENCSR340NAL)

summary:
H3K27ac ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 6 hours.

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


title: DNase-seq from A549 (ENCSR294XUZ)

summary:
DNase-seq on A549 cell line treated with 100 nM dexamethasone for 3 hours.

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


title: ChIP-seq from A549 (ENCSR288EPV)

summary:
BCL3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 12 hours.

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


title: ChIP-seq from A549 (ENCSR330IJE)

summary:
FOSL2 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 1 hours.

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


title: ChIP-seq from A549 (ENCSR285FZP)

summary:
H3K4me3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 7 hours.

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


title: ChIP-seq from A549 (ENCSR310TYO)

summary:
Control ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 10 hours.

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


title: ChIP-seq from A549 (ENCSR356YXW)

summary:
HES2 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 0.5 hours.

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


title: ChIP-seq from A549 (ENCSR274VPI)

summary:
Control ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 8 hours.

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


title: ChIP-seq from A549 (ENCSR274WRI)

summary:
FOSL2 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 2 hours.

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


title: ChIP-seq from A549 (ENCSR260WCE)

summary:
EP300 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 0.5 hours.

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


title: polyA mRNA RNA-seq from A549 (ENCSR255VBV)

type: Expression profiling by high throughput sequencing

summary:
mRNA-seq on A549 cell line treated with 100 nM dexamethasone for 6 hours.

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


title: ChIP-seq from A549 (ENCSR269IUA)

summary:
CEBPB ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 12 hours.

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


title: ChIP-seq from A549 (ENCSR242TBH)

summary:
H3K27ac ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 1 hours.

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


title: ChIP-seq from A549 (ENCSR242EWU)

summary:
FOSL2 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 8 hours.

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


title: ChIP-seq from A549 (ENCSR252FZA)

summary:
H3K4me3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 2 hours.

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


title: ChIP-seq from A549 (ENCSR250EHC)

summary:
H3K27ac ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 8 hours.

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


title: ChIP-seq from A549 (ENCSR225AOO)

summary:
H3K4me1 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 5 hours.

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


title: ChIP-seq from A549 (ENCSR317VER)

summary:
Control ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 7 hours.

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


title: ChIP-seq from A549 (ENCSR215DID)

summary:
H3K4me2 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 0.5 hours.

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


title: ChIP-seq from A549 (ENCSR215UXN)

summary:
BCL3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 1 hours.

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


title: polyA mRNA RNA-seq from A549 (ENCSR224PTG)

summary:
mRNA-seq on A549 cell line treated with 100 nM dexamethasone for 10 hours.

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


title: ChIP-seq from A549 (ENCSR186IQL)

summary:
BCL3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 6 hours.

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


title: ChIP-seq from A549 (ENCSR299ILN)

summary:
CEBPB ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 1 hours.

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


title: ChIP-seq from A549 (ENCSR182OZC)

summary:
CEBPB ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 2 hours.

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


title: ChIP-seq from A549 (ENCSR216GEB)

summary:
CEBPB ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 3 hours.

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


title: ChIP-seq from A549 (ENCSR180YHA)

summary:
H3K27ac ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 10 hours.

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


title: polyA mRNA RNA-seq from A549 (ENCSR154TDP)

summary:
mRNA-seq on A549 cell line treated with 100 nM dexamethasone for 12 hours.

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


title: DNase-seq from A549 (ENCSR136DNA)

summary:
DNase-seq on A549 cell line treated with 100 nM dexamethasone for 0 hours.

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


title: ChIP-seq from A549 (ENCSR190VMK)

summary:
CEBPB ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 10 hours.

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


title: ChIP-seq from A549 (ENCSR255CTA)

summary:
NR3C1 (GR) ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 10 hours.

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


title: ChIP-seq from A549 (ENCSR171ZJG)

summary:
H3K4me1 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 3 hours.

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


title: ChIP-seq from A549 (ENCSR147APP)

summary:
Control ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 2 hours.

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


title: ChIP-seq from A549 (ENCSR145YCX)

summary:
EP300 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 4 hours.

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


title: ChIP-seq from A549 (ENCSR124VXG)

summary:
EP300 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 12 hours.

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


title: ChIP-seq from A549 (ENCSR124YCC)

summary:
H3K4me2 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 2 hours.

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


title: ChIP-seq from A549 (ENCSR111ZXV)

summary:
FOSL2 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 5 hours.

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


title: ChIP-seq from A549 (ENCSR203XPU)

summary:
H3K4me3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 0 hours.

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


title: ChIP-seq from A549 (ENCSR103UVU)

summary:
FOSL2 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 3 hours.

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


title: ChIP-seq from A549 (ENCSR102XUM)

summary:
H3K27ac ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 0.5 hours.

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


title: ChIP-seq from A549 (ENCSR047EVQ)

summary:
EP300 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 3 hours.

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


title: polyA mRNA RNA-seq from A549 (ENCSR070IYV)

summary:
mRNA-seq on A549 cell line treated with 100 nM dexamethasone for 0.5 hours.

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


title: ChIP-seq from A549 (ENCSR067XTW)

summary:
FOSL2 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 12 hours.

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


title: ChIP-seq from A549 (ENCSR037DAC)

summary:
H3K9me3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 4 hours.

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


title: ChIP-seq from A549 (ENCSR078POK)

summary:
HES2 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 4 hours.

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


title: DNase-seq from A549 (ENCSR077EYC)

summary:
DNase-seq on A549 cell line treated with 100 nM dexamethasone for 6 hours.

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


title: ChIP-seq from A549 (ENCSR032SCO)

summary:
H3K9me3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 6 hours.

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


title: ChIP-seq from A549 (ENCSR013RTF)

summary:
H3K9me3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 10 hours.

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


title: ChIP-seq from A549 (ENCSR139DGM)

summary:
H3K4me3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 10 hours.

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


title: ChIP-seq from A549 (ENCSR013KHB)

summary:
BCL3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 0.5 hours.

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


title: ChIP-seq from A549 (ENCSR005CRY)

summary:
Control ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 12 hours.

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


title: Rapid Recall Ability of Memory T cells is Encoded in their Epigenome

city: Cincinnati

first: Artem

last: Barski

state: OH

address: 3333 Burnet Av

department: Allergy

institute: Cincinnati Children's Hospital

summary: Even though T-cell receptor (TCR) stimulation together with co-stimulation is sufficient for the activation of both naïve and memory T cells, the memory cells are capable of producing lineage specific cytokines much more rapidly than the naïve cells. The mechanisms behind this rapid recall response of the memory cells are still not completely understood. Here, we performed epigenetic profiling of human resting naïve, central and effector memory T cells using ChIP-Seq and found that unlike the naïve cells, the regulatory elements of the cytokine genes in the memory T cells are marked by activating histone modifications even in the resting state. Therefore, the ability to induce expression of rapid recall genes upon activation is associated with the deposition of positive histone modifications during memory T cell differentiation. We propose a model of T cell memory, in which immunological memory state is encoded epigenetically, through poising and transcriptional memory.

overall_design: Chromatin state of resting Human Naive, Central memory (TCM) and Effector Memory (TEM) T cells was analyzed by ChIP-Seq; Gene expression in resting and activated for 40 min, 150 min and 15hrs Naive, TCM and TEM cells was analyzed by RNA-Seq

first: Keji

last: Zhao

first: Andrey

last: Kartashov

first: Suresh

last: Cuddapah


title: DNase-seq from A549 (ENCSR128IVG)

summary:
DNase-seq on A549 cell line treated with 100 nM dexamethasone for 10 hours.

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


title: Maedi-visna virus (MVV) preferrentially integrates into genes and generates 6-bp duplications

city: London

first: Peter

middle: P

last: Cherepanov

address: 1 Midland Road

country: United Kingdom

institute: The Francis Crick Institute

summary: We sequenced MVV integration sites in acutely infected primary sheep cells and compared them to a control set of integration sites generated using recombinant MVV intasomes and deproteinized genomic sheep DNA. Alignment of the integration sites revealed symmetric sequence preferences that are consistent with integration of viral ends across 6 bp in target DNA in both conditions. As expected for a lentivirus, MVV displayed a strong preference for transcription units, with 70.2% integration sites found within predicted sheep genes, compared to 43.7% in the in vitro generated control condition.

overall_design: Integration sites obtained by infection of sheep choroid plexus cells with pathogenic MVV strain KV1772 or by incubation of deproteinised sheep DNA with recombinant intasome (in vitro control condition) were amplified by linker-mediated PCR and sequenced using Illumina technology.

first: Erik

last: Serrao

first: Allison

last: Ballandras-Colas

first: Daniel

last: Maskell

first: Stefán

last: Jónsson

first: Valgerdur

last: Andrésdóttir

first: Alan

middle: N

last: Engelman


title: ChIP-seq from A549 (ENCSR109KEL)

summary:
H3K9me3 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 0.5 hours.

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


title: ChIP-seq from A549 (ENCSR016PSC)

summary:
H3K4me2 ChIP-seq on A549 cell line treated with 100 nM dexamethasone for 7 hours.

