title: Gene expression profile of human peritoneal mesothelial cells (HPMC) treated with TGF-b1

status: Public on Oct 18 2018

city: Gwangju

first: Joo Young

last: Huh

address: 77 Yongbong-ro

department: College of Pharmacy

institute: Chonnam National University

summary: Long-term peritoneal dialysis is associated with progressive fibrosis of the peritoneum. Epithelial-mesenchymal transition (EMT) of mesothelial cells is an important mechanism involved in peritoneal fibrosis, and TGF-b1 is considered central in this process. We conducted network-based integrated analysis of transcriptomic data to systemically characterize the molecular signature of TGF-b1-stimulated human peritoneal mesothelial cells (HPMCs).

overall_design: Total RNA was extracted from HPMCs cultured under 1 ng/mL TGF-b1 for 6 and 24 h using Trizol (Invitrogen) according to standard methods. For microarray analysis, 0.5 mg of total RNA was used to make biotin-labeled cRNA using the Ambion Illumina cRNA amplification and labeling kit (Ambion, Austin, TX, USA) . cRNA was then column purified and the quality verified by Agilent 2100 Bioanalyzer (Palo Alto, CA, USA) prior to hybridization. Biotin-labeled cRNA was labeled with Cy3 (Amersham, Piscataway, NJ, USA) and hybridized onto a HumanRef-8 24 K Expression Array Bead Chip (Illumina, San Diego, CA, USA). The arrays were then scanned by an Illumina Bead Station laser scanning imaging system. The data were analyzed using Genespring software from Agilent after normalization.

first: Hunjoo

last: Ha

first: Sandun

last: Choi

first: Joo-Young

first: Soo-Min

last: Han


title: Expression data from PDGF-B induced murine gliomas transplanted in NOD/SCID mice

status: Public on Oct 22 2018

city: Genoa

first: Paolo

last: Malatesta

address: Largo Rosanna Benzi 10

country: Italy

institute: IRCCS Ospedale Policlinico San Martino

summary: The different phases of tumor immunoediting in vivo were dissected thanks to a murine model of glioma induced by PDGF-B overexpression. We show that low-grade gliomas are highly immunostimulatory and that the adaptive immune system prevents the development of secondary tumor in syngeneic mice. During tumor progression, glioma cells downregulate immunostimulatory genes and the immune infiltrate becomes pro-tumorigenic. We showed that glioma cells are able to progress towards a high-grade phenotype even in immunodeficient mice, albeit more slowly and this progression invariably requires a downregulation of immunostimulatory genes.

overall_design: Cells derived from early onset / low grade murine gliomas induced with PDGF-B overexpression were serially transplanted in immunodeficient NOD/SCID mice where they can root. Upon the development of secondary and tertiary gliomas, tumor cells were explanted, dissociated and sorted by FACS, basing on the expression of the EGFP transgene expressed togheter with PDGF-B oncogene as a bicistronic transcript. EGFP-positive cells were then either processed for RNA estraction.

first: Irene

last: Appolloni


title: Modulation of gene expression in rat muscle cells following treatment with nanoceria in different gravity regimes

city: Pontedera (PI)

first: Gianni

last: Ciofani

address: Viale Rinaldo Piaggio 34

institute: Istituto Italiano di Tecnologia

summary: The study evaluates potential protective effects of cerium oxide nanoparticles (nanoceria) against oxidative stress in muscle tissue, both on ground and in space

overall_design: Rat muscle cells (H9c2) were cultured on Earth or aboard the International Space Station, with or without nanoceria treatment. Samples were fixed, RNA was extracted and microarray (Clariom S Pico arrays, ThermoFisher Scientific 902936) analyses were performed, using 30 ng of total RNA for reverse transcription (with 500 pg of HeLa cell RNA as control). The study comprises four experimental classes (ground vs space, with or without nanoceria treatment), and a total of eight arrays: B1504, B1509 as ground, untreated samples;  B1505, B1506, B1507 as ground, treated samples; B1501 as space, untreated sample; B1502, B1503 as space, treated samples

first: Giada

middle: G

last: Genchi

first: Andrea

last: Degl’Innocenti

first: Alice

middle: R

last: Salgarella

first: Ilaria

last: Pezzini

first: Attilio

last: Marino

first: Arianna

last: Menciassi

first: Sara

last: Piccirillo

first: Michele

last: Balsamo


title: CFP1 safeguards male meiotic progression by regulating meiotic gene expression [array]

status: Public on Oct 16 2018

city: Seoul

first: Chanhyeok

last: Park

address: 5, Hwarang-ro 14-gil

department: Brain Science Institute

country: South Korea

institute: KIST (Korea Institute of Science and Technology)

summary: Microarray analysis revealed that Cfp1 conditional depletion in spermatongonia using Stra8-cre perturbs gene expression; 3233 genes were down-regulated, whereas 3967 genes were up-regulated in conditional knockout testes.

overall_design: We performed microarray analysis in postnatal day 14 (P14) Cfp1 KO and littermate control testes.

first: B

last: Ki

first: C

middle: H

first: K

last: Hong

first: Y


title: Changes in the liver transcriptome of farmed Atlantic salmon (Salmo salar) fed diets based on terrestrial alternatives to fish meal and fish oil

city: St. John's

first: Albert

last: Caballero Solares

state: NL

address: 0 Marine Lab Road

department: Ocean Sciences

country: Canada

institute: Memorial University of Newfoundland

summary: After a 14-week feeding trial, Atlantic salmon fed a diet based on animal by-product meal and vegetable oil (ABP) showed lower growth rates compared to others fed an FM/FO-based diet (MAR). Interestingly, feeding a vegetable meal/oil-based diet (VEG) resulted in growth rates similar to the FM/FO-based diet. A 44K microarray experiment conducted on liver total RNA samples from these three dietary groups identified 46 genes related to metabolic and growth-relevant pathways, 25 immune-related, and 12 related to oxidation-reduction processes.

overall_design:
Atlantic salmon were fed the three experimental diets (MAR, ABP, and VEG) for 14 weeks. Four tanks were dedicated to each experimental diet. At the end of the feeding trial, liver samples were collected from five individuals per tank. Each dietary group contributed liver RNA samples of eight individual fish (two from each tank) to the microarray experiment (i.e., 24 fish in total). Differences among dietary groups in the liver transcriptome of fish were assessed by contrasting individual RNA samples against a common reference pool of equal quantities of RNA from all 24 fish. Test samples were labeled with Cy5, whereas the reference pool was labeled with Cy3.
Please note that sample titles represent 'tissue_diet_tank number_individual fish number' for each sample.

last: Caballero-Solares

first: Xi

last: Xue

first: Christopher

middle: C

last: Parrish

first: Richard

last: Taylor

first: Maryam

last: Beheshti Foroutani

first: Matthew

middle: L

last: Rise


title: Alterations of miRNAs in Goat skin fibroblast cells (GSF cells) in response to Orf virus infection

status: Public on Oct 25 2018

city: Haikou

first: Feng

last: Pang

address: Renmin Road 58

country: China

institute: Hainan University

type: Non-coding RNA profiling by high throughput sequencing

summary: To find out differently expressed miRNAs in GSF cells in response to Orf virus infection and to construct circRNA-miRNA networks

overall_design: Three mock GSF samples and three ORFV-infected GSF samples (OV samples)

first: Fengyang

last: Wang


title: (Epi)genetic regulation of zebrafish intestinal development

status: Public on Oct 24 2018

city: Nijmegen

first: Leonie

middle: M

last: Kamminga

address: Geert Grooteplein 28

department: Molecular Biology

country: Netherlands

institute: Radboud University

type: Expression profiling by high throughput sequencing

type: Genome binding/occupancy profiling by high throughput sequencing

summary: The goal of the experiment was to characterize the wild type larval intestine in zebrafish. Tg(cldn15la:GFP) intestine-specific transgene was used to ease dissections. RNAseq was performed at 5, 7, 9 dpf on wild type dissected intestines to characterize the transcriptome. ChIPseq was performed at 5, 7, 9 dpf on wild type dissected intestines to check the intestinal presence of active (H3K4me3) and repressive (H3K27me3) chromatin marks and to correlate their presence with intestinal gene expression.

