title: Transcriptomes of E2F7/8 DKO liver tumors

city: Utrecht

first: Michal

last: Mokry

address: Lundlaan 6

institute: Wilhelmina Children's Hospital, University Medical Center Utrecht

summary: E2F transcriptional activators and repressors regulate cell cycle-dependent gene expression. Using a series of E2f loss- and gain-of-function mice we show that development is relatively insensitive to alterations in individual E2F levels and composition. However, modest increases in E2F transcriptional output (E2f7Δ/Δ;E2f8Δ/Δ, E2f1KI/1KI and E2f3bKI/3bKI) resulted in spontaneous hepatocellular carcinoma (HCC) without additional organ involvement, whereas decreases (E2f1-/- and E2f3b-/-) protected against HCC. DNA binding domain-, cell type- and temporal-specific gene ablation strategies defined a cell autonomous oncogenic role for E2F1/3B and a tumor suppressor role for E2F8 in hepatocytes during early post-natal liver development. Chromatin binding and expression profiling revealed a mechanism involving activation by E2F1/3B and repression by E2F7/8 to antagonistically regulate a common set of target genes associated with HCC progression. Thus, while development is sufficiently robust to withstand changes in E2F composition and activity, the liver is uniquely sensitive to perturbations in E2Fs.  In summary, precise E2F transcriptional output in hepatocytes during early adolescence is critical to foster a cancer-free life span.

overall_design: Transcriptomes of four E2F7/8 DKO liver tumors, four Wt livers and four E2F7/8 DKO livers


title: Differentiation of human embryonic stem cells to HOXA+ hemogenic vasculature that resembles the aorta-gonad-mesonephros

status: Public on Oct 17 2016

city: Parkville

first: Belinda

last: Phipson

state: VIC

address: 1G Royal Parade

department: Bioinformatics

country: Australia

institute: WEHI

type: Expression profiling by high throughput sequencing

summary: The production of definitive haematopoietic stem/progenitor cells from human pluripotent stem cells (hPSCs) remains a significant challenge. Using reporter lines to track the endothelial (SOX17) to haematopoietic (RUNX1C) transition, we found that hPSC differentiated in growth factor supplemented serum free medium generated RUNX1C+CD34+ clonogenic cells that homed to the bone marrow, but did not engraft. Compared to repopulation-competent cord blood CD34+ cells, RUNX1C+CD34+ progenitors lacked HOXA gene expression, indicating incorrect mesoderm patterning. This deficiency was ameliorated by a timed pulse of WNT activation combined with ACTIVIN antagonism. Significantly, these HOXA+ cultures now formed complex SOX17+ vessels that produced fetal liver-like haematopoietic cells, similar to the human aorta-gonad-mesonephros (AGM). Comparison of transcriptional profiles of these nascent haematopoietic stem/progenitors with cells isolated from human AGM confirmed significant similarities, consistent with the assignment of our in vitro generated cells to the definitive human haematopoietic lineage. Our findings argue that HOXA codes established early in differentiation predict cellular potential and provide correct cell patterning for the specification of definitive haematopoietic lineages from hPSCs.

overall_design: mRNA profiles of 26 samples were obtained for 5 different cell populations and 2 different treatments.

first: Andrew

middle: G

last: Elefanty


title: A tissue checkpoint regulates type 2 immunity

city: San Francisco

first: Rachel

last: Gate

state: CA

address: 533 Parnassus Ave

country: USA

institute: UCSF

summary: Innate pattern recognition receptors for conserved structural elements play critical roles in immunity against viruses, bacteria and fungi, but analogous pathways linking innate recognition of diverse allergens or helminths with type 2 immunity remain elusive.  The discovery of group 2 innate lymphoid cells (ILC2s), which produce similar cytokines as CD4+ T helper 2 (Th2) cells1, has suggested models whereby ILC2s directly or indirectly induce adaptive Th2 cells,2-8 but current understanding of how these cells interact in tissue microenvironments to coordinate allergic immunity is limited.  Here, we show that tissue Th2 cells differentiate independently of ILC2s, but that both cell types share overlapping transcriptional and functional programs, which require exposure to the tissue-derived cytokines such as interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP).  Combined loss of these epithelial cytokines affects neither Th2 cell priming nor T cell-dependent antibody production, but abrogates allergic lung inflammation due to requirements for local tissue signals to promote differentiation of effector function in both ILC2s and Th2 cells.  Our findings reveal how diverse perturbations, including proteases, venoms and mechanical irritants, converge on common pathways to activate type 2 immune responses, thus uncovering a shared checkpoint that can be exploited to control both innate and adaptive allergic inflammation.

overall_design: ATAC-seq on ILC2 and Tcells from lymph node and lung tissues in WT and cytokine KO

middle: E


title: Small-RNA transcriptome sequencing of individual cells

city: Stockholm

first: Ilgar

last: Abdullayev

address: Nobels väg 3

department: Cell and Molecular Biology

country: Sweden

institute: Karolinska Institutet

type: Non-coding RNA profiling by high throughput sequencing

summary: Several classes of small RNAs have been described, however to molecularly profile them require large numbers of cells. Here, we developed a method for single-cell small-RNA sequencing that we applied to naïve and primed human embryonic stem cells and to cancer cells. Single-cell profiling of microRNAs and fragments of tRNAs and snoRNAs revealed that, in particular, microRNAs have unrecognized potential to separate cell types and states.

sample_organism:
Homo sapiens
synthetic construct

platform_organism:
Homo sapiens
synthetic construct

overall_design: Small-RNA transcriptome sequencing (Small-seq) is a method designed to capture all small RNAs at single cells

first: Omid

middle: R

last: Faridani

first: Rickard

last: Sandberg


title: naive T cell heterogeneity after neonatal thymectomy

status: Public on Oct 18 2016

country: Netherlands

summary: The generation of new naive T-cells is dependent on thymic output, but in adults the naive T-cell pool is primarily maintained by peripheral proliferation. Naive T-cells have long been regarded as relatively quiescent cells but recently it was shown that IL-8 production is a signatory effector function of naïve T-cells, at least in newborns. With human aging naïve CD4 T-cell numbers decline but it is not clear whether this is accompanied by (functional) differentiation of naïve T-cells and loss of true naivety. Using a unique cohort of children and adolescents who underwent neonatal thymectomy, we demonstrate that the naive CD4 T-cell compartment in healthy humans is functionally heterogeneous and that this functional diversity is lost after neonatal thymectomy. Thymic regeneration later in life resulted in functional restoration of the naïve T-cell compartment. These data shed further light on functional differentiation within the naive T-cell compartment and the importance of the thymus in naive T-cell homeostasis.

overall_design: Rna-seq analysis of immune cells derived from healthy controls and thymectomy patients


title: Photorespiration is crucial to the dynamic response of photosynthetic metabolism and stomatal movement to altered CO2 availability

status: Public on Oct 15 2016

city: Düsseldorf

first: Andreas

middle: PM

last: Weber

address: Universitätsstr. 1

department: Institute for Plant Biochemistry

country: Germany

institute: Heinrich-Heine-University

summary: The photorespiratory pathway, short photorespiration, is an essential process in oxygenic photosynthetic organisms but also reduces the efficiency of photosynthetic carbon assimilation and is hence frequently considered as a wasteful process. By comparing the response of wild-type plants and mutants impaired in photorespiration to a shift in ambient CO2 concentrations, we demonstrate that photorespiration also plays a beneficial role during short-term acclimation to reduced CO2 availability. Wild-type plants responded with few differentially expressed genes, mostly involved in drought stress, which is likely a consequence of enhanced opening of stomata and concomitant water loss upon shift toward low CO2. In contrast, mutants with impaired activity of photorespiratory enzymes were highly stressed and not able to adjust stomatal conductance to reduced external CO2 availability. The mutants´ transcriptional response was congruent, indicating a general reprogramming to deal with the consequences of reduced CO2 availability, signaled by enhanced oxygenation of ribulose-1,5 bisphosphate and amplified by the artificially impaired photorespiratory metabolism. Central in this reprogramming was the pronounced reallocation of resources from growth processes to stress responses. In conclusion, we demonstrate that unrestricted photorespiratory metabolism is a prerequisite for rapid physiological acclimation to a reduction in CO2 availability.

overall_design: Leaf transcriptomes of Arabidopsis thaliana wild-type (WT) and photorespiratory mutants hpr1, shm1, glyk1, and pglp1, grown under high CO2 (HC; 1% CO2) conditions and shifted for 8 h to low CO2 (LC; 0.038% CO2) conditions. WT samples were sequenced in biological triplicates, all other samples in biological duplicates.

first: Marion

last: Eisenhut

first: Andrea

last: Bräutigam

first: Stefan

last: Timm

first: Alexandra

last: Florian

first: Takayuki

last: Tohge

first: Alisdair

last: Fernie

first: Hermann

last: Bauwe

middle: P


title: Targeted differentiation of regional ventral neuroprogenitors and related neuronal subtypes from human pluripotent stem cells

city: Shanghai

first: Xiaoqing

last: Zhang

address: 1239 Siping Road

country: China

institute: Tongji University

summary:
Purpose: To find the mechanism for the differences in cell fates between the EB (embryoid body) and AD (adherent) culture conditions
Methods: hESCs were cultured in different methods, and RNA-seq were generated , in triplicate, using Illumina GAIIx. The sequence reads  were analyzed  with Weighted gene correlation network analysis (WGCNA) and  Gene Ontology (GO) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays
Results: We totally found roughly 600 genes which were specifically enriched in both day 4 EB cells and day 4 EB cells treated with SB431542 and LDN193189. Meanwhile, there were around 1000 genes which showed significant higher expression in AD cells
Conclusions: complex intracellular cell contexts and extracellular components work together and define the distinct differentiation potencies of the AD and EB cells upon SHH patterning.

overall_design: mRNA from hESCs cultured in AD and EB conditions were analysed, in triplicate, using Illumina HiSeq 2000.

first: Ling

last: Liu


title: RNAseq data from mouse beta-cells expressing mutant (GCK Y214C) versus wild-type Glucokinase

city: Jerusalem

first: Sharona

last: Tornovsky Babaey

address: Jerusalem 91120, Israel

department: Endocrinology and Metabolism

country: Israel

institute: Hebrew University-Hadassah Medical Center

summary: The goal of this study is to compare the transcriptome of mouse beta-cells expressing mutant constitutively active Glucokinase versus wild-type Glucokinase.

overall_design: RNA profiles of pancreatic  islets from 5-6 week old transgenic mice expressing mutant GCK ( Y214C)  (Pdx1Cre-ER; Rosa-LSL-Y214C-GCK) and from their control littermates  (Rosa-LSL-Y214C-GCK) were generated by deep sequencing

first: Benjamin

last: Glaser

first: Yuval

last: Dor

last: Tornovsky-Babaey


title: Direct conversion of rodent fibroblasts into myelinating induced Schwann cells

status: Public on Oct 16 2016

city: Milano

first: Luca

last: Massimino

state: MI

address: Via Olgettina, 58

department: Gastroenterology

country: Italy

institute: Ospedale San Raffaele

summary: Transcriptome analysis of rodent fibroblast-derived induced Schwann cells

overall_design: 3 samples of source primary fibroblasts, 3 samples of primary Schwann cells as reference, and 3 samples of induced Schwann cells have been used for transcriptome analysis.

first: Pietro

last: Mazzara

first: Vania

last: Broccoli


title: ChIP-seq from hindbrain (ENCSR984OHL)

status: Public on Oct 14 2016

city: Stanford

first: ENCODE

last: DCC

address: 300 Pasteur Dr

institute: ENCODE DCC

type: Genome binding/occupancy profiling by high throughput sequencing

summary:
H3K27me3 ChIP-seq on embryonic 10.5 day mouse hindbrain

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: TSS-EMOTE, a refined protocol for a more complete and less biased global mapping of transcription start sites in bacterial pathogens.

city: Geneva

first: Julien

last: Prados

address: Rue Michel Servet 1

department: SCMU

country: Switzerland

institute: University of Geneva

summary:
Background
Bacteria rely on efficient gene regulatory mechanisms to switch between genetic programs when they are facing new environments. Although this regulation can occur at many different levels, one of the key steps is the initiation of transcription. Identification of the first nucleotide transcribed by the RNA polymerase is therefore essential to understand the underlying regulatory processes, since this provides insight on promoter strength and binding sites for transcriptional regulators, and additionally reveals the exact 5' untranslated region of the transcripts, which often contains elements that regulate translation.
Results
Here we present data from a novel TSS-EMOTE assay (Transcription Start Specific Exact Mapping Of Transcriptome Ends) to precisely map the transcription initiation sites of four entire transcriptomes. TSS-EMOTE is a variation of the dRNA-seq method, which has been combined with the EMOTE protocol, in order to increase detection of longer transcripts and limit biases introduced by PCR amplification of the Illumina sequencing library. Using TSS-EMOTE, 2018 promoters were detected in the opportunistic pathogen Staphylococcus aureus, and detailed consensus sequences could be obtained for the RNA polymerase recognition elements (e.g. sigma factor binding sites). The data also revealed a 94 nt median length of the 5' untranslated region in S. aureus, giving important insights for future work on translational regulation. Additionally, the transcriptomes of three other opportunistic pathogens, Staphylococcus epidermidis, Acinetobacter baumannii and Enterobacter aerogenes, were examined, and the identified promoter locations were then used to generate a map of the operon structure for each of the four organisms.
Conclusions
Mapping transcription start sites, and subsequent correlation with the genomic sequence, provides a multitude of important information about the regulation of gene expression, both at the transcriptional and translational level, by defining 5' untranslated regions and sigma-factor binding sites. We have here mapped transcription start sites in four important pathogens using TSS-EMOTE, a method that works with both long and 3'-phosphorylated RNA molecules, and which incorporates Unique Molecular Identifiers (UMIs) to allow unbiased quantification.

sample_organism:
Acinetobacter baumannii
Klebsiella aerogenes
Staphylococcus aureus
Staphylococcus epidermidis

overall_design: Each TSS-EMOTE assay consists of two library for the same sample: one library where RppH is added (+RppH) to allow ligation of the adapter at 5' end, one library without RppH added (-RppH) to establish the background signal. All TSS-EMOTE assays are performed in duplicate.

first: Patrick

last: Linder

first: Peter

last: Redder


title: A genome-wide map of polyadenylation sites in primary human breast tissue

city: Aurora

last: Kabos

state: CO

address: 12801 E. 17th Avenue

department: Division of Medical Oncology

institute: University of Colorado School of Medicine

summary: We used a modified PAS-Seq protocol to map sites of polyadenylation genome-wide in primary breast tissue. Here, we present a map of breast poly(A)-sites derived from six ER+ tumors, six ER- tumors, and adjacent normal tissue from each of the 12 tumor donors.

overall_design: Modified PAS-seq in 12 pairs of matched patient tumor/normal tissue samples (6 ER-, 6 ER+).

first: Austin

last: Gillen

first: Heather

middle: M

last: Brechbuhl

first: Tomomi

last: Yamamoto

first: Enos

last: Kline

first: Jay

last: Hesselberth


title: ChIP-seq from Karpas-422 (ENCSR978BQI)

summary: 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 forebrain (ENCSR992SHK)

summary:
H3K4me1 ChIP-seq on embryonic 10.5 day mouse forebrain

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 midbrain (ENCSR989LUY)

summary:
H3K27ac ChIP-seq on embryonic 10.5 day mouse midbrain

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 fibroblast of arm (ENCSR922FLS)


title: ChIP-seq from Karpas-422 (ENCSR963HAR)


title: ChIP-seq from SK-N-SH (ENCSR914QOK)


title: ChIP-seq from embryonic facial prominence (ENCSR914QGB)

summary:
H3K4me1 ChIP-seq on embryonic 10.5 day mouse embryonic facial prominence

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 limb (ENCSR906RTN)

summary:
H3K27me3 ChIP-seq on embryonic 10.5 day mouse limb

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 fibroblast of arm (ENCSR866KFY)


title: ChIP-seq from Karpas-422 (ENCSR910XKX)


title: ChIP-seq from limb (ENCSR863VHE)

summary:
H3K27ac ChIP-seq on embryonic 10.5 day mouse limb

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 OCI-LY1 (ENCSR859JNA)


title: ChIP-seq from Karpas-422 (ENCSR867UKC)


title: ChIP-seq from OCI-LY3 (ENCSR867TPP)


title: ChIP-seq from midbrain (ENCSR966TCN)

summary:
H3K27me3 ChIP-seq on embryonic 10.5 day mouse midbrain

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: WGBS from GM12878 (ENCSR890UQO)

type: Methylation profiling by high throughput sequencing

summary:
HAIB Whole Genome Bisulfite Sequencing GM12878

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 HCT116 (ENCSR810BDB)


title: ChIP-seq from midbrain (ENCSR842LMA)

summary:
Control ChIP-seq on embryonic 10.5 day mouse midbrain

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 hindbrain (ENCSR962MBB)

summary:
H3K36me3 ChIP-seq on embryonic 10.5 day mouse hindbrain

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 heart (ENCSR782DGO)

summary:
H3K4me1 ChIP-seq on embryonic 10.5 day mouse heart

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 DOHH2 (ENCSR784AQY)


title: Human liver RNA-seq data corresponding to uninfected non-malignant, HCV infected non-malignant, and HCV+ HCC tissue

city: Bronx

first: Neil

middle: Ari

last: Wijetunga

state: NY

address: 1301 Morris Park Ave

department: Genetics

institute: Albert Einstein College of Medicine

summary: We aimed to identify epigenetic regulators of transcription that may be involved in the development and the progression of HCV-associated HCC.  We used directional RNAseq for transcriptome profiling that we correlate with genome wide DNA methylation data.

overall_design: RNAseq for liver biopsies of 10 uninfected, 9 non-neoplastic infected and 8 HCV infected HCC samples.

first: N

middle: A

first: John

last: Greally


title: ChIP-seq from heart (ENCSR782DEA)

summary:
H3K4me3 ChIP-seq on embryonic 10.5 day mouse heart

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 forebrain (ENCSR825ZJV)

summary:
H3K27ac ChIP-seq on embryonic 10.5 day mouse forebrain

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 forebrain (ENCSR776WPN)

summary:
Control ChIP-seq on embryonic 10.5 day mouse forebrain

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 embryonic facial prominence (ENCSR765JWZ)

summary:
H3K4me3 ChIP-seq on embryonic 10.5 day mouse embryonic facial prominence

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: WGBS from K562 (ENCSR765JPC)

summary:
HAIB Whole Genome Bisulfite Sequencing K562

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 OCI-LY7 (ENCSR752KQT)

summary: 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 fibroblast of arm (ENCSR914AWT)


title: ChIP-seq from fibroblast of arm (ENCSR906NGD)


title: ChIP-seq from MCF-7 (ENCSR768LHG)


title: WGBS from HepG2 (ENCSR881XOU)

summary:
HAIB Whole Genome Bisulfite Sequencing HepG2

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 OCI-LY3 (ENCSR857GMX)


title: ChIP-seq from midbrain (ENCSR747ZXL)

summary:
H3K36me3 ChIP-seq on embryonic 10.5 day mouse midbrain

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 DOHH2 (ENCSR741STU)


title: ChIP-seq from forebrain (ENCSR737JHU)

summary:
H3K9me3 ChIP-seq on embryonic 10.5 day mouse forebrain

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 hindbrain (ENCSR703TBR)

summary:
H3K9me3 ChIP-seq on embryonic 10.5 day mouse hindbrain

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 limb (ENCSR687ALB)

summary:
Control ChIP-seq on embryonic 10.5 day mouse limb

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 embryonic facial prominence (ENCSR682UEM)

summary:
Control ChIP-seq on embryonic 10.5 day mouse embryonic facial prominence