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


title: RNA immunoprecipiation identifies novel targets of DAZL in human fetal ovary

city: Edinburgh

first: Roseanne

last: Rosario

address: 47 Little France Crescent

institute: University of Edinburgh

summary: We identified 429 potential RNA targets of DAZL in the human fetal ovary (padj<0.01), with function in synaptonemal complex formation and recombination (SYCP1, SYCP3, HORMAD1, TRIP13, TEX11), structural maintenance of chromosomes/cohesin formation and spindle assembly checkpoint (SMC1B, RAD21L, MAD2L1), and DNA repair (RAD18, RAD51, RAD54B).

overall_design: Immunoprecipitation of endogenous DAZL from 17weeks gestational age (wga) human fetal ovarian tissue. DAZL-bound RNAs were purified and sequenced.

first: Richard

middle: A

last: Anderson


title: Arabidopsis thaliana treatments to trigger somatic embryo formation under RNAseq

city: Alicante

first: Angel

last: Barco

address: Ramon y Cajal

department: Neuro Plasticity

country: Spain

institute: NeuroSciences Institute of Alicante CSIC

summary: Arabidopsis clf/swn mutant is able to form somatic embryos under the proper treatment conditions. In order to get more information about the process, we compared the expression profiles of wt and clf/swn in absence of treatment, Injury, Auxin, and Auxin+Injury treatments

overall_design: Comparison of gene expression between the clf/swn mutant and wt under different treatments

first: Lars

last: Hennig

first: Iva

last: Mogzová

first: Rafael

middle: M

last: Viana


title: Removable insulator facilitates higher-order chromatin remodeling and selective gene expression in the HOXA locus via the retinoic acid signaling

city: Kumamoto

first: Ko

last: Ishihara

address: 2-2-1 Honjyo

department: Priority Organization for Innovation and Excellence

country: Japan

institute: Kumamoto University

type: Genome binding/occupancy profiling by genome tiling array

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

overall_design: Refer to individual Series


title: DNA methylation on type-specific human skeletal muscle fibers

city: Muncie

first: Scott

last: Trappe

state: IN

address: 2000 W University Ave

institute: Ball State University

type: Methylation profiling by high throughput sequencing

summary:
Purpose: Reduced Representation Bisulfite Sequencing (RRBS) DNA input requirements become a challenge when working with small pools of tissue-specific cell types. We describe an application of the RRBS method to assess DNA methylation on low-DNA input from human slow-twitch (MHC I) and fast-twitch (MHC IIa) skeletal muscle fibers.
Methods : Fiber-type specific (MHC I and MHC IIa muscle fibers) total DNA was extracted from vastus lateralis muscle biopsies of 8 young physically active men (~25 yrs). A total of 16 DNA samples were generated : 8 DNA samples from pure MHC I and 8 DNA samples from pure MHC IIa muscle fibers. An equal quantity of DNA (4 ng) from each sample was combined to generate a "pooled" DNA sample representing all 8  subjects for each fiber type. Two fiber-type specific "pooled" samples of 32 ng of DNA were generated for library construction and sequencing, creating a Type 1 (MHC I muscle fibers) and Type 2a (MHC IIa muscle fibers) sample. Sequencing was performed using the HiSeq 2500 (Illumina) with 50 bp paired-end read parameters. Minimum sequencing read coverage of 5 (5x) was used as the cutoff for CpG-sites inclusion in the DNA methylation analysis. Fisher’s exact test was performed on CpG-sites that overlapped (i.e. identified in both samples) Type 1 and Type 2a samples to obtain p-values that indicate the likelihood of the site being a differentially methylated CpG-site (DMS). DMS with p<0.05 were classified as hypermethylated or hypomethylated if they were more or less methylated than the Type 1 sample, which was used as the reference sample.
Results: The 32 ng of DNA from fiber-type specific muscle samples  (Type 1 and 2a) used in this study ensured similar sequencing quality as compared to other studies using greater DNA input (>50 ng). Mapping ratios of ~47% and  bisulfite conversion rates of ~97-98% were obtained.The unique and best alignment was successfully assessed for each of 17,376,728 CpG-sites in the Type 1 sample and 17,006,993 in the Type 2a sample, which represents ~30% of the total CpG number  in the human genome. We identified 143,160 differentially methylated CpG-sites (DMS) across 14,046 genes among MHC I and MHC IIa muscle fibers.  The analysis revealed that some genes predominantly expressed in MHC I were hypermethylated in MHC IIa muscle fibers.
Conclusion: This study validates a low-DNA input RRBS method for human skeletal muscle samples to investigate the methylation patterns at a fiber-type specific level. These are the first fiber-type specific methylation data reported from human skeletal muscle. Considering the metabolic and structural differences between MHC I and MHC IIa muscle fibers, this technique could provide novel insights into the skeletal muscle methylation profile in relation to health, performance, disease or disuse.

overall_design: Comparison of DNA methylation profiles in slow-twitch (MHC I) and fast-twitch (MHC IIa) human skeletal muscle fibers.

first: Gwenaelle

last: Begue

first: Ulrika

last: Raue

first: Bozena

last: Jemiolo


title: Removable insulator facilitates higher-order chromatin remodeling and selective gene expression in the HOXA locus via the retinoic acid signaling [ChIP-seq]

summary: Chromatin insulators partition the genome into the functional units to control gene expression especially in complex chromosomal regions. The CCCTC-binding factor (CTCF) is an insulator-binding protein which functions for transcriptional regulation and higher-order chromatin formation. Here we report that a removable CTCF insulator is responsible for the retinoic acid (RA)-mediated higher-order chromatin remodeling and selective gene expression in the human HOXA gene locus. Our detailed chromatin analyses characterized multiple CTCF-enriched sites and RA-responsive enhancers in this locus. These regulatory elements and transcriptionally silent HOXA genes were closely positioned under the basal condition. Notably, upon the RA signaling, the transcription factor RAR/RXR induced the loss of an adjacent CTCF binding and changed the higher-order chromatin conformation of the overall locus, establishing transcriptionally active, poised and repressive domains that were separated by stably localizing CTCF insulators. This study uncovers that removable insulator spatiotemporally switches higher-order chromatin and multiple gene activities at the chromosomal domain levels, via the cooperation of CTCF and key transcription factors.

overall_design: In total 6 samples; 2 input samples and 4 ChIP-seq samples

first: Mitsuyoshi

last: Nakao

first: Masafumi

last: Nakamoto


title: The Pseudomonas syringae type III effector HopBB1 fine tunes pathogen virulence by degrading host transcriptional repressors

city: Piracicaba

first: Paulo

last: Teixeira

state: SP

address: Av. Pádua Dias, 11

department: Biology

country: Brazil

institute: University of São Paulo (ESALQ/USP)


title: The role of miR-17-92 in the miRegulatory landscape of Ewing Sarcoma

city: Vienna

first: Maximilian

last: Kauer

address: Zimmermannplatz 10

department: Molecular Biology

country: Austria

institute: CCRI, St.Anna Children Cancer Research Institute


title: The role of miR-17-92 in the miRegulatory landscape of Ewing Sarcoma (PARCLIP-Seq)

summary: MicroRNAs serve to fine-tune gene expression and play an important regulatory role in tissue specific gene networks. The identification and validation of miRNA target genes in a tissue still poses a significant problem since the presence of a seed sequence in the 3´UTR of an mRNA and its expression modulation upon ectopic expression of the miRNA do not reliably predict regulation under physiological conditions. The chimeric oncoprotein EWS-FLI1 is the driving pathogenic force in Ewing Sarcoma. miR-17-92, one of the most potent oncogenic miRNAs, was recently reported to be the top EWS-FLI1 activated miRNA. Using a combination of AGO2 pull-down experiments by PAR-CLIP (Photoactivatable-Ribonucleoside-Enhanced Crosslinking and Immunoprecipitation) and of RNAseq upon miRNA depletion by ectopic sponge expression, we aimed to identify the targetome of miR-17-92 in Ewing sarcoma. Intersecting both datasets we found an enrichment of PAR-CLIP hits for members of the miR-17-92 cluster in the 3´UTRs of genes up-regulated in response to mir-17-92 specific sponge expression. Strikingly, approximately a quarter of these genes annotate to the TGFB/BMP pathway, the majority mapping downstream of SMAD signalling. Taken together, our findings shed light on the complex miRegulatory landscape of Ewing Sarcoma pointing miR-17-92 as a key node connected to TGFB/BMP pathway

overall_design: PAR-CLIP of AGO2 of 3 samples of clone the Ewing Sarcoma celline A673 harboring an inducible sh mediated knockdown of EWS-FLI1

first: Raphaela

last: Schwentner

first: David

last: Herrero-Martin

middle: O

first: Anna

last: Katschnig

first: Cornelia

last: Mutz

first: Grzegorz

last: Sienski

first: Javier

last: Alonso

first: Heinrich

last: Kovar


title: The role of miR-17-92 in the miRegulatory landscape of Ewing Sarcoma (RNA-Seq)

overall_design: mRNA profiles of a Ewings Sarcoma cellline (clone of A673 with inducible sh EWS-FLI1 knockdown) treated with microRNA sponges and controls


title: RNA-seq of zebrafish ZMEL1 melanoma cells versus BRAF inhibitor resistant ZMELR1 melanoma cells

status: Public on Jan 09 2017

city: New York

first: Richard

middle: Mark

last: White

state: NY

address: 1275 York Avenue MB 424

department: Cancer Biology & Genetics

institute: Memorial Sloan Kettering Cancer Center

summary: We report how the zebrafish melanoma cell line ZMEL1 changes after 4 month exposure to the BRAF inhibitor PLX4032 (1uM)

overall_design: Examination of ZMEL1 vs. ZMELR1 cells growing in vitro

first: Emily

last: Kansler


title: Direct control of regulatory T cells by keratinocytes

city: Charlestown

first: Katia

last: Georgopoulos

state: MA

address: 1st and 13th St

department: CBRC

institute: Harvard Medical School

summary: Environmental challenges to epithelial cells trigger gene expression changes that elicit context-appropriate immune responses. Here we show that the chromatin remodeler Mi-2β controls epidermal homeostasis by holding genes involved in keratinocyte and immune-cell activation at an inactive state. Mi-2β depletion caused rapid deployment of both a pro-inflammatory and an immunosuppressive response in the skin. A key target of Mi-2β in keratinocytes was the pro-inflammatory cytokine Thymic Stromal Lymphopoietin (TSLP). Loss of TSLPR signaling specifically in regulatory T cells (Treg) prevented their activation and permitted rapid progression from a skin pro-inflammatory response to a lethal systemic condition. Thus, in addition to their well-characterized role in pro-inflammatory responses, keratinocytes also directly support immune-suppressive responses that are critical for re-establishing organismal homeostasis.

overall_design: 9 RNAseq samples

first: Mariko

last: Kashiwagi


title: Normalisation Against Circadian and Age-related Disturbances Enables Robust Detection of Gene Expression Changes in Liver of Aged Mice

city: Fribourg

first: Sara

middle: S

last: Fonseca Costa

address: Chemin du Musée 5

country: Switzerland

institute: University of Fribourg

summary: Pilot experiment to uncover age-related changes of the mouse liver transcriptome derived from healthy male mice. To avoid bias, RNA samples from multiple time points over the day were combined.

overall_design: For each age point, we pooled equal amounts of liver RNA from six time points per day and from four animals each.