overall_design: RNAseq of wild type dissected Danio rerio intestines, pools of 10 intestines in triplicates at 5, 7, and 9 dpf. ChIPseq of wild type dissected Danio rerio intestines, pools of 25 intesines (+5 set aside for input DNA) in duplicates at 5, 7, and 9 dpf for H3K4me3 and H3K27me3.

first: Bilge

last: San

first: Marco

last: Aben

first: Dei

last: Elurbe

first: Kai

last: Völtzke

first: Marjo

last: den Broeder

first: Juliette

last: Legler

first: Julien

last: Rougeot


title: Liver regeneration after cholestatic damage induced by Rbpj deletion

status: Public on Oct 17 2018

city: Ulm

first: André

last: Lechel

address: Albert-Einstein-Allee 23

department: Department of Internal Medicine I

country: Germany

institute: University hospital Ulm

summary:
Liver cholestasis is a chronic liver disease (CLD) which belongs to a major health problem. Cholestasis is characterised by a decrease in bile flow due to impaired secretion by hepatocytes or by obstruction of bile flow through intra- or extrahepatic bile ducts. Thereby cholestasis can induce ductal proliferation, hepatocyte injury and liver fibrosis. Notch signalling promotes the formation and maturation of ductular reactions. We investigated the liver regeneration process in the context of cholestasis induced by disruption of the Notch signalling pathway.  Liver-specific deletion of Rbpj, which represents a key regulator of Notch signalling, induces severe cholestasis through impaired IHBD maturation, severe necrosis and increased lethality. Deregulation of the biliary compartment and cholestasis are associated with change of several signalling pathways including the Hippo pathway resulting in upregulation of SOX9, which is associated with transdifferentiation of hepatocytes. SOX9 upregulation in cholestatic liver injury in vitro is independent of Notch signalling. We could comprehensively address that Rbpj depletion is followed by deregulation of YAP/TEAD, which influences transdifferentiation of hepatocytes and thereby contributing to liver regeneration.
In this study the liver regeneration process was analyzed in 4 weeks old Rbpj knockout mice and compared to 4 weeks old Rbpj wildtype mice.

overall_design: RNA from whole liver derived from 4 weeks old Rbpj-/- and 4 weeks old Rbpj+/+ mice on a C57BL/6J background was used. Agilent Mouse Gene Expression Microarrays 8x60K were used.

first: Umesh

last: Tharehalli


title: Longitudinal Stratification of Gene Expression Data Reveals Three SLE Groups of Disease Activity Progression.

status: Public on Oct 15 2018

city: GRANADA

first: Daniel

last: Toro

state: Spain

address: Avenida de la Ilustracion

department: Bioinformatics

country: Spain

institute: GENYO

summary:
The highly heterogeneous clinical presentation of lupus is characterized by the unpredictable appearance of flares of disease activity and important organ damage. Attempts to stratify lupus patients have been limited to clinical information, leading to unsuccessful clinical trials and controversial research results. Our aim was to develop and validate a robust method to stratify patients with lupus according to longitudinal disease activity and whole-genome gene expression data in order to establish subgroups of patients who share disease progression mechanisms.
We applied a clustering-based approach to stratify SLE patients based on the correlation between disease activity scores and longitudinal gene expression information. Clustering robustness was evaluated by bootstrapping and the clusters were characterized in terms of clinical and functional features.Using two independent sets of patients, one pediatric and another adult, our results show a clear partition into three different disease clusters not influenced by treatment, race or other source of bias. Two of the clusters differentiate into a neutrophil correlated disease group and a lymphocyte correlated disease group, while the third that correlated to a lesser extent with neutrophils, was functionally more heterogeneous. The neutrophil-driven clusters were associated with increased development towards proliferative nephritis.
We found three subgroups of patients that show different mechanisms of disease progression and are clinically differentiated. Our results have important implications for treatment options, the design of clinical trials, the etiology of the disease, and the prediction of severe glomerulonephritis.

overall_design: We calculate a correlation matrix between each gene and the activity of the disease through the different visits for each patient. We select the best genes to stratify patients and perform clustering analysis. Finally, the clinical characterization of each cluster obtained was carried out.

last: Toro-Dominguez

first: Jordi

last: Martorell-Marugán

last: Goldman

first: Michelle

last: Petri

first: Pedro

last: Carmona-Sáez

first: Marta

middle: E

last: Alarcón-Riquelme


title: Cycling CD4+  T cells in HIV-infected immune nonresponders have mitochondrial dysfunction

city: Cleveland

first: AARTHI

last: TALLA

state: OH

address: 2103 Cornell Rd

department: Pathology

country: USA

institute: Case Western Reserve University School of Medicine

summary: Immune nonresponder (INR) HIV-1–infected subjects are characterized by their inability to reconstitute the CD4+ T cell pool after antiretroviral therapy. This is linked to poor clinical outcome. Mechanisms underlying immune reconstitution failure are poorly understood, although, counterintuitively, INRs often have increased frequencies of circulating CD4+ T cells in the cell cycle. While cycling CD4+ T cells from healthy controls and from HIV+ patients with restored CD4+ T cell numbers show complete cell division in vitro, cycling CD4+ T cells from INRs do not. Here, we show that cells with the phenotype and transcriptional profile of Tregs were enriched among cycling cells in health and in HIV infection. Yet there were diminished frequencies and numbers of Tregs among cycling CD4+ T cells in INRs, and cycling CD4+ T cells from INR subjects displayed transcriptional profiles associated with the impaired development and maintenance of functional Tregs. Flow cytometric assessment of TGF-β activity confirmed the dysfunction of Tregs in INR subjects. Transcriptional profiling and flow cytometry revealed diminished mitochondrial fitness in Tregs among INRs; cycling Tregs from INRs had low expression of mitochondrial biogenesis regulators, the peroxisome proliferator–activated receptor γ coactivator 1-α (PGC1α), and the transcription factor for mitochondria (TFAM). In vitro exposure to IL-15 allowed cells to complete division, restored the expression of PGC1α and TFAM, and regenerated mitochondrial fitness in the cycling Tregs of INRs. Our data suggest that rescuing mitochondrial function could correct the immune dysfunction characteristic of Tregs in HIV-1–infected subjects who fail to restore CD4+ T cells during antiretroviral therapy

overall_design: Sort-purified CD45RA-CD71- and CD45RA-CD71+ cells from 6 HIV- healthy controls, 6 HIV+ Immune non-responders and 6 HIV+ Immune responders

first: Souheil-Antoine

last: Younes

first: Aarthi

last: Talla

first: Susan

middle: P

last: Ribeiro

first: Evgeniya

middle: V

last: Saidakova

first: Michael

last: Lederman

first: Rafick-Pierre

last: Sekaly


title: Phloem associated foliar translatomes in Prunus domestica L.

city: College Park

first: James

middle: N

last: Culver

state: MD

address: 4291 Fieldhouse Dr.

department: Plant Science and Landscape Architecture

institute: University of Maryland, College Park

summary: In this study, we used vascular specific promoters and a translating ribosome affinity purification strategy to identify phloem associated translatomes in Prunus domestica L. Three different promoter:FLAG-RPL18 lines were used. These included two phloem specific promoters (pSUC2 and pSULTR2;2), as well as the more ubiquitously expressed cauliflower mosaic virus 35S promoter (p35S). Immunopurification of ribosome-mRNA complexes was accomplished by the method described in Reynoso et al. (Plant Functional Genomics: Methods and Protocols, 185-207; 2015). The dataset includes samples from plum leaves taken at 2, 4 and 6 weeks post vernalization.

overall_design: 27 samples, 3 time points (2, 4, and 6 weeks), 3 promoter lines, 3 biological replicates.

first: Tamara

middle: D

last: Collum

first: Christopher

last: Dardick


title: Integrated functional genomics and craniofacial morphogenesis within the FaceBase Consortium: Alk5 mutant (or control) at embryo stage E12.5

status: Public on Oct 13 2018

city: Los Angeles

last: Kesling

address: 2250 Alcazar Street

institute: University of Southern California

summary: Congenital malformations in facial bones significantly impact the overall representation of the face. Establishing correlations between gene expression and morphogenesis of craniofacial structures may lead to new discoveries of molecular mechanisms of craniofacial development. Thus in the present investigation, we will generate gene expression profiles of facial bones at embryo stage 12.5 to establish their roles in regulating craniofacial development.