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 Karpas-422 (ENCSR660IQS)


title: ChIP-seq from hindbrain (ENCSR731KRE)

summary:
H3K4me3 ChIP-seq on embryonic 10.5 day mouse hindbrain

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 forebrain (ENCSR735VEJ)

summary:
H3K27me3 ChIP-seq on embryonic 10.5 day mouse forebrain

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 SUDHL6 (ENCSR694PMV)


title: microRNA-seq from fibroblast of arm (ENCSR697KHQ)

summary:
miRNA-seq on human fibroblast of arm

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: WGBS from mammary epithelial cell (ENCSR656TQD)

summary:
HAIB Whole Genome Bisulfite Sequencing HMEC

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 heart (ENCSR681NQF)

summary:
Control ChIP-seq on embryonic 10.5 day mouse heart

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: microRNA-seq from HCT116 (ENCSR650SEP)

summary:
miRNA-seq on human HCT116

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 hindbrain (ENCSR608QBO)

summary:
H3K4me1 ChIP-seq on embryonic 10.5 day mouse hindbrain

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 DOHH2 (ENCSR627TNG)


title: ChIP-seq from OCI-LY3 (ENCSR604JFH)


title: ChIP-seq from SUDHL6 (ENCSR587FCM)


title: ChIP-seq from OCI-LY1 (ENCSR597UDW)


title: ChIP-seq from OCI-LY3 (ENCSR638FRE)


title: ChIP-seq from heart (ENCSR582SPN)

summary:
H3K27ac ChIP-seq on embryonic 10.5 day mouse heart

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 OCI-LY1 (ENCSR569IIN)


title: ChIP-seq from midbrain (ENCSR581EJK)

summary:
H3K4me3 ChIP-seq on embryonic 10.5 day mouse midbrain

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 forebrain (ENCSR558NWQ)

summary:
H3K36me3 ChIP-seq on embryonic 10.5 day mouse forebrain

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 embryonic facial prominence (ENCSR538DPG)

summary:
H3K36me3 ChIP-seq on embryonic 10.5 day mouse embryonic facial prominence

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 OCI-LY3 (ENCSR548PZS)

summary: 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 SUDHL6 (ENCSR494LJG)


title: ChIP-seq from SUDHL6 (ENCSR511OIE)


title: DNase-seq from OCI-LY7 (ENCSR489NAM)


title: ChIP-seq from fibroblast of arm (ENCSR479HKJ)


title: ChIP-seq from DOHH2 (ENCSR460SEN)


title: ChIP-seq from MCF-7 (ENCSR493NBY)


title: ChIP-seq from hindbrain (ENCSR594JGI)

summary:
H3K27ac ChIP-seq on embryonic 10.5 day mouse hindbrain

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 Karpas-422 (ENCSR367UDO)


title: WGBS from fibroblast of arm (ENCSR440MLE)

summary:
HAIB Whole Genome Bisulfite Sequencing Fibroblast of Arm

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 OCI-LY1 (ENCSR449AYM)


title: ChIP-seq from OCI-LY7 (ENCSR447ZGY)


title: ChIP-seq from OCI-LY7 (ENCSR389WWC)


title: ChIP-seq from heart (ENCSR455REA)

summary:
H3K9me3 ChIP-seq on embryonic 10.5 day mouse heart

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 OCI-LY3 (ENCSR361GKY)


title: microRNA-seq from MCF-7 (ENCSR343HIX)

summary:
miRNA-seq on human MCF-7

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 limb (ENCSR318QFY)

summary:
H3K4me3 ChIP-seq on embryonic 10.5 day mouse limb

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 OCI-LY1 (ENCSR422JNY)


title: ChIP-seq from midbrain (ENCSR272GNQ)

summary:
H3K4me1 ChIP-seq on embryonic 10.5 day mouse midbrain

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 Karpas-422 (ENCSR306VSH)


title: ChIP-seq from limb (ENCSR242PHH)

summary:
H3K36me3 ChIP-seq on embryonic 10.5 day mouse limb

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 heart (ENCSR266JQW)

summary:
H3K27me3 ChIP-seq on embryonic 10.5 day mouse heart

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 OCI-LY7 (ENCSR243AIS)


title: ChIP-seq from embryonic facial prominence (ENCSR285IQN)

summary:
H3K27me3 ChIP-seq on embryonic 10.5 day mouse embryonic facial prominence

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 limb (ENCSR238SGC)

summary:
H3K4me1 ChIP-seq on embryonic 10.5 day mouse limb

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 fibroblast of arm (ENCSR217TAW)


title: ChIP-seq from midbrain (ENCSR769ITO)

summary:
H3K9me3 ChIP-seq on embryonic 10.5 day mouse midbrain

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 hindbrain (ENCSR191XBS)

summary:
Control ChIP-seq on embryonic 10.5 day mouse hindbrain

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 HCT116 (ENCSR198WIH)


title: ChIP-seq from forebrain (ENCSR368RJD)

summary:
H3K4me3 ChIP-seq on embryonic 10.5 day mouse forebrain

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 SUDHL6 (ENCSR179YLS)


title: ChIP-seq from SK-N-SH (ENCSR185OHN)


title: ChIP-seq from ES-E14 (ENCSR095IPH)

summary:
Control ChIP-seq on E0 mouse ES-E14

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 heart (ENCSR328WMV)

summary:
H3K36me3 ChIP-seq on embryonic 10.5 day mouse heart

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 OCI-LY7 (ENCSR063AUO)


title: ChIP-seq from OCI-LY3 (ENCSR581LZU)


title: ChIP-seq from OCI-LY1 (ENCSR189AGR)


title: ChIP-seq from SK-N-SH (ENCSR000FDA)

summary:
Control ChIP-seq on human SK-N-SH

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 embryonic facial prominence (ENCSR151APL)

summary:
H3K27ac ChIP-seq on embryonic 10.5 day mouse embryonic facial prominence

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 fibroblast of arm (ENCSR007YOT)

summary: 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 OCI-LY7 (ENCSR060WGK)


title: ChIP-seq from SUDHL6 (ENCSR316KHQ)


title: ChIP-seq from SK-N-SH (ENCSR000FCV)

summary:
H3K36me3 SK-N-SH ChIP-Seq

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 HCT116 (ENCSR000FCQ)

summary:
H3K36me3 HCT116 ChIP-Seq

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 SK-N-SH (ENCSR000FCR)

summary:
H3K4me1 SK-N-SH ChIP-Seq

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 SK-N-SH (ENCSR000FCU)

summary:
H3K27ac SK-N-SH ChIP-Seq

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 HCT116 (ENCSR000FCP)

summary:
H3K9me3 HCT116 ChIP-Seq

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 SK-N-SH (ENCSR000FCS)

summary:
H3K4me3 SK-N-SH ChIP-Seq

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 Panc1 (ENCSR000FCO)

summary:
H3K27me3 ChIP-seq on human PANC1

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 SK-N-SH (ENCSR000FCT)

summary:
H3K9me3 SK-N-SH ChIP-Seq

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 Panc1 (ENCSR000FCN)

summary:
H3K9me3 PANC1 ChIP-Seq

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 Panc1 (ENCSR000FCM)

summary:
H3K36me3 PANC1 ChIP-Seq

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 HCT116 (ENCSR000EUX)

summary:
Control ChIP-seq on human HCT-116

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 Karpas-422 (ENCSR019JDO)


title: ChIP-seq from Panc1 (ENCSR000EXM)

summary:
Control ChIP-seq on human PANC-1

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 K562 (ENCSR000CPH)

summary:
The libraries contained in this experiment come from the whole cell fraction of independent growths of cell line K562. They are stranded PE76 Illumina GAIIx RNA-Seq libraries from rRNA-depleted Poly-A+ RNA > 200 nucleotides in size.

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 OCI-LY7 (ENCSR005SXO)


title: polyA mRNA RNA-seq from HepG2 (ENCSR000CPE)

summary:
The libraries contained in this experiment come from the whole cell fraction of independent growths of cell line HepG2. They are stranded PE76 Illumina GAIIx RNA-Seq libraries from rRNA-depleted Poly-A+ RNA > 200 nucleotides in size.

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 HeLa-S3 (ENCSR000CPR)

summary:
The libraries contained in this experiment come from the whole cell fraction of independent growths of cell line HeLa-S3. They are stranded PE76 Illumina GAIIx RNA-Seq libraries from rRNA-depleted Poly-A+ RNA > 200 nucleotides in size.

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 OCI-LY1 (ENCSR184QUS)


title: microRNA-seq from GM12878 (ENCSR000AEK)

summary:
RNA Evaluation GM12878 micro RNA-seq  from Mortazavi

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 GM12878 (ENCSR000COQ)

summary:
The libraries contained in this experiment come from the whole cell fraction of independent growths of cell line GM12878. They are stranded PE76 Illumina GAIIx RNA-Seq libraries from rRNA-depleted Poly-A+ RNA > 200 nucleotides in size.

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: MBNL1 HITS-CLIP in MDA-MB-231 breast cancer cells

first: Hani

last: Goodarzi

department: Biochemistry and Biophysics

summary: HITS-CLIP was performed to identify endogenous MBNL1 binding sites on RNAs in MDA-MB-231 breast cancer cells.

overall_design: A previously published method was used to perform HITS-CLIP for endogenous MBNL1 in MDA-MB-231 breast cancer cells (Moore et al. 2014. Nat Protoc. 9:263-293.)

first: Lisa

last: Fish

first: Nora

last: Pencheva

first: Hien

last: Tran

first: Mitsukuni

last: Yoshida

first: Sohail

middle: F

last: Tavazoie


title: MBNL1-dependent modulation of gene expression in MDA-MB-231 breast cancer cells

summary: To identify MBNL1-dependent changes in gene expression, MDA-MB-231 cells expressing either control or MBNL1-targeting shRNAs were transcriptomically profiled.

overall_design: MDA-MB-231 cells stably expressing a control or two independent MBNL1-targeting shRNAs were sequenced in biological duplicate.


title: Muscleblind-like 1 suppresses breast cancer metastatic colonization and stabilizes metastasis suppressor transcripts

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

overall_design: Refer to individual Series


title: microRNA-seq from K562 (ENCSR000AET)

first: ENCODE

last: DCC

summary:
RNA Evaluation K562 micro RNA-seq from Mortazavi

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: Discovery and Differential Expression of miRNAs in Fusarium Wilt Resistant and Susceptible Banana Varieties

city: Haikou

first: XIn

last: Chen

address: 4th College Road

institute: catas

summary: MicroRNAs (miRNAs) are a class of endogenous non-coding small RNAs that regulate targeted mRNAs by degrading or repressing translation, considered as post-transcrption regulators. So far, a large number of miRNAs have been discovered in model plants, but little information is available on miRNAs in banana. In this study, by sequencing the small RNA (sRNA) transcriptomes of Fusarium wilt resistant and susceptible banana varieties, 139 members in 38 miRNA families were discovered, and six out of eight new miRNAs were confirmed by RT-PCR. According to the analysis of sRNA transcriptome data and qRT-PCR verification, some miRNAs were differentially expressed between Fusarium wilt resistant and susceptible banana varieties. Two hundred and ninety-nine and 31 target genes were predicted based on the draft maps of banana B genome and Fusarium oxysporum (FOC1, FOC4) genomes respectively. Specifically, two important pathogenic genes in Fusarium oxysporum genomes, feruloyl esterase gene and proline iminopeptidase gene, were targeted by banana miRNAs. These novel findings may provide a new strategy for the prevention and control of Fusarium wilt in banana.

sample_organism:
Musa acuminata AAA Group
Musa AAB Group

platform_organism:
Musa acuminata AAA Group
Musa AAB Group

overall_design: miRNA-seq on leaf and root tissue from a fusarium wilt-resistant and wilt-susceptible banana variety.

first: Wenquan

last: Wang

first: Zhiqiang

last: Jin

first: Shun

last: Song

first: Xin


title: polyA mRNA RNA-seq from A549 (ENCSR000CON)

summary:
The libraries contained in this experiment come from the whole cell fraction of independent growths of cell line A549. They are stranded PE76 Illumina GAIIx RNA-Seq libraries from rRNA-depleted Poly-A+ RNA > 200 nucleotides in size.

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: The evolution of N6-methyladenosine in primates

city: Chicago

first: Kevin

middle: P.

last: White

state: IL

address: 900 E. 57th STR. 10th FL.

department: Institute for Genomics and Systems Biology

institute: University of Chicago

summary: Phenotypic differences within populations and between closely related species are often driven by variation and evolution of gene expression. However, most analyses have focused on the effects of genomic variation at cis-regulatory elements such as promoters and enhancers that control transcriptional activity, and little is understood about the influence of post-transcriptional processes on transcript evolution. Post-transcriptional modification of RNA by N6-methyladenosine (m6A) has been shown to be widespread throughout the transcriptome, and this reversible mark can affect transcript stability and translation dynamics. Here we analyze m6A mRNA modifications in lymphoblastoid cell lines (LCLs) from human, chimpanzee and rhesus, and we identify patterns of m6A evolution among species. We find that m6A evolution occurs in parallel with evolution of consensus RNA sequence motifs known to be associated with the enzymatic complexes that regulate m6A dynamics, and expression evolution of m6A-modified genes occurs in a parallel evolutionary pattern with m6A evolution. Further, genes modified by evolved m6A in humans are significantly enriched in transcriptional regulatory processes and disease related pathways, suggesting an important role in human biology for the evolution of m6A modification.

sample_organism:
Macaca mulatta
Pan troglodytes
Homo sapiens

overall_design: Perform m6A-seq in human, chimpanzee and rhesus, and identify m6A evolutionary mode in primates.

first: Lijia

last: Ma


title: Quantifying RNA binding sites transcriptome-wide using DO-RIP-seq

status: Public on Oct 13 2016

city: Durham

first: Matthew

middle: Burk

last: Friedersdorf

state: NC

address: 207 Research Drive

department: Molecular Genetics & Microbiology

institute: Duke University

summary: RNA-binding proteins (RBPs) and non-coding RNAs orchestrate post-transcriptional processes through the recognition of specific sites on targeted transcripts. Thus, understanding the connection between binding to specific sites and active regulation of the whole transcript is essential. Many immunoprecipitation techniques have been developed that identify either whole transcripts or binding sites of RBPs on each transcript using cell lysates. However, none of these methods simultaneously measures the strength of each binding site, and quantifies binding to whole transcripts. In this study, we compare current procedures and present Digestion Optimized (DO)-RIP-seq, a simple method that locates and quantifies RBP binding sites using a continuous metric. We have used the RBP HuR/ELAVL1 to demonstrate that DO-RIP-seq can quantify HuR binding sites with high coverage across the entire human transcriptome, thereby generating metrics of relative RNA binding strength. We demonstrate that this quantitative enrichment of binding sites is proportional to the relative in vitro binding strength for these sites. Also, we used DO-RIP-seq to quantify and compare HuR's binding to whole transcripts, thus allowing for seamless integration of binding site data with whole transcript measurements. Finally, we demonstrate that DO-RIP-seq is useful for identifying functional mRNA target sets, and binding sites where combinatorial interactions between HuR and AGO-microRNAs regulate the fate of the transcripts. Our data indicate that DO-RIP-seq will be useful for quantifying RBP binding events that regulate dynamic biological processes.

overall_design: Three HuR immunoprecipitation replicates and three matched negative control immunoprecipitation replicates.

middle: B

first: Cindo

middle: O

last: Nicholson

first: Jack

middle: D

last: Keene


title: Individual-nucleotide resolution CLIP and high-throughput sequencing for FOX2, TDP43 and hnRNP M in WT and P-KO H9 cells

first: Li

last: Yang

address: 131 Dong-An Road

department: Institutes of Biological Sciences

institute: Fudan University

summary: Individual-nucleotide resolution UV-crosslinking and immunoprecipitation (iCLIP) combined with high-throughput sequencing was used to generate a transcriptome-wide binding map of TDP43, FOX2 and hnRNP M in WT and P-KO H9 cells.

overall_design: Two biological replicates for FOX2, TDP43 and hnRNP M co-immunoprecipitated RNA after UV-crosslinking in WT and P-KO cells

first: Zheng

last: Luo

first: Qing-Fei

last: Yin

first: Huang

last: Wu

first: Ling-Ling


title: Gene expression profiling of adipocyte precursor cells in response to Pdgfa

city: New Haven

first: Valerie

last: Horsley

state: CT

address: 266 Whitney avenue

department: MCDB

institute: Yale University

summary: Adipocyte precursor cells were treated with Pdgfa during 1 or 2 hours in vitro to identify early changes in transciprion in response to treatment. This experiment supports the evidence that Pdgfa induces proliferation and maintenance of adipocyte stem cells.

overall_design: Adipocyte precursor cells were isolated by FACS and treated with 30ng/ml of recombinant mouse Pdgfa for 1 or 2 hours.

first: Guilermo

middle: C

last: Rivera-Gonzalez


title: Effect of Mef2 knockdown in Drosophila fat body

city: London

first: Marc

last: Dionne

address: Level 0, Flowers Building

department: Life Sciences

country: United Kingdom

institute: Imperial College London

overall_design: 10 samples: 5 (biological replicate) controls (whole male Drosophila, 5-10 days post-eclosion, genotype w[1118] ; c564 / +) and 5 (biological replicate) Mef2 knockdowns (whole male Drosophila, 5-10 days post-eclosion, genotype w[1118] ; c564 / UAS-Mef2-IR[GD15549])

middle: S


title: Therapeutic targeting of GCB- and ABC-DLBCLs by rationally designed BCL6 inhibitors

first: Huimin

last: Geng

address: 513 Parnassus Ave., MSB HSW 1201

department: Department of Laboratory Medicine

summary: BCL6 inhibitor induces derepression of BCL6 target genes and shows a similar transcriptional program to BCL6 siRNA

overall_design: Genome-wide profiling of mRNA transcript levels in human DLBCL cell line with BCL6 inhibitor and DMSO control.

first: Mariano

last: Cardenas

first: Ari

last: Melnick


title: Loss of CREBBP results in gene expression repression in lymphoma cells

summary: KD of CREBBP at lymphoma cell line, MD901, results in reduced expression

overall_design: Genome-wide profiling of total RNA transcript levels in human cell line MD901 (CREBBP wild type) with shCREBBP and scramble control.

first: Yanwen

last: Jiang


title: FXR cistrome in mouse liver

city: Lille

first: Jérôme

last: Eeckhoute

address: Bâtiment J&K, Faculté de Médecine de Lille-Pôle Recherche, Boulevard du Professeur Leclerc

country: France

institute: CNRS

summary: FXR ChIP-seq was performed using the liver from adult male C57Bl6 mice

overall_design: Liver from control mice or mice treated with taurocholic acid (TCA), metformin or both were used to perform FXR ChIP-seq

first: Jerome

first: Celine

last: Gheeraert


title: ATAC-Seq to investigate the spatial choreography of the accessible genome

city: Palo Alto

first: Xingqi

last: Chen

address: 269 Campus Drive

institute: Stanford University

summary: Understanding the spatial choreography of the acessible genome in the intact nucleus

overall_design: We had perfored the ATAC-seq in FACS sorted GM12878

first: Ying

last: Shen

first: Howard

middle: Y

last: Chang


title: Loss of CREBBP results in H3K27ac loss at enhancers in lymphoma cells

city: San Francisco

institute: UCSF

summary: KD of CREBBP at lymphoma cell line, MD901, results in reduced H3K27ac enrichment at a subset of promoters and enhancers.

overall_design: Genome-wide H3K27Ac ChIPseq binding sites in human cell line MD901 (CREBBP wild type) with shCREBBP (11027 and 3752) and scramble control.


title: Loss of CREBBP results in H3K27ac loss at enhancers in mouse lymphoma cells

summary: KD of Crebbp at mouse cells results in reduced H3K27ac enrichment at a subset of promoters and enhancers.

overall_design: Genome-wide H3K27Ac ChIPseq binding sites in mouse cells with shCrebbp and scramble control.


title: A balance between secreted inhibitors and edge-sensing controls gastruloid self-organization

city: New York

first: Albert

last: Ruzo

address: 1230 York Avenue

department: Laboratory of Stem Cell Biology and Molecular Embryology

institute: The Rockefeller University

summary: The earliest aspects of human embryogenesis remain mysterious. To model patterning events in the human embryo we used colonies of human embryonic stem cells (hESCs) grown on micropatterned substrate and differentiated with BMP4. These recapitulate the embryonic arrangement of the mammalian germ layers and provide an assay to assess the structural and signaling mechanisms patterning the human gastrula.  Structurally, high-density hESCs relocalize their TGF-β receptors to their lateral side in the center of the colony, while maintaining apical localization of receptors at the edge. This relocalization insulates central cells from apically applied ligands while maintaining response to basally presented ones. Additionally, BMP4 directly induces the expression of its own inhibitor, Noggin, generating a reaction-diffusion mechanism that underlies patterning. We develop a quantitative model that integrates edge sensing and inhibitors, to predict human fate positioning in micropatterns, and potentially the human embryo.

overall_design: We performed RNAseq of human embryonic stem cells cultured in micropatterned colonies at different time points after the addition of BMP4.

first: Ali

middle: H

last: Brivanlou


title: ALKBH1-Mediated Transfer RNA Demethylation

first: Guan-Zheng

last: Luo

address: 929 E 57th St

department: Chemistry

institute: UChicago

summary: Transfer RNA (tRNA) is a central component of protein synthesis and cell signaling network. One salient feature of tRNA is its heavily modified status, which can critically impact its function. Here we show that mammalian ALKBH1 is a tRNA demethylase. It mediates the demethylation of N1-methyladenosine (m1A) in tRNAs. The ALKBH1-catalyzed demethylation of the target tRNAs results in their reduced partition in polysomes and their decreased usage in protein synthesis. This process is dynamic and responds to glucose availability to affect translation. Our results uncover reversible methylation of tRNA as a new regulatory mechanism of post-transcriptional gene expression.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design:
Profile the binding RNA of ALKBH1 by CLIP-seq.
tRNA-seq wild-type and Alkbh1 KOMEF

first: Fange

last: Liu

first: Chuan

last: He

first: Jiangbo

last: Wei


title: Maternal dietary vitamin A deficiency and diet dependent liver gene expression in mice

status: Public on Oct 12 2016

city: Madison

first: Colin

last: Jefcoate

state: WI

address: 1111 Highland Ave

department: Cell and Regenerative Biology

institute: UW-Madison

summary: Initiation of a vitamin A deficient diet in mid-gestation, maintained in the post-weaning diet is sufficient to cause liver and serum retinoid depletion. Wild type C57Bl/6J timed mated pregnant dams were administered either a defined vitamin A sufficient low fat (12 percent kcal from fat) diet or matched vitamin A deficient diet from embryonic day 10.5. Vitamin A sufficient offspring were weaned onto either a high fat diet (60 percent kcal from fat) or maintained on the low fat 12 percent kcal from fat diet for 11 weeks (14 weeks of age). Gestational vitamin A deficient offspring were maintained on the same vitamin A deficient diet until 14 weeks of age. The impact of the maternal diet  on a post-weaning high fat diet was compared to a standard maternal breeder diet followed by the post-weaning high fat diet.

overall_design: Three comparison experiment. Liver expression of WT C57Bl/6J mice at 14 weeks of age from dams fed a particular maternal diet (X) and weaned onto a post-weaning diet (Y) such that diets are presented X-Y. Breeder diet - High fat diet compared to Low fat 12 percent kcal vitamin A sufficient - High fat diet. Low fat 12 percent kcal vitamin A sufficient - High fat diet compared to Low fat 12 percent kcal vitamin A sufficient - Low fat 12 percent kcal vitamin A sufficient. Low fat 12 percent kcal vitamin A sufficient - Low fat 12 percent kcal vitamin A sufficient compared to Low fat 12 percent kcal vitamin A deficient - Low fat 12 percent kcal vitamin A deficient.

first: C


title: Transcriptome analysis of alternative splicing events in WT and P-KO H9 cells

city: Shanghai

first: Li

last: Yang

summary: We have used RNA-seq to explore alternative splicing events in WT and P-KO H9 cells

overall_design: RNA-seq for wild type (WT) and SPA paternal KO (P-KO) H9 cells

first: Zheng

first: Qing-Fei

last: Yin

first: Huang

last: Wu

first: Ling-Ling


title: Role of SMAR1 in global gene regulation through interaction with tumor suppressor p53

city: Pune

first: Samit

last: Chattopadhyay

state: Maharashtra

address: Ganeshkhind

department: Chromatin and disease biology lab

country: India

institute: National Centre For Cell Science

summary: Scaffold Matrix Attachment Region binding protein 1, SMAR1 has vital role to play as a general repressor of transcription. SMAR1 is known to retard cell cycle progression and delay tumor growth in mice. Further, it forms a ternary complex with p53-Mdm2 and inhibit p53-mediated transcription. Thus, SMAR1 can potentially alter p53 function and orchestrate different set of genes in p53-dependent and p53-independent manner. The present study aims to decipher the potential role of SMAR1 in global transcription regulation and to study role of p53 in the process. Towards this objective, chromatin immunoprecipitation combined Next-generation sequencing (ChIP-Seq) was performed using HCT116 and HCT116 p53-/- cell samples. The α-SMAR1 antibody was used for such ChIP experiments which was already tested by Wastern blot assays and found to be SMAR1 specific. The sequence data generated was then analyzed and the results obtained are (1) Higher genomic occupancy of SMAR1 in HCT116 (wild type) than HCT116 p53-/- (P53 null) data set (2) For peaks within ±5kb of TSS, SMAR1 had the highest predisposition to bind upstream of the TSS in close proximity, i.e., -1 to 0 kb that represents the promoter region of the gene (3) SMAR1 was found to target 5617 genes (unique in Wild type) , 8198 genes (unique in Null) and 1876 genes that were common in both the samples (4) In silico motif search indicated that SMAR1 binds to a dinucleotide T(C/G) repeat sequence (5) Functional Annotation of targets revealed that the predicted target genes are involved in apoptosis, epigenetics, cell cycle, cell signalling, neuronal genes, transcription, metabolism etc. The target also include noncoding RNAs genes such as microRNAs /lincRNAs.

overall_design: Chromatin immunoprecipitation was carried out using ChIP grade α-SMAR1 antibody (immune fraction) and Rabbit IgG (mock) in HCT116 p53+/+ (Wild type)  and HCT116 p53-/- (null) cell lines. It was followed by massively parallel sequencing using Illumina GAIIx Analyzer.

first: Jinumary

last: Mathai

first: Smriti

last: Mittal

first: Abhijeet

last: Kulkarni

first: Smita

last: Saxena


title: Loss of CREBBP results in H3K27Ac loss at enhancers and gene expression repression in lymphoma cells

first: Huimin

last: Geng

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

overall_design: Refer to individual Series


title: Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Bcl6-/- helper T cell Transcriptomes

city: Kisarazu

first: Osamu

last: Ohara

state: Chiba

address: 2-6-7 Kazusa-Kamatari

department: Technology Development

country: Japan

institute: Kazusa DNA Research Institute

summary: Virus infection induces T follicular helper (TFH) and T helper 1 (TH1) cells. Although TFH cells are important in anti-viral humoral immunity, the role of TH 1 cells is still elusive. IgG2 antibodies predominate in the response to vaccination with inactivated Influenza A virus (IAV) and were responsible for protective immunity to lethal challenge with pathogenic H5N1 and pandemic H1N1 IAVs even in mice lacking TFH cells owing to B or T cell-specific ablation of the Bcl6. We demonstrate that IL-21 and IFN-γ secreted from TH1 cells were essential for greater persistence and higher titers of IgG2 protective antibodies. These results suggest that TH1 induction could be a promising strategy to induce effective neutralizing antibodies against emerging influenza viruses.

overall_design: TH1 or TFH cells of wild type (WT) and conditional Bcl6-/- mice were sorted and analyzed the transcriptome using Illumina HiSeq1500.

first: Kosuke

last: Miyauchi

first: Masato

last: Kubo


title: Fibrillarin RIP-seq in PA1 cells

summary: We have used fibrillarin RIP-seq to explore snoRNA related transcripts in PA1 cells.

overall_design: RNA-Immunoprecipitation sequencing of Fibrillarin.

last: Luo

last: Chen


title: Transcriptomic analyses for the CSC-like properties under monolayer and sphere culture conditions in 293T and MCF-7 cells

city: Seoul

first: Jung Min

last: Kim

address: Gangnam-gu Teheran-ro 216

department: Department of Health Genomics

country: South Korea

institute: NAR Center, Inc. & Genoplan, Inc.

summary: In order to verify the CSC-like properties in 3D spheres of 293T cells as compared to monolayer, MCF-7 breast cancer cells under monolayer and sphere culture conditions were used as a control. Corresponding author: Chul Geun Kim, Department of Life Science, Hanyang University, Seoul 133-791, Korea (e-mail, cgkim@hanyang.ac.kr).

overall_design: mRNA profiles of the 293T and MCF-7 cells [monolayer (mMCF-7 and m293T) and sphere (sMCF-7 and s293T) culture conditions] were generated by deep sequencing using Illumina GAIIx.

first: Dae

last: Ha

first: Chang

last: Lim

first: Jung

first: Chul

middle: G


title: RNA-seq analysis of transcriptomes at 5 day after sexual induction in Fusarium graminearum strains

first: Hokyoung

last: Son

address: Daehak-dong, Gwanak-gu

department: Center for Food and Bioconvergence

institute: Seoul National University

summary: Fusarium graminearum (teleomorph Gibberella zeae) is a prominent pathogen that infects major cereal crops, such as wheat, barley, and maize. To dissect molecular mechanisms of small non-coding RNA-mediated gene regulation during ascospore production, we compared transcriptomes of fungal cultures harvested from F. graminearum wild-type strain Z-3639 and RNAi component mutants at 5 days after sexual induction.

overall_design: 7 samples examined: Fungal cultures harvested from Fusarium graminearum wild-type strain Z-3639, Fgdicer1, Fgdicer2, Fgdicer1 Fgdicer2, Fgago1, Fgago2, and Fgago1 Fgago2 at 5 days after sexual induction.

first: Jae

first: Yin-Won

last: Lee


title: small RNA-seq analysis of transcriptomes at 5 day after sexual induction in Fusarium graminearum strains

summary: Fusarium graminearum (teleomorph Gibberella zeae) is a prominent pathogen that infects major cereal crops, such as wheat, barley, and maize. To dissect molecular mechanisms of small non-coding RNA-mediated gene regulation during ascospore production, we compared small RNA transcriptomes of fungal cultures harvested from F. graminearum wild-type strain Z-3639 and RNAi component mutants at 5 days after sexual induction.

first: Jae-Yun


title: E2F coregulates an essential HSF developmental program that is distinct from the heat-shock response

city: Evanston

first: Jian

last: Li

address: 2205 Tech Drive, Hogan 2-100

department: Molecular Biosciences

institute: Northwestern University


title: Loss of CREBBP results in gene expression represssion in mouse lymphoma cells

summary: KD of Crebbp at mouse cells results in reduced expression

overall_design: Genome-wide profiling of total RNA transcript levels in  in mouse cells with shCrebbp and scramble control.

first: Yanwen

last: Jiang

first: Ari

last: Melnick


title: ChIP-seq of HSF-1 and Pol II in C. elegans larval development and heat shock

summary: To understand the function and regulation of the C. elegans heat shock factor (HSF-1) in larval development, we have used ChIP-seq to analyze the occupancy of HSF1 and RNA Pol II in L2 larvae and young adult (YA) animals grown at 20°C or upon heat shock at 34°C for 30 min. In addition, we have used RNA-seq to analyze the transcriptomes of wild type (N2), hsf-1(ok600) mutants and hsf-1(ok600); rmSi1[hsf-1::gfp]  L2 larvae grown at 20°C and characterized the gene expression change by heat shock in wild type (N2) animals at L2 stage.

overall_design: Experiment type: ChIP-seq. Biological Source: strain: AM1061; developmental dtage: L2 Larva, young adult (YA). Experimental Factors: temperature: 20 degree celsius, 34 degree celsius; antibodies: anti-GFP (clontech, #632592), anti-AMA-1 (Novus, #38520002).

first: Richard

middle: I

last: Morimoto


title: RNA-seq analysis in C. elegans larval development and heat shock

summary: To understand the function and regulation of the C. elegans heat shock factor (HSF-1) in larval development, we have used ChIP-seq to analyze the occupancy of HSF1 and RNA Pol II in L2 larvae and young adult (YA) animals grown at 20°C or upon heat shock at 34°C for 30 min. In addition, we have used RNA-seq to analyze the transcriptomes of wild type (N2), hsf-1(ok600) mutants and hsf-1(ok600); rmSi1[hsf-1::gfp]  L2 larvae grown at 20°C and characterized the gene expression change by heat shock in wild type (N2), hsf-1(sy441) and hsf-1(sy441);rmSi1[hsf-1::gfp] animals at L2 stage.

overall_design: Experiment type: RNA-seq. Biological Source: strain: N2, hsf-1(sy441), hsf-1(sy441);rmSi1[hsf-1::gfp]; developmental dtage: L2 Larva. Experimental Factors: temperature: 20 degree celsius, 34 degree celsius.


title: RNA-seq analysis of hsf-1 mutant in C. elegans larval development

overall_design: Experiment type: RNA-seq. Biological Source: strain: N2, OG576, AM1061; developmental dtage: L2 Larva. Experimental Factors: temperature: 20 degree celsius.


title: An H4K16 histone acetyltransferase mediates decondensation of the X chromosome in C. elegans males

city: Ann Arbor

first: Gyorgyi

last: Csankovszki

address: 830 N. University Ave.

institute: University of Michigan

summary: In C. elegans, in order to equalize gene expression between the sexes and balance X and autosomal expression, two steps are believed to be required. First, an unknown mechanism is hypothesized to upregulate the X chromosome in both sexes. This mechanism balances the X to autosomal expression in males, but creates X overexpression in hermaphrodites. Therefore, to restore the balance, hermaphrodites downregulate gene expression twofold on both X chromosomes. While many studies have focused on X chromosome downregulation, the mechanism of X upregulation is not known. To gain more insight into X upregulation, we studied the effects of chromatin condensation and histone acetylation on gene expression levels in male C. elegans. We have found that the H4K16 histone acetyltransferase MYS-1/Tip60 mediates dramatic decondensation of the male X chromosome as measured by FISH. However, RNA-seq analysis revealed that MYS-1 contributes only slightly to upregulation of gene expression on the X chromosome. These results suggest that the level of chromosome decondensation does not necessarily correlate with the degree of gene expression change in vivo. Furthermore, the X chromosome is more sensitive to MYS-1-mediated decondensation than the autosomes, despite similar levels of H4K16ac on all chromosomes, as measured by ChIP-seq. H4K16ac levels weakly correlate with gene expression levels on both the X and the autosomes, but highly expressed genes on the X chromosome do not contain exceptionally high levels of H4K16ac.These results indicate that H4K16ac and chromosome decondensation influence regulation of the male X chromosome; however, they do not fully account for the high levels of gene expression observed on the X chromosomes.

overall_design:
ChIP-seq profiles of C. elegans H4K16ac histone modification in 3 replicates from L3 wild type XX hermaphrodites and her-1;sdc-2 XO hermaphrodies. Corresponding inputs are labeled with 'Input" plus ChIP name.
ChIP-seq profiles of C. elegans. Strains are N2 Bristol strain (wild type) and TY1072 her-1(e1520) V;sdc-2(y74) X.
RNA-seq profiles of C. elegans L3 wild type XX hermaphrodites, dpy-21 XX hermaphrodties, her-1;sdc-2 vector RNAi XO hermaphrodies, and her-1;sdc-2 mys-1 RNAi XO hermaphrodies.
RNA-seq profiles of C. elegans. Strains are N2 Bristol strain (wild type), TY1072 her-1(e1520) V;sdc-2(y74) X, and EKM71 dpy-21(e428). Biological replicates for each strain listed separately.

first: Alyssa

last: Lau

first: Kevin

last: Zhu

first: Elizabeth

last: Brouhard

first: Michael

last: Davis


title: Therapeutic targeting of GCB- and ABC-DLBCL by rationally designed BCL6 inhibitor

first: Matt

last: Teater

address: 445 E 69th St

institute: Weill Cornell Medical College

summary: Rationale: The BCL6 oncogene is constitutively activated by chromosomal translocations and amplification in ABC-DLBCLs, a class of DLBCLs that respond poorly to current therapies. Yet the role of BCL6 in maintaining these lymphomas has not been investigated. BCL6 mediates its effects by recruiting corepressors to an extended groove motif. Development of effective BCL6 inhibitors requires compounds exceeding the binding affinity of these corepressors. Objectives: To design small molecule inhibitors with superior potency vs. endogenous BCL6 ligands for unmet putative therapeutic needs such as targeting ABC-DLBCL. Findings: We used an in silico drug design functional-group mapping approach called SILCS to create a specific BCL6 inhibitor with 10-fold greater potency than endogenous corepressors. The compound, called FX1, binds in such a way as to occupy an essential region of the BCL6 lateral groove. FX1 disrupts BCL6 repression complex formation, reactivates BCL6 target genes, and mimics the phenotype of mice engineered to express BCL6 with lateral groove mutations. This compound eradicated established DLBCLs xenografts at low doses. Most strikingly, FX1 suppressed ABC-DLBCL cells as well as primary human ABC-DLBCL specimens ex vivo. Conclusions: ABC-DLBCL is a BCL6 dependent disease that can be targeted by novel inhibitors able to exceed the binding affinity of natural BCL6 ligands.

overall_design: gene expression profiles of DLBCL cases

first: Mariano

last: Cardenas

first: Olivier

last: Elemento


title: Estrogen receptor α promotes breast cancer by reprogramming cell metabolism

city: Huddinge

first: Karin

last: Dahlman-Wright

address: Blickagången 16

department: Department of Biosciences and Nutrition

institute: Karolinska Institutet


title: The germ cell fate of cynomolgus monkeys is specified in the amnion

city: Kyoto

first: Yukihiro

last: Yabuta

state: Kyoto

address: Yoshida-Konoe-cho, Sakyo-ku

department: Anatomy and Cell Biology

institute: Kyoto University, Graduate school of medicine

summary: The germ cell lineage ensures reproduction, heredity and evolution. However, the mechanism for germ cell specification in primates, including humans, has been unknown. In primates, the pluripotent epiblast segregates the amnion upon implantation and thereafter initiates gastrulation to generate three germ layers. Here, we show that in cynomolgus monkeys, the SOX17/BLIMP1/TFAP2C-positive primordial germ cells (cyPGCs) arise from the dorsal amnion at embryonic day (E) 11. cyPGCs then migrate down beneath the epiblast and expand their numbers, through proliferation and continuous recruitment from the posterior amnion, around posterior yolk sac endoderm by E17. Remarkably, the amnion itself expresses BMP4, a cytokine potentially critical for PGC specification, thereby inducing cyPGCs in an autocrine fashion. Consistently, the amnion expresses T, a key mesodermal factor, prior to the onset of gastrulation. Our study demonstrates the origin of cyPGCs in the amnion, which undergoes a unique morphogenetic event prior to and independent from the gastrulation.

overall_design: Single cell transcriptome analysis of cynomolgus monkey embryo E13-20 using SC3-seq technology.

first: Kotaro

last: Sasaki

first: Tomonori

last: Nakamura

first: Ikuhiro

last: Okamoto

first: Chizuru

last: Iwatani

first: Hideaki

last: Tsuchiya

first: Naoto

last: Shiraki

first: Tetsuya

last: Takakuwa

first: Takuya

last: Yamamoto

first: Mitinori

last: Saitou


title: Insights into the adaptive stress response of Arabidopsis thaliana to thermal stress by ribosomal profiling

city: Potsdam

first: Radoslaw

last: Lukoszek

address: Karl-Liebknecht-Strasse 24-25

institute: University of Potsdam

summary: Environmental stress is detrimental to plants viability and requires an adequate reprogramming of cellular activities to maximize plant survival. We present a global analysis of the adaptive stress response of Arabidopsis thaliana to prolonged heat stress. We combine deep sequencing of RNA and ribosome protected fragments to provide genome wide map of adaptation to heat stress on at transcriptional and translational level. Our analysis shows that the genes with the highest upregulation upon heat stress are known heat-responsive gene, chaperons and other genes involved in protein folding control. Majority of these genes exhibits increase on both transcriptional and translational level. No translational inhibition or ribosome stalling was observed, which can be observed in the early thermal stress response, indicating that plants alter their cellular composition in order to adapt to the prolonged exposure to increased temperatures.

overall_design: Comparing global transcriptional and translational control by RNA-Seq and Ribosome Profiling (mRNA-Seq of ribosome protected fragments – RPF).

first: Peter

last: Feist

first: Ignatova

last: Zoya


title: ATF7IP-mediated stabilization of the histone methyltransferase SETDB1 is essential for heterochromatin formation by the HUSH complex

status: Public on Oct 11 2016

city: Cambridge

first: Richard

last: Timms

address: Cambridge Biomedical Campus, Hills Road

department: CITIID, Department of Medicine

institute: University of Cambridge


title: Assessing the impact of loss of ATF7IP and SETDB1 on the transcriptome

summary: By comparing HeLa cells lacking ATF7IP or SETDB1 generated through CRISPR/Cas9-mediated gene disruption to wild-type HeLa cells, the goal of the experiment was to determine the effect of loss of the SETDB1•ATF7IP complex on the transcriptome.

overall_design: Total RNA-seq of three independent knockout HeLa clones lacking either ATF7IP or SETDB1

middle: T

first: Iva

last: Tchasovnikarova

first: Paul

middle: J

last: Lehner


title: Transcriptome of mouse preimplantation development [C57BL/6 x Cast; WT]

city: Worcester

first: Ingolf

last: Bach

state: MA

address: 364 Plantation St

department: Molecular, Cell and Cancer Biology

institute: University of Massachusetts Medical School

summary:
Purpose:  The goals of this study are to establish a dynamic roadmap of imprinted X chromosome inactivation and the role of Xist by elucidation of the transcriptome of  Xist KO embryos during mouse preimplantation development
Methods: mRNA profiles of the preimplantation embryos WT and KO for Xist were elucidated by RNA-seq at various stages. Trophoblasts isolated from blastocyst outgrowths were also included. The sequence reads that samples where gender could be determined and that passed quality filters were analyzed at the level of autosomes, X chromosome as well as single genes. Effects of genetic background on the kinetics of iXCI was evaluated by RNA-seq on E3.5 embryos with a hybrid C57BL/6 x Cast background.
Results: Female embryos fail to silence the X chromosome at late preimplantation development. General autosomal gene expression is not affected in embryos lacking Xist.
Conclusions: Xist is crucial for iXCI. In preimplantation embryos the main in vivo function of Xist is to regulate iXCI in females. Genetic background does not significantly influence kinetics of iXCI.

overall_design: Global mRNA profiles of single preimplantation embryos were generated by deep sequencing.

first: Bach

last: Ingolf


title: Molecular analysis of renal cell carcinoma with unclassfied histology [gene expression]

first: Jeffrey

last: Zhao

address: 1275 York Avenue

department: Genomics Core

institute: Memorial Sloan Kettering Cancer Center

summary: Renal cell carcinomas with unclassified histology (uRCC) constitute a significant portion of aggressive non-clear cell RCC (nccRCC) that have no standard therapy. The oncogenic drivers in these tumors are unknown. We performed a molecular analysis of 62 high-grade primary uRCC, incorporating targeted cancer gene sequencing, RNA sequencing, Single Nucleotide Polymorphism array, fluorescence in-situ hybridization, immunohistochemistry, and cell-based assays. We identified recurrent somatic mutations in 29 genes, including NF2 (18%), SETD2 (18%), BAP1 (13%), KMT2C (10%), and MTOR (8%). Integrated analysis revealed distinct molecular subsets, including a subset of 26% uRCC characterized by NF2-loss, dysregulated Hippo-YAP pathway and worse survival.

overall_design: Analysis of RNA from uRCC with or without NF2-loss

first: Ying-Bei

last: Chen

first: Anders

last: Skanderup

first: Victor

middle: E

last: Reuter

first: James

last: Hsieh


title: Assessing the impact of loss of ATF7IP and SETDB1 on the global distribution of H3K9me3

summary: By comparing HeLa cells lacking ATF7IP or SETDB1 generated through CRISPR/Cas9-mediated gene disruption to wild-type HeLa cells, the goal of the experiment was to determine the effect of loss of the SETDB1•ATF7IP complex on the distribution of the repress

overall_design: H3K9me3 ChIP-seq analysis of wild-type HeLa cells compared to ATF7IP knockout and SETDB1 knockout HeLa cells.


title: Identification of Differentially Expressed Genes involved in Thermal Adaptation of the Hong Kong Oyster by Digital Gene Expression Profiling

city: Guangzhou

first: Jun

last: Li

state: Guangdong

address: xingangxilu 164hao

department: South China Sea Institute of Oceanology

institute: Chinese Academy of Sciences

summary: Thermal exposure of sessile marine animals inhabiting estuarine intertidal regions is a matter of serious concern. The Hong Kong oyster, Crassostrea hongkongensis is one of the dominant sessile inhabitants of marine intertidal region which undergoes large seasonal temperature fluctuations every year. The oyster has developed several adaptation mechanisms to cope with acute thermal stress. However, the genetic basis of these mechanisms remain largely unclear. To better understand how acute thermal exposure affects the biology of the oyster, two cDNA libraries obtained from the gill of oysters exposed to thermal stress and ambient temperature were sequenced using the Digital Gene Expression (DGE) tag profiling strategy. In total, 5.9 and 6.2 million reads were obtained for thermal stress and control libraries respectively, with approximately 74.25% and 75.02 % of the reads mapping to the C. hongkongensis reference sequence. A total of 605 differentially expressed transcripts could be detected in the thermal stress group as compared to the control group, of which 378 are up-regulated and 227 are down-regulated. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that these Differentially Expressed Genes (DEGs) were enriched with a broad spectrum of biological processes and pathways, including those associated with chaperones, antioxidants, immunity, apoptosis and cytoskeletal reorganization. Among these significantly enriched pathways, protein processing in the endoplasmic reticulum was the most affected metabolic pathway, which plays an important role in the unfolded protein response (UPR) and ER-associated degradation (ERAD) processes. Our results demonstrate the complex multi-modal cellular response to thermal stress in C. hongkongensis.

overall_design: Digital gene expression tag profiling analysis of the Hong Kong oyster

first: Yang

last: Zhang

first: Ziniu

last: Yu


title: HMGB2 orchestrates the chromatin landscape of senescence-associated secretory phenotype gene loci.

city: Philadelphia

first: Priyankara

last: Wickramasinghe

state: PA

address: 3601 Spruce Street

department: Bioinformatics

institute: The Wistar Institute

summary: Cellular senescence is a stable cell growth arrest that is characterized by silencing of proliferation-promoting genes through compaction of individual chromosomes into senescence-associated heterochromatin foci (SAHF).  Paradoxically, senescence is also accompanied by increased expression of certain secreted factors such as cytokines and chemokines, known as senescence-associated secretory phenotype (SASP). How SASP genes are excluded from SAHF-mediated global gene silencing remains unclear.  Here we report that HMGB2 orchestrates the chromatin landscape of SASP gene loci.  HMGB2 preferentially localizes to SASP gene loci during senescence.  Loss of HMGB2 during senescence blunts SASP gene expression by allowing for spreading of repressive heterochromatin into SASP gene loci.  This correlated with incorporation of SASP gene loci into SAHF.  Our results establish HMGB2 as a novel master regulator that orchestrates SASP through preventing heterochromatin spreading to allow for exclusion of SASP gene loci from a global heterochromatin environment during senescence.

overall_design: HMGB2 CHIP-seq in senescent and growing IMR90 cells

first: Katherine

middle: M

last: Aird

first: Rugang


title: RNA-seq of human fibroblasts after irradiation

city: Jena

first: JenAge

last: Project

address: Beutenbergstr. 11

institute: Leibniz Institute for Age Research - Fritz Lipmann Institute

summary:
Comparing gene expression level by Illumina sequencing of fibroblasts after irradiation

Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)

overall_design: 6 samples, 3 samples per group, 2 groups: 1) MRC-5 cells population doublings (PD) 16 and irradiation (20GY) and 2) HFF cells PD32 and irradiation (20GY)

first: Shiva

last: Marthandan

first: Uwe

last: Menzel

first: Steffen

last: Priebe

first: Marco

last: Groth

first: Reinhard

last: Guthke

first: Matthias

last: Platzer

first: Peter

last: Hemmerich

first: Christoph

last: Kaether

first: Stephan

last: Diekmann


title: Molecular analysis of renal cell carcinoma with unclassfied histology

first: Jeffrey

last: Zhao

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

overall_design: Refer to individual Series


title: Aberrant blood DNA methylation reveals reproductive hormone imbalances in firefighters

city: Cincinnati

first: Mario

last: Medvedovic

state: OH

address: 3223 Eden Av. ML 56

department: Department of Environmental Health

institute: University of Cincinnati

summary: Constant exposure to toxic combustion byproducts distresses firefighters and puts them at risk of developing adverse health conditions. Epigenetic alternations have been identified as one of the major mechanisms linked to environment-induced diseases. We found DUSP22 which was epigenetically activated in heavy traffic exposure cohort, also showed similar alternations in firefighters, suggesting that some common components in the exposure such as PAH exist could be the major epigenetic modifier in both cohorts. We hypothesize that occupation-related exposure causes aberrant methylation changes in blood and eventually affects health outcome in firefighters. Therefore, we performed a genome wide DNA methylation profiling on firefighter blood samples using methylated CpG island recovery assay with next generation sequencing. We found firefighters, showed significant DNA hypomethylation in a set genes which are functionally related to cancer, organismal injury and abnormalities, reproductive system diseases, and developmental disorders. Methylation changes in the top four genes (TRDR6, KLHL17, PDIA2, and PTCHD3) had been confirmed through bisulfite sequencing. Interestingly, GO-KEEG pathway analyses suggest reproductive system and spermatogenesis related pathway as the top gene network. Blood AMH level of firefighters was 1.43-times higher than that of the non-firefighters Our data, for the first time, showed the constant exposure to firefighting environment induces changes in blood DNA methylation and reproductive hormones, which explain why firefighters suffer certain poor health outcomes.

overall_design: Pooled six firefighters versus pooled four non-firefighter controls

first: Bin

last: Ouyang

first: Yuet-Kin

last: Leung

first: C

last: Baxter

first: Jun

last: Ying

first: Ana

last: Cheong

first: Jacek

last: Biesiada

first: Jing

last: Chen

first: Shuk-mei

last: Ho


title: Polycomb Underlies Transcriptional Heterogeneity in Lineage Priming of Embryonic Stem Cells

city: Edinburgh

first: Rob

last: Illingworth

state: Midlothian

address: Centre for Regenerative Medicine

department: Centre for regenerative Medicine

institute: The University of Edinburgh


title: Polycomb Underlies Transcriptional Heterogeneity in Lineage Priming of Embryonic Stem Cells [ChIP-Seq and GRO-Seq]

summary: Chromatin Immunoprecipitation (ChIP) for the histone modification H3K4me3 and H3K27me3 and Genome Wide Run-on seq (GROseq) were performed on subpopulations of the HexVenus reporter mouse ES cell line (clone HV1.5) growing under self-renewing conditions. Subpopulations were identified and isolated based on the expression of the ES cell surface marker SSEA 1 and the expression of the venus protein. At approximately 70% confluence, cells were trypsinised, resuspended in FACs buffer (10%FCS in PBS) and incubated with a mouse monoclonal antibody to SSEA 1 (MC-480, Developmental Hybridoma Studies Bank, University of Iowa). Cells were then incubated with an Alexa-647 conjugated anti-mouse IgM antibody (Invitrogen) and subpopulations were fractionated by flow cytometry prior to further processing specific to each method. The aim was to determine if differential gene expression between these populations is primarily mediated at the level of transcription and if these changes are concomitant with changes in chromatin state.

overall_design: mESCs carrying a fluorescently tagged Hhex-Venus (HV) reporter construct were FACS sorted into Ssea1+HV- and Ssea1+HV+ populations. Nuclei were prepared from these populations immediately following FACS sorting and then further processed as per the relevant protocol. Two independent biological replicates were prepared for each sample and sequencing libraries were the pooled prior to sequencing or combined bioinformatically following sequencing as outlined for each sample.

first: Robert

first: Jurriaan

last: Hölzenspies

first: Wendy

middle: A

last: Bickmore

first: Joshua

last: Brickman


title: Transcriptome of mouse preimplantation development [Rlim KO]

first: Ingolf

last: Bach

summary:
Purpose: The goals of this study are to establish a roadmap of XCI and compare the transcriptomes of WT and Rlim KO embryos during X chromosome inactivation.

Methods: mRNA profiles of 175 preimplantation embryos WT and KO for Rlim were elucidated by RNA-seq at various stages. Trophoblasts isolated from blastocyst outgrowths were also included. The sequence reads that samples where gender could be determined and that passed quality filters were analyzed at the level of autosomes, X xhromosomes as well as single genes.

Results: Using single cell RNA-seq technology on 175 whole preimplantation embryos, we obtained about 2.95 million sequence reads per sample. Reads were normalized to autosomal gene expression. Gender of each embryo was determined by expression of Y-linked genes and Xist. Data analysis showed normal expression profiles of marker genes for epiblast and trophoblast cell types during preimplantation development. Comparing Xist expression profiles in embryos WT and KO shows that Rlim is not required for initiation of Xist transcription but for upregulation of Xist expression. Moreover, our results identify two waves of XCI during preimplantation development: One that occurs at Morula stages that is Rlim-independent and one at blastocyst stages that in dependent on Rlim.

Conclusions: Our study represents the first detailed mouse preimplantation transcriptome. Our results show that Rlim is required for a second wave of imprinted XCI that occurs in female embryos at blastocyst stages.

overall_design: Global mRNA profiles of whole preimplantation embryos were generated by deep sequencing.


title: Transcriptome of mouse preimplantation development [Xist KO]

summary:
Purpose: The goals of this study are to establish a dynamic roadmap of imprinted X chromosome inactivation and the role of Xist by elucidation of the transcriptome of Xist KO embryos during mouse preimplantation development.

Methods: mRNA profiles of the preimplantation embryos WT and KO for Xist were elucidated by RNA-seq at various stages. Trophoblasts isolated from blastocyst outgrowths were also included. The sequence reads for samples where gender could be determined and that passed quality filters were analyzed at the level of autosomes, X chromosome as well as single genes.

Results: Female embryos fail to silence the X chromosome at late preimplantation development. General autosomal gene expression is not affected in embryos lacking Xist.

Conclusions: Xist is crucial for iXCI. In preimplantation embryos, the main in vivo function of Xist is to regulate iXCI in females.

first: Bach

last: Ingolf


title: Arabidopsis FORGETTER1 sustains stress-induced transcription through nucleosome remodeling

status: Public on Oct 10 2016

first: Isabel

last: Bäurle

address: Karl-Liebknecht-Str. 24-25

department: Institut für Biochemie und Biologie

institute: Universität Potsdam

summary: Plants as sessile organisms can adapt to environmental stress to mitigate its adverse effects. As part of such adaptation they maintain an active memory of heat stress for several days that mediates a more efficient response to recurring stress. We identified a mutant that is specifically affected in this heat stress memory. The forgetter1 (frg1) mutant is defective in the Arabidopsis orthologue of Strawberry notch and displays reduced maintenance of heat-induced gene expression. FRG1 globally associates with the promoter region of actively expressed genes in a heat-dependent fashion. FRG1 interacts with chromatin remodelers of the SWI/SNF and ISWI families, which also display reduced heat stress memory. Accordingly, nucleosome dynamics at loci with altered maintenance of heat-induced expression are affected in frg1. Thus, FRG1 is required to sustain a transcription-competent chromatin environment by nucleosome positioning. Our findings suggest a mechanism for the highly conserved Strawberry notch proteins in development and pathologies.

overall_design: Chromatin binding of FRG1.

first: Krzysztof

last: Brzezinka

first: Simone

last: Altmann

first: Hjördis

last: Czesnick

first: Philippe

last: Nicolas

first: Eileen

last: Benke

first: Tina

last: Kabelitz

first: Christian

last: Kappel


title: Transcriptomic profiles and RNA half-life of M. acetivorans growing in acetate, methanol, and trimethylamine

city: Urbana

first: Zaida

last: Luthey-Schulten

address: 600 South Mathews Avenue

department: Chemistry

institute: University of Illinois at Urbana-Champaign

summary: The goal of this work was to measure the half-lives of RNA transcripts and identify which genes in Methanosarcina acetivorans C2A were differentially expressed between methylotrophic and acetitrophic growth substrates. We used this data to predict metabolic phenotype under different growth condition and hypothesize whether key metabolic genes were transcriptionally or degradationally regulated.

overall_design: The mRNA from Methanosarcina acetivorans C2A grown on acetate, methanol and trimethylamine was harvested, sequenced and mapped to the M. acetivorans genome.  For each condition, mRNA was harvested at 6 or 7 timepoints after halting transcription with actinomycin D.  Degradation rates were computed genome-wide for the three growth substrates. Genes differentially expressed genes between each condition were identified.

first: Joseph

middle: R

last: Peterson

first: William

middle: W

last: Metcalf


title: Estrogen receptor α promotes breast cancer by reprogramming cell metabolism [ChIP-seq]

first: Karin

last: Dahlman-Wright

summary: Estrogen receptor α (ERα) is a key regulator of breast growth and breast cancer development. However, the role of ERα in metabolic reprogramming, a hallmark of cancer, is not well documented. In this study, using an integrated approach combining genome-wide mapping of chromatin bound ERα with estrogen induced transcript and metabolic profiling, we demonstrate that ERα reprograms metabolism upon estrogen stimulation, including changes in aerobic glycolysis, nucleotide and amino acid synthesis, and choline metabolism. We show, for the first time, that the ERα target gene choline phosphotransferase 1 (CHPT1) plays an essential role in estrogen induced increases in phosphatidylcholine (PtdCho) levels and that CHPT1 promotes tumorigenesis and proliferation. Furthermore, we show that CHPT1 is overexpressed in tumors compared to normal breast. We also demonstrate that ERα promotes aerobic glycolysis through increased expression of glycolytic genes. In conclusion, this study highlights the importance of ERα for metabolic alterations in breast cancer cells. Furthermore, overexpression of the ERα target CHPT1 in breast cancer supports its potential as a therapeutic target.

overall_design: Examination of ERα DNA binding sites in T47D, a breast cancer cell line.

first: Min

last: Jia

first: Trygve

last: Andreassen

first: Siver

last: Moestue

first: Indranil

last: Sinha

first: Hui

last: Gao

first: Tone

middle: F

last: Bathen

first: Chunyan

last: Zao


title: Multi-parametric profiling of non-small cell lung cancers reveals distinct immunophenotypes

city: Boston

first: Ruben

last: Dries

address: 360 Longwood Ave

department: Computational Biology

institute: DFCI


title: Single-cell profiling of non small cell lung cancer associated B-cells.

summary: Background: Immune checkpoint blockade improves survival in a subset of patients with non-small cell lung cancer (NSCLC), but robust biomarkers that predict response to PD-1 pathway inhibitors are lacking.  Furthermore, our understanding of the diversity of the NSCLC tumor immune microenvironment remains limited.    Methods: We performed comprehensive flow-cytometric immunoprofiling on both tumor and immune cells from 51 NSCLCs and integrated this analysis with clinical and histopathologic characteristics, next generation sequencing, mRNA expression, and PD-L1 immunohistochemistry (IHC).    Results:  Cytometric profiling identified an immunologically “hot” cluster with abundant CD8+ T cells expressing high levels of the PD-1 and TIM-3, and an immunologically “cold” cluster with lower relative abundance of CD8+ T cells and expression of inhibitory markers.  The “hot” cluster was highly enriched for expression of genes associated with T cell trafficking and cytotoxic function, and high PD-L1 expression by IHC.  There was no correlation between immunophenotype and KRAS or EGFR mutation, or patient smoking history, but we did observe an enrichment of squamous subtype and tumors with higher mutation burden in the “hot” cluster.  Additionally, ~20% of cases had high B cell infiltrates with a subset producing IL-10.    Conclusions: Our results support the use of immune-based metrics to study response and resistance to immunotherapy in lung cancer.   Background: Immune checkpoint blockade improves survival in a subset of patients with non-small cell lung cancer (NSCLC), but robust biomarkers that predict response to PD-1 pathway inhibitors are lacking.  Furthermore, our understanding of the diversity of the NSCLC tumor immune microenvironment remains limited.    Methods: We performed comprehensive flow-cytometric immunoprofiling on both tumor and immune cells from 51 NSCLCs and integrated this analysis with clinical and histopathologic characteristics, next generation sequencing, mRNA expression, and PD-L1 immunohistochemistry (IHC).    Results:  Cytometric profiling identified an immunologically “hot” cluster with abundant CD8+ T cells expressing high levels of the PD-1 and TIM-3, and an immunologically “cold” cluster with lower relative abundance of CD8+ T cells and expression of inhibitory markers.  The “hot” cluster was highly enriched for expression of genes associated with T cell trafficking and cytotoxic function, and high PD-L1 expression by IHC.  There was no correlation between immunophenotype and KRAS or EGFR mutation, or patient smoking history, but we did observe an enrichment of squamous subtype and tumors with higher mutation burden in the “hot” cluster.  Additionally, ~20% of cases had high B cell infiltrates with a subset producing IL-10.    Conclusions: Our results support the use of immune-based metrics to study response and resistance to immunotherapy in lung cancer.

overall_design: Single-cell comparison of normal and tumor infiltrated B-cells.

first: Patrick

last: Lizotte

first: Elena

last: Ivanova