first: Daniel

last: Wegmann

first: Jürgen

last: Ripperger


title: Glucocorticoid receptor regulates the ANGPTL4 gene in a CTCF-mediated chromatin context in human hepatic cells

first: Ko

last: Ishihara

summary: Glucocorticoid plays an essential role in various stress responses and metabolism, which is mediated by the glucocorticoid receptor (GR) in cells. This hormonal action is integrated to transcriptional control of the GR target genes in cell type-specific and condition-dependent manners. In this study, we report that GR regulates the angiopoietin-like 4 (ANGPTL4) gene in a CCCTC-binding factor (CTCF)-mediated chromatin context in human hepatic HepG2 cells. There were at least four CTCF-enriched sites and two GR-binding sites in the ANGPTL4 locus. Among them, major CTCF-enriched site was positioned nearly GR-bound enhancer of this gene. Using treatment with the synthetic glucocorticoid dexamethasone (Dex), our data showed that CTCF is required for proper induction and subsequent silencing of ANGPTL4 gene. Interestingly, this gene induction was diminished under the long-term Dex pretreatment. Although ANGPTL4 locus maintains stable higher-order chromatin conformation at the basal and the Dex-treated states, liganded GR activated the ANGPTL4 gene, but not the neighboring three genes, via the interactions between enhancer, promoter and CTCF sites. These results reveal that liganded GR spatiotemporally controls ANGPTL4 gene in the chromosomal context.

overall_design: In total 2 samples; 1 input sample and 1 ChIP-seq sample

first: Masafumi

last: Nakamoto

first: Mitsuyoshi

last: Nakao


title: Gene expression changes after LOC550643 silencing

city: West Haven

first: Sarah

last: Slavoff

state: Connecticut

address: Yale University West Campus-Building 600

department: Chemistry

institute: Yale University- West Campus

summary: Differential analysis of gene expression in HEK293T cells treated with a pool of siRNA targeting LOC550643, or non-silencing siRNA.

overall_design: LOC550643 encodes a polypeptide that binds to EDC4, and therefore may regulate RNA decay. This experiment tests whether steady-state gene expression levels are different in HEK293T cells treated with non-silencing siRNA, or with siRNA targeting LOC550643, by performing differential expression analysis of total RNA from both of these samples (triplicates of each).

first: Alexandra

last: Khitun


title: Mouse neural stem cells heterozyous or null for Dgcr8

city: Rochester

first: Hu

last: Li

state: MN

address: 200 First Street, Gonda Building G19-408

department: Molecular Pharmacology & Experimental Therapeutics

institute: Mayo Clinic

summary: We isolated and characterized mouse neural stem cells that are heterozygous or null for Dgcr8 from E13.5 embryonic brain;

overall_design: Examination transcriptional profiles of mouse neural stem cells heterozyous or null for Dgcr8

first: Zhong

last: Liu

first: Rui

last: Zhao

first: Cheng

last: Zhang


title: RNA sequencing of organoids isolated from pancreatic cancer mouse model KRASG12D; p53R172H; Ptf1a-Cre.

city: zurich

first: Cédric

last: Cortijo

address: Otto-Stern-Weg 7

department: HPL

institute: ETHZ

summary: We studied the transcriptomics of pancreatic ductal adenocarcinoma (PDAC) and the role of a splicing factor called SF3B1 in this context. We generated mice that will develop PDAC via an inducible expression of KRASG12D; p53R172H specifically in the pancreas using a Ptf1a-Cre.

overall_design:
We have isolated organoids from:
KrasG12D; p53R172H (KP),
KrasG12D; p53R172H; Ptf1a-Cre (KPC) ,
KrasG12D; p53R172H; SF3b1 Fl/+ (KPS),
and KrasG12D; p53R172H; Ptf1a-Cre; SF3b1 Fl/+ (KPCS) mice.

We have 3 organoids per group, representing 3 biological replicates. We have exposed the organoids to normoxia (21% O2) or hypoxia (3%O2).

first: C

first: W

last: Krek


title: DNA sequence properties that determine susceptibility to epiallelic switching

city: Birmingham

first: Marco

last: Catoni

address: Edgbaston

department: School of Biosciences

institute: University of Birmingham

type: Expression profiling by genome tiling array


title: Transcriptome profile of yeast adapted to the toxic effect of manganese

city: Pushchino

first: Ivan

middle: V

last: Kulakovskiy

address: Institutskaya 4

country: Russia

institute: Institute of Protein Research

summary: Transcriptome analysis shows that the adaptation of S. cerevisiae yeast cells to the growth at a toxic concentration of manganese ions involves multiple mechanisms, including the activation of transport systems responsible for manganese compartmentalization, the systems of phosphorus transport and polyphosphates accumulation, as well as other transport proteins.

overall_design: RNA-Seq in control and manganese-adapted yeast cells.

first: Tatiana

last: Kulakovskaya


title: Small RNAome profiling from human skeletal muscle: Novel miRNAs and their targets associated with cancer cachexia

city: Edmonton

first: Sambasivarao

last: Damaraju

state: Alberta

address: 11560 University Ave

department: Laboratory medicine and pathology

country: Canada

institute: University of Alberta

type: Non-coding RNA profiling by high throughput sequencing

summary: Background: MicroRNAs (miRs) are small non-coding RNAs that regulate gene (mRNA) expression. Although pathological role of miRs have been studied in muscle wasting conditions such as age, obesity, starvation and muscular dystrophy, their roles in Cancer Cachexia CC are still emerging. Objectives: (i) to profile human skeletal muscle expressed miRs; (ii) to identify differentially expressed (DE) miRs between cachectic and non-cachectic cancer patients; (iii) to identify mRNA targets for the DE miRs to gain mechanistic insights and (iv) to investigate if miRs show potential prognostic and predictive value. Methods: 43 cancer patients were included, of which 19 were cachectic cases exhibiting pre-illness weight loss ≥ 5% and 24 non-cachectic cancer controls who were weight stable in the preceding 6 months. Total RNA isolated from muscle biopsies were subjected to next generation sequencing (NGS). Results: 781 miRs were profiled and 82 miRs with read counts of ≥ 5 in 80% of samples were retained for analysis. We identified 7 DE miRs (up-regulated, fold change of ≥1.4 at p< 0.05). Potential mRNA targets for the DE miRs were identified using previously described human skeletal muscle mRNA expression data (n=90) and identified 212 potential mRNA targets. Ingenuity Pathway Analysis identified 41 pathways (p<0.05) including pathways of myogenesis and inflammation. qRT-PCR analysis of representative miRs, showed similar direction of effect (p<0.05) as in NGS. And lastly, we evaluated the identified miRs for prognostic and predictive value. Conclusions: We identified seven novel miRs associated with CC and pathways that are regulated in CC.

overall_design: Identification of miRs for cancer Cachexia using human skeletal muscle biopsies

first: Sanbasivarao

first: Ashok

last: Narasimhan

first: Cynthia

last: Stretch

first: Russell

last: Greiner

first: Oliver

middle: F

last: Bathe

first: Vickie

middle: E

last: Baracos


title: Ribosome profiling of synchronous, non-arrested yeast cells identifies translational control of lipid biosynthesis enzymes in the cell cycle

city: College Station

first: Rodolfo

last: Aramayo

state: Texas

address: Room 412, Biological Sciences Building West (BSBW)

institute: Texas A&M University

summary: The translational efficiency of mRNAs in cells progressing synchronously through the mitotic cell cycle and having to meet their growth requirements for cell division has not been interrogated. Here, we used ribosome profiling of a cell-size series from the time of cell birth, to identify for the first time yeast mRNAs under periodic translational control. Late in the cell cycle, there was coordinate translational activation of mRNAs encoding lipid biosynthesis enzymes. An upstream open reading frame (uORF) mediates the translational control of ACC1, the mRNA encoding the rate-limiting enzyme acetyl-CoA carboxylase. The ACC1 uORF also adjusts Acc1p protein levels in different nutrients. Mutating the ACC1 uORF delayed cell cycle progression, reduced cell size and suppressed the replicative longevity of cells lacking the Sch9p protein kinase, the yeast S6 kinase ortholog. These findings reveal unexpected links between lipogenesis and protein synthesis in mitotic cell divisions

overall_design: We used centrifugal elutriation to isolate growing, highly synchronous, unbudded, early G1 cell populations and scored the elutriated cultures over time microscopically, recording the percentage of budded cells with a particle counter that directly measures their volume (channelyzer). Generation of both the Ribosome Profile (RP) and Transcriptional Profile (TP) libraries require at least ≥2E+09 yeast cells per sample. Such sample size could not be collected following a typical time-series experiment because only a small minority of the total cell population is in early G1 at any given moment. Instead, we allowed the entire cell population of each elutriated fraction to progress in the cell cycle until it reached a given cell size (e.g., 40 fl), at which point the sample was harvested. Elutriated cells of the same size were pooled together until enough cells per sample were obtained. This pool of same-size cells defined one experimental replicate (e.g., Sample01A). We harvested cells with 5fl cell size increments, from the time they are born (40 fl -- Sample01), until the end of the cell cycle (75 fl -- Sample08). In total we generated three independent Experimental Replicates for each cell size (A, B and C). We have: Sample01A, 01B and 01C (40 fl); Sample02A, 02B and 02C (45 fl), Sample03A, 03B and 03C (50 fl), Sample04A, 04B and 04C (55 fl), Sample05A, 05B and 05C (60 fl), Sample06A, 06B and 06C (65 fl), Sample07A, 07B and 07C (70 fl) and Sample08A, 08B and 08C (75 fl). Samples are divided into two series: Ribosome Profile (RP) and Transcriptional Profile (TP).

first: Heidi

last: Blank

first: Ricardo

last: Perez

first: Chong

last: He

first: Nairita

last: Maitra

first: Richard

last: Metz

first: Joshua

last: Hill

first: Yuhong

last: Lin

first: Charles

middle: D

last: Johnson

first: Vytas

last: Bankaitis

first: Brian

middle: K

last: Kennedy

first: Michael

last: Polymenis


title: Epigenetic siRNA and chemical screens identify SETD8 inhibition as a new therapeutic strategy of p53 reactivation in high-risk Neuroblastoma.

city: Bethesda

first: Veronica

last: veschi

state: MD

address: 10 Center Dr. MSC-1105

department: NCI

institute: NIH

summary:
Purpose: The intergration of genetic and chemical screens identified SETD8 as a new druggable target in neuroblastoma tumor. The goal of this study is to evaluate the transcriptome profiling (RNA-seq) of Neuroblastoma cell lines after genetic and pharmacological inhibition of SETD8.
Methods: mRNA profiles of NB cells after genetic and pharmacological inhibition of SETD8 were generated by deep sequencing in duplicate with Ilumina HiSeq2500 using Illumina TruSeq V4. The sequence reads were analyzed with software Trimmomatic, STAR and edgeR to determine the differetially expressed genes. qRT–PCR validation was performed using SYBR Green assays.
Results:  About 60 million sequence reads per sample were mapped to the human genome (hg19).  Approximately 10% of the transcripts showed differential expression between the control and the treated samples, with a fold change ≥1.5 and p value <0.05. Altered expression of 12 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to SETD8 function.
Conclusions: Our study identifies SETD8 as a new therapeutic target in Neuroblastoma tumor. RNA-seq transcriptome analyses and functional studies revealed that SETD8 ablation rescued the proapoptotic and cell-cycle arrest functions of p53 through reactivation of the p53 canonical pathway by decreasing p53k382me1.

overall_design: mRNA profiles of Neuroblastoma cells after genetic and pharmacological inhibition of SETD8 were generated by deep sequencing in duplicate with Ilumina HiSeq2500 using Illumina TruSeq V4.

last: Veschi

first: Carol

middle: J

last: Thiele

first: Chunhua

last: Yan

first: Ying

last: Hu


title: Integrated analysis of molecular and systems level function of the Crp regulon [RNA-Seq]

city: La Jolla

first: Haythem

last: Latif

state: California

address: 417 Powell-Focht Bioengineering Hall, 9500 Gilman Drive

institute: University of California San Diego

summary: A fundamental goal of biological research is to connect molecular events with macroscopic physiological phenomena. By incorporating a multi-scale approach that accounts for mechanistic properties of promoters and maps those findings to a genome-scale metabolic-regulatory network, the Escherichia coli Crp regulon is revealed, enabling systems analytics to be applied to delineate its governing role in regulating cellular carbon flow. Genome-wide promoter functions were characterized using ChIP-exo elucidating stable intermediates formed during transcription initiation and distinctions between transcriptional activators and repressors. Genome-wide analysis of Crp regulated genes showed a coordinate regulation of catabolism, anabolism, and energy-generating chemiosmotic processes. Examination of the functional state of the reconstructed regulon during growth on multiple substrates revealed a coherent quantitative adjustment of these overall metabolic processes based on substrate quality, revealing the detailed mechanistic basis for the phenomenologically observed homoeostatic response. Thus, a multi-scale relationship from individual molecular mechanisms to physiological properties is established.

overall_design: RNA-Seq

first: Stephen

last: Federowicz

first: Ali

last: Ebrahim

first: Janna

last: Tarasova

last: Szubin

first: Jose

last: Utrilla

first: Karsten

last: Zengler

first: Bernhard

last: Palsson


title: Integrated analysis of molecular and systems level function of the Crp regulon [ChIP-exo]

overall_design: A total of 13 different experimental conditions are included yielding a total of 43 individual ChIP-exo samples. Invidividual conditions were produced with a minimum of 2 biological replicates. All samples were collected at mid-exponential phase from shake flasks grown on M9 minimal media supplemented with glucose, fructose, or glycerol. Crp, delta Crp, and the Crp mutants delAr1, delAr2, delAr1delAr2, and RpoD ChIP studies were conducted aerobically. ArcA and Fnr ChIP studies were conducted under anaerobi conditions. Delta Crp was generated as a control for ChIP studies of Crp.

first: Richard


title: Integrated analysis of molecular and systems level function of the Crp regulon

overall_design: Refer to individual Series


title: Neuronal activity modifies the chromatin accessibility landscape in the adult brain (RNA-Seq)

status: Public on Jan 08 2017

city: Philadelphia

first: Yijing

last: Su

state: PA

address: Levy 326

department: Department of Oral Medicine

institute: University of Pennsylvania

summary: We generated RNA profiling datasets from adult mouse dentate gyrus  upon neuronal activation at three different time point

overall_design: Examination of chromatin accessibility changes and RNA expression changes in mouse dentate gyrus upon neuronal activation

first: Hongjun

last: Song


title: Neuronal activity modifies the chromatin accessibility landscape in the adult brain (ATAC-Seq)

summary: We generated the chromatin accessibility profiling datasets from adult mouse dentate gyrus upon neuronal activation at 3 different time points

overall_design: Examination of chromatin accessibility changes in mouse dentate gyrus upon neuronal activation


title: Neuronal activity modifies the chromatin accessibility landscape in the adult brain

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


title: Global transcriptome changes after nitrogen replenishment following or not a rapamycin treatment in S288c yeast strain

city: Montpellier

first: Bruno

last: Blondin

address: 2 place Pierre Viala

country: France

institute: INRA


title: Neuronal activity modifies the chromatin accessibility landscape in the adult brain (ATAC-Seq OE)

summary: We generated the chromatin accessibility profiling datasets from adult mouse dentate gyrus with cFos knockdown and overexpression upon neuronal activation (E0 and E1)


title: Neuronal activity modifies the chromatin accessibility landscape in the adult brain (ATAC-Seq KD)

summary: We generated the chromatin accessibility profiling datasets from adult mouse dentate gyrus with cFos knockdown  upon neuronal activation (E0 and E1)


title: Neuronal activity modifies the chromatin accessibility landscape in the adult brain (RNA-Seq OE)

summary: We generated RNA profiling datasets from adult mouse dentate gyrus with cFos knockdown and/or overexpression upon neuronal activation


title: Neuronal activity modifies the chromatin accessibility landscape in the adult brain (RNA-Seq WT)


title: DNA sequence properties that determine susceptibility to epiallelic switching [Bisulfite-Seq]

first: Marco

last: Catoni

summary: Transgenerationally heritable epialleles are defined by the stable propagation of alternative transcriptional states through mitotic and meiotic cell cycles. Given that the propagation of DNA methylation at CpG sites, mediated in Arabidopsis by MET1, plays a central role in epigenetic inheritance, we examined genome-wide DNA methylation in partial and complete loss-of-function met1 mutants. We interpreted the data in relation to transgenerational epiallelic stability and provide evidence that DNA sequence features such as density of CpGs and genomic repetitiveness of the loci largely determine their susceptibility to epiallelic switching. The importance of this rule was confirmed by analyses of common epialleles in natural Arabidopsis accessions and verified in rice.

overall_design: Examination of DNA methylation of 2 met1 mutant alleles, 2 replicates of F2 plants obtained by crossing met1-3 with WT, and 2 transgenic MET1 complemented met1-1 lines.


title: Neuronal activity modifies the chromatin accessibility landscape in the adult brain (ATAC-Seq WT)


title: Long noncoding RNAs transcribed by ERV-9 LTR retrotransposon act in cis to modulate long-range LTR enhancer function [ChIRP-Seq]

status: Public on Jan 07 2017

city: Augusta

first: Justin

last: Choi

state: GA

address: 1410 Laney Walker Blvd.

department: Cancer Center

institute: Georgia Regents University

summary: LTR retrotransposons are repetitive DNA elements comprising ~10% of the human genome.However, Whether or how the LTR lncRNAs serve biological functions is largely unknown. Here we show that in primary human erythroblasts, lncRNAs transcribed from the LTR retrotransposons of ERV-9 human endogenous retrovirus regulated transcription of key erythroid genes. Genome wide ChIRP-Seq was carried out to detect the association of ERV-9 lncRNAs with the genomic DNA in the Day 13 erythroid cells from in vitro culture and phenylhydrazine treated Day 5 spleen cells from transgenic mice in vivo.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Examination by ChIRP-seq of ERV-9 LTR lncRNA interaction with genomic DNA in day 13 human erythroblasts cultured ex vivo from peripheral blood CD34+ cells and day 5 phenylhydrazine treated  transgenic mice spleen cells

first: Tianxiang

first: Dorothy

last: Tuan

first: Jeong-Hyeon


title: Long noncoding RNAs transcribed by ERV-9 LTR retrotransposon act in cis to modulate long-range LTR enhancer function [RNA-Seq]

summary: LTR retrotransposons are repetitive DNA elements comprising ~10% of the human genome. However, Whether or how the LTR lncRNAs serve biological functions is largely unknown. Here we show that in primary human erythroblasts, lncRNAs transcribed from the LTR retrotransposons of ERV-9 human endogenous retrovirus regulated transcription of key erythroid genes. Global knock-down of ERV-LTR lncRNAs was performed in the in vitro erythropoiesis system of human CD34 cells, and genome wide RNA-seq was carried out to detect the effect on transcription.

overall_design: Examination of transcriptome changes of 2 shRNA knock-down cells and a scrambled control knock-down cells


title: Endothelial transcriptome in response to pharmacological methyltransferase inhibition

city: Melbourne

first: Mark

last: Ziemann

state: VIC

address: 85 Commercial Rd

department: Bioinformatics Working Group

country: Australia

institute: Burnet Institute

summary: The enzymatic activities of protein methyltransferases serve to write covalent modifications on histone and non-histone proteins in the control of gene transcription. Here, we describe gene expression changes in human endothelial cells caused by treatment with methyltransferase inhibitors 7,7'-carbonylbis (azanediyl) bis(4-hydroxynaphthalene-2 -sulfonic acid (AMI-1) and disodium-2-(2,4,5,7- tetrabromo-3-oxido-6-oxoxanthen-9-yl) benzoate trihydrate (AMI-5). Deep sequencing of mRNA indicated robust change on transcription following AMI-5 treatment compared with AMI-1. Functional annotation analysis revealed that both compounds suppress the expression of genes associated with translational regulation, suggesting arginine methylation by protein arginine methyltransferases (PRMTs) could be associated with regulation of this pathway. Interestingly, AMI-5 but not AMI-1 was found to decrease methylation of H3 histones at lysine 4 and down-regulate gene expression associated with interleukin-6 (IL-6) and activator protein-1 (AP-1) signaling pathways. These results imply that inhibition of protein methylation by AMI-1 and AMI-5 can differentially regulate specific pathways with potential to interrupt pathological signaling in the vascular endothelium.

overall_design: HMEC-1 cells were treated with either 7,7'-carbonylbis (azanediyl) bis(4-hydroxynaphthalene-2 -sulfonic acid (AMI-1) or disodium-2-(2,4,5,7- tetrabromo-3-oxido-6-oxoxanthen-9-yl) benzoate trihydrate (AMI-5). These compounds were dissolved in DMSO and added to cells to make a final concentration of 100 μM. As a control, cells were exposed to DMSO only. Exposure time was 16 h.

first: Jun

last: Okabe

first: Ana

last: Fernandez

first: Sam

last: Keating

first: Aneta

last: Balcerczyk

first: Assam

last: El-Osta


title: RNA-Seq analysis of coding and long non-coding RNAs in the sub-chronic and chronic stages of spinal cord injury

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:
Background: Chronic spinal cord injury (SCI) remains one of the most debilitating neurological disorders and the majority of SCI patients are in the chronic phase. Previous studies of SCI that were limited by resources and technology have usually focused on few genes and pathways at a time. Thus, a comprehensive view of the complex molecular changes underlying SCI pathophysiology is needed. In particular, the biological roles of long non-coding RNAs (lncRNAs), a class of regulatory RNAs, have never been characterized systemically in SCI.
Results: This study is the first to investigate alterations in the expression of both coding and long non-coding genes in the sub-chronic and chronic stages of SCI using RNA-Sequencing. Our data revealed differentially expressed genes, canonical pathways, and networks unique to particular time points or common to multiple time points in the progression of SCI. For example, a network of multiple critical genes responsible for astrogliosis and fibrosis was identified among differentially expressed genes common to three time points (1month, 3months, and 6 months after SCI). Moreover, the potential functions of rat lncRNAs in SCI were extensively analyzed. First, a comprehensive annotation database was compiled for rat lncRNAs that revealed several interesting characteristics of lncRNAs in the rat genome. Then, by correlating the temporal expression patterns of lncRNAs with those of protein-coding genes, we identified lncRNAs that are associated with functional categories such as signaling pathways, immune response, epigenetic modification, nervous system, and extracellular matrix. The expression patterns of some lncRNAs are highly correlated with those of their most proximal protein-coding genes, so it is possible that these lncRNAs regulate the expression of their protein-coding neighbors. Finally, we searched for transcription factor motifs enriched in the upstream regulatory regions of differentially expressed lncRNAs, and identified differentially expressed lncRNAs that are homologous to human genomic regions harboring molecular variants associated with human neurological diseases.
Conclusions: Overall, our study provides an unprecedented resource for the study of sub-chronic and chronic SCI that will help the research community identify new molecular targets for future functional investigation.

overall_design: Time-series gene expression profiles of protein-coding and long non-coding genes were generated after sequencing transcriptomes obtained from spinal cord control samples and injured spinal cords (SCI) at different  phases of sub-chronic and chronic injury: 1 month, 3 months, and 6 months. Samples were obtained from 36 Sprague-Dawley female rats randomly assigned to control or injury groups. Tissues from 3 rats were pooled to form a biological replicate. Three replicates for control and injury groups were performed.

last: Cuevas-Diaz Duran

first: Han

last: Yan

first: Yiyan

last: Zheng

first: Xingfan

last: Huang

first: Raymod

last: Grill

first: Dong

middle: H

last: Kim

first: Qilin

last: Cao

first: Jiaqian

last: Wu


title: Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies [RNA-Seq]

city: Durham

first: Gregory

last: Crawford

state: NC

address: 101 Science Drive

department: Center for Genomic and Computational Biology

institute: Duke University

summary: MyoD is known to transdifferentiate fibroblasts into muscle-like cells. Despite phenotypic resemblance and expression of myogenic marker genes in transdifferentiated cells, our global gene expression data suggests that ~100 genes, many involved in muscle development and function, remain non-reprogrammed. To understand this incomplete reprogramming, we characterized genome-wide chromatin accessibility and MyoD binding in human primary myoblasts and in MyoD-induced skin fibroblast cells. Our analyses revealed thousands of sites with incomplete chromatin reprogramming.Combined analyses of gene expression and epigenetic profiles revealed that many myogenic genes not upregulated during the transdifferentiation process have undergone MyoD-dependent chromatin remodeling, but to a significantly lower extent than reprogrammed genes. Our findings suggest that incomplete MyoD-induced transdifferentiation is due to chromatin-remodeling deficiencies, and that additional factors are required to transdifferentiate cells into a state more similar to myoblasts.

overall_design: Fibroblast cells were transduced with a vector carrying human MyoD gene and induced by tetracycline for expression. Dnase-seq, ChIP-seq and RNA-seq were used to identify transcription factors binding, differential chromtin structural change, and differential expression at on-target and off-target sites.

first: Dinesh

last: Manandhar

first: Lingyun

last: Song

first: Ami

last: Kabadi

first: Lee

last: Edsall

first: Melanie

last: Ehrlich

first: Koji

last: Tsumagari

first: Charles

last: Gersbach

first: Raluca

last: Gordan


title: Net silencing by let-7i in Postural Tachycardia Syndrome

first: Mark

last: Ziemann

summary: While strongly implicated in Postural Tachycardia Syndrome (POTS), considerable controversy exists regarding norepinephrine transporter (NET) loss-of-function. POTS is characterized by the clinical symptoms of orthostatic intolerance, light-headedness, tachycardia and syncope or near syncope with upright posture. Abnormal sympathetic nervous system activity is typical, of a type which suggests dysfunction of the NET, with evidence the gene responsible is under tight epigenetic control. Using RNA of isolated chromatin combined with sequencing (RICh-Seq) we show let7i miRNA suppresses NET by MeCP2. Vorinostat restores epigenetic control and NET expression in POTS.

overall_design: We used biotin labeled locked nucleic acid oligonucleotides to pull-down three regions of the NET (SLC6A2) gene promoter from sheared chromatin. These NET enriched fractions underwent small RNA library preparation and Illumina sequencing (labeled “NET_rep1-3”). As a negative control, we used a pool of scrambled probes (labeled “scrambled_rep1-3”). We also sequenced small RNA from chromatin that did not undergo enrichment (labeled “input_rep1-3”).

first: Abdul

middle: W

last: Khan

first: Susan

last: Corcoran

first: K

last: Harikrishnan

first: Jun

last: Okabe

first: Haloom

last: Rafehi

first: Scott

last: Maxwell

first: Murray

last: Esler

first: Assam

last: El-Osta


title: Specificity of Pitx3-Dependent Gene Regulatory Networks in Subsets of Midbrain Dopamine Neurons

city: Montreal

first: Panojot

last: Bifsha

state: QC

address: 3175 Chemin de la Côte Ste-Catherine

department: Pediatrics

institute: CHU Sainte-Justine

summary: Global binding patterns of Pitx3 on genomic DNA of human dopaminergic cells revealed that Pitx3 is often co-recruited to regions that foster the formation of GATA-bHLH-BRN complexes, which usually involve Lmo co-regulatory proteins

overall_design: ChIP assay followed by high throughput sequencing (ChIP-seq)

first: Aurelio

last: Balsalobre

first: Jacques

last: Drouin


title: Brown adipocytes can display a mammary basal myoepithelial cell phenotype in vivo

city: Dallas

first: Li

last: Li

state: TX

address: 5323 Harry Hines Boulevard

institute: UT Southwestern Medical Center

summary:
A comparison of the mRNAs analysis in lactation mammary myoepithelial cells (GFP+/GFP-) and brown adipocytes (GFP+)  from Myf5-Cre-ROSAmTmG and Ucp1-iCre-ROSAmTmG mice.
Results provide the gene expression signature in the brown origin (UCP1/Myf5-positive) myoepithelial cells in vivo.

overall_design:
Mammary myoepithelial cells and brown adipocytes were isolated by FACS sorting based on the cell surface markers and total RNA were immediately.
GFP+ mammary myoepithelial cells (Lin−:CD24+:CD29hi) from lactation day 10 Myf5-Cre-ROSAmTmG mice (n=2).
GFP- mammary myoepithelial cells (Lin−:CD24+:CD29hi) from lactation day 10 Myf5-Cre-ROSAmTmG mice (n=2).
GFP+ mammary myoepithelial cells (Lin−:CD24+:CD29hi) from lactation day 10 Ucp1-iCre-ROSAmTmG mice (n=2).
GFP- mammary myoepithelial cells (Lin−:CD24+:CD29hi) from lactation day 10 Ucp1-iCre-ROSAmTmG mice (n=2).
GFP+ brown adipocytes from 8-week old female  Myf5-Cre-ROSAmTmG mice (n=2).
GFP+ brown adipocytes from 8-week old female Ucp1-iCre-ROSAmTmG mice (n=2).

first: Baoguo

first: John

middle: R

last: Speakman


title: Incomplete MyoD-induced transdifferentiation is mediated by chromatin remodeling deficiencies [ChIP-Seq]

first: Gregory

last: Crawford

first: Dinesh

last: Manandhar

first: Lingyun

last: Song

first: Ami

last: Kabadi

first: Lee

last: Edsall

first: Melanie

last: Ehrlich

first: Koji

last: Tsumagari

first: Charles


title: Epigenetic variation between urban and rural populations of Darwin’s finches

city: Pullman

first: Michael

last: Skinner

state: WA

address: Abelson 507

department: SBS

institute: WSU

summary: The molecular basis of evolutionary change is assumed to be genetic variation. However, growing evidence suggests that epigenetic mechanisms, such as DNA methylation, may also be involved in evolutionary change. An important first step in evaluating this hypothesis is to test for the presence of epigenetic variation between natural populations living under different environmental conditions. In the current study we explored variation between populations of Darwin’s finches living in adjacent “urban” and “rural” environments on Santa Cruz Island in the Galápagos. We tested for morphological, genetic, and epigenetic differences between the urban and rural populations of each of two species of ground finches, Geospiza fortis and G. fuliginosa. Using data collected from more than 1000 birds, we found significant morphological differences between populations of G. fortis, but not G. fuliginosa. We did not find genetic differences between populations of either species, based on comparisons of copy number variation (CNV). In contrast, we did find epigenetic differences between the urban and rural populations of both species, based on DNA methylation analysis. We explored genomic features and gene associations of the differentially methylated regions (DMR), as well as their possible functional significance. In summary, our study documents local population epigenetic variation within species of Darwin’s finches.

sample_organism:
Geospiza fortis
Geospiza fuliginosa

platform_organism:
Geospiza fortis
Geospiza fuliginosa

overall_design: Red blood cell and sperm samples were collected from two species of finch (Geospiza fortis and Geospiza fuliginosa) from two different locations (rural and urban). Samples from individual birds were combined into pooled samples for sequencing. For erythrocyte samples, three pools of five individuals each were created for each site. For sperm samples, three pools of two individuals each were created for each site. The methylation characteristics of the pooled samples was estimated using a methylated DNA immunoprecipitation (MeDIP) followed by PE50 sequencing on an Illumina HiSeq 2500 platform.

first: Sabrina

last: McNew

first: Daniel

last: Beck

first: Ingrid

last: Sadler-Riggleman

first: Sarah

last: Knutie

first: Jennifer

last: Koop

first: Dale

last: Clayton


title: Transcriptomic profiles of human foreskin fibroblast cells in response to orf virus

city: Guangzhou

first: Daxiang

last: Chen

state: Guangdong

address: 1838 N. Guangzhou Avenue

country: China

institute: Southern Medical University

summary: Using RNA sequencing technology, we compared speciﬁc changes in the transcriptomic proﬁles in human foreskin fibroblast cells (HFF-1) following ORFV infection. ORFV speciﬁcally upregulated and downregulated a variety of genes, including genes involved in antiviral immune response, apoptosis, cell cycle and a series of signaling pathways, such as the IFN and p53-signaling pathways. A range of genes were downregulated at early stage. In contrast, the virus up-regulates a number of cellular genes at late stage.

overall_design: HFF-1 mRNA profiles of 0, 3, and 8 hours post infection with orf virus were generated by deep sequencing, in triplicate, using Illumina Hiseq2500.

first: Shuhong

last: Luo


title: Checkpoint-independent Regulation of Origin Firing by Mrc1 through Interaction with Hsk1 kinase

status: Public on Jan 06 2017

city: Tokyo

first: Yutaka

last: Kanoh

address: 2-1-6 Kamikitazawa, Setagaya-ku

department: Genome Medicine

institute: Tokyo Metropolitan Institute of Medical Science

summary: Mrc1 is a conserved checkpoint mediator protein that transduces replication-stress signal to downstream effector kinase. Loss of mrc1 checkpoint activity results in aberrant activation of late/dormant origins in the presence of hydroxyurea. Mrc1 was also suggested to regulate orders of early-origin firing in a checkpoint-independent manner, but its mechanism was unknown. Here we identify HBS (Hsk1 Bypass Segment) on Mrc1. ∆HBS does not suppress late/dormant origin firing in the presence of hydroxyurea but causes precocious and enhanced activation of weak early-firing origins during normal S-phase progression, and bypasses the requirement of Hsk1 for growth. This may be caused by disruption of intramolecular binding between HBS and NTHBS (N-terminal-Target-of-HBS). Hsk1 binds to Mrc1 through HBS and phosphorylates a segment adjacent to NTHBS, disrupting intramolecular interaction. We propose that Mrc1 exerts “brake” on initiation (through intra-molecular interaction) and this brake can be released (upon loss of intra-molecular interaction) by either Hsk1-mediated phosphorylation of Mrc1 or deletion of HBS (or phosphomimic mutation) which can bypass the function of Hsk1 for growth. The “brake” mechanism may explain the checkpoint-independent regulation of early origin firing in fission yeast.

overall_design: Replication profile by ChIP-seq of BrdU-incorporation in wild-type, mrc1∆, mrc1-3A, mrc1∆hbs. And the location of the potential replication origins by ChIP-seq of Mcm4

first: Seiji

last: Matsumoto

first: Michie

last: Shimmoto

first: Motoshi

last: Hayano

first: Kyosuke

last: Ueda

first: Rino

last: Fukatsu

first: Naoko

last: Kakusho

first: Hisao

last: Masai


title: Nat1 promotes translation of specific proteins that induce differentiation of mouse embryonic stem cells [ribosome profiling]

city: Kyoto

first: Shinya

last: Yamanaka

address: 53 Kawahara-machi, Shogoin, Sakyo-ku

institute: Center for iPS Cell Research and Applicaton (CiRA), Kyoto University

summary: Nat1 (also known as p97/Dap5/Eif4g2) is a ubiquitously expressed cytoplasmic protein that is homologous to the C-terminal two thirds of eukaryotic translation initiation factor 4G (also known as Eif4g1). We previously showed that Nat1-null mouse embryonic stem cells (mESCs) were resistant to differentiation. In the current study, we found that Nat1 and Eif4g1 share many binding proteins, such as Eif3s, Eif4s and ribosomal proteins. However, Nat1 did not bind to Eif4e or poly A binding proteins, which are critical for cap-dependent translation initiation. In contrast, Nat1 binds to Eif2s, Fmr and related proteins, and Prrc2 proteins more preferentially than does Eif4g1. We also found that Nat1-null mESCs possess a status partially similar to ground state, which is established in wild-type mES cells when treated with inhibitors of the ERK and GSK3 signaling pathways. In Nat1-null mESCs, the ERK pathway is suppressed even without inhibitors. Ribosomal profiling revealed that translation of Map3k3 and Sos1 is suppressed in the absence of Nat1. Forced expression of Map3k3 induced differentiation of Nat1-null mESCs. These data collectively showed that Nat1 is involved in translation of proteins that are required for cell differentiation.

overall_design: Examining ribosome-protected mRNA fragments (RPF) and total RNA in replicate WT ESCs (n=2), Nat1+/- mESCs (n=3) and Nat1-null ESCs (n=3).

first: H

last: Sugiyama

first: K

last: Takahashi


title: Analysis of gene expression (RNAseq) from shTP53:RB1 LNCaP/AR cell lines

first: Ping

last: Mu

address: 6000 Harry Hines Blvd., NA6.308A

department: Human Oncology and Pathogenesis

summary: Some cancers evade targeted therapies through a mechanism known as lineage plasticity, whereby tumor cells acquire phenotypic characteristics of a cell lineage whose survival no longer depends on the drug target. Here we show, using in vitro and in vivo prostate cancer models, that these tumors can develop resistance to the antiandrogen drug enzalutamide by a phenotypic shift from androgen receptor (AR) dependent luminal epithelial cells to AR independent basal-like cells. This lineage plasticity is enabled by loss of TP53 and RB1 function, is mediated by increased expression of the reprogramming transcription factor SOX2 and can be reversed by restoring TP53 and RB1 function or by inhibiting SOX2 expression. Thus, mutations in tumor suppressor genes can create a state of increased cellular plasticity that, when challenged with antiandrogen therapy, promotes resistance through lineage switching.

overall_design: LNCaP/AR prostate cell line was transduced with shNT or shTP53:RB1 hairpins and then RNA was harvested from these cell lines for gene epxression analysis.

first: Charles

middle: L

last: Sawyers


title: Fetal and adult progenitors give rise to unique populations of CD8+ T cells

city: Ithaca

first: Andrew

last: Grimson

address: 445 Biotechnology Building

department: Molecular Biology & Genetics

institute: Cornell University

summary: Neonatal CD8+ T cells are unable to form long-lived memory cells in response to infection due to cell-intrinsic reasons; however, the underlying basis for this difference is unclear.  Here,  using intrathymic transfers with fetal and adult progenitor cells, in conjunction with gene expression profiling and functional assays, we demonstrate that because neonatal CD8+ T cells are derived from a distinct progenitor cell population, they behave differently than adult cells from the time they are generated. These progenitor cells have higher Lin28 expression than adult progenitor cells. We found that adult CD8+ T cells generated from progenitor cells with induced Lin28 expression do not form memory cells, similar to neonatal cells. These findings suggest that neonatal and adult CD8+ T cells belong to separate lineages of CD8+ T cells and potentially explains why it is challenging to elicit memory CD8+ T cells in early life.

overall_design: Gene expression analysis of adult and neonatal CD8+ T cells in the thymus, the spleen, and splenic cell subsets (naïve and innate memory). Small RNA analysis of CD8+ T cells expressing exogenous Lin28b.

first: Erin

last: Wissink


title: MYC Mediates mRNA Cap Methylation of Canonical Wnt/beta-catenin Signaling Transcripts by Recruiting CDK7 and RNA Methyltransferase

city: Lebanon

first: Michael

last: Cole

state: NH

address: One Medical Center Dr

institute: Geisel School of Medicine at Dartmouth

summary: We performed an RNA pulldown against a methyl group on the mRNA cap using a fusion protein, GST-eIF4E, highly specific for a m7G-mRNA cap. We performed RNA-seq on both the pulldowns and inputs and normalized our pulldown to input in order to determine which genes MYC targets for mRNA cap methylation above and beyond any affect at the transcriptional level. We found that MYC targets approximately 30% of transcripts for enhanced mRNA cap methylation above 1.2 fold on a global scale following 24 h of MYC induction, specifically transcripts involved in the canonical Wnt/β-catenin signaling pathway. We used this dataset to validate transcripts targeted by MYC for mRNA cap methylation and to help us determine the mechanism responsible for this phenomenon.

overall_design: Examination of MYC-mediated mRNA cap methylation on a global scale by isolating methyl-capped (m7G) mRNA from P493-6 cells with varying MYC levels for further analysis.

first: Valeriya

last: Posternak


title: Nat1 promotes translation of specific proteins that induce differentiation of mouse embryonic stem cells

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

overall_design: Refer to individual Series


title: p53 coordinates Wnt and TGF-β inputs on mesendoderm differentiation genes

city: Hangzhou

first: Yilong

last: Zou

state: Zhejiang

address: Shilongshan Road #18, Cloud Town, Xihu District

department: School of Life Sciences

institute: Westlake University

summary: The TGF-β superfamily member Nodal triggers mesendoderm differentiation in embryonic stem (ES) cells. This transition however requires cooperating Wnt signaling inputs. Here we report that p53, a powerful tumor suppressor in adult tissues, orchestrates this cooperation. We show that p53, which is released from inhibition as mouse ES cells exit from pluripotency, acts as a direct inducer of Wnt3 expression. Wnt-activated Tcf3 then converges with Nodal-activated Smad transcriptional complexes on mesendoderm specification super-enhancers. p53 and its homolog p73 act redundantly in Wnt induction. When p53 and p73 are depleted, the ES cells fail to secrete autocrine Wnt ligands, Tcf and Nodal-activated Smads fail to bind to mesendoderm gene enhancers, and the cells adopt ectoderm rather than mesendoderm identity. Enforced Wnt3 expression or addition of Wnt3a rescues mesendoderm differentiation in p53/p73-depleted ES cells. Thus, independently of their established role as tumor suppressors that guard genome integrity in mature cells, p53 and p73 serve a primordial role in ES cell differentiation by driving a cooperation of Wnt and TGF-β transcriptional inputs on mesendoderm identity gene enhancers.

overall_design: In this study, 14 RNA-Seq samples and 20 ChIP-Seq samples are included.

first: Qiong

last: Wang

first: Joan

last: Massagué


title: Therapeutic targeting MLL degradation pathways in MLL-rearranged leukemia

city: Chicago

first: Ali

last: Shilatifard

state: IL

address: 320 E Superior St

department: Department of Biochemistry and Molecular Genetics

institute: Northwestern University Feinberg School of Medicine

summary: Chromosomal translocations of the mixed-lineage leukemia (MLL) gene with various partner genes result in aggressive leukemia with dismal outcomes. Despite similar expression at the mRNA level from the wild-type and chimeric MLL alleles, the chimeric protein is more stable. We report that UBE2O functions in regulating the stability of wild-type MLL in response to interleukin-1 signaling. Targeting wild-type MLL degradation impedes MLL leukemia cell proliferation, and it downregulates a specific group of target genes of the MLL chimeras and their oncogenic cofactor, the super elongation complex. Pharmacologically inhibiting this pathway substantially delays progression, and it improves survival of murine leukemia through stabilizing wild-type MLL protein, which displaces the MLL chimera from some of its target genes and, therefore, relieves the cellular oncogenic addiction to MLL chimeras. Stabilization of MLL provides us with a paradigm in the development of therapies for aggressive MLL leukemia and perhaps for other cancers caused by translocations.

overall_design: Determination of factors affecting MLL stability using a genome-wide shRNA screen in HEK293 cells. Examination of MLL, MLL chimera, and Super Elongation complex in HEK293 and leukemia cells with and without knockdown, or chemical inhibition, of proteins affecting MLL stability. Control cells such as MLL WT and knockout MEF were used to test MLL antibody specificity specificity

first: Kaiwei

last: Liang

first: Edwin

last: Smith


title: TGF-β inhibitors stimulate red blood cell production by enhancing self-renewal of BFU-E erythroid progenitors

city: Rochester

first: Hu

last: Li

address: 200 First Street, Gonda Building G19-408

department: Molecular Pharmacology & Experimental Therapeutics

institute: Mayo Clinic

summary: Erythroid progenitor BFU-Es are so-named based on their ability to generate in methylcellulose culture large colonies of erythroid cells that consist of “bursts” of smaller erythroid colonies derived from the later CFU-E Epo- dependent progenitors. “Early” BFU-E cells forming large BFU-E colonies presumably have higher capacities for self-renewal than do those forming small BFU-E colonies. In order to understand the mechanism underlying this heterogeneity, we conducted single cell transcriptome analysis on BFU-E cells purified from mouse embryos. Our analyses showed that there are two principal subgroups of mouse BFU-E cells and that the type III TGFβ receptor (TβRIII) is a potential marker that distinguishes “early” and “late” BFU-Es.  Expression of TβRIII is correlated with that of GATA1, a gene encoding an erythroid transcription factor induced during the BFU-E to CFU-E transition. The mouse and human BFU-E sub populations (TßRIII10%lo) expressing the 10% lowest amount of surface TβRIII are indeed enriched for early BFU-Es, and are significantly more responsive to glucocorticoid stimulation, which promotes BFU-E self-renewal, as compared to the total BFU-E population. The TßRIII10%lo BFU-E subpopulation presumably represents earlier BFU-Es with maximal capacity for self-renewal. Consistent with this notion, signaling by the TGFβ receptor kinases RI and RII increases during the transition from early (TßRIII10%lo) to late  (TßRIII10%hi) BFU-Es and then decreases in CFU-E cells. Blocking TGF-β signaling by receptor kinase inhibitors increase TßRIII10%lo BFU-E cell self-renewal and increases total erythroblast production, suggesting the use of this type of drug in treating Epo unresponsive anemias.

overall_design: Discovery of BFU-E subpopulations

first: Xiaofei

last: Gao

first: Sherry

last: Lee


title: Genome-wide mapping of p300 binding in resting and activated human naïve and memory CD8 T cells

status: Public on Jan 05 2017

city: Shanghai

first: Cheng

last: Yang

address: 227 Chongqing South Road, Luwan District

institute: Shanghai Jiaotong University School of Medicine

summary: Memory T cells (TM) play a prominent role in protective and auto-immunity because they mount a more effective response than naïve T cells (TN), by rapidly expressing a large number of immune response genes upon stimulation. Previous studies have shown a correlation between increased histone acetylation levels and rapid gene expression at specific loci in CD8+ TM. However, the underlying mechanisms of histone acetylation remodeling in TM and its role in regulating global gene expression are not well defined, particularly in human TM cells. In this study, we examined the global level of histone acetylation and the expression of histone acetyltransferases and deacetylases , and found no differences between human CD8+ TN and TM cells. Through Genomegenome-wide mapping of the histone acetyltransferase p300 in human CD8+ TN and TM cells, recruitment of p300 was found to be positively correlated with the expression of 213 genes in TM and 516 genes in TN cells at rest, and was positively correlated with the expression of 556 genes in TM and 330 genes in TN cells after 4 hrs’ stimulation. Importantly, genes which have positive correlations between expression levels and p300 occupancy in TM were significantly enriched in effector functions of CD8+ T cells, while those in TN cells were over-presented in nucleic acid processing and cell differentiations. At IFNG locus, specifically, the recruitment of p300 was significantly higher in CD8+ TM than TN and cells that were correlated with increased levels of histone acetylation at this locus, and robust IFN-g expression by CD8+ TM cells. Selective inhibition of p300 and deletion of p300 binding sites within the IFNG promoter resulted in decreased histone acetylation at this locus and the lower expression level of IFN-g in CD8+ TM cells. These results suggest that recruitment of the histone acetyltransferase p300 modifies histone acetylation and allows rapid expression of IFNG, and likely a large set of immune response genes, in human CD8+ TM, which in turn contribute to the enhanced functionality of human CD8+ TM cells.

overall_design: Human naïve and memory T cells were isolated from peripheral blood of healthy individuals by FACS, and were triggered through CD3/CD28 signaling for 0 hr or 4 hr. Chromatin were fixed with 1% formaldehyde, fragmented by sonication, and fragments that were bound by p300 were immuno-precipitated with a p300 specific antibody. Immuno-precipitated DNA was analyzed by Illumina/Solexa ChIP-Sequencing.

first: Hao

last: Shen


title: Enrichment of Wolbachia Endosymbiont Transcripts from Host Nematode RNA by Cappable-seq

city: Ipswich

first: Barton

last: Slatko

state: Massachusetts

address: 240 County Road

institute: New England Biolabs

summary: We report the application of Cappable-seq to selectively enrich prokaryotic endosymbiont transcripts from mixed host-symbiont total RNA.

overall_design: Comparison of total RNA and Cappable-seq enriched RNA from Brugia malayi.

first: Ashley

last: Luck

first: Jeremy

last: Foster


title: Impact of nonalcoholic fatty liver disease on toxicokinetics of tetrachloroethylene in mice

city: College Station

first: Ivan

last: Rusyn

address: 4458 TAMU

institute: Texas A&M University

summary:
We report the effect of NAFLD on liver gene expression changes that could impact tetrachloroethhylene metabolism
Methods: We fed male C57Bl/6J mice a base diet (BD), high fat (HFD), or methionine/choline/folate deficient high fat diet (MCD) for 8 weeks and then treated them with vehicle or tetrachloroethylene (PERC, 300 mg/kg ig). We only report "basal" differences herein (aka vehicle-treated).
Results: We report that there were diet-specific differences in xenobiotic metabolizing genes, and that these genes may be responsible for NAFLD-induced disruption in PERC metabolism

overall_design: Examination of liver left lobe gene expression for 3 different diets fed to C57Bl/6J male mice

first: Joe

last: Cichocki


title: Long noncoding RNAs transcribed by ERV-9 LTR retrotransposon act in cis to modulate long-range LTR enhancer function

city: Augusta

first: Justin

last: Choi

address: 1410 Laney Walker Blvd.

institute: Georgia Regents University


title: Encoding of Contextual Fear Memory Requires De Novo Proteins in the Prelimbic Cortex

city: New York

first: Doron

last: Betel

state: NY

address: 1305 York Avenue (Box 140)

department: Medicine

institute: Weill Cornell Medical College

summary: Time dependent coordinated hippocampal-prefrontal cortical interactions are required for the long-term storage of memories. However, the role of prefrontal cortex (PFC) in encoding of long-term memories remains elusive. Here, we discover a critical role of PFC in the encoding of contextual memories in mice. We demonstrate that specific pools of mRNAs are translated in the PFC following one and six hours of behavioral training. Moreover, disruption of protein synthesis in the prelimbic region of PFC immediately after training inhibits encoding contextual fear memories, whereas disruption at six hours after training is ineffective. Thus, early protein synthesis in the PFC is necessary and critical for the encoding of contextual fear memories. These findings establish key role for the prelimbic cortex in encoding of contextual memories.

overall_design: Examination of polyribosome associated mRNAs in the prefrontal cortex of 8 adult mice following one hour and six hour after contextual fear conditioning.

first: Sathya

last: Puthanveettil


title: Genome-wide identification of transcription factor ATOH1 target genes in adult small intestine and colon.

city: Houston

first: Yuan-Hung

last: Lo

address: One Baylor Plaza

institute: Baylor College of Medicine

summary: We generated three mRNA expression profiles by RNA-Seq of (i) wild-type crypts, (ii) Atoh1 knockout crypts, and (iii) purified ATOH1-positive cells.

overall_design: We isolated Atoh1 knockout and littermate wild-type crypts from 6-8 week old Atoh1lox/lox;VilCreERT2 and Atoh1lox/WT;VilCreERT2 mice, respectively. In addition, ATOH1-positive cells were isolated by flow cytometry of 7AAD-negative (live), GFP-positive cells from either ileal or colonic crypts of Atoh1GFP/GFp mice (which express a functional ATOH1::GFP protein and are phenotypically normal).

first: Joo-Seop

last: Park

first: Noah

last: Shroyer


title: Genome-wide identification of transcription factor ATOH1 target genes in adult small intestine and colon (ChIP-Seq)

summary: We identify targets of ATOH1 binding in the adult intestinal epithelium.

overall_design: Ileal or colonic crypts were isolated from 10~12 week old adult Atoh1GFP/GFP mice (which express a functional ATOH1::GFP protein and are phenotypically normal) followed by ATOH1, H3K27Ac and H3K27me3 ChIP-Seq.


title: Alveolar Macrophages Prevent Lethal Influenza Pneumonia By Inhibiting Infection Of Type-1 Alveolar Epithelial Cells

city: Charlottesville

first: Thomas

last: Braciale

state: Virginia

address: 345 Crispell Dr

department: Pathology

institute: University of Virginia

summary: Examine differences in Type-1 alveolar epithelial cells with and without alveolar macrophages during influenza infection

overall_design: Type-1 alveolar epithelial cells were isolated from mice with and without alveolar macrophages at day 2 post-infection with influenza a virus

first: Amber

last: Cardani

first: Adam

last: Boulton


title: Genome-wide identification of transcription factor ATOH1 target genes in adult small intestine and colon


title: The molecular response of the white-rot fungus Dichomitus squalens to wood and non-woody biomass as examined by transcriptome and exoproteome analyses

city: Utrecht

first: Ronald

last: de Vries

address: Uppsalalaan 8

department: fungal physiology

country: Netherlands

institute: Centre of fungal biodiversity

summary: The ability to obtain carbon and energy is a major requirement to exist in any environment. For several ascomycete fungi (post-)genomic analyses have shown that species that occupy a large variety of habitats possess a diverse enzymatic machinery, while species with a specific habitat have a more focused enzyme repertoire that is well-adapted to the prevailing substrate. White-rot basidiomycete fungi also live in a specific habitat, as they are found exclusively in wood. In this study we evaluated how well the white-rot fungus Dichomitus squalens has adapted to degrade its natural wood substrate. The transcriptome and exoproteome of D. squalens were analysed after cultivation on two natural substrates, aspen and spruce wood, and two non-woody substrates, wheat bran and cotton seed hulls. D. squalens produced ligninolytic enzymes mainly at the early time point of the wood cultures, indicating the need to degrade lignin to get access to wood polysaccharides. Surprisingly, the response of the fungus to the non-woody polysaccharides was nearly as good match to the substrate composition as observed for the wood polysaccharides. This indicates that D. squalens has preserved its ability to efficiently degrade plant polysaccharides not present in its natural habitat.

overall_design: This study compares the gene expression of D. squalens growing on different plant biomass at two different time points. The culture medium was supplemented with spruce wood (Picea abies) sawdust, aspen wood (Populus tremula) sawdust, powdered wheat bran or powdered cotton seed hulls respectively. Samples were taken after 9 and 16 days of culture.

first: Johanna

last: Rytioja

first: Kristiina

last: Hildén

first: Marcos

last: Di Falco

first: Miaomiao

last: Zhou

first: Maria Victoria

last: Aguilar-Pontes

first: Outi-Maaria

last: Sietiö

first: Adrian

last: Tsang

middle: P

first: Miia

last: Mäkelä


title: Genome-wide H2B monoubiquitination regulates gene expression by coordinating H3K4me3 and H3K27me3 [RNA-Seq Data Set]

city: Göttingen, Niedersachsen

first: Steven

last: Johnsen

state: Niedersachsen

address: Robert Koch Strasse 40

department: Clinic for General, Visceral and Pediatric Surgery

country: Germany

institute: University Medical Center Göttingen

summary: Gene body-associated monoubiquitination of H2B (H2Bub1) coupled with promoter-associated active histone modifications such as trimethylation H3 on lysine 4 (H3K4me3) and acetylation H3 on lysine 27 (H3K27ac) facilitate gene transcription. However, surprisingly, only a subset of genes is altered in their expression following knockdown of H2B ubiquitin-protein ligases RNF20 or RNF40 in human cells. In order to obtain a more complete genome- and transcriptome-wide understanding of the role of H2Bub1 in gene transcription, we generated tamoxifen-inducible Rnf40 knockout mouse embryonic fibroblasts (MEFs). Mapping of H2Bub1, H3K4me3, H3K27me3, and H3K27ac occupancy identified an “ascending” gene cluster including bivalent genes, which is occupied by low to moderate amounts of H2Bub1 and exhibits high variability in transcription. We provide evidence that the variation in expression is highly associated with the variations in H3K4me3, H3K27me3, and H3K27ac occupancy. Moreover, these variably marked “ascent” genes are selectively regulated in Rnf40-deficient MEFs. Consistent with previous studies, the effect of Rnf40 loss on the expression of genes within this cluster is also variable with some genes demonstrating increased while others decreased mRNA levels following Rnf40 deletion. Importantly, we identified the Ezh2 gene as an Rnf40/H2Bub1 target whose expression significantly decreased in Rnf40-deficient MEFs. Notably, we show that genes upregulated following Rnf40 deletion are enriched for H3K27me3, which is decreased following Rnf40 deletion, and these effects can be mimicked by treating with a small molecule EZH2 inhibitor. On the other hand, consistent with findings in many eukaryotic systems, genes whose expression decreases following Rnf40 deletion show an enrichment of H3K4me3 and decreased levels following deletion. Together, we provide mechanistic information by which Rnf40, presumably via H2Bub1, modulates gene expression via coordination of the active and repressive marks H3K4me3 and H3K27me3.

overall_design: mRNA profiles of  Rnf40+/+ and Rnf40-/- mouse embroynic fibroblasts were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000

first: Wanhua

last: Xie


title: BTBD18 licenses piRNA-generating loci to support mouse germ cell development

city: Bethesda

first: Bertram

last: Canagarajah

state: Maryland

address: 9000 Rockville Pike

department: NIDDK

institute: NIH

summary: PIWI-interacting RNAs (piRNAs) are small non-coding RNAs essential for animal germ cell development. Despite intense investigation of post-transcriptional processing, piRNA biogenesis at the chromatin level remains enigmatic. Here we document that BTBD18 is a pachytene nuclear protein in mouse testes that occupies intergenic pachytene piRNA-producing loci with remarkable genome-wide specificity. Deficiency of Btbd18 in mice results in disrupted piRNA biogenesis and male sterility. Transcriptome profiling, chromatin accessibility and RNA polymerase II occupancy demonstrate that BTBD18 facilitates expression of pachytene piRNA precursors by promoting transcription elongation. Therefore, we conclude that BTBD18 functionally licenses genomic sources of piRNAs for transcription activation in mice, and propose that piRNA precursor biogenesis is regulated by transcriptional elongation.

overall_design: RNA-seq, small RNA-seq, ChIP-seq, and ATAC-seq were performed using mouse testes or purified testicular cells with indicated genotypes.

first: Liquan

first: Jurrien

last: Dean


title: Genome-wide H2B monoubiquitination regulates gene expression by coordinating H3K4me3 and H3K27me3 [ChIP-Seq Data Set]

overall_design: examination of H2Bub1, H3K4me3, H3K27me3, and H3K27ac in Rnf40+/+ and Rnf40-/- mouse embryonic fibroblasts were generated by deep sequencing


title: Genome-wide DNA Methylation Analysis in Lung Fibroblasts Co-cultured with Silica-exposed Alveolar Macrophages

status: Public on Jan 04 2017

city: Zhengzhou city

first: Juan

last: Li

state: Henan

address: kexue road

department: college of public health

institute: Zhengzhou University

summary: In the present study, we used MeDIP coupled with next-generation sequencing to profile the whole genome DNA methylation patterns of fibroblast from the co-culture model in vitro. We analyzed the data to identify possible biological pathways for fibroblast differentiating into myofibroblast as well as the interactions of related genes.

overall_design: The co-culture was established of AMs and fibroblasts. Seeding fibroblasts into six-well plates and incubated for one or two days until approximately 60% confluence was achieved. AMs were seeding into the inserts and placed the insert into the six-well dish and then exposed to 100µg/ml SiO2 for 0-, 24-, and 48 hours

first: Changfu

last: Hao

first: Jianyong

last: Hou


title: ChIP-seq from HEK293 (ENCSR688NWK)

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

institute: ENCODE DCC

summary:
Input ChIP-seq on eGFP-ZFP62 tagged human HEK293 cells.

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


title: Proliferation-independent regulation of organ size by Notch signaling

city: Kansas City

first: Agne

last: Kozlovskaja-Gumbriene

state: MO

institute: Stowers Institute for Medical Research

summary:
Purpose: To identify genes that are transcriptionally controlled by Notch signaling during zebrafish lateral line proneuromast formation.
Methods: We isolated primordium cells from dissected tails of 36 hpf Tg((cldnB:GFP);Tg(cldnB:gal4) x Tg(UAS:nicd)) and sibling Tg((cldnB:GFP);Tg(cldnB:gal4)) embryos by FACS and performed RNASeq analysis.
Results: Using an optimized data analysis workflow, we mapped about 26 million sequence reads per sample to the zebrafish genome (build danRer10) and identified 32,105 transcripts in the dissociated tails of WT and NICD zebrafish with TopHat workflow. Approximately 2% of the transcripts showed differential expression between the WT and NICD tails, with a fold change ≥0.5 and p value <0.01.
Conclusion: RNASeq analyses revealed that Notch signaling cell-autonomously induces apical constriction and cell adhesion.

overall_design: Zebrafish lateral line mRNA profiles of 36 hours wild type (WT) and NICD embryos were generated in triplicate, using HiSeq 2500 (Illumina).

first: Yi

last: Ren

first: Alexander

last: Richard

first: Jiskra

last: Ryan

first: Nagelberg

last: Danielle

first: Knaut

last: Holger

first: McClain

last: Melainia

first: Piotrowski

last: Tatjana


title: Genome-wide H2B monoubiquitination regulates gene expression by coordinating H3K4me3 and H3K27me3

first: Steven

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

overall_design: Refer to individual Series