title: K8 CLIP-Seq in KSHV reactivated BCBL-1 cells

city: guangzhou

first: Dongcheng

last: Liu

state: guangdong

address: zhongshan 2nd road

department: Institute of Human Virology and Ministry of Education Key Laboratory of Tropical Disease Control

institute: Sun Yat-sen University

summary: KSHV K8 is required for  KSHV DNA replication and is found to be an RNA binding protein. To understand the molecular mechanism of K8 in regulation of DNA replication, we examine the binding RNAs of  K8 protein in BCBL-1 cells using CLIP-Seq analysis.

sample_organism:
Homo sapiens
Human gammaherpesvirus 8

platform_organism:
Homo sapiens
Human gammaherpesvirus 8

overall_design: KSHV K8 CLIP was performed in TPA-induced BCBL-1 cells. K8-immunoprecipitation of UV cross-linked K8-RNA complexes, followed by RNA isolation, library construction, and high-throughput sequencing (Illumina HiSeq 2500); we performed 2 biological replicates, three technical replicates of each biological replicate. Technical replicates were pooled before library construction. The two biological replicates for the IgG and BJAB samples did not produce enough material for sequencing each replicate independently so they were combined into a single sample each for IgG and BJAB.

first: Yan

last: Wang

last: Yuan


title: OKF6/Tert2 Human oral cells : Control vs transfected with E6E7 HPV16

status: Public on Oct 05 2017

city: Santiago

first: Ulises

last: Urzua

address: Independencia 1027

department: Basic and Clinical Oncology

country: Chile

institute: University of Chile

summary: Transcriptional profiling of OKF6/Tert2 oral cell transfected with E6E7 HPV-16 genes using pLXSN vector. Control cells were transfected with the empty pLXSN  vector

overall_design: Two-condition experiment, OKF6/Tert2 E6E7 vs OKF6/tert2 V. Two dye-swap Cy3/Cy5 replicates per sample.

first: Juan Pablo

last: Muñoz

first: Diego

last: Carrillo

first: Francisco

last: Aguayo


title: Cohesin loss eliminates all loop domains

city: Houston

first: Suhas

last: Rao

state: TX

address: 1 Baylor Plaza

department: Molecular and Human Genetics

country: USA

institute: Baylor College of Medicine

type: Genome binding/occupancy profiling by high throughput sequencing

type: Expression profiling by high throughput sequencing

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

overall_design: Refer to individual Series


title: Rapid reversal of innate immune dysregulation in blood of patients and liver of humanized mice with HCV following DAA therapy

city: Aurora

first: Matthew

middle: Alan

last: Burchill

state: Colorado

department: Department of Medicine

institute: University of Colorado - Anschutz Medical Campus

summary: Analysis of transcriptional changes in the peripheral blood of patients prior to and following DAA treatment of HCV infection

overall_design: Peripheral Blood Mononuclear cells from patients with chronic HCV treated with direct acting antiviral therapy. This series contains only the human blood samples.

first: Hugo

last: Rosen


title: Expression data from mouse MDSC with interference or overexpression of lncMDSC

status: Public on Oct 04 2017

city: tianjin

first: Yunhuan

last: Gao

address: Wei Jin Road No. 94

department: School of Medicine

country: China

institute: Nankai University

summary:
Myeloid-derived suppressor cells (MDSCs) have emerged as major regulators of immune responses in cancer and other pathological conditions. At the epigenetic level, lncRNA play an important role in cell differentiation and function. We identify a novel long non-coding RNA (lncRNA) termed as lnc-mdsc in MDSCs, which may tightly control the development of MDSCs.
We used microarrays to detail the global programme of gene expression and identified distinct classes of up or down regulated genes in MDSC interference or overexpression the lncMDSC.

overall_design: The transfected MDSC were selected for RNA extraction and hybridization on Affymetrix microarrays. MDSC transfection control shRNA lentivirus as siNC group,MDSC transfection shlncMDSC lentivirus as SilncRNA group, MDSC transfection overexpression control lentivirus as NC group, MDSC transfection lncMDSC overexpression lentivirus as lncRNA group.

first: Rongcun

last: Yang


title: Expression data from mouse MDSC with interference of lncMDSC

summary:
Myeloid-derived suppressor cells (MDSCs) have emerged as major regulators of immune responses in cancer and other pathological conditions. At the epigenetic level, lncRNA play an important role in cell differentiation and function. We identify a novel long non-coding RNA (lncRNA) termed as lnc-mdsc in MDSCs, which may tightly control the development of MDSCs.
We used microarrays to detail the global programme of gene expression and identified distinct classes of up or down regulated genes in MDSC interference the lncMDSC.

overall_design: The transfected MDSC were selected for RNA extraction and hybridization on Affymetrix microarrays. MDSC transfection control siRNA as Si-NC group, MDSC transfection silncMDSC  as Si-B group.


title: Gene expression analysis of RNAs isolated from TPEN-untreated and TPEN-treated human keratinocytes

city: Pohang

first: Bhin

last: Jin-hyuk

address: Ji-gok research center, hyoja-dong, Nam-gu

department: Department of Chemical engineering

country: South Korea

institute: POSTECH

summary: In order to identify the zinc responsive genes, we performed a gene expression microarray analysis for the RNAs isolated from TPEN-untreated and TPEN-treated human keratinocytes

overall_design: Duplicate experiments were performed for TPEN-untreated and TPEN-treated human keratinocytes. Total RNA was isolated from tissues using Qiazol (QIAGEN) following the manufacturers’ protocols.

first: Bum-Ho

last: Bin

first: Jinhyuk

last: Bhin


title: Cohesin loss eliminates all loop domains [HiC]

summary: The human genome folds to create thousands of intervals, called “contact domains,” that exhibit enhanced contact frequency within themselves. “Loop domains” form because of tethering between two loci – almost always bound by CTCF and cohesin – lying on the same chromosome. “Compartment domains” form when genomic intervals with similar histone marks co-segregate. Here, we explore the effects of degrading cohesin. All loop domains are eliminated, but neither compartment domains nor histone marks are affected. Loss of loop domains does not lead to widespread ectopic gene activation, but does affect a significant minority of active genes. In particular, cohesin loss causes superenhancers to co-localize, forming hundreds of links within and across chromosomes, and affecting the regulation of nearby genes. We then restore cohesin and monitor the re-formation of each loop. Although re-formation rates vary greatly, many megabase-sized loops recovered in under an hour, consistent with a model where loop extrusion is rapid.

overall_design: we use in situ Hi-C, ChIP-Seq and PRO-Seq to probe nuclear architecture, the epigenome and transcription during cohesin loss and recovery

first: Erez

last: Lieberman Aiden


title: Chemical reprogramming of mouse embryonic and adult fibroblast into endoderm lineage

city: Guangzhou

first: Lihui

last: Lin

state: Guangdong

address: No.190, Kaiyuan Street

department: Stem cell

institute: Guangzhou Institutes Of Biomedicine and Health Chinese Academy Of Science

summary: We report here an approach to redirect somatic cell fate under chemically defined conditions without transcription factors. We start by converting mouse embryonic fibroblasts (MEFs) to epithelial-like cells (ciELC) with chemicals and growth factors.  Subsequent cell fate mapping reveals a robust induction of SOX17 in the resulting ELCs that can be further reprogrammed to endodermal progenitor cells (ciEPC).  Interestingly, these cells can self-renew in vitro and further differentiate into albumin-producing hepatocytes that can rescue mice from acute live injury. Our results demonstrate a rational approach to convert MEFs to hepatocytes and suggest that this mechanism-driven approach may be generalized for other cells.

overall_design: Examination of mouse  fibroblasts, ciEPCs, ciHeps, ESC derived EPCs and primary hepatocytes

first: Jing

first: Duanqing

last: Pei


title: Expression data from glioblastoma tissue

city: Odense

first: Bjarne

middle: Winther

last: Kristensen

address: Winsloewsparken 15

department: Dept. of Pathology

country: Denmark

institute: Odense University Hospital

summary:
Glioblastomas are among the most lethal cancers; however, recent advances in survival have increased the need for better prognostic markers. microRNAs (miRNAs) hold great prognostic potential being deregulated in glioblastomas and highly stable in stored tissue specimens. Moreover, miRNAs control multiple genes representing an additional level of gene regulation possibly more prognostically powerful than a single gene. The aim of the study was to identify a novel miRNA signature with the ability to separate patients into prognostic subgroups. Samples from 40 glioblastoma patients were included retrospectively; patients were comparable on all clinical aspects except overall survival enabling patients to be categorized as short-term or long-term survivors based on median survival.
A miRNome screening was employed, and a prognostic profile was developed using leave-one-out cross-validation. We found that expression patterns of miRNAs; particularly the four miRNAs: hsa-miR-107_st, hsa-miR-548x_st, hsa-miR-3125_st and hsa-miR-331-3p_st could determine short- and long-term survival with a predicted accuracy of 78%. Heatmap dendrograms dichotomized glioblastomas into prognostic subgroups with a significant association to survival in univariate (HR 8.50; 95% CI 3.06-23.62; p<0.001) and multivariate analysis (HR 9.84; 95% CI 2.93-33.06; p<0.001). Similar tendency was seen in The Cancer Genome Atlas (TCGA) using a 2-miRNA signature of miR-107 and miR-331 (miR sum score), which were the only miRNAs available in TCGA. In TCGA, patients with O6-methylguanine-DNA-methyltransferase (MGMT) unmethylated tumors and low miR sum score had the shortest survival. Adjusting for age and MGMT status, low miR sum score was associated with a poorer prognosis (HR 0.66; 95% CI 0.45-0.97; p=0.033). A Kyoto Encyclopedia of Genes and Genomes analysis predicted the identified miRNAs to regulate genes involved in cell cycle regulation and survival.  In conclusion, the biology of miRNAs is complex, but the identified 4-miRNA expression pattern could comprise promising biomarkers in glioblastoma stratifying patients into short- and long-term survivors.

overall_design: miRNA expression data from primary glioblastoma tissue; 40 patient samples were analyzed. One sample was omitted from further analysis due to low intensity on the chip (Patient ID 10). Another sample (Patient ID 21) had a mutation in isocitrate dehydrogenase 1 and was therefore omitted from further analysis due to potential confounding.

first: Simon

middle: K

last: Hermansen

first: Mia

middle: D

last: Sørensen

first: Anker

last: Hansen

first: Steen

last: Knudsen

first: Alvaro

middle: G

last: Alvarado

first: Justin

last: Lathia

middle: W


title: Genomic alterations activating KLF5 [RNA-Seq]

city: Salt Lake City

first: Xiaoyang

last: Zhang

address: 1950 CIrcle of Hope

institute: University of Utah

summary: Using RNA-seq to identify genes that regulated by KLF5 and KLF5 mutants

overall_design: RNA-seq of BICR31 cells treated with siNC or siKLF5. RNA-seq of HCC95 cells over-expressing empty vector, KLF5 WT or KLF5 E419Q.


title: Bicoid binding along anteroposterior axis of Drosophila Melanogaster embryos

city: Berkeley

first: Mustafa

last: Mir

state: CA

address: 1951 Oxford St., Room 485, Li Ka Shing Center

institute: University of California, Berkeley

summary: ChIP-Seq against Bicoid on manually dissected posterior thirds of Drosophila Melanogaster early stage 5 embryos.

sample_organism:
Drosophila melanogaster
Drosophila pseudoobscura

overall_design: Embryos were collected from a population cage for 90 minutes and then aged for 2 hours in order to enrich for embryos at developmental stage five. Embryos were then fixed with formaldehyde as previously described (Li et al. 2008) and sorted by morphology for those at early stage 5. The posterior thirds of embryos were sliced off by hand with a scalpel. A pool of the embryo segments from approximately 300 embryos was combined with 20 µg of whole Drosophila pseudoobscura embryos at stage 5 (to serve as carrier), and homogenized in homogenization buffer containing 15mM NaCl, 15mM TrisHCl pH 7.5, 60mM KCl, 1mM EDTA, and 0.1% Triton-X100, with 1mM DTT, 0.1 mM PMSF, and protease inhibit cocktail (Roche) added before use. After homogenization, 0.5% NP40 was added, and following a 5 minute incubation, samples were spun down at a low speed. Nuclei in the pellet were then washed once with the homogenization buffer containing 0.2M NaCl. The low speed centrifugation was repeated, and the recovered nuclei pellet was then re-suspended in nuclear lysis buffer (10 mM TrisCl, pH 7.9, 100 mM NaCl, 1 mM EDTA, 0.5 % Sarkosyl) +1%SDS, +1.5% sarkosyl. The chromatin was recovered by spinning the sample at full speed in a micro-centrifuge at 4oC for 1 hour and was re-suspended in a small volume of nuclear lysis buffer. Chromatin was sheared to an average size of 300bp using a Covaris sonicator (peak power= 140, duty factor = wo, cycle burst = 200, time = 2:20 minutes). Chromatin immunoprecipitation was performed using 72ng of chromatin and 1.5ug of an anti-Bicoid polyclonal antibody described previously (Li et al. 2008). The Bicoid antibody was coupled to Dynabead M-280 sheep anti-rabbit magnetic beads and the immunoprecipitation was conducted with the standard protocol from the manufacturer. DNA libraries for the chromatin immunoprecitation samples were prepared using the Rubicon genomics thru-plex DNA-seq kit using 16 PCR cycles and sequenced using Illumina High-seq with 2500 rapid run100bp single end reads. The sequencing reads were aligned to a combined D. pseudoobscura (Flybase Release 1.0) and D. melanogaster genome (Flybase Release 5) using Bowtie2 with options set as bowtie2 -5 5 -3 5 -N 1 -X 2000. The aligned reads were converted to wig files using custom scripts available upon request. Wig files were normalized to 10 million mapped reads.

first: Jenna

last: Haines

first: Xiao-Yong

last: Li

first: Michael

middle: B

last: Eisen

first: Xavier

last: Darzacq


title: Global gene occupancy by nuclear WASp during T cell development

city: Stockholm

first: Nik

middle: V

last: Kuznetsov

address: Nobels vag 16

country: Sweden

institute: Karolinska Institute

summary: To investigate a role of nuclear WASp in T cell development we performed WASp chromatin immunoprecipitation and deep sequencing (ChIP-Seq) in thymocytes and spleen CD4+ T cells. To pre-process raw ChIP-Seq data, the total number of reads were normalized and aligned against the mouse genome. WASp was enriched at transcription start sites of a large number of protein-coding genes. Many of the WASp-enriched genes were associated with RNA Polymerase II-enriched genes and active epigenetic marks of transcription; H3K4m3, H3K9a, H3K27a, and with the epigenetic mark for active enhancers H3K4m1. To study the distribution of overactive WASpI296T in the thymocyte genome and to identify regions enriched in WASpI296T binding, we performed second round of ChIP-Seq analysis using the WASp F-8 antibody. To detect differences in gene enrichment between thymocytes expressing wildtype WASp or WASpI296T, we applied stringent conditions and subtracted common genes between the two samples. Using this approach, we identify 70 WASpI296T-enriched genes. Functional clustering of these genes revealed that WASpI296T was associated with RNA Polymerase II genes in 11 functional groups of genes.thymocytes and spleen CD4+ T cells. WASp was enriched at transcription start sites of a large number of protein-coding genes.

overall_design: Examination of enriched gene sequences in WASp I296T and wildtype mice thymocytes and spleen CD4+ T cells

first: Nikolai

first: Lisa

middle: S

last: Westerberg


title: Genomic alterations activating KLF5


title: Differential Expression Analysis of wildtype, E12-/- and E47-/- neuronal stem cells

city: Freising

first: Franziska

last: Greulich

address: Gregor-Mendel-Str. 2

department: Metabolic Programming

country: Germany

institute: TU München

summary: RNA sequencing of neuronal stem cells from wildtype, E12-/- and E47-/- mice isolated at E14.5

overall_design: RNA from 3 replicates of E12+/+, E47+/+, E12-/- and E47-/- E14.5 neuronal stem cells each were sequenced

first: Sabrina

last: Pfurr

first: Christian

last: Schachtrup


title: Over-expression of BAG-1 in head and neck squamous cell carcinomas (HNSCC) is associated with cisplatin-resistance

city: BETHESDA

first: PING

last: JIN

state: MD

address: 9000 ROCKVILLE PIKE

department: DTM

institute: CC/DTM/NIH

summary:
In order to improve therapy for head and neck squamous cell carcinoma (HNSCC), biomarkers associated with local and/or distant tumor relapses and cancer drug resistance are urgently needed. This study identified a potential biomarker, BAG-1 (Bcl-2 associated athanogene-1), that is implicated in HNSCC insensitive to cisplatin and tumor progression.
Advanced HNSCC cells revealed resistant to cisplatin accompanied by increased expression of BAG-1 protein. siRNA knockdown of BAG-1 expression resulted in significant improvement of HNSCC sensitivity to cisplatin. BAG-1 expression enhanced stability of BCL-xL and conferred cisplatin resistant to the HNSCC cells. In addition, high levels of expression of phospho AKT, BAG-1, and BCL- xL were observed in advanced HNSCC compared to in that of primary HNSCC. Conclusion: Increased expression of BAG-1 was associated with cisplatin resistance and tumor progression in HNSCC patients and warrants further validation in larger independent studies. Over expression of BAG-1 may be a biomarker for cisplatin resistance in patients with primary or recurrent HNSCCs and targeting BAG-1 could be helpful in overcoming cisplatin resistance.

overall_design: Primary and advanced (relapsed from parental) University of Michigan squamous cell carcinoma (UMSCC) cell lines were tested for sensitivity to cisplatin and gene expression profiles were compared between primary (cisplatin sensitive) and the relapsed (cisplatin resistant) cell lines by using Agilent microarrays.

first: Shutong

last: Liu

first: Bo

last: Ren

first: Hang

last: Gao

first: Suchan

last: Liao

first: Ying-Xian

last: Zhai

first: Shirong

first: Xue-Jin

last: Su

first: Ping

last: Jin

first: David

last: Stroncek

first: Zhixiang

last: Xu

first: Qinghua

last: Zeng

first: Yulin


title: MicroRNAs clustered within the 14q32 locus are associated with endothelial damage and microparticle secretion in bicuspid aortic valve disease

city: Reus

first: Neus

last: Martínez-Micaelo

address: Avda. de la Universitat, 1

country: Spain

institute: Pere Virgili Health Research Institute

summary: To identify the miRNAs associated with endothelial microparticles in plasma, we have employed SurePrint G3 Human v16 miRNA 8x60K Microarray to determine miRNAs in plasma from healthy donors and bicuspid aortic valve patients. Expression of 7 miRNAs (let-7d, let-7g, miR-130a, miR-337, miR-409, miR-494 and miR-718) from this signature was quantified in the same RNA samples by real-time PCR, confirming microarray results.

overall_design: miRNA expression profile was measured in plasma of healthy individuals and BAV patients (n=36)

first: J

middle: M

last: Alegret

first: M


title: Cardiomayocyte specific translating RNA sequencing from mice in heart failure

first: John

last: Leach

summary: Mammalian organs vary widely in regenerative capacity, and poorly regenerative organs, such as the heart are particularly vulnerable to organ failure. Once established, heart failure commonly results in in considerable mortality and early demise. The Hippo pathway, a kinase cascade that prevents adult cardiomyocyte proliferation and regeneration, is upregulated in human heart failure. We show that deletion of the Hippo pathway component Salvador (Salv) in mouse hearts with established ischemic heart failure after myocardial infarction induced a reparative genetic program characterized by increased scar border vascularity, reduced fibrosis, and recovery of pumping function to that of sham-operated controls. To isolate cardiomyocyte specific translating mRNA we used TRAP (translating ribosomal affinity purification) followed by RNA sequencing. Hippo deficient cardiomyocytes had increased expression of proliferative, and stress response genes. Interestingly the mitochondrial quality control gene, Park2 was among the stress response genes. Further genetic studies indicated that Park2 was essential for heart repair in both the neonatal mouse and the adult Salv conditional knockout mouse. Thus, suggesting a requirement for mitochondrial quality control in the regenerating myocardium. Our findings indicate that the failing heart has a previously unrecognized capacity for repair involving more than cardiomyocyte renewal.

overall_design: Cardiac mRNA profiles of total whole-heart RNA and translating ribosomal affinity purified (TRAP) cardiomyocyte specific RNA from adult wild type control (ctrl) and Salv cKO (mut) mice that underwent sham or left anterior descending coronary artery ligation were generated by sequencing, in triplicate, using the Proton Ion Torret.

middle: P

first: James

middle: F

last: Martin


title: Evaluating the relative potency and mechanism of action of azoles in the rat Whole Embryo Culture

city: Bilthoven

first: Jeroen

last: Pennings

address: A. van Leeuwenhoeklaan 9

country: Netherlands

institute: Natl. Inst. Public Health & Environment

summary: We evaluated the effect of azoles on embryonic development in the rat whole embryo culture (WEC). Using the total morphological scoring system (TMS), we calculated the effective dose for 10% decrease in TMS. We collected transcriptomics data for rat WEC exposed to azoles at their ID10 for 4 hours. Results revealed shared expressions responses in genes involved in the retinoic acid (RA) and sterol biosynthesis pathways, which are respectively representatives of developmental toxicity and desired fungicidal action of the azoles. Azoles with more pronounced effects on the regulation of RA-associated genes were generally characterized as more potent embryotoxicants.

overall_design: 109 samples hybridized to Affymetrix arrays, multiple replicates per group

first: Myrto

last: Dimopoulou


title: Genome-wide gene expression analysis of hNAC1-dependent time course rescue of Nac1 null abnormal reprogrammed cells

city: beijing

first: liang

middle: sheng

last: xian

address: shuangqing road

institute: chinese academy of science

summary: In this study, we dissected the functional contribution of NAC1 in establishing pluripotency during somatic cell reprogramming. We identified a critical role for NAC1 in transcriptionally and post-transcriptionally modulating E-cadherin expression during the generation of iPSCs. In the absence of NAC1 functions, reprogramming is diverted to an anomalous state that can be fully rescued with the re-expression of Nac1.

overall_design: This study containes 6 microarrays from day 0, 2, and 5 samples  of the hNAC1 time course rescue experiments from two in-house generated null iPS lines: Nac1 null iPS clone #5 and Nac1 null iPS clone #7

first: Francesco

last: Faiola

first: Jianlong

last: Wang


title: Transcriptomic analysis of salt-stress response in Aspergillus nidulans

city: Huzhou

first: Sha

address: No.759 Er Huan East Rd

institute: Huzhou University

summary: Adaptation to changes in the environment is crucial for the viability of all organisms. Although the importance of calcineurin in the stress response has been highlighted in filamentous fungi, little is known about the involvement of ion-responsive genes and pathways in conferring salt tolerance without calcium signaling. In this study, high-throughput RNA-seq was used to investigate salt stress-induced genes in the parent, ΔcnaB, and ΔcnaBΔcchA strains of Aspergillus nidulans, which differ greatly in their salt adaption under salt stress. In total, 2,884 differentially expressed genes including 1,382 up- and 1,502 down-regulated genes were identiﬁed. Secondary transporters, which were up-regulated to a greater extent in ΔcnaBΔcchA than in the parent or ΔcnaB strains, are likely to play important roles in response to salt stress. Furthermore, 36 genes were exclusively up-regulated in the ΔcnaBΔcchA mutant under salt stress. Functional analysis of differentially expressed genes revealed that genes involved in transport, heat shock protein binding, and cell division processes were exclusively activated in ΔcnaBΔcchA. Overall, our findings reveal that secondary transporters and stress-responsive genes may play crucial roles in salt tolerance to bypass the requirement for the CchA-calcineurin pathway, contributing to a deeper understanding of the mechanisms that influence fungal salt stress adaption in Aspergillus.

overall_design: mRNA profiles of wild type (WT)， ΔcnaB, and ΔcnaBΔcchA strains of Aspergillus nidulans treated with or without NaCl were generated by deep sequencing

first: Shengwen

last: Shao

first: Hongchang

last: Zhou

first: Jun

last: Wu

first: Jiangyu

last: Han

first: Shasha

last: Li


title: Immune repertoire after immunization as seen by next generation sequencing and proteomics

city: Rotterdam

first: Martijn

middle: Maurice

last: vanDuijn

state: ZH

address: Wytemaweg 80

department: Neurology

institute: ERASMUS MEDICAL CENTER

summary: We study the repertoire of immunoglobulin sequences after immunization in a cohort of rats. Animals were immunized with dinitrophenol modified KLH or with recombinant human HuD. In the immune reprtoire, and also in the matching proteomics data, we observe that the  animals produce a repertoire that has many shared motifs for those immunized with the same antigen. Cluster analysis allows the samples to be segregated according to the immunogen used.

overall_design: 5 animals were immunized with DNP-KLH and 5 animals were immunized with human recombinant HuD. The immunoglobulin heavy chain variable domain was amplified from splenocyte cDNA, and sequenced with a 2x300bp paired end method

first: Lennard

last: Dekker

first: Wilfred

middle: J

last: van Ijcken

first: Peter

middle: A

last: Sillevis-Smitt

first: Theo

last: Luider

first: Luider

last: Theo


title: Mrg15 allosterically activates Ash1’s H3K36 methyltransferase activity and facilitates Ash1’s trithorax group protein function in Drosophila

city: Beijing

first: Zhuqiang

last: Zhang

address: 15 Datun Road, Chaoyang District.

institute: Institute of Biophysics, CAS

summary: Ash1 is a classic Trithorax group protein possessing an H3K36-specific histone methyltransferase activity. Ash1 plays a critical role in antagonizing Polycomb silencing and its loss-of-function mutations lead to inactivation of certain Hox genes and homeotic transformation. Here, we report the purification of Ash1 complex with the identification of two novel subunits, Mrg15 and Nurf55. Interestingly, Mrg15 stimulates the enzymatic activity of Ash1 in vitro, and such stimulation is independent of the chromo domain of Mrg15. In vivo, Mrg15 is recruited by Ash1 to their common target genes and Mrg15 is essential for the proper deposition of H3K36me2 at these regions.

overall_design: We measured Ash1/Mrg15 genomic binding by ChIP-seq in fly S2 cell lines with WT, siAsh1 and siMrg15 conditions, respectively. Expression profiles by RNA-seq were also done in WT, siAsh1 and siMrg15 S2 cells.

first: Chang

last: Huang

first: Fu

last: Yang

first: Jing

first: Gaihong

last: Cai

first: Ling

first: Yong

last: Zheng

first: She

last: Chen

first: Rongwen

last: Xi

first: Bing

last: Zhu


title: Genome-wide E2A binding map in murine neuronal stem cells

first: Franziska

last: Greulich

summary: Chromatin-Immunoprecipitation followed by next generation sequencing (ChIP-Seq) for E2A in murine neuronal stem cells

overall_design: ChIP-Seq against E2A and appropriate input control in wildtype, E12-/- and E47-/- E12.5 neuronal stem cells.

first: Sabrina

last: Pfurr

first: Christian

last: Schachtrup


title: Genomic alterations activating KLF5 [ChIP-Seq]

first: Xiaoyang

summary: We used ChIP-seq to map the binding sites of wild-type and mutant KLF5. In addition, by performing H3K27ac ChIP-seq, we mapped the enhancer regions in cell lines of head and neck squamous cell carcinomas, esophageal carcinomas, and stomach adenocarcinomas.

overall_design: ChIP-seq of H3K27ac in head and neck squamous cell carcinoma cell lines (BHY, BICR6, BICR16, BICR31, CAL33, Detroit562, HSC4, YD8), esophagel carcinoma cell lines (TE6, TE10, TT) and stomach adenocarcinoma cell lines (AGS, GSU, KATOIII). ChIP-seq of KLF5 and p300 in BICR31 cells. ChIP-seq of V5 in HEK293T cells over-expressing, V5-Empty, V5-KLF5-WT and V5-KLF5-mutants. ChIP-seq of V5 and H3K27ac in HCC95 cells over-expressing V5-Empty, V5-KLF5-WT and V5-KLF5-E419Q.


title: Co-transplantation of CAR-gene Engineered Precursor T Cells Leads To Suppressed T Cell Development and Increased NK Cell-based CAR-mediated Anti-leukemic Activity

status: Public on Oct 03 2017

city: Braunschweig

first: Robert

last: Geffers

address: Inhoffenstr. 7

department: Dep. Molecular Bacteriology

institute: HCI - Helmholtz Centre for Infection Research

summary: CAR gene expression on precursor T cells (preTs) that have been generated in vitro from engineered hematopoietic stem cells may reduce the risk of leukemia relapse upon co-transplantation in an MHC-independent manner. Setting the expression of an anti-murine CD19 CAR under the control of an inducible promoter allowed time-dependent assessment of its impact on in vivo development. Adoptive transfer of engineered preTs along with T cell-depleted bone marrow resulted in potent anti-leukemia effects even in fully MHC-class I and II mismatched recipients. Anti-leukemia effects entirely relied on the in vivo development of CAR-expressing natural killer cells since NK cell depletion after transplantation resulted in a complete abrogation of anti-leukemic efficacy. Gene expression profiling revealed that enforced CAR expression on preTs led to an activated shift of transcriptional key factors to those being associated with NK cell development such as Nfil3, Id2, and Eomes. In contrast, CAR expression on preTs blocked thymic seeding completely and prevented further T cell development. The CAR-expressing NK cell progeny of transferred preTs persisted for up to 60 days post transplantation allowing for complete B-cell recovery thereafter. Taken together, we provide new functional insights for the use of CAR-engineered preTs allowing for potent anti-leukemia efficiency within a limited time window for on target/off tumor effects.

overall_design: Microarray data analysis of sorted CAR preTs and Ctrl preTs from in vitro culture (day 20 preTs previous to transplantation) and of their respective progenies harvested from the mouse on day 28 after transplantation were performed.

first: M

last: Maluski

last: Sauer

first: R


title: Discovery of pan-Histone Acetyltransferase Inhibitors with Potent Antitumor Activity in vivo

city: shanghai

first: cheng

last: luo

address: zuchongzhi road 555

institute: shanghai institute of material medica

summary: we use MV4-11 as cellular models to analyze differential gene expression.

overall_design: 4 samples including 20uM G47 treatment and DMSO control, repeat for 2 times

first: Cheng

last: Luo

first: Wenchao

last: Lu


title: Epigenetic mechanisms underlying maternal diabetes-associated risk of congenital heart disease

city: Columbus

first: Vidu

last: Garg

state: OH

address: 700 Children's Drive WB4239

department: Cardiovascular Research

institute: Research Institute at Nationwide Children's Hospital

summary: Maternal hyperglycemia increases the risk of CHD and is further sensitized by haploinsufficiency of Notch1 supporting a gene-environment interaction model. To gain insights into chromatin accessible status by which hyperglycemia affects molecular pathways regulating cardiac development, we performed ATAC-seq on embryonic AV cushion mesenchymal cells maintained in normal and high glucose.

overall_design: ATAC sequencing of mouse embryonic atrioventricular mesenchymal cells in the setting of normoglycemia and hyperglycemia

first: Madhumita

last: Basu

first: Stephanie

last: LaHaye

first: Kai

last: Jiao


title: Expression data from keratinocytes treated either with IL-22 or combination of tofacitinib (JAK1/3 inhibitor) and IL-22 at 6 hours

first: Ankit

last: Srivastava

state: - Select a State -

address: CMM L8:02

institute: Karolinska Institutet

summary:
JAK inhibitors like tofacitinib were thought to act primarily on T cells. However, our data and recent research suggest that JAK receptors are also present on keratinocytes. Here, we show effect of tofacitinib on primary keratinocytes, which could explain effects of topical tofacitinib treatment in psoriasis.
We have performed whole transcriptome analysis (using microarray) on RNA isolated from cultured primary keratinocytes treated either with IL-22 alone or combination of tofacitinb and IL-22 at 6 hours

overall_design: Primary keratinocytes were cultured in-vitro and pretreated with tofacitinib (0.6μM) for 1 hour followed by IL-22 (20 ng/ml) treatment for 6 hours. Total RNA was isolated and whole transcriptomic analysis was performed.

first: Andor

last: Pivarcsi

first: Enikö

last: Sonkoly


title: Genome-wide analysis of genes induced by thrombin at 2 hour and 8 hour in human aortic smooth muscle cells

city: Memphis

first: Gadiparthi

middle: N

last: Rao

state: TN

address: 71 S Manassas Street, #309 TSRB

department: Physiology

institute: UTHSC

summary: Human aortic smooth muscles are quiesced for 24 hours followed by treatment with thrombin for 2 hours and 8 hours in presence or absence of cyclosporin A (10 micromolar) to analyze the effect of thrombin on expression pattern of various genes in presence of cyclosporin A.

overall_design: Total RNA obtained from control and 2 hour or 8 hour of thrombin treatment

first: Gadiparth

first: Nikhlesh

last: Singh


title: Gene Expression Regulation by Lung Cancer Oncogenes

city: Suita

first: Izumi

last: Nagatomo

state: Osaka

address: 2-2 Yamada-oka

department: Respiratory Medicine and Clinical Immunology

country: Japan

institute: Osaka University Graduate School of Medicine

summary: To characterize gene expression changes induced by oncogenes implicated in human lung adenocarcinoma, we analyzed the whole transcriptome of NIH3T3 cells expressing mutant EGFR (exon 19 deletion) or wild-type EGFR. Expression levels of several genes from this list were validated by quantitative RT-PCR using the same RNA samples.

overall_design: Total RNA expression profiling was performed by MBL Co., Ltd. RNA was isolated and purified from WT-EGFR– and Mut-EGFR– expressing NIH3T3 cells using the AllPrep DNA/RNA Mini kit (Qiagen). Two independent experiments were performed in obtaining T7-cDNA for each sample.


title: Alignment of Mitotic Chromosomes in Human Cells Involves SR-Like Splicing Factors Btf and TRAP150

city: Dayton

first: Michael

last: Markey

address: 3640 Colonel Glenn Hwy.

department: Biochemistry and Molecular Biology

institute: Wright State Unviersity

summary:
Here we show that depletion of the homologous non-classical serine-arginine-rich (SR) splicing factors Btf (BCLAF1) and TRAP150 causes mitotic defects.
We propose that, in addition to their previously reported roles in maintaining mRNA distribution, Btf and TRAP150 control abundance of transcripts encoding mitotic regulators thereby affecting mitotic progression in human cells.

overall_design: Affymetrix Exon 1.0 ST microarrays were performed according to the manufacturer's directions with mRNA isolated from cultured HeLa cells treated with siRNA targeting Btf, TRAP150, or a control siRNA.

first: Markey

last: Michael P.

first: Bubulya

last: Paula


title: A radiolabeling-free, qPCR-based method for locus-specific pseudouridine detection

first: Chengqi

last: Yi

address: 5 Yiheyuan Road, Haidian District

institute: Peking University

summary: Pseudouridine (Ψ) is the most abundant post-transcriptional RNA modification. Various methods have been developed to achieve locus-specific Ψ detection; however, the existing methods often involve radiolabeling of RNA, require advanced experimental skills and can be time-consuming. Herein we report a radiolabeling-free，qPCR-based method to detect locus-specific Ψs in rRNA and mRNA. This method is based on Ψ chemical adduct (Ψ-CMC) induced mutation/deletion during reverse transcription (RT), leading to qPCR products of different melting temperatures. Utilizing high-throughput sequencing, we demonstrate that such misincorporation is a general feature of Ψ-CMC adduct during our improved RT conditions. We validated this method on known Ψ sites in rRNA and showed that the melting curves correlate with the modification level. Moreover, we successfully detected Ψs in mRNA and lncRNA of different abundance, and identified Ψ synthase that targets mRNA. Our facile method takes only 1.5 days to complete, and with slight adjustment it can be applied to detect other epitranscriptomic marks in the transcriptome.

overall_design: Here we report a radiolabeling-free, qPCR based method to rapidly detect Ψ in a locus-specific manner. The method is based on Ψ labelling adduct induced misincorporation during reverse transcription (RT), generating qPCR products of different melting temperatures. To demonstrate that read-through induced misincorporation is a general feature of Ψ sites under our improved RT condition, we utilized high-throughput sequencing to comprehensively examine the pattern of misincorporation for all Ψ sites in rRNA using HEK293T cells. Besides, to address the detection resolution of the method, three qPCR amplicons examined with our locus-specific approach were subjected to high-throughput sequencing (for MALAT1, EEF1A1 and 18S rRNA).

first: Zhixin

last: Lei


title: miRNA-transcriptome profiling of growth plate cartilage

city: Cologne

first: Bent

last: Brachvogel

address: Joseph-Stelzmann Street 52

institute: University of Cologne

summary:
Cartilage originates from mesenchymal cell condensations that differentiate into chondrocytes of transient growth plate cartilage or permanent cartilage of the articular joint surface and trachea. MicroRNAs fine-tune the activation of entire signaling networks and thereby modulate complex cellular responses, but so far only limited data are available on miRNAs that regulate cartilage development.
Here we characterize an miRNA which promotes the biosynthesis of a key component in the RAF/MEK/ERK pathway in cartilage. Specifically, by transcriptome profiling we identified miR-322 to be upregulated during chondrocyte differentiation. Among the various miR-322 target genes in the RAF/MEK/ERK pathway, only Mek1 was identified as a regulated target in chondrocytes. Surprisingly, an increased concentration of miR-322 stabilizes Mek1-mRNA to arise protein levels and dampen ERK1/2 phosphorylation, while cartilage-specific inactivation in mice linked the loss of miR-322 to decreased MEK1 levels and increased RAF/MEK/ERK pathway activation. Such mice died perinatally due to tracheal growth restriction and respiratory failure. Hence, a single miRNA can stimulate the production of an inhibitory component of a central signaling pathway to impair cartilage development.

overall_design: Total RNA from microdissected material of the epiphyseal growth plate cartilage of 12-day-old C57BL/6 mice was extracted with phenol-chloroform using standard methods and the RNA integrity was determined (2100 Bioanalyzer, Agilent) according to the manufacturer’s specifications. The material from five epiphyseal growth plates was pooled and the Agilent protocol was applied to label and hybridize 100ng of total RNA per single microarray of a mouse 8x15K-miRBaseV14 slide. After scanning and extraction, data was analyzed using GeneSpring XII software (Agilent). Due to the limited amount of starting material, only two independent hybridization experiments could be performed.


title: Identification , functional expression in Saccharomyces cerevisiae and characterization of a Penicillium chrysogenum high-affinity L-arabinose transporter

city: Delft

first: Jean-Marc

last: Daran

address: Julianalaan 67

department: Department of Biotechnology

institute: Delft University of Technology

summary:
L-Arabinose occurs at economically relevant levels in lignocellulosic hydrolysates. Especially at low concentrations of L-arabinose, its uptake via the Gal2 galactose transporter is an important rate-controlling step in the complete conversion of these feedstocks by engineered, pentose-metabolizing Saccharomyces cerevisiae strains.
Chemostat-based transcriptome analysis yielded 16 putative sugar transporter genes in the filamentous fungus Penicillium chrysogenum whose transcript levels were at least three-fold higher in L-arabinose-limited cultures than in glucose-limited and ethanol-limited cultures. Of five genes that showed an over 30-fold higher transcript level in arabinose-grown cultures, only one (Pc20g01790) restored growth on L-arabinose upon expression in an engineered L-arabinose-fermenting S. cerevisiae strain in which GAL2 had been deleted. Sugar-transport assays indicated that Pc20g01790this transporter, designated as PcAraT,  encodes functions as a high-affinity (Km = 0.13 mM) L-arabinose-proton symporter that does not transport xylose or glucose. An L-arabinose-metabolizing S. cerevisiae strain co-expressing Pc20g01790PcAraT and GAL2 showed lower residual substrate concentrations in L-arabinose-limited chemostat cultures (4 mg L-1) than a congenic strain in which L-arabinose import exclusively depended on Gal2 (1.8 g L-1). Inhibition of L-arabinose transport by these sugars was less pronounced than observed with Gal2. A hexose-phosphorylation-deficient, L-arabinose-metabolizing S. cerevisiae strain expressing PcAraT Pc20g0190 grew on 20 g L-1 L-arabinose in the presence of 20 g L-1 glucose, which completely inhibited growth on L-arabinose of a congenic strain dependent on L-arabinose transport via Gal2.
Its high affinity and specificity for L-L-arabinose, combined with limited sensitivity to inhibition by glucose and D-D-xylose make PcAraT/ Pc20g01790 a valuable transporter gene for application in metabolic engineering strategies aimed at engineering S. cerevisiae strains for efficient conversion of lignocellulosic hydrolysates.

overall_design: The goal of this study was to explore the P. chrysogenum genome for L-arabinose transporters that can be functionally expressed in S. cerevisiae and support glucose- and D-xylose insensitive, high-affinity transport of L-arabinose. To this end, transcriptomes of L-arabinose-, ethanol- and glucose-limited chemostat cultures of P. chrysogenum were compared, and putative L-arabinose transporter genes were tested for their ability to support L-arabinose transport upon expression in an S. cerevisiae strain engineered for L-arabinose fermentation in which GAL2 had been deleted. A P. chrysogenum transporter identified in this screen, PcAraTPc20g01790, was subjected to more detailed analysis, including kinetic sugar-uptake studies with radiolabelled substrates, in vivo studies on uptake inhibition, and physiological studies with engineered S. cerevisiae strains in L-arabinose-limited chemostat cultures.

first: Jasmine

last: Bracher

first: Maarten

last: Verhoeven

first: Wouter

last: Wisselink

first: Jack

middle: T

last: Pronk

first: Barbara

last: Crimi

first: Antonius

last: van Maris


title: Effects of inhibition of topoisomerase I or HSP90 in primary melanoma cell lines

city: Houston

first: Zhiqiang

last: Wang

state: Texas

address: 7455 Fannin St.

department: Lymphoma and Myeloma

institute: University of Texas MD Anderson Cancer Center

summary:
Using 4 primary melanoma cell lines for which autologous tumor-infiltrating T lymphocytes (TILs) were available, a screen of clinically-relevant small-molecule inhibitors (SMIs) was performed to find SMIs that could synergistically enhance tumor cell killing by autologous TILs. Among positive results were SMIs targeting topoisomerase I (TOP1) or HSP90. Of note, as implied by the fact that these SMIs had synergistic effects, there was relatively little direct cytotoxicity of the SMIs when used alone.
Gene expression profiling was undertaken to identify changes induced by SMIs of TOP1 or HSP90. SN38 is the active metabolite of irinotecan, a standard-of-care clinical TOP1 inhibitor. Ganetespib is a newer generation HSP90 inhibitor, reported to exhibit greater potency in preclinical tumor models and reduced toxicity in rodents, compared to other 1st and 2nd generation HSP90 inhibitors, consistent with its favorable safety profile in patients.

overall_design: Each of the 4 primary melanoma cell lines was cultured in duplicate with either SN38, ganetespib, or DMSO control.

first: Jodi

last: McKenzie

first: Rina

last: Mbofung

first: Min

last: Zhang

first: R

middle: E

last: Davis

first: Patrick

last: Hwu


title: Transcriptional response of C. albicans to weak organic acids, carbon source and MIG1 inactivation.

city: Singapore

first: Norman

last: Pavelka

address: 8A Biomedical Grove, Immunos Building, Level 4

department: Singapore Immunology Network

country: Singapore

institute: Agency for Science, Technology and Research

summary: Candida albicans is a resident fungus of the human intestinal microflora. Commonly isolated at low abundance in healthy people, C. albicans outcompetes local microbiota during candidiasis episodes. Under normal conditions, members of the human gastrointestinal microbiota were shown to keep C. albicans colonization under control. By releasing weak organic acids (WOAs), bacteria are able to moderate yeast growth. This mechanism displayed a synergistic effect in vitro with the absence of glucose in medium of culture, which underline the complex interaction that C. albicans faces in its natural environment. Inactivation of the transcriptional regulator MIG1 in C. albicans results in a lack of sensitivity to this synergistic outcome. To decipher C. albicans transcriptional responses to glucose, WOAs and the role of MIG1, we performed RNA sequencing on four biological replicates exposed to combinations of these 3 parameters. We were able to characterise the i) glucose response, ii) response to acetic and butyric acid, iii) MIG1 regulation of C. albicans and iv) genes responsible for WOAs resistance. We identified a group of 6 genes linked to WOAs sensitivity in a glucose-MIG1-dependent manner and inactivated one of these genes, the putative glucose transporter HGT16, in a SC5314 wild-type background. As expected, the mutant displayed a partial complementation to WOAs resistance in absence of glucose. This result points towards a mechanism of WOAs sensitivity in C. albicans involving membrane transporters which could be exploited to control yeast colonisation in human body niches.

overall_design: 48 samples: 2 strains (SC5314 and mig1), 2 media (YPD and YPM), 3 conditions (no acids, acetic acid, butyric acid), 4 replicates (1, 2, 3, 4)

first: Fabien

last: Cottier

first: Alrina Shin Min

last: Tan

first: Marina

last: Yurieva

first: Webber

last: Liao

first: Josephine

last: Lum

first: Michael

last: Poidinger

first: Francesca

last: Zolezzi


title: N6-Methyladenine DNA Modification in Human Genome

status: Public on Oct 02 2017

city: Guangzhou

first: Minghui

last: He

address: International Biotech Island

department: Bioinformatics Department

institute: Forevergen Biosciences Co., Ltd

summary: In human cells, 5-methylcytosine (5mC) DNA modification plays an important role in gene regulation. However, N6-methyladenine (6mA) DNA modification, which is predominantly present in prokaryotes, is considered to be absent in human genomic DNA. Here, using single molecule real-time (SMRT) sequencing on human blood, we show that DNA 6mA modification is extensively present in human genome, accounting for ~0.051% of the total adenines. [G/C]AGG[C/T] was the most significant motif associated with 6mA modification. 6mA sites are enriched in the exon coding regions and are associated with transcriptional activation. DNA N6-methyladenine and N6-demethyladenine modification in human are mediated by methyltransferase N6AMT1 and demethylase ALKBH1, respectively. The 6mA abundance is significantly lower in cancer tissues compared to adjacent normal tissues, which is accompanied with decreased N6AMT1 and increased ALKBH1 levels. Decrease of 6mA modification level stimulated tumorigenesis in human. Collectively, our results demonstrate that 6mA DNA modification is present in human tissues, and we describe a potential role of the N6AMT1/ALKBH1-6mA regulatory axis in the progression of human cancer.

overall_design: DNA IP-seq of HuaXia1 (HX1) PBMC sample

first: Chuanle

last: Xiao


title: Binding to RNA regulates Set1 function [ChIP-seq]

city: Marseille

first: Abdessamad

last: EL KAOUTARI

state: France

address: 27 boulevard Lei Roure

country: France

institute: INSERM

summary: The Set1 family of histone H3 lysine 4 (H3K4) methyltransferases is highly conserved from yeast to humans. Here we show that the Set1 complex (Set1C) directly binds RNA in vitro through the regions that comprise the double RNA recognition motifs (dRRM) and N-SET domain within Set1 and its subunit Spp1. To investigate the functional relevance of RNA binding, we performed UV RNA cross-linking (CRAC) for Set1 and RNA polymerase II in parallel with ChIP-seq experiments. Set1 binds nascent transcripts through its dRRM. RNA binding is important to define the appropriate topology of Set1C distribution along transcription units and correlates with the efficient deposition of the H3K4me3 mark. In addition, we uncovered that Set1 binds to different classes of RNAs to levels that largely exceed the levels of binding to the general population of transcripts, suggesting the Set1 persists on these RNAs after transcription. This class includes RNAs derived from SET1, Ty1 retrotransposons, specific transcription factors genes and snRNAs. We propose that Set1 modulates adaptive responses, as exemplified by the posttranscriptional inhibition of Ty1 retrotransposition.

overall_design: Investigation of the functional relevance of RNA binding in yeast using RNA cross-linking (CRAC) for Set1 and RNA polymerase II and ChIP-seq experiments.

first: Pierre

last: Luciano

first: Jongcheol

last: Jeon

last: El Kaoutari

first: Drice

last: Challal

first: Amandine

last: Bonnet

first: Mara

last: Barucco

first: Tito

last: Candelli

first: Frederic

last: Jourquin

first: Pascale

last: Lesage

first: Jaehoon

last: Kim

first: Domenico

last: Libri

first: Vincent

last: Géli


title: Binding to RNA regulates Set1 function [CRAC-seq]

overall_design: Investigation of the functional relevance of RNA binding in yeast using RNA cross-linking (CRAC) for Set1 and ChIP-seq experiments.


title: The Nasal Methylome: A Key to Understanding Allergic Asthma [Illumina]

city: Aurora

first: Ivana

last: Yang

state: CO

institute: University of Colorado Anschutz Medical Campus

type: Methylation profiling by genome tiling array

summary:
The goal of this investigation was to establish proof of concept that nasal epithelium can be used as a proxy for  the airway epithelium in studies of allergic asthma. We collected PBMCs, nasal epithelia, and bronchial epithelia from 12 subjects with allergic asthma and 12 control subjects without asthma, all non-Hispanic white nonsmoker adults.
We conclude that genomic profiling of nasal epithelia captures most disease-relevant changes identified in airway epithelia  but also provides additional targets that are most likely influenced by exposures. Thus, epigenetic marks in nasal epithelia may prove useful as a biomarker of disease severity and response to  treatment or as a biosensor of the environment in asthma.

overall_design: To determine the effect of allergic asthma–associated methylation changes on gene expression, we examined array-based (Agilent 8x60k) measures of expression of genes nearest DMPs as a function of methylation change across 72 expression arrays and 72 Methylation arrays.

first: Adam

last: Richards

first: Elizabeth

last: Davidson

first: Allen

last: Stevens

first: Christena

last: Kolakowski

first: Richard

last: Martin

first: David

last: Schwartz


title: The Nasal Methylome: A Key to Understanding Allergic Asthma [Agilent]


title: Binding to RNA regulates Set1 function

first: Abdessamad

last: EL KAOUTARI

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

overall_design: Refer to individual Series


title: The Arabidopsis DNA methylome is relatively impervious to abiotic stress

city: Philadelphia

first: Diep

middle: R

last: Ganguly

state: PA

address: 433 S University Ave

department: Department of Biology

institute: University of Pennsylvania

type: Methylation profiling by high throughput sequencing

summary: Improving plant stress response holds great agricultural potential. One promising, yet speculative, possibility is the formation of plant stress memory facilitating enhanced responses to recurring stress. One possibility is the involvement of environmentally-induced variation in reversible chromatin marks, such as DNA methylation, leading to the altered regulation of underlying genetic elements that promote enhanced stress tolerance. Such potential has spurred numerous investigations yielding conflicting results, thus it remains unclear whether robust stress-induced chromatin variation can encode plant stress memory conveying enhanced stress tolerance. Herein we investigate for the possibility of stress-induced alterations in DNA methylation to convey stress memory, both on mitotic and transgenerational timescales, such that previously stressed plants show improved stress tolerance with correlated alterations in DNA methylation at stress-responsive loci. We find that although the experience of stress may be stored mitotically, it does not appear to be transmitted meiotically and is independent of DNA methylation changes. Overall, the DNA methylome appears to be robust against stress-induced variation and is unlikely to contribute to any form of stress memory.

overall_design: Whole genome bisulfite sequencing was performed on plants exposed to a nine day drought stress ('mitotic drought', 3 biological replicates), repeated excess light stress over 1 week (1xWLRS, 3 biological replicates) and on progeny of 5th generation plants ('G5', 6 biological replicates per treatment) from independent lineages that were propagated by single seed descent under control conditions ('Watered') or with a recurring drought stress ('Drought') every generation.

first: Peter

last: Crisp

first: Steven

last: Eichten

first: Barry

last: Pogson


title: The Nasal Methylome: A Key to Understanding Allergic Asthma


title: Expression data from highly efficient polycystic kidney disease cystogenesis in kidney organoids derived from CRISPR-mutant human pluripotent stem cells (hPSCs)

city: Toronto

first: York

middle: PC

last: Pei

state: Ontario

address: 8N838, 585 University Avenue

department: Department of Medicine

country: Canada

institute: University of Toronto

summary: Computational identification of gene expression pathways in cysts alongside tubular organoids

overall_design: Using Affymetrix Human Gene 2.0 ST Arrays, the global gene profiling of seven paired samples (cysts and remnant tubules from the same organoid) at 71-87 days was performed

first: Benjamin

last: Freedman


title: DNA-methylation analysis of response to P.falciparum infection in Fulani and Mossi ethnic groups, Burkina Faso

city: Stockholm

first: Ann-Kristin

last: Östlund-Farrants

address: Svante Arrheniusväg 20C

department: Department of Molecular Biosciences, The Wenner-Gren Institute

institute: Stockholm University

summary: The Fulani ethnic group is relatively protected from Plasmodium falciparum malaria, however a genetic basis for this is unknown. Therefore, we have performed a pilot study to examine global transcription and DNA methylation patterns in specific immune cell populations in the Fulani, compared to a sympatric ethnic group, the Mossi. When we compared uninfected and infected individuals in Fulani and Mossi, a strong transcriptional response was only detected in the monocyte fraction of Fulani, and this was not related to differences in DNA methylation.

overall_design:
RNA sequencing analysis of CD14+ (monocyte) and CD14- (predominantly lymphocyte), and DNA-methylation analysis of CD14+ (monocyte) fractions of PBMCs,  from of Fulani and Mossi individuals, uninfected or infected with P.falciparum.
This Series represents the DNA-methylation dataset.


title: Methyaltion array and RNA-Seq analysis of response to P.falciparum infection in Fulani and Mossi ethnic groups, Burkina Faso


title: Single-cell RNA-Seq of the geniculate ganglion from Mus musculus

city: Miami

first: Nirupa

last: Chaudhari

state: FL

address: 1600 NW 10th Ave

department: Physiology & Biophysics

institute: University of Miami Miller School of Medicine

summary: We use comprehensive and unsupervised transcriptome analyses to provide molecular classifications of sensory neurons in the mouse geniculate ganglion. 96 neurons were isolated on a C1 Fluodigm chip, underwent RNA-Seq, and iteratively clustered into sub-classes.

overall_design: RNA-Seq analysis of 96 geniculate ganglion neurons collected on two 96-well C1 Fluodigm chips.

first: Gennady

last: Dvoryanchikov

first: Damian

last: Hernandez


title: Transcriptome analysis of CD4+ T cells differentiated from wild-type and CD4cre IRF8flox mice

city: Dijon

first: Romain

last: Boidot

address: 1, rue Pr Marion

institute: CGFL

summary: We report that the Th9 differenciation program is alterated in absence of IRF8 protein

overall_design: Examination of the expression profile of CD4+ T cells after 1 and 2 days of differentiation

first: Etienne

last: Humblin

first: Frédérique

last: Végran

first: Lionel

last: Apetoh

first: François

last: Ghiringhelli


title: CD4+ T cells


title: Chromatin interaction analysis of transcription factors and IRF8 in CD4+ T cells differentiated from wild-type mice

summary: We report that the IRF8 protein is able to interact with chromatin during Th9 differenciation

overall_design: Examination of the interaction of IRF8 and transcription factors during early stages of Th9 CD4+ T cell differentiation


title: Drug toxicology models by using hiPSC-derived alveolar organoids (AOs)

city: Kyoto

first: Shimpei

last: Gotoh

address: 53 Kawaharacho, Shogoin, Sakyo-ku

department: Center for iPS cell Research and Application

institute: Kyoto University

summary: Microarray analysis was performed to obtain the transcriptomes of GNE7915-, amioarone- and vehicle control-treated hiPSC-derived SFTPC+ cells.

overall_design: AOs harboring SFTPC+ cells were generated from isolated CPMhigh cells by coculturing with human fetal lung fibroblasts. SFTPC+ cells were passaged in AOs. After passaged three times every two weeks, AOs were treated with 5 µM of GNE7915, 10 µM of amiodarone, or vehicle control (DMSO) for 10 days. SFTPC+ cells in each condition were isolated on Day 77 (n = 3 biological replicates).

first: Yuki

last: Yamamoto


title: Catabolite repression by intracellular succinate in Campylobacter jejuni

status: Public on Oct 01 2017

city: Albany

first: Craig

last: Parker

address: 800 Buchanan St

department: PSM

institute: USDA ARS

summary: Bacteria have evolved different mechanisms to catabolize carbon sources from a mixture of nutrients. They first consume their preferred carbon source, before others are used. Regulatory mechanisms adapt the metabolism accordingly to maximize growth and to outcompete other organisms.   The human pathogen Campylobacter jejuni is an asaccharolytic Gram-negative bacterium that catabolizes amino acids and organic acids for growth. It prefers serine and aspartate as carbon sources, however it lacks all regulators known to be involved in regulating carbon source utilization in other organisms. In which manner C. jejuni adapts its metabolism towards the presence or absence of preferred carbon sources is unknown.  In this study, we show with transcriptomic analysis and enzyme assays how C. jejuni adapts its metabolism in response to its preferred carbon source serine. In the presence of serine as well as lactate and pyruvate C. jejuni represses the utilization of other carbon sources, by repressing the expression of a number of central metabolic enzymes. The regulatory proteins RacR, Cj1000 and CsrA play a role in the regulation of these metabolic enzymes. This metabolism dependent transcriptional repression correlates with an accumulation of intracellular succinate. Hence, we propose a demand-based catabolite repression mechanism in C. jejuni, which depends on the intracellular succinate level.

overall_design: Comparison of growth conditions, C. jejuni strain 81116 grown under microaerophilic (5% Oxygen) condition in HI broth compared to  C. jejuni strain 81116 grown in HI broth with 25mM serine, or HI broth with 25mM aspartate. Log phase and early stationary phase were examined.

first: A

middle: X

last: van der Stel

first: C

middle: H

last: van de Lest

first: S

last: Huynh

first: J

last: van Putten

first: M

last: Wösten


title: Gene expression changes in response to ancestral maternal obesity

city: Darlinghurst

first: Paul

last: Young

state: NSW

address: 405 Liverpool Street

country: Australia

institute: Victor Chang Cardiac Research Institute

summary: Maternal obesity can program offspring metabolism across multiple generations. It is not known whether multigenerational effects reflect true inheritance of the induced phenotype, or are due to serial propagation of the phenotype through repeated exposure to a compromised gestational milieu. Here we sought to distinguish these possibilities, using the Avy mouse model of maternal obesity. In this model, F1 sons of obese dams display a predisposition to hepatic insulin resistance which remains latent unless the offspring are challenged with a Western diet. We find that F2 grandsons and F3 great-grandsons of obese dams also carry the latent predisposition to metabolic dysfunction, but remain metabolically normal on a healthy diet. Given that the breeding animals giving rise to F2 and F3 were maintained on a healthy diet, the latency of the phenotype permits exclusion of serial programming; we also confirmed that F1 females remained metabolically healthy during pregnancy. Molecular analyses of male descendants identified upregulation of hepatic Apoa4 as a consistent signature of the latent phenotype across all generations. Our results exclude serial programming as a factor in transmission of the metabolic phenotype induced by ancestral maternal obesity, and indicate inheritance through the germline, probably via some form of epigenetic inheritance.

overall_design: samples were performed in quadruplicate with 3 groups including control mice, and grandsons and great-grandsons of obese Avy/a females

first: Sally

last: Eaton

first: Alastair

last: Aiken

first: Joshua

middle: W

last: Ho

first: Jennifer

last: Cropley

first: Catherine

last: Suter


title: Establishment of a tumour progression model in chordoma

city: Ulm

first: Kevin

last: Mellert

address: Albert-Einstein-Allee 23

department: Institute of Pathology

institute: University Hospital Ulm

summary: mRNA profiling of three novel chordoma cell lines out of the same patient. The gene expression profiles of the primary tumour derived cell line U-CH17P was compared to the gene expression profiles of the metastases derived cell lines  U-CH17S and U-CH17M in order to spot differently expressed genes, that are involved in the formation of metastases in chordoma.

overall_design: Comparative analysis

first: Daniela

last: Jäger

first: Thomas

last: Barth


title: Histone H3K4 monomethylation catalyzed by Trr and mammalian COMPASS-like proteins at enhancers is dispensable for development and viability

city: Chicago

first: Ali

last: Shilatifard

state: IL

address: 320 E Superior St

department: Department of Biochemistry and Molecular Genetics

institute: Northwestern University Feinberg School of Medicine

summary: Histone H3 lysine 4 monomethylation (H3K4me1) is an evolutionarily conserved feature of enhancer chromatin catalyzed by the COMPASS-like methyltransferase family that includes Trr in Drosophila melanogaster and MLL3 (encoded by KMT2C) and MLL4 (encoded by KMT2D) in mammals. Here we demonstrate that Drosophila embryos expressing catalytically deficient Trr eclose and develop to productive adulthood. Parallel experiments with a trr allele that augments enzyme product specificity show that conversion of H3K4me1 at enhancers to H3K4me2 and H3K4me3 is also compatible with life and results in minimal changes in gene expression. Similarly, loss of the catalytic SET domains of MLL3 and MLL4 in mouse embryonic stem cells (mESCs) does not disrupt selfrenewal. Drosophila embryos with trr alleles encoding catalytic mutants manifest subtle developmental abnormalities when subjected to temperature stress or altered cohesin levels. Collectively, our findings suggest that animal development can occur in the context of Trr or mammalian COMPASS-like proteins deficient in H3K4 monomethylation activity and point to a possible role for H3K4me1 on cis-regulatory elements in specific settings to fine-tune transcriptional regulation in response to environmental stress.

sample_organism:
Drosophila melanogaster
Mus musculus

platform_organism:
Drosophila melanogaster
Mus musculus

overall_design: ChIP-seq and RNA-seq experiments were conducted in Drosophila wing imaginal discs and adult brain tissues from transgenic flies expressing either a catalytic-deficient (Trr-C2398A) or catalytic-hyperactive (Trr-Y2383F) Trr enzyme. ChIP-seq and RNA-seq were also conducted in mouse embryonic stem cells in which CRISPR-Cas9 was used to delete the SET domain of both MLL3 and MLL4 (MLL3/4-delSET).

first: Ryan

last: Rickels

first: Clayton

middle: K

last: Collings


title: Array comparative genomic hybridization of 18 pancreatic ductal adenocarcinomas and their autologous metastases

city: Duesseldorf

first: Valentin

last: Rausch

address: Moorenstr. 5

department: Department of General, Visceral, and Pediatric Surgery

institute: Heinrich-Heine-University and University Hospital

summary:
Background: Mortality rates of pancreatic cancer remain high, which is mainly due to advanced disease and metastasis. We hypothesized that DNA copy number alteration are enriched in metastatic cells compared to autologous primary tumors, which may inform on cancer-related pathways possibly serving as potential targets for specific therapies. We investigated 18 pancreatic ductal adenocarcinomas, including 39 lymph node and 5 distant metastases after surgical resection. Analysis was performed with array-based comparative genomic hybridization.
Results: Metastases acquire a higher frequency of CNAs with the highest in distant metastasis (OM: median=42, LNM: median=23, PT: median=17). In LNM, gains were prevalent on chromosome bands 8q11.23-q24.3, 12q14.1, 17p12.1, 21q22.12, and losses on 3p21.31, 4p14, 8p23.3-p11.21,17p12-11.2. Genes on amplified regions are involved in cancer-related pathways such as WNT-signaling, also involved in metastasis.
Conclusions: Pancreatic cancers show a high degree of intratumor heterogeneity, which could lead to resistance of chemotherapy and worse outcome. ACGH analysis reveals regions preferentially gained or lost in synchronous metastases encoding for genes involved in cancer-related pathways, which could lead to novel therapeutic opportunities.

overall_design: Array CGH experiment: DNA of 18 primary tumor cells (PT), 39 lymph node metastases (M) and 5 distant organ metastases (OM) of 18 pancreatic ductal adenocarcinomas (Cy3) versus control DNA (Cy5)

first: Andreas

last: Krieg

first: Jordi

last: Camps

first: Bianca

last: Behrens

first: Manfred

last: Beier

first: Darawalee

last: Wangsa

first: Kerstin

last: Heselmeyer-Haddad

first: Stephan

last: Baldus

first: Wolfram

last: Knoefel

last: Ried

first: Nikolas

last: Stoecklein


title: Sensors, Pathways and Transcription factors regulating IR-induced inflammatory transcriptional output [RNA-seq data set 2]

city: los angeles

first: Prabhat

middle: Kumar

last: Purbey

state: California

address: 675 Charles E. Young Drive South

department: MIMG

institute: UCLA

summary: RNA-seq of mRNA from five stimulation time point (LipidA, 100ng/ml) of bone marrow-derived macrophages from C57Bl/6 mice.

first: Stephen

last: Smale


title: CD15-positive tumor-derived glioblastoma cells

city: Cleveland

first: Briana

last: Prager

address: 9500 Euclid Ave.

institute: Cleveland Clinic


title: Genome-wide maps of chromatin state in CD15-positive tumor-derived glioblastoma cells [ChIP-seq]

summary: We report that these features are associated with distinct transcriptional programs, with vascular regions showing a proneural profile and hypoxic regions a mesenchymal pattern.  As these regions harbor glioma stem cells (GSCs), we investigated the epigenetic regulation of these two niches.  Proneural, perivascular GSCs activated EZH2, whereas mesenchymal GSCs in hypoxic regions expressed BMI1 protein. To determine the differential regional activation of EZH2 and BMI1 function, we performed chromatin immunoprecipitation followed by deep sequencing (ChIP-seq) with H3K27me3 (histone modification by EZH2) or H2AK119Ub (histone modification by BMI1) antibodies in CD15-postive GSCs from enhancing and necrotic regions of two GBM specimens, and found over 80% of regional specific target genes displayed distinct H3K27me3 or H2AK119Ub marks, indicating distinct PRC function in GSCs residing in different regions. H3K27me3, generally associated with inhibition of transcription, marked neuronal and cellular development targets in both the enhancing and necrotic regions, albeit without substantial overlap in gene identity, with EZH2/SUZ12/H3K27me3 targets most significantly in the enhancing regions.  In contrast, H2AK119Ub marked very different targets in the enhancing and necrotic regions, with H2AK119Ub in CD15-positive GSCs from the hypoxia (necrotic) regions marking genes strongly associated with mesenchymal subtype signaling pathways, such as TGFb, NFkB, and WNT, indicating probable microenvironment-specific functions of EZH2 and BMI1.

overall_design: Examination of 2 different histone modifications in in CD15-positive GSCs from enhancing and necrotic regions of two glioblastoma specimens.

first: Xun

last: Jin

middle: C

last: Gimple


title: Microarray of S100β-v-erbB/p53-/- cells cultured in normoxia, hypoxia, hypoxia with Brefeldin A (0.1uM) and hypoxia EHT-1864 (1uM).

city: Lebanon

first: Damian

last: Almiron Bonnin

state: NH

address: 1 Medical Center Drive

department: Molecular and Systems Biology

institute: Geisel School of Medicine at Dartmouth College

summary: High-grade gliomas (HGGs) include the most common and the most aggressive primary brain tumor of adults and children. Despite multimodality treatment, most high grade gliomas eventually recur and are ultimately incurable. Several studies suggest that the initiation, progression, and recurrence of gliomas are driven, at least partly, by cancer stem-like cells. A defining characteristic of these cancer stem-like cells is their capacity to self-renew. We have identified a hypoxia-induced pathway that utilizes the Hypoxia Inducible Factor 1α (HIF-1α) transcription factor and the JAK1/2-STAT3 (Janus Kinase 1/2 - Signal Transducer and Activator of Transcription 3) axis to enhance the self-renewal of glioma stem-like cells. Hypoxia is a commonly found pathologic feature of HGGs. Under hypoxic conditions, HIF-1α levels are greatly increased in glioma stem-like cells. Increased HIF-1α activates the JAK1/2-STAT3 axis and enhances tumor stem-like cell self-renewal. Our data further demonstrate the importance of Vascular Endothelial Growth Factor (VEGF) secretion for this pathway of hypoxia-mediated self-renewal. Brefeldin A and EHT-1864, agents that significantly inhibit VEGF secretion, decreased stem cell self-renewal, inhibited tumor growth, and increased the survival of mice allografted with S100β-v-erbB/p53-/- glioma stem-like cells. These agents also inhibit the expression of a hypoxia gene expression signature that is associated with decreased survival of HGG patients. These findings suggest that targeting the secretion of extracellular, autocrine/paracrine mediators of glioma stem-like cell self-renewal could potentially contribute to the treatment of HGG.

overall_design: Three independent S100β-v-erbB/p53-/- TSC1 cell cultures were treated with either DMSO control, BFA (1uM), or EHT-1864 (1uM) grown in hypoxia or normoxia (16h). Then collected for Trizol mRNA, and microarray analysis on the Clarion S mouse array.

last: Almiron  Bonnin


title: Epigenetic silencing of the dual-role signal mediator, ANGPTL4 in tumor tissue and its overexpression in the urothelial carcinoma microenvironment

city: Chia-Yi

first: Yu Ming

last: Chuang

address: 168 University Road,Min Hsiung

department: Department of Biomedical Science

country: Taiwan

institute: National Chung Cheng University

summary: To investigate the effect of ANGPTL4 expression on bladder cancer cells, expression profile was compared in BFTC 905 cells overexpressed with control vector vs human full length ANGPTL4 gene.

overall_design: BFTC 905 bladder cancer cells were transfected with pcDNA3.1 (vector control) or plasmid overexpressing ANGPTL4 (treatment).

first: Michael

last: Chan

first: Chin

last: Li

first: Ru-Inn

last: Lin

first: Yu-Ming


title: Expression of receptors for inflammatory mediators in murine vagal nodose versus jugular capsaicin-sensitive  (Trpv1-positive) C-fiber neurons

city: Gaithersburg

first: Jingya

last: Wang

state: Maryland

address: 1 Medimmune Way

department: Early respiratory and immunology

institute: Astrazeneca

summary: Capsaicin-sensitive (Trpv1-positive) sensory C-fibers derived from vagal ganglia innervate the visceral organs, and respond to inflammatory mediators and noxious stimuli. These neurons play an important role in maintenance of visceral homeostasis, and contribute to the symptoms of visceral inflammatory diseases. Vagal sensory neurons are located in two ganglia, the jugular ganglia (derived from the neural crest), and the nodose ganglia (from the epibranchial placodes). The functional difference, especially in response to immune mediators, between jugular and nodose neurons is not fully understood. In this study, we microscopically isolated murine nodose and jugular capsaicin-sensitive / Trpv1-expressing C-fiber neurons and performed transcriptome profiling using ultra-low input RNA sequencing.

overall_design: Examination of gene expression in nodose and jugular capsaicin-sensitive C-fiber neurons

first: Bradley

last: Undem

first: Roland

last: Kolbeck

first: Marian

last: Kollarik


title: Transcriptome-based association study reveals a regulatory network for the shape of garlic clove

city: Changsha

first: Touming

last: Liu

address: NO.348, western road of xianjia lake

department: Institute of Bast Fiber Crops

institute: Chinese Academy of Agricultural Sciences

summary: A total of 102 garlic accession were performed for mRNA sequencing, and then were used for scoring the variations in both gene sequence (SNPs) and expression (GE) in this population. Thereafter, SNPs and GE are used for carrying out association analysis with the phenotype of shape of garlic clove, respectively, which comes to a joint decision for the candidate genes that are involved in trait. In addition, SNPs and GE data is used as genotype and phenotype, respectively, for performing eQTL analysis to ascertain the interaction among trait-controlled genes, which finally brings a regulatory network for the shape of garlic clove.

overall_design: Firstly, a total of 102 garlic accession were performed for mRNA-seq by Illumina sequencing. Then, the read sequencing were aligned into the referenced transcriptome, which resulted in the identification of the variations in both gene sequence (SNPs) and expression (GE).

first: Chan

first: Siyuan

last: Zhu


title: The orphan nuclear receptor NR4A3 is involved in the function of dendritic cells

city: Tokyo

first: Chiharu

last: Nishiyama

address: 6-3-1 Niijuku, Katsushika-ku

department: Biological Science and Technology

institute: Tokyo University of Science

summary:
Transcriptome analysis of LPS-stimulated bone marrow-derived dendritic cells with NR4A3 gene silencing
The NR4A3/NOR1 belongs to the NR4A subfamily of the orphan nuclear hormone receptor superfamily, which is activated in a ligand-independent manner. To examine the role of NR4A3/NOR1 in gene expression of dendritic cells (DCs), we introduced NR4A3 siRNA into bone marrow-derived DCs (BMDCs) and determined the expression levels of mRNA and proteins of cytokines, cell surface molecules, NFκB signaling-related proteins, and transcription factors. The expression level of NR4A3 was markedly up-regulated by TLRs-mediated stimulation in DCs. NR4A3 knockdown significantly suppressed LPS, CpG, or poly I:C-mediated up-regulation of CD80, CD86, IL-10, IL-6, and IL-12. Proliferation and IL-2 production levels of T cells co-cultured with NR4A3-knocked down DCs were significantly lower than that of T cells co-cultured with control DCs. Furthermore, the expression of IKKβ, IRF4, and IRF8 was significantly decreased in NR4A3 siRNA-introduced BMDCs. The knockdown experiments using siRNAs for IKKβ, IRF4, and/or IRF8 indicated that LPS-induced up-regulation of IL-10 and IL-6 was reduced in IKKβ knocked down cells, and that the up-regulation of IL-12 was suppressed by the knockdown of IRF4 and IRF8. Taken together, these results indicate that NR4A3 is involved in TLR-mediated activation and gene expression of DCs.

overall_design: We analyzed gene expression profiles of LPS-stimulated or unstimulated bone marrow-derived dendritic cells with or without NR4A3 gene silencing using the Affymetrix Mouse Gene 1.0 ST platform. Array data was processed and analyzed by GeneSpring software. No techinical replicates were performed.

first: Masanori

last: Nagaoka

first: Takuya

last: Yashiro

first: Yuna

last: Uchida

first: Tomoaki

last: Ando

first: Mutsuko

last: Hara

first: Hajime

last: Arai

first: Hideoki

last: Ogawa

first: Ko

last: Okumura

first: Kazumi

last: Kasakura


title: Preconception Urinary Phthalate Concentrations and Sperm DNA Methylation Profiles among Men Undergoing IVF Treatment: A Cross-Sectional Study

city: Amherst

first: Haotian

last: Wu

state: MA

address: 686 N. Pleasant Street Room 128

institute: UMass Amherst

summary: To answer the question of whether preconception phthalate and phthalate replacements associated with sperm differentially methylated regions (DMRs) among men undergoing in-vitro fertilization, genome-wide DNA-methylation profiles of 48 human sperm samples were generated by  bisulfite-based Illumina 450K BeadChip arrays. The sperm DNA methylation is then correlated with urinary phthalate metabolite concentrations.

overall_design:
A cross-sectional study of urinary phthalate metabolite concentrations and sperm genomic DNA methylation generated from Illumina 450K. The sperm was from participants recruited from an IVF and the urinary phthalate metabolite concentrations are measured via mass spec.

Please note that [1] the 'Exposure_Matrix.csv' contains the data used for analysis and necessary for differentiating samples and [2] the'readme_for_Exposure_Matrix.txt' contains the column header information.

first: Molly

middle: S

last: Estill

first: Alexander

last: Shershebnev

last: Suvorov

first: Stephen

last: Krawetz

first: Brian

last: Whitcomb

first: Holly

last: Dinnie

first: Tayyab

last: Rahil

first: Cynthia

last: Sites

first: J

last: Pilsner


title: Mapping histone acylations in mouse liver

city: Neuherberg

first: Robert

last: Schneider

address: Ingolstaedter strasse 1

department: Institute of Functional Epigenetics

institute: Helmoltz Zentrum Muenchen

summary: Comparison of histone acylations in liver from fed and fasted mice. We have mapped H3K9ac, H3K14pr and H3K14bu by ChIP-seq in livers of either re-fed or 48h fasted mice.

overall_design: ChIP-seq of histone acylations H3K9ac, H3K14pr and H3K14bu in mouse liver.

first: Adam

middle: F

last: Kebede


title: Detailed Longitudinal Sampling of Glioma Stem Cells In Situ Reveals Chr7 Gain and Chr10 Loss As Repeated Events in Primary Tumor Formation and Recurrence (SNP)

city: Istanbul

first: mehmet

last: baysan

address: Kuşbakışı Caddesi No: 27 34662 Altunizade – Üsküdar – İstanbul Office: East Campus 108

department: Department of Computer Science

country: Turkey

institute: Istanbul Sehir university

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

summary: In this study, we developed an extensive dataset for a GBM case via the generation of polyclonal and monoclonal glioma stem cell lines from initial diagnosis, as well as from multiple sections of distant tumor locations of the deceased patient’s brain following tumor recurrence. Our analyses revealed the tissue-wide expansion of a new clone in the recurrent tumor as well as chromosome 7 gain and chromosome 10 loss as repeated genomic events in primary and recurrent disease. Moreover, chromosome 7 gain and chromosome 10 loss produced similar alterations in mRNA expression profiles in primary and recurrent tumors despite possessing other highly heterogeneous and divergent genomic alterations between the tumors. We identified ETV1 and CDK6 as putative candidate genes, and NFKB (complex), IL1B, IL6, Akt and VEGF as potential signaling regulators, as potentially central downstream effectors of chr7 gain and chr10 loss. Finally, the differences caused by the transcriptomic shift following gain of chromosome 7 and loss of chromosome 10 were consistent with those generally seen in GBM samples compared to normal brain in large-scale patient-tumor data sets.

overall_design:
Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from patient tumor and cell lines.
Copy number analysis of Affymetrix CSHD arrays was performed for 46 samples from a GBM patient

first: Mehmet

last: Baysan


title: Transcriptome analysis and mapping histone acylations in fasted mouse livers

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

overall_design: Refer to individual Series


title: Detailed Longitudinal Sampling of Glioma Stem Cells In Situ Reveals Chr7 Gain and Chr10 Loss As Repeated Events in Primary Tumor Formation and Recurrence (expression)

overall_design: Affymetrix U133P2 arrays were performed according to the manufacturer's directions on DNA extracted from patient tumor and cell lines.


title: Detailed Longitudinal Sampling of Glioma Stem Cells In Situ Reveals Chr7 Gain and Chr10 Loss As Repeated Events in Primary Tumor Formation and Recurrence

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


title: Genome-wide analysis of prostatic tissue gene expression from patients with benign prostatic hyperplasia

city: Boston

first: Keyan

last: Salari

address: Gray/Bigelow Rm 1102, 55 Fruit Street

institute: Massachusetts General Hospital

summary: Analysis of gene expression in prostatic tissue from BPH patients with and without SRD5A2 gene methylation. The hypothesis is that BPH patients with DNA methylation of the SRD5A2 gene promoter have impaired conversion of testosterone to dihydrotestosterone, and therefore may use an alternative signaling pathway for prostatic tissue growth. Here, we compare gene expression profiles of SRD5A2-methylated vs. unmethylated prostatic tissue to nominate alternative biological pathways relevant in each molecular subtype of BPH.

overall_design: 22 unique patient samples were analyzed (12 SRD5A2-methylated, 10 SRD5A2-unmethylated). All samples were transitional zone prostatic tissue obtained during transurethral resection of prostate (TURP) surgery.

first: Aria

last: Olumi


title: Alterations in gene expression in response to different regimes of Shiga toxin 2

city: Jena

first: S.

last: Lambeck

address: Erlanger Allee 101

institute: JUH

summary:
The microarray data provided here belong to a study that describes two different Shiga toxin (Stx) induced models of hemolytic uremic syndrome (HUS) in mice. Although several rodent models of HUS were published, it still remains difficult to reproduce all clinical features of human HUS.
Here, two different Stx2 regimes combined with volume resuscitation were tested in C57BL/6J wild type mice. Animals were euthanized because of kidney injury after 3 or 7 days respectively. Kidneys were removed for histological evaluation and RNA extraction. Kidney injury was confirmed histologically and by laboratory parameters in plasma. Data for the respective vehicle treated groups are also provided here.

overall_design: Overall, gene expression data from 16 C57BL/6J kidneys were collected. The mice were randomly subjected to 4 different groups: sham day 3, Stx2 day 3, sham day 7, Stx2 day 7.

first: Sina

middle: M

last: Coldewey

first: Sophie

last: Dennhardt

first: Sandro

last: Lindig

first: Wiebke

last: Pirschel

first: Bianka

last: Wissuwa


title: Sensors, Pathways and Transcription factors regulating IR-induced inflammatory transcriptional output [ChIP-seq]

first: Prabhat

last: Purbey

summary: Radiation induced interferon response is mediated by IRF1 but not by the IRF3. Phosphorylated p53 binds strongly within 1kb of TTS of p53 dependent genes that are potently induced by ionizing radiation.

overall_design: Bone marrow-derived macrophages were irradiated with 6Gy IR for 0, 0.5h, 1h, 2h and 6h. Chromatin from 0, 1h, 2h and 6h was immunoprecipitated with antibodies against IRF1 or IRF3. For p-p53 ChIP-seq, chromatin were prepared from 0, 0.5h, 1h, 2h and 6h time points.

first: Stephen

last: Smale


title: Comparison of gene expression profiling among shRNAs-mediated RUNX1 knockdown in MV4-11 cells with various knockdown efficacies

city: Kyoto

first: Junichi

last: Taniguchi

address: Kitashirakawa-Oiwakecho, Sakyo-Ku

department: Department of Chemistry, Graduate School of Science

institute: Kyoto University

summary: The primary function of RUNX1 in leukemogenesis has been controversial since classical understanding of RUNX1 as an oncosuppressor was challenged by our recent discovery of novel oncogenic features of RUNX1. Here we provide insight into the dual function of RUNX1 through determining the significance of total RUNX expressions in AML cells. Our data indicate that moderately attenuated RUNX1 expression induces increased total RUNX expressions, which subsequently enhances proliferation of AML cells via GSTA2-mediated intracellular ROS removal. Indeed, inhibiting GSTA2 function in vivo prolonged the overall survival period of mice xeno-transplanted with human AML cells. These findings suggest that modulation of RUNX-GST-ROS axis could potentially be a novel therapeutic target in the poorest-prognostic AML patients with intermediate RUNX1 expression levels.

overall_design: MV4-11 cells were transduced with series of shRNAs targeting RUNX1 at various efficacies (Moderate knockdown; MV4-11_sh_Rx1_moderate, Profound knockdown; MV4-11_sh_Rx1_profound_#1 and #2). Control shRNA targets luciferase sequence (sh_Luc.).

first: Ken

last: Morita

first: Shintaro

last: Maeda

first: Kensho

last: Suzuki

first: Hiroki

last: Kiyose

first: Hiroshi

last: Sugiyama

first: Souichi

last: Adachi

first: Yasuhiko

last: Kamikubo


title: Sensors, Pathways and Transcription factors regulating IR-induced inflammatory transcriptional output [RNA-seq data set 1]

summary: Bone marrow-derived macrophages derived from C57Bl/6, Myd88-/- and Trif-/-, Ifnar-/-, Atm-/-, Sting-/-, Scid,  Irf3-/-, Irf1-/-, p53-/-, Nrf2-/-mice were irradiated with 6Gray ioninzing radiation; C57Bl/6 macrophages were Irradiated in the presence of MAPK inhibitors or Reactive Oxygen Species Scavenger (N-Acetyl Cysteine), Two biological replicates were generated for each time point. RNA samples were collected at 0 (unirradiated), 0.5, 1, 2, 6, and 24h post irradiation except where ever mentioned.


title: Trichostatin A preferentially reverses the upregulation of gene expression levels induced by gain of chromosome 7 in colorectal cancer cell lines

city: Bethesda

first: Yue

last: Hu

state: MD

address: 50 South Drive, Bldg. 50, Rm. 1408

department: Genetic

institute: NCI

summary: Epithelial cancers are defined by a tumor-specific distribution of chromosomal aneuploidies that are maintained when cells metastasize and are conserved in cell lines derived from primary tumors. Correlations between genomic copy number and gene expression have been observed for different tumors including, colorectal (CRC), breast and pancreatic cancer. These ploidy-driven transcriptional deregulations are characterized by low-level expression changes of most genes on the affected chromosomes. The emergence of these aberrations at an early stage of tumorigenesis and the strong selection for the maintenance of these aneuploidies suggests that aneuploidy-dependent transcriptional deregulations might contribute to cellular transformation and maintenance of the malignant phenotype. The histone deacetylase inhibitor (HDACi) Trichostatin A (TSA) has anticancer effects and is well known to lead to large scale gene expression changes. Here we assessed if TSA could disrupt the aneuploidy-driven gene expression in the aneuploid colon cancer cell line SW480 and the artificially generated aneuploid cell line DLD-1+7. We found that TSA increases transcriptional activity throughout the genome, yet inhibits aneuploidy-induced gene expression changes on chromosome 7. Among the TSA affected genes on chromosome 7 we identified potential CRC oncogenes. These experiments represent the first attempt to explain how histone acetylation affects aneuploidy-driven gene expression changes.

overall_design: 6 samples are compared in total. There are 3-5 replicates per condition. Conditions are: 1. DLD1; 2. DLD1 + TSA; 3. DLD1+chr7; 4. DLD1+chr7 + TSA; 5. SW480; 6. SW480 + TSA

first: Floryne

middle: O

last: Buishand

first: Eric

last: Cardin

first: Thomas

last: Ried


title: Sensors, Pathways and Transcription factors regulating IR-induced inflammatory transcriptional output


title: Genome wide maps of H3K4me3, H3K27me3 and H3K27ac in Brachyury mutants and RNA-seq data of Brachyury mutants

city: Frankfurt am Main

first: Phillip

last: Grote

state: Hessen

address: Paul-Ehrlich-Str. 42-44

department: Genome Regulation

institute: Georg-Speyer-Haus

summary: The transcription factor BRACHYURY is the founding member of the T-box family of proteins. A conserved residue (Y88 in BRACHYURY) was previously suggested to be important for interaction with KDM proteins that demethylate H3K27me3. We generated Brachyury mutant mouse embryonic stem cell (ESC) lines. For a wild type control (Thet) we derived an embryonic stem cell line from blastocysts, containing a single wild type copy of the Brachyury locus (T +/2J; 2J is a large genomic deletion of the entire Brachyury locus). We mutated the remaining wild type copy of Brachyury to code for Alanin instead of the conserved tyrosine (Y88) residue (T_Y88A). We derived embryos from these ESCs, compare expression profiles (RNAseq) from Thet and TY88A caudal end mesoderm of early embryos (stages: TS12 and TS13), and complement the expression data with histone methylation ChIPseq data for H3K4me3, HeK27me3 and H3K27ac. Of note: due to the different requirements of cellular material for RNAseq and ChIPseq we differentiated the same ESC used for the embryo generation (in vivo, RNA-seq) to generate early caudal end mesoderm in vitro (ChIPseq). In addition, this dataset contains a ChIPseq track for BRACHURY in wild type ESCs, differentiated into early mesoderm in vitro with the same protocol as for the histone ChiIPseq.

overall_design: Comparison of RNAseq expression profile early mesoderm, extracted from of T_het (wild type) and T_Y88A (mutant) mouse embryos. These RNAseq data are complemented with H3K4me3, H3K27me3 and H3K27ac ChIPseq data from in vitro generated early mesoderm of the same genotype.

first: Arica

last: Beisaw


title: CTCF-mediated enhancer-promoter interaction is a critical regulator of cell-to-cell variation of gene expression

first: Keji

last: Zhao

address: 9000 Rockville Pike

department: Systems Biology Center

institute: NHLBI,NIH

summary: Recent studies indicate that even a homogeneous population of cells display heterogeneity in gene expression and response to environmental stimuli. Although promoter structure critically influences the cell-to-cell variation of gene expression in bacteria and lower eukaryotes, it remains unclear what controls the gene expression noise in mammals. Here we report that CTCF decreases cell-to-cell variation of expression by stabilizing enhancer-promoter interaction. We show that CTCF binding sites are interwoven with enhancers within topologically-associated domains (TADs) and a positive correlation is found between CTCF binding and the activity of the associated enhancers. Deletion of CTCF sites using CRISPR/Cas9 compromises enhancer-promoter interactions. Using single-cell flow cytometry and single-molecule RNA-FISH assays, we demonstrate that knocking down of CTCF or deletion of a CTCF binding site results in increased cell-to-cell variation of gene expression, indicating that long-range promoter-enhancer interaction mediated by CTCF plays an important role in controlling the cell-to-cell variation of gene expression in mammalian cells.

overall_design:
¬	3e Hi-C is a robust technique to measure genome-wide chromatin interactions
¬	CTCF binding is positively correlated with the activity of enhancers and their interaction with target promoters
¬	Knocking down CTCF expression or deletion of CTCF binding sites results in decreased enhancer-promoter interaction and increased cell-to-cell variation of gene expression
¬	CTCF stabilizes enhancer-promoter interaction and controls gene expression noise.

first: Gang

last: Ren

first: Wenfei

last: Jin

first: Kairong

last: Cui


title: RNA-Seq of hematopoietic stem cells from vehicle and estrogen-treated mice

city: Houston

first: Daisuke

last: Nakada

address: One Baylor Plaza

department: Molecular and Human Genetics

institute: Baylor College of Medicine

summary:
Purpose: The goals of this study were to determine genes in HSCs that are regulated by estrogen.
Methods: mRNA profiles of vehicle and estrogen treated wild-type (WT) and Esr1fl/fl;Mx1-Cre (ERa-KO) HSCs were generated by deep sequencing using Illumina HiSeq 2000 and Ion Torrent Proton platforms. The sequence reads that passed quality filters were analyzed at the transcript isoform level using DE-Seq2. qRT–PCR validation was performed using SYBR Green assays

overall_design: mRNA profiles of vehicle and estrogen treated wild-type (WT) and Esr1fl/fl;Mx1-Cre (ERa-KO) HSCs were generated by deep sequencing using Ion Torrent platform

first: Richard

last: Chapple

first: Kevin

last: Hoegenauer


title: The diphenylpyrazol compound anle138b blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology.

status: Public on Sep 30 2017

city: Göttingen

first: Gaurav

last: Jain

state: Lower Saxony

address: Von-Siebold-Str. 3a, Office no: 2.212

institute: The German Center for Neurodegenerative Diseases (German: Deutsches Zentrum für Neurodegenerative Erkrankungen DZNE)

summary: Alzheimer’s disease is a devastating neurodegenerative disease eventually leading to dementia. An effective treatment does not yet exist. Here we show that oral application of the compound anle138b restores hippocampal synaptic and transcriptional plasticity as well as spatial memory in a mouse model for Alzheimer’s disease, when given orally before or after the onset of pathology. At the mechanistic level we provide evidence that anle138b blocks the formation of conducting Aβ pores without changing the membrane embedded Aβ-oligomer structure. In conclusion, our data suggest that anle138b is a novel and promising compound to treat AD-related pathology that should be investigated further.

overall_design: APPdelta9 and Wildtype mouse treated with anle138b or placebo

first: Ana

last: Hernandez

first: Andre

last: Fischer