overall_design: To perform global gene expression profiling analysis of mandible and maxilla development and integrate these datasets with cell lineage and quantitative 3D dynamic imaging analyses. In collaboration with the ontology group within the FaceBase consortium, we will define anatomical landmarks and morphometric parameters of the developing mandible and maxilla. Wnt1cre;Alk5fl/+ mice were mated with Alk5fl/fl mice and pregnant females were sacrificed at embryonic day 12.5 (E12.5), with observance of a vaginal plug denoting E0. Mutant embryos were identified by the presence of cleft palate and calvarial defect. The mandible and maxilla were dissected away from mutant embryos and control litter mates, then each mandible and maxilla was divided into its distal and proximal ends.

first: Yang

last: Chai

first: Jingyuan

last: Li

first: Yuan

last: Yuan

first: Bridget

last: Samuels

first: Thach

last: Ho


title: Integrated functional genomics and craniofacial morphogenesis within the FaceBase Consortium: Tgfbr2 mutant (or control) at embryo stage E13.5

summary: Congenital malformations in facial bones significantly impact the overall representation of the face. Establishing correlations between gene expression and morphogenesis of craniofacial structures may lead to new discoveries of molecular mechanisms of craniofacial development. Thus in the present investigation, we will generate gene expression profiles of facial bones at embryo stage 13.5 to establish their roles in regulating craniofacial development.

overall_design: To perform global gene expression profiling analysis of mandible and maxilla development and integrate these datasets with cell lineage and quantitative 3D dynamic imaging analyses. In collaboration with the ontology group within the FaceBase consortium, we will define anatomical landmarks and morphometric parameters of the developing mandible and maxilla. Wnt1cre;Tgfbr2fl/+ mice were mated with Tgfbr2fl/fl mice and pregnant females were sacrificed at embryonic day 13.5 (E13.5), with observance of a vaginal plug denoting E0. Mutant embryos were identified by the presence of cleft palate and calvarial defect. The mandible and maxilla were dissected away from mutant embryos and control litter mates, then each mandible and maxilla was divided into its distal and proximal ends.


title: Integrated functional genomics and craniofacial morphogenesis within the FaceBase Consortium: Tgfbr2 mutant (or control) at embryo stage E12.5

overall_design: To perform global gene expression profiling analysis of mandible and maxilla development and integrate these datasets with cell lineage and quantitative 3D dynamic imaging analyses. In collaboration with the ontology group within the FaceBase consortium, we will define anatomical landmarks and morphometric parameters of the developing mandible and maxilla. Wnt1cre;Tgfbr2fl/+ mice were mated with Tgfbr2fl/fl mice and pregnant females were sacrificed at embryonic day 12.5 (E12.5), with observance of a vaginal plug denoting E0. Mutant embryos were identified by the presence of cleft palate and calvarial defect. The mandible and maxilla were dissected away from mutant embryos and control litter mates, then each mandible and maxilla was divided into its distal and proximal ends.


title: Integrated functional genomics and craniofacial morphogenesis within the FaceBase Consortium: Alk5 mutant (or control) at embryo stage E13.5

overall_design: To perform global gene expression profiling analysis of mandible and maxilla development and integrate these datasets with cell lineage and quantitative 3D dynamic imaging analyses. In collaboration with the ontology group within the FaceBase consortium, we will define anatomical landmarks and morphometric parameters of the developing mandible and maxilla. Wnt1cre;Alk5fl/+ mice were mated with Alk5fl/fl mice and pregnant females were sacrificed at embryonic day 13.5 (E13.5), with observance of a vaginal plug denoting E0. Mutant embryos were identified by the presence of cleft palate and calvarial defect. The mandible and maxilla were dissected away from mutant embryos and control litter mates, then each mandible and maxilla was divided into its distal and proximal ends.


title: Gene expression analysis of hematopoietic stem progenitor cells from transgenic mice that express the constitutively active form of IKK2 protein in HSCs

city: Kyoto

first: Masahiro

middle: Marshall

last: Nakagawa

address: Yoshidakonoecho, Sakyo-ku, Kyoto,

country: Japan

institute: Kyoto University

summary: To understand molecular mechanisms that are deregulated in  hematopoietic stem progenitor cells from transgenic mice that express the constitutively active form of IKK2 protein in HSCs (CA/CA mice), we isolated Flt3 low Lin-Sca1+c-Kit+ (LSK) cells from control and CA/CA  mice and performed microarray analysis using the Illumina's MouseWG-6 v2.0 Expression BeadChip platform.

overall_design: 2 Samples

first: C

last: Rathinam

first: M


title: The differences in local translatome across distinct neuron types is mediated by both baseline cellular differences and post-transcriptional mechanisms

status: Public on Oct 12 2018

city: St Louis

first: Joseph

last: Dougherty

state: Missouri

address: 4566 Scott Ave, box 8232

department: Genetics and Psychiatry

institute: Washington University

summary: Local translation in neurites is a phenomenon that enhances spatial segregation of proteins and their functions away from the cell body, yet it is unclear how local translation varies across neuronal cell types. Further, it is unclear if differences in local translation across cell types simply reflect differences in transcription or if there is also a cell type specific posttranscriptional regulation of the location and translation of specific mRNAs. Most of the mRNAs discovered as locally translated have been identified from hippocampal neurons because their laminar organization facilitates neurite specific dissection and microscopy methods. Given the diversity of neurons across the brain, studies have not yet analyzed how locally translated mRNAs differ across cell types, particularly those with neurites intertwined into other cell types. Here, we used the SynapTRAP method to harvest two broad cell types in the forebrain: GABAergic neurons and pyramidal neurons. While some transcripts overlap, the majority of the local translatome is not shared across these cell types. While most differences are driven by baseline expression levels in the respective cells, some transcripts also evidence cell type specific post transcriptional regulation of localization. Finally, we provide evidence that GABAergic neurons specifically localize mRNAs for peptide neurotransmitters, including somatostatin and cortistatin, suggesting localized production of these key signaling molecules in the neurites of GABAergic neurons. Overall, this work suggests that differences in local translation in neurites across neuronal cell types are poised to contribute substantially to the variability between cells.

overall_design: 5 Replicates of 4 sample types, collect from two cell types each in the brain.

first: Yating

last: Liu

first: Rebecca

last: Ouwenga


title: Loss of the Mia40a oxidoreductase leads to hepato-pancreatic insufficiency in the zebrafish

status: Public on Oct 10 2018

city: bad nauheim

first: Stefan

last: Günther

address: ludwigtr. 43

institute: MPI for heart and lung research

summary: Development and function of tissues and organs are powered by the activity of mitochondria. In humans, inherited genetic mutations that lead to progressive mitochondrial pathology often manifest during infancy and can lead to death, reflecting the indispensable nature of mitochondrial function and biogenesis. Here, we describe a zebrafish mutant for the gene mia40a, the life-essential homologue of the evolutionarily conserved Mia40 oxidoreductase which drives the biogenesis of cysteine-rich mitochondrial proteins. We report that mia40a mutant animals undergo progressive cellular respiration defects and develop enlarged mitochondria in skeletal muscles before their ultimate at the larval stage. We generated a rich transcriptomic and proteomic resource that allowed us to identify abnormalities in the development of endodermal organs, in particular the liver and pancreas. We identify the acinar cells of the exocrine pancreas to be severely affected by mutations in the MIA pathway. Our data contribute to a better understanding of the molecular, cellular and organismal effects of mitochondrial deficiency, important for the accurate diagnosis and future treatment strategies of these diseases.

overall_design: Embryos obtained from an in-cross of heterozygous mia40awaw1/+ siblings were genotyped at 3 dpf. Pools of five mia40+/+ or mia40waw1/waw1 larvae, derived from the same clutch, were collected at indicated time-points for RNA extraction and transcriptomic profiling. Larvae used in 8 dpf experiments were subjected to external feeding from 5dpf before being collected for the analysis at 8dpf.

first: Anna

last: Sokol

first: Barbara

last: Uszczynska-Ratajczak

first: Michelle

last: Collins

first: Michal

last: Bazala

first: Ulrike

last: Topf

first: Sreedevi

last: Sugunan

last: Guenther

first: Carsten

last: Kuenne

first: Johannes

last: Graumann

first: Sherine

middle: S

last: Chan

first: Didier

middle: Y

last: Stainier

first: Agnieszka

last: Chacinska


title: Maternal high-protein and low-protein diets perturb hypothalamus and liver transcriptome and metabolic homeostasis in adult mouse offspring

status: Public on Oct 01 2018

first: Calvin

last: Pan

address: 675 Charles Young Dr South

institute: UCLA

summary: Early life nutritional imbalances are risk factors for metabolic dysfunctions in adulthood, but the effects of perinatal exposure to high versus low protein diets are poorly understood. We exposed C57BL/6 offspring to a high protein/low carbohydrate (HP/LC) or low protein/high carbohydrate (LP/HC) diet during gestation and lactation, and measured metabolic phenotypes between birth and ten months of age in male offspring. Perinatal HP/LC and LP/HC exposures resulted in a decreased ability to clear glucose in the offspring, with reduced baseline insulin and glucose levels in the LP/HC group and a reduced insulin response post-glucose challenge in the HP/LC group. The LP/HC diet group also showed reduced weight at birth and at weaning age, whereas the HP/LC offspring showed an increased weight at weaning and increased adiposity after 5 months of age. Gene expression profiling of hypothalamic and liver tissues indicated alterations of diverse molecular pathways by both diets. Specifically, hypothalamic transcriptome and pathway analyses indicate perturbations of MAPK and hedgehog signaling, processes associated with neural restructuring and transmission, and phosphate metabolism by perinatal protein imbalances. Liver transcriptome data revealed changes in purine and phosphate metabolism, hedgehog signaling, and circadian rhythm pathways. Our results support that maternal protein imbalances perturb molecular pathways in central and peripheral metabolic tissues and predispose offspring to metabolic dysfunctions.

overall_design: The LP/HC diet (D02041002, Research Diets Inc. New Brunswick, NJ) contains 9% protein, 4.4% fat, and 77% carbohydrates (6). The HP/LC diet (D02041001, Research Diets Inc. New Brunswick, NJ) has 23% protein, 4.4% fat and 64% carbohydrate by weight. Standard chow diet (TD 7013, Harlan Teklad. Placentia, CA), containing 18% protein, 6% fat, and 75% carbohydrate by weight, was used as the control diet. The diets were matched by total caloric content.    As most dams cannibalized first litters, all the offspring were from second litters from multiple dams 10 to 12 weeks old.  C57BL/6 females were mated overnight with males between 10 and 16 weeks of age. Gestational day 0 (GD0) was determined by the detection of a vaginal plug in the morning. On GD8, pregnant females were placed on a LP/HC, HP/LC, or chow diet. Pups were weaned at 28 days of age into cages of four animals per cage, separated by sex and maternal environment.  In order to maintain the four animal-per-cage requirements, some cages had mice from different treatments. A total of 22, 27, and 20 male offspring from the LP/HC, HP/LC, or chow diet group, respectively, were examined.    Hypothalamus and liver were dissected between 10 AM and 12 PM from male mice at 10 months of age, placed immediately into liquid nitrogen, and stored at -80oC until RNA was extracted with the RNAeasy kit (Qiagen).    At 9 months GTT were done, Body Composition was measured at day 2 and monthly thereafter.

first: Aldons

middle: J

last: Lusis

first: Xia

last: Yang

first: Lisa

last: Martin


title: Single cell RNA-sequencing of innate lymphoid cells isolated from mouse skin layers

status: Public on Oct 04 2018

city: Bethesda

first: Tetsuro

last: Kobayashi

address: 9000 Rockville Pike, Bldg 10, Rm12N256

institute: NIAMS/NIH

summary:
Purpose: Determine the layer-specific indentities and heterogeneity of innate lymphoid cells in the skin by single cell transcriptomic analysis

Methods: Innate lymphoid cells were sorted from epidermis, dermis and subcutis of adult B6 mice and subjected to droplet based single-cell captureing and RNA isolation and library preparation.

Results: 3,431, 3,356 and 1,061 innate lymphoid cells from epidermis, dermis, and subcutis were analyzed. Unsupervised clustering of the combined data set performed in Seurat identified 6 distinct ILC clusters.

Conclusions: This study reveals skin layer-specific transcriptomic signature of innate lymphoid cells

overall_design: Transcriptome profiles of skin innate lymphoid cells were generated by droplet-based single cell RNA-seq

first: Benjamin

last: Voisin

first: Keisuke

last: Nagao


title: Screening for potential target genes of microRNA-548ac using HTA 2.0 microarrays

status: Public on Oct 03 2018

city: Rostock

first: Michael

last: Hecker

address: Gehlsheimer Str. 20

department: Department of Neurology

institute: University of Rostock

summary: We screened for target genes of hsa-miR-548ac by transcriptome profiling. The miRNA was overexpressed in HeLa cells by transient transfection of a precursor miRNA expression plasmid. High-density Affymetrix Human Transcriptome Arrays (HTA) 2.0 were used for the gene expression analysis. This GEO entry provides the microarray data preprocessed according to the gene level workflow.

overall_design: HeLa cells were transiently transfected with a non-viral precursor miRNA expression plasmid (HmiR1085-MR04, GeneCopoeia). As negative control, a plasmid with scrambled sequence (CmiR0001-MR04, GeneCopoeia) was used. RNA samples were obtained 24 h and 48 h after transfection of the mir-548ac plasmid (n=3 replicates) or the control plasmid (n=2 replicates). For all 10 RNA samples, transcript levels were measured with Affymetrix HTA 2.0 microarrays.

first: Dirk

last: Koczan

first: Nina

last: Boxberger

first: Uwe

middle: K

last: Zettl


title: Mouse models with defective DNA damage repair

city: Heidelberg

first: Kwong Leong

last: Wong

state: Germany (DEU)

address: Im Neuenheimer Feld 280

department: Molecular genetics

institute: DKFZ

summary:
Chromothripsis and chromoanasynthesis are one-off catastrophic events leading to clustered genomic rearrangements.
Expression profiling were performed on brain tissues with Medulloblastoma (n=9) and  normal Cerebellum (n=4) to compare the expression of Double strain break DNA repair pathways.

overall_design: Chromothripsis or chromoanasynthesis were frequently observed in brain tumors in mice deficient for Homologous-Recombination-Repair or Non-Homologous-End-Joining factors. Expression profiling were performed on brain tissues with Medulloblastoma (n=9) and  normal Cerebellum (n=4) to compare the expression of Double strain break DNA repair pathways.

first: Ratnaparkhe

last: Manasi

first: John


title: PPARg Deficiency Suppresses the Release of IL-1b and a in Macrophages via a Type 1 Interferon Dependent Mechanism

city: St. Louis

first: Joel

last: Schilling

state: MO

address: 660 S. Euclid Ave

department: Internal Medicine

institute: Washington University School of Medicine

summary: TG elicited Peritoneal macrophages from WT and PPARgamma KO mice were treated with control or lipid inflammatory stress in triplicate

overall_design: LysM-Cre (cre) controls) or LysM-PPARg (ppar) were treated with vehicle (BSA-PBS; bp) or palmitate (250 uM) with LPS (100 ng/ml); pl for 8h and RNA was extracted


title: ATO treatment on mesenchymal stem cells (MSCs) interacting breast cancer cells

city: Buffalo

first: Hai

last: Wang

state: NY

address: Elm and Carlton Streets, MRC 328

department: Molecular and Cellular Biology

institute: Roswell Park Cancer Institute

summary: Based on next generation RNA-seq, we examed Arsenic trioxide treatment (ATO) effect on MSCs-interacting MCF7 cells in 3D cultures. We found gap junction protein Cx43 is dramatically downregulated after ATO treatment..

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: human breast cancer cell line MCF-7 cells cocultured with mouse MSCs in 3D culture, with or without ATO treatment, are subject to NGS and then analyzed.

first: Zhang

last: Xiang

first: Wang

last: Hai


title: Development of Trypanosoma congolense IL3000 in the host bloodstream

city: Edinburgh

first: Alasdair

last: Ivens

address: Kings Buildings

country: United Kingdom

institute: Centre for Immunity, Infection and Evolution

summary: Trypanosoma congolense IL3000 parasites were grown in adult MF1 mice with parasites harvested on day 5 post infection ('ascend') or on day 6/7 post infection ('peak').

overall_design: Three replicates each of two conditions (ascending, peak) were analysed. 'Peak' samples were each derived from single infections; 'ascend' samples were derived from pooling, but with independent pools for each replicate, a total of 8 infections used overall to generate sufficient material for analysis.  All samples were analysed for their cell cycle status by scoring the number of kinetoplasts and nuclei in parasites.

first: Eleanor

last: Silvester

first: Keith

last: Matthews


title: Comparison of the mRNA profile of GDC0032-resistant and GDC0032-sensitive IGROV1 cells

city: Beer Sheva

first: Jonathan

last: Zorea

address: Ben Gurion blvd

country: Israel

institute: Ben Gurion University

summary: The goal was to find pathways which were enriched in the resistant group of cells.

overall_design: mRNA profiles of both cell lines were generated by deep sequencing, in triplicate, using Illumina GAIIx.

first: Moshe

last: Elkabets


title: Ribonucleotide excision repair prevents intestinal tumorigenesis

city: Kiel

first: Neha

last: Mishra

address: Rosalind-Franklin-Str. 12

institute: Institute of Clinical Molecular Biology

summary:
Insufficient repair of DNA lesions results in the acquisition of somatic mutations and displays the driving force in cancerogenesis. Ribonucleotide incorporation by eukaryotic DNA polymerases occurs during every round of genome duplication and represents by far the most frequent type of naturally occurring DNA lesions. RNAse H2 removes misincorporated ribonucleotides from genomic DNA in a process termed ribonucleotide excision repair (RER). Whether intestinal epithelial proliferation requires RER and whether abrogation of RER is involved in the etiology of cancerogenesis at all is unknown.

Mice with an epithelial specific deletion of RNase H2 subunit b (H2bΔIEC) and co-deletion of the tumor suppressor p53 (H2b/p53ΔIEC) were generated and phenotyped at young and old age. RNA sequencing was performed in isolated epithelial cells and intestinal organoids. Mutational signature of spontaneous tumors from H2b/p53ΔIEC mice were characterized using exome sequencing. Association of tumor RNase H2 expression and patient survival was assessed in transcriptome data from 467 CRC patients.

H2bΔIEC mice display chronic epithelial DNA damage and develop a p53-dependent proliferative exhaustion of the intestinal stem cell compartment. H2b/p53ΔIEC mice have restored epithelial proliferation and spontaneously develop small intestinal carcinomas. Resulting tumors display a distinct mutational signature characterized by T>G base substitutions at GpTpG trinucleotides. Transcriptome data from human colorectal cancer patients indicate that reduced RNase H2 expression is associated with poor survival in CRC.

Conclusion: We propose a hitherto unappreciated role for RNase H2 as a tumor suppressor gene in CRC. Our mouse model provides a novel tool to study the impact of abrogated RER on intestinal carcinogenesis.

overall_design: RNA sequencing of i) isolated epithelial crypts from aged H2Bfl/fl and H2BdIEC mice, ii) intestinal organoids from H2Bfl/fl, H2BdIEC and H2B/p53dIEC and iii)  tumor tissue and surrounding unaffected tissue of H2B/p53dIEC and H2B/p53fl/fl

first: Aden

last: Konrad

first: Philip

last: Rosenstiel


title: Hepatic gene expression profiles in persimmon peel extract administrated KK-Ay mice

city: Aomori

first: Yuji

last: Nakai

state: Aomori

address: 2-1-1, Yanagawa

department: Institute of Regional Innovation

institute: Hirosaki University

summary: We have shown in a previous study that the intake of persimmon peel (PP) extract altered hepatic gene expression of insulin signaling and enhanced tyrosine phosphorylation of insulin receptors in nonobese type 2 diabetic Goto–Kakizaki rats. We also showed the alteration of gene expression in fatty acid synthesis and metabolism. To evaluate the effect of PP extract on obese diabetic KK-Ay mice, we fed them a diet mixed with 0.1% of the extract for 8 weeks. The plasma total ketone bodies level of the treated mice were significantly lower than that of the untreated mice. The hepatic gene expression profiles of treated mice indicated upregulation of fatty acid biosynthesis-associated gene expression. Hepatic nonesterified palmitic acid content was higher in treated mice than in untreated mice. These results suggest that the intake of PP extract enhances hepatic fatty acid biosynthesis of KK-Ay mice, reducing their plasma total ketone bodies level.

overall_design: Five-week-old male KK-Ay/TaJcl mice were purchased from CREA Japan, Inc. (Tokyo, Japan). They were individually housed in plastic cages and maintained at 22 ± 1°C under a 12-h light/dark cycle (lights on from 08:00 to 20:00 daily). They were fed a commercial diet (AIN-93G, Oriental Yeast, Co., Ltd., Tokyo, Japan) for a week and then divided into two groups with similar average body weight: a control diet (CD) group (n = 7) fed a commercial diet and a PP extract diet (PD) group (n = 6) fed a commercial diet containing 1 g/kg of PP extract. The mice were allowed free access to food and drinking water. In both groups, the feeding period was 8 weeks, and body weights and food intakes were measured every day during the feeding period.  After 8 weeks, each mouse was fasted for 3 h and then anesthetized with pentobarbital. Blood was collected from the carotid artery and treated with heparin. The blood was centrifuged at 800×g, and supernatants were collected and stored at−20°C until use. Livers were excised and treated with RNAlater for subsequent RNA analysis. The remaining liver tissues were frozen in liquid nitrogen and stored at −80°C until use. The protocol for the animal experiments was approved by the Animal Use Committee of the Faculty of Agriculture, University of Tokyo.

first: Ryoichi

last: Izuchi

first: Tomoko

last: Ishijima

first: Shinji

last: Okada

first: Keiko

last: Abe


title: Expression date from endothelial cells stimulated with anti-HLA class I and anti-A antibody

status: Public on Sep 28 2018

city: Nagoya

first: Kenta

last: IWASAKI

state: Aichi

address: 65 Tsurumai-cho, Showa-ku

department: Department of Transplant Immunology

institute: Nagoya University School of Medicine

summary:
While donor specific antibody (DSA) against HLA class II could frequently cause chronic antibody-mediated rejection (ABMR) in organ transplantation, anti-A/B antibody would not do so, because blood group ABO-incompatible transplantation has shown favorable graft outcome. Recently, an increasing attention has been paid to the importance of direct allorecognition of CD4 T-cells against HLA-class II expressed on graft endothelial cells. However, the effect of allo-antibody binding on its allorecognition remains unclear.
Microarray analysis and molecular profiling demonstrated that CD275 (PD-L1) expression was increased by anti-A/B ligation-mediated ERK inactivation in endothelial cells despite IFNγ stimulation.

overall_design: Endothelial cells were stimulated with anti-A antibody for 48hyrs. Total RNA were purified and then subjected to microarray experiments

last: Iwasaki

first: Takaaki

last: Kobayashi


title: Experimental replacement therapy counters decreased IGF-1 levels in Huntington’s disease

city: Seattle

first: James

middle: William

last: MacDonald

state: WA

address: 4225 Roosevelt Way NE

department: Environmental and Occupational Health Sciences

institute: University of Washington

summary: Huntington’s disease (HD) is a monogenetic neurodegenerative disorder caused by the expansion of a polyglutamine (polyQ) stretch in huntingtin (htt). Here we show that mutant htt reduces the transcription of insulin-like growth factor 1 (IGF-1) and leads to loss of IGF-1 in HD brains, HD mouse models and mutant htt-transgenic microglial cells. IGF-1 replacement therapy by transplantation of genetically engineered mouse neuronal precursor cells (mNPCs) in a mouse model of HD reverted the motor phenotype and countered striatal neuronal loss.

overall_design: 4 arrays, 2 experimental groups: 25Q (express 25Q htt) and 72Q (express 72Q htt).

first: Richard

last: Beyer

first: Theodor

last: Bammler

first: Aurelio

last: Silvestroni

first: Elsa

last: Raibon

first: Allison

last: Ebert

last: Lee

first: Wanda

last: Kwan

first: Sarah

middle: B

last: Swarts

first: Amelia

last: Barber

first: Albert

last: LaSpada

first: Wenzhen

last: Duan

last: Faull

first: Flaviano

last: Giorgini

first: Paul

last: Muchowski

first: Gillian

last: Bates

first: Clive

last: Svendsen

first: Thomas

last: Möller


title: Jarid2 Functions as a Tumor Suppressor in Myeloid Neoplasms by Repressing Self-Renewal in Hematopoietic Progenitor Cells

status: Public on Sep 30 2018

first: Hamza

last: CELIK

address: 660 S Euclid Ave

institute: Washington University in St Louis

summary: How specific genetic lesions contribute to transformation of non-malignant myeloproliferative neoplasms (MPN) and myelodysplastic syndromes (MDS) to secondary acute myeloid leukemia (sAML) are poorly understood.  The JARID2 gene is lost by chromosomal deletions in a proportion of MPN/MDS patients who progress to sAML.  In this study, genetic mouse models and patient-derived xenografts (PDX) demonstrated that Jarid2 acts as a tumor suppressor in chronic myeloid disorders.  Genetic deletion of Jarid2 either reduced overall survival of MPN, or drove transformation to sAML, depending on the timing and context of co-operating mutations.  Mechanistically, Jarid2 recruits PRC2 to epigenetically repress self-renewal pathways in hematopoietic progenitor cells.  These studies establish Jarid2 as a bona fide hematopoietic tumor suppressor and highlight new therapeutic targets.

overall_design: Hematopoietic stem cells (HSCs) and multipotent progenitors (MPPs) were sorted from Vav-CRE: Control and Vav-CRE:Jarid2-KO or Mx1-CRE: Control, Mx1-CRE: Jarid2-KO, and Max1-CRE: Jarid2-KO - Jak2-V617F mice for RNA-seq to determine gene expression.   Hematopoietic stem cells (HSCs) and multipotent progenitors (MPPs) were sorted from Vav-CRE: Control and Vav-CRE:Jarid2-KO to determine H3K27me3 chromatin profile by ChIPmentation.

last: Celik

first: Grant

middle: A

last: Challen


title: Genome-wide chromatin profiling using ATAC-seq of diabetic or non-diabetic murine haematopoietic stem cells (HSC)

status: Public on Sep 27 2018

city: Oxford

first: Laurienne

last: Edgar

address: L6 West Wing, John Radcliffe Hospital, Headley Way

department: Cardiovascular Medicine, Radcliffe Department of Medicine

institute: University of Oxford

summary: To understand the underlying mechanisms and predict transcription factors implicated in the generation and sustained pro-inflammatory memory within HSCs, ATAC-seq was performed on bone marrow HSCs isolated from either diabetic or non-diabetic control mice. Differential peak analyses indicated that cells form diabetic mice had an altered chromatin structure, and pathway analysis of these differential sites revealed pathways associated with inflammation. Peak motif enrichment analysis implicated Runt-related transcription factor 1 (RUNX1), among others, to be significantly enriched.

overall_design: 4 diabetic mice samples and 4 non-diabetic control mice samples were used. Each sample was split in half, one half submitted as a baseline, unstimulated control and the other was stimulated with IL-1β.

last: Krausgruber

first: Madeleine

last: Lemieux

first: Robin

last: Choudhury


title: TIP55, a splice isoform of the KAT5 acetyltransferase, is essential for developmental gene regulation and organogenesis

city: Worcester

last: Fazzio

state: MA

address: 364 Plantation street

institute: UMMS

summary: Multiple varieties of most chromatin regulatory complexes are expressed in mammals, resulting from a combination of alternative splicing, differential incorporation of accessory subunits, and other processes. Despite this complexity, chromatin regulators are usually characterized in vivo using mutants that affect multiple forms. Here we examine the developmental functions of the TIP55 isoform of the KAT5 (TIP60) histone acetyltransferase. In contrast to the preimplantation developmental arrest of mice deficient for all four Kat5 transcripts, mice specifically deficient for Tip55 die around E11.5 and fail to develop beating hearts . Prior to developmental arrest, mice exhibit altered proliferation and cell death in heart and neural tube, respectively. Consistent with these findings, transcriptome profiling prior to the onset of overt morphological abnormalities reveals alterations in multiple tissue types. These findings reveal that although Tip55 is dispensable for the pre- and early post-implantation roles of Kat5, it is essential for organogenesis. Targeted mutations of additional Kat5 isoforms will be necessary to understand their specific functions. Furthermore, targeted mutations of individual isoforms of other chromatin remodeling enzymes will likely uncover new biological functions.

overall_design: The data represent RNA-seq experiments examining gene expression changes in Tip55 knockout embryos relative to controls.

first: Diwash

last: Acharya

first: Bernadette

last: Nera

first: Zachary

last: Milstone

first: Lauren

last: Bourke

first: Yeonsoo

last: Yoon

first: Jaime

last: Rivera-Pérez

first: Chinmay

last: Trivedi

middle: G


title: Histone methylation regulator PTIP is required to maintain normal and leukemic bone marrow niches

status: Public on Sep 24 2018

city: Houston

first: Margarida

last: Almeida Santos

state: Texas

address: 1515 Holcombe Blvd Mail code 1000

department: Epigenetics and Molecular Carcinogenesis

institute: UT MD Anderson Cancer Center

summary: The bone is essential for locomotion, calcium storage and harboring the hematopoietic stem cells (HSCs) that supply the body with mature blood cells throughout life. HSCs reside at the interface of the bone and bone marrow (BM), where active bone remodeling takes place. Although the cellular components of the BM niche have been characterized, little is known about its epigenetic regulation. Here we find that the histone methylation regulator PTIP (Pax interaction with transcription-activation domain protein-1) is required to maintain the integrity of the BM niche by promoting osteoclast differentiation. PTIP directly promotes chromatin changes required for the expression of Pparg  (Peroxisome proliferator-activated receptor-γ), a transcription factor essential for osteoclastogenesis. PTIP deletion leads to a drastic reduction of HSCs in the BM and induces extramedullary hematopoiesis. Furthermore, exposure of acute myeloid leukemia cells to a PTIP-deficient BM microenvironment leads to a reduction in leukemia initiating cells (LICs) and increased survival upon transplantation. Taken together, our data identify PTIP as a novel epigenetic regulator of osteoclastogenesis that is required for the integrity of the BM niche to sustain both normal hematopoiesis and leukemia.

overall_design: RNA-seq data from osteoclast progenitors isolated from fresh bone marrow of WT Mx-1Cre and Ptip flox/flox Mx-1Cre mice, two independent replicates.

first: Prosun

last: Das

first: Kylee

last: Veazey

first: Hieu

last: Van

first: Saakshi

last: Kaushik

first: Kevin

last: Lin

first: Yue

last: Lu

first: Masaru

last: Ishii

first: Junichi

last: Kikuta

first: Kai

last: Ge

first: Andre

last: Nussenzweig


title: Intracellular activation of complement C3 leads to PD-L1 antibody treatment resistance via modulating tumor-associated macrophages

status: Public on Sep 21 2018

city: Chongqing

first: Haoran

last: Zha

address: Shaping Street #31

institute: Institute of Cancer, Xinqiao Hospital,Third Military Medical University

summary: Mounting evidence has highlighted the importance of complement in the construction of an immunosuppressive tumor microenvironment (TME). Tumor cell-derived C3 has been previously reported, however, whether and how it acts on anti-tumor immunity remains to be elucidated. Here, we describe a unique role of tumor cell-derived C3 in suppressing anti-tumor immunity. Tumor cell-derived C3 was activated intracellularly, which results in generation of C3a. C3a could modulate tumor-associated macrophages (TAMs) via C3a-C3aR-PI3Kγ signaling, thereby repressing anti-tumor immunity. More importantly, deletion of C3 in tumor cells with high C3 expression is sufficient to enhance the efficacy of ɑPD-L1 treatment. Collectively, our present results suggest tumor cell-derived C3 may serve as a novel target in cancer immunotherapy, specifically targeting C3 in tumor cells to enhance anti-tumor immunity.

overall_design: Tumor-associated macrophages were isolated from CT26 Sg-Con or CT26 Sg-C3 tumors on day 15 post tumor challenge. The RNA were quantified by RNA-seq.

first: Bo

last: Zhu


title: Gene expression alterations in Danshen-treated rats eye

status: Public on Sep 20 2018

city: Beijing

first: Qian

last: Zhang

address: No. 1 Shuaifuyuan, Dongcheng District

institute: Peking Union Medical College Hospital

summary: Diabetic rats changes gene expression in Danshen-treated rats eye.

overall_design: We performed microarray analyses of Danshen-treated rats eye.

first: Xinhua

last: Xiao

first: Jia

last: Zheng

first: Ming

last: Li

first: Miao

last: Yu

first: Fan

last: Ping

first: Zhixin

last: Wang

first: Cuijuan

last: Qi

first: Tong

first: Xiaojing


title: Analysis of Ronin knockout related gene expression changes in mouse embryonic stem cells.

status: Public on Sep 16 2018

city: New York

first: Marion

middle: Dejosez

last: Zwaka

address: 1425 Madison Ave

department: Black Family Stem Cell Institute

institute: Icahn School of Medicine at Mount Sinai

summary: Ronin knockout is embryonic lethal and Ronin knockout ES cells are not viable. Here we used CreER2; Roninflox/flox mouse ES cells to induce Ronin knockout by tamoxfien treatment in comparison to control Roninflox/flox cells to study Ronin knockout related transcriptional changes.

overall_design: Roninflox/flox (control) or CreERT2; Roninflox/flox mouse ES cells were plated at a density of 100,000 cell per 10 cm2 and cultured in standard mouse ES cell medium. Cells were treated with 0.25 µM tamoxifen for 1.5, 3 or 6 days and total RNA was isolated to study gene expression changes.

first: Thomas

last: Dejosez


title: Gene expression profiling of mouse HSCs treated with Eltrombopag

status: Public on Sep 17 2018

city: Bronx

first: Britta

last: Will

state: NEW YORK

address: 1300 Morris Park Ave

department: Department of Cell Biology

institute: Albert Einstein College of Medicine

summary: Eltrombopag, a small molecule thrombopoietin receptor (TPO-R) agonist and potent intracellular iron chelator, has shown remarkable efficacy to stimulate sustained multilineage hematopoiesis in patients with bone marrow failure syndromes, suggesting an effect at the most immature hematopoietic stem and multipotent progenitor level. While the functional and molecular effects of Eltrombopag on megakaryopoiesis have been carefully studied in the recent past, insights into its mechanistic impact on the earliest stages of hematopoiesis have been limited. Additionally, previous studies also revealed molecular pathway of Eltrombopag apart from stimulation of TPO signaling, detail characterization remains to be addressed. In this study, we investigated the effects of Eltrombopag, in comparison with TPO, on highly-purified primary hematopoietic stem cells (HSCs) from healthy human donors. The binding of Eltrombopag to TPO-R is species-specific to human and primate cells. we also utilized HSCs isolated mouse as separation-of-function models to directly assess the molecular effect of Eltrombopag on HSCs independent of TPOR stimulation.

overall_design: For isolation of mouse HSCs, bone marrow cells were isolated from tibiae, femurs, pelvic bones and vertebrae of 6 to 10-week-old mice. Low-density mononuclear cells (LDMNCs) were enriched by density gradient centrifugation using Histopague 1083 (Sigma-Aldrich, MO). Prospective HSCs (Lin−Sca-1+c-Kit+CD150+CD48−) were sorted on either FACS Aria II (Becton Dickinson, Franklin Lakes, NJ) or MoFlo Astrios (Beckman Coulter, Indianapolis, IN)

first: Yun-Ruei

last: Kao

first: Ulrich

last: Steidl


title: RNA-Seq as part of a study to investigate impact of Atg16l on Il22 signalling in the intestinal mucosa

status: Public on Sep 18 2018

first: Robert

last: Haesler

address: Schittenhelmstr. 12

department: IKMB / 1st Dept. of Medicine

institute: University Clinic of Schleswig Holstein

summary: A coding variant of the inflammatory bowel disease (IBD) risk gene ATG16L1 has been associated with defective autophagy and deregulation of endoplasmic reticulum (ER) function. IL-22 is a barrier protective cytokine by inducing regeneration and antimicrobial responses in the intestinal mucosa. We show that ATG16L1 critically orchestrates IL-22 signaling in the intestinal epithelium. IL-22 stimulation physiologically leads to transient ER stress and subsequent activation of STING dependent type I interferon (IFN-I) signaling, which is augmented in Atg16l1ΔIEC intestinal organoids. IFN-I signals amplify epithelial TNF production downstream of IL-22 and contribute to necroptotic cell death. In vivo, IL-22 treatment in Atg16l1ΔIEC and Atg16l1ΔIEC/Xbp1ΔIEC mice potentiates endogenous ileal inflammation and causes widespread necroptotic epithelial cell death. Therapeutic blockade of IFN-I signaling ameliorates IL-22 induced ileal inflammation in Atg16l1ΔIEC mice. Our data demonstrate an unexpected role of ATG16L1 in coordinating the outcome of IL-22 signaling in the intestinal epithelium.

overall_design: Organoids from Atg16l intestinal knockout vs. Wildtype

last: Häsler

first: Konrad

last: Aden


title: Effects of LSD1 inhibitors on enhancer functions in T-ALL cells

status: Public on Sep 22 2018

city: Shimotsuke

first: Yusuke

last: Furukawa

state: Tochigi

address: 3311-1 Yakushiji

department: Center for Molecular Medicine

institute: Jichi Medical University

summary: We treated the T-ALL cell line MOLT4  with a novel LSD inhibitor and performed ChIP-seq analysis using anti-histoneH3K27ac antibody to assess the enhancer function.

overall_design: We isolated fixed chromatin from MOLT4 cells treated with the LSD1 inhibitor S2157 and performed immunoprecipitation with anti-H3K27ac antibody, followed by deep sequencing.

first: Jiro

last: Kikuchi


title: P. aeruginosa TY1-PA3898 ChIP-seq

city: Honolulu

first: Tung

last: Hoang

state: HI

address: 1800 East-West Road

department: Microbiology

institute: University of Hawaii at Manoa

summary: We present here a transcriptional regulator, PA3898, which controls biofilm formation and multidrug efflux-pumps in P. aeruginosa. A mutant of this regulator significantly reduced the ability of P. aeruginosa to produce biofilm in vitro, and affected its in vivo fitness and pathogenesis in Drosophila melanogaster and BALB/c mouse lung infection models. Transcriptome analysis revealed that PA3898 modulates essential virulence genes/pathways, including multidrug efflux-pumps and phenazine biosynthesis.ChIP-seq identified its DNA binding sequences and confirmed PA3898 directly interacts with promoter regions of four genes/operons, two of which are mexAB-oprM and phz2.

overall_design: PAO1 strain contains TY1-tagged PA3898 was used to identify DNA sequences that interact with regulator via ChIP-seq

first: Yun

last: Heacock-Kang


title: Fzd6 knockout skin E15.5

status: Public on Sep 14 2018

city: Madison

first: Hao

last: Chang

state: WI

address: 1300 University Ave

department: Dermatology

institute: University of Wisconsin-Madison

summary:
The hair follicle misorientation phenotype in Fzd6-/- mice appears to act through the PCP signaling system, but the downstream effectors of Fzd6 remain mysterious.
We used microarrays to search for potential downstream effectors of the Fzd6 signaling pathway in regulating hair follicle orientation.

overall_design: We profiled the transcriptomes of back skins from E15.5 Fzd6+/– and Fzd6–/– embryos by hybridization of three independent samples to Affymetrix MOE430 2.0 gene chips.

first: Bo

last: Dong

first: Samantha

last: Vold

first: Cristina

last: Olvera-Jaramillo


title: Expression data of mouse (C57BL/6) Achilles tendon samples

city: Ghent

first: Isabelle

last: Cambré

address: De Pintelaan 185

country: Belgium

institute: Ugent

summary:
Biomechanical stress is an underestimated factor in rheumatic diseases. In this study the influence of extra activity on gene expression is investigated in healthy mice.
We used microarrays to determine the deregulation in gene expression induced by activity.

overall_design: Micro-dissected Achilles tendon samples were freshly collected and RNA was extracted for hybridization on Affymetrix microarrays. Mice had either been in a normal or a increased activity (voluntary running) condition

first: Dirk

last: Elewaut


title: Transcriptomes of microglia in experimental cerebral malaria in mice in the presence and absence of Type I Interferon signaling

status: Public on Sep 07 2018

city: London

first: Richard

middle: James

last: Mitter

state: LONDON

address: 1 Midland Road

department: Bioinformatics & Biostatistics

institute: The Francis Crick Institute

summary:
Plasmodium berghei ANKA infection in mice is used as a model for human cerebral malaria, the most severe complication of Plasmodium falciparum infection. The response of brain cells such as microglia has been little investigated, and may play a role in the pathogenesis or regulation of cerebral malaria.   We showed previously that microglia are activated in P. berghei infections, and that Type 1 Interferon signaling is important for activation. This dataset contains the transcriptome of brain microglia of infected mice in the presence and absence of Type I interferon signaling, with the aim of identifying the genes involved in this pathway in microglia during experimental cerebral malaria. Refererence: Capuccini et al 2016, Scientific Reports, 6:39258
The global gene expression profiles from RNA of microglia isolated from uninfected and P berghei-infected wild-type C57BL/6 mice and and IFNA Receptor Knock-out mice using Illumina Beadarrays.

overall_design: Total RNA from Female C57BL/6 wildtype and IFNA Receptor knock-out mice injected with 105 Plasmodium berghei ANKA infected red blood cells intraperitoneally compared to untreated mice of the same genotype.

first: Jean

last: Langhorne

first: Carlos

middle: T

last: Lopez

first: Jingwen

last: Lin

first: Barbara

last: Capuccini


title: Effect of Trim9 deficiency on adult retina

status: Public on Sep 12 2018

city: Ames

first: Jeff

last: Trimarchi

state: IA

address: 2437 Pammel Drive

department: Genetics, Development and Cell Biology

institute: Iowa State University

summary: Analysis of adult retinas from tripartite motif-containing domain 9 knockouts and wild type littermates.  Trim9 belongs to the TRIM family of E3 ubiquitin ligases. Results provide insight into possible roles for Trim9 in the retina.

overall_design: To investigate potential phenotypes in Trim9-KO retinas, microarrays were performed on adult retinas isolated from n=3 Trim9-KO mice and WT littermates.

first: Rebecca

last: Chowdhury

first: Lauren

last: Laboissonniere

first: Andrea

last: Wester

first: Madison

last: Muller

first: Jeffrey

middle: M


title: Modulation of microglia-mediated amyloid-beta clearance with nanoformulated polyphenol through the SIRT1-LDLR pathway

city: Shanghai

first: Hu

last: Meng

address: 160 Pujian Road, Pudong New Area, Shanghai

institute: Department of Pharmacy, Ren Ji Hospital, School of Medicine，Shanghai Jiaotong University

summary:
Light-controlled in situ synthesis of DNA microarrays (Affymetrix GeneChip® Mouse Genome 430 2.0) were performed to determine the altered gene expression. Affymetrix algorithm and multiple analysis comparison software were used for assessing gene expression differences, and mRNAs that increased or decreased in the brains of NP(α-M)-treated mice relative to that in the brains of Blank-NP-treated mice were identified.
For the assay, total RNA was extracted using Takara RNAiso Plus Kit (Cat#9109, Takara, DaLian, LiaoNing, CN) following the manufacturer’s instructions and checked for a RIN number to inspect RNA integrity by an Agilent Bioanalyzer 2100 (Agilent technologies, Santa Clara, CA, US). Qualified total RNA was further purified by RNeasy mini kit (Cat#74106, QIAGEN, GmBH, Germany) and RNase-Free DNase Set (Cat#79254, QIAGEN, GmBH, Germany). Array hybridization and wash was performed using GeneChip® Hybridization, Wash and Stain Kit (Cat#900720, Affymetrix, Santa Clara, CA, US) in Hybridization Oven 645 (Cat#00-0331-220V, Affymetrix, Santa Clara, CA, US) and Fluidics Station 450 (Cat#00-0079, Affymetrix, Santa Clara, CA, US) followed the manufacturer’s instructions. Slides were scanned by GeneChip® Scanner 3000 (Cat#00-00212, Affymetrix, Santa Clara, CA, US) and Command Console Software 4.0 (Affymetrix, Santa Clara, CA, US) with default settings. Raw data were normalized by MAS 5.0 algorithm, Gene Spring Software12.6.1 (Agilent technologies, Santa Clara, CA, US).

overall_design: To elucidate the regulatory mechanism of NP(α-M) on LDLR expression, we conducted gene microarray analysis, and interpreted the data via Ingenuity Pathway Analysis, finding that the key genes related to LDLR expression were SIRT1, sterol regulatory element binding protein-2 (SREBP2), cAMP-response element binding protein (CREB) and proprotein convertase subtilisin/kexin type 9 (PCSK9).

first: Meng

last: Hu

first: Xiao

last: Gu

first: Jianrong

last: Xu

first: Hongzhuan

last: Chen

first: Xiaoling

last: Gao


title: RNA expression of stretched versus unstretched primary murine sinusoidal endothelial cells.

status: Public on Sep 06 2018

city: Rochester

first: Aditya

last: Bhagwate

state: MN

address: 200 1st Street SW

institute: Mayo Clinic

summary: Primary murine sinusoidal endothelial cells were subjected to cyclic stretch and their gene expression profiles assessed by RNA-sequencing.

overall_design: Primary sinusoidal endothelial cells were isolated from mouse liver and then plated on Flexcell plates coated in collagen IV.  The cells were serum starved and then subjected to cyclic stretch.  RNA was isolated and RNA-sequencing was done to compare changes in gene expression which occur secondary to cyclic stretch.

first: Moira

last: Hilscher


title: Expression data from acd, p53 and double mutant mouse embryos

city: Ankara

first: Ceren

last: Sucularli

address: Sihhiye

country: Turkey

institute: Hacettepe University

summary:
In mouse, the adrenocortical dysplasia (acd) phenotype shows limb and body axis anomalies, as a result of p53-dependent apoptosis, and perinatal lethality. The p53 deficiency partially rescues anomalies, but not perinatal lethality, implicating the involvement of p53-independent mechanisms in the acd phenotype. Differentially expressed genes in acd mutant and double mutant embryos were identified. p53-dependent and –independent pathways contributing to acd phenotype were characterized.
We used microarrays to analyze gene expression profiles of acd and double mutant embryos and to identify p53 dependent and –independent mechanisms underlying acd phenotype.

overall_design: Microarray analysis was performed with wild type (wt), acd mutant (Acdacd/acd), p53-/-, and double mutant (Acdacd/acd, p53-/-) embryos at E10.5. CEL files were normalized using justRMA algorithm and differentially expressed genes were selected using BRB-Array tools version 4.4.0. p53-dependent and –independent pathways contributing to the acd phenotype were identified.

first: Catherine

middle: E

last: Keegan


title: Effect of ALOXE3 overexpression on primary murine hepatocyte gene expression profiles

city: St. Louis

first: Brian

middle: Jesse

last: DeBosch

address: 660 S. Euclid Ave, Box 8208

department: Pediatrics and Cell Biology & Physiology

institute: Washington University School of Medicine

summary: We demonstrate the effects of ALOXE3 overexpression on primary murine hepatocyte gene expression by high-throughput RNA sequencing

overall_design: Examination of transcriptome in primary murine hepatocytes 24h after infection with adenovirus encoding beta galactosidase or ALOXE3


title: Seh1 Interacts with Olig2 and Brd7 to Promote Oligodendrocyte Differentiation and Myelination (RNA-Seq)

city: xiamen

first: Liu

last: Zhixiong

state: Fujian

address: Xiangan Nanlu 4221-120

department: School of Life Sciences

institute: Xiamen University

summary: Nuclear pore complex components (Nups) are involved in neural development and alterations in Nup genes are linked to human neurological diseases. However, the physiological functions of specific Nups and the underlying mechanisms involved in these processes remain elusive. Here we show that tissue-specific depletion of nucleoporin Seh1 causes dramatic myelination defects in the Central Nervous System (CNS). Seh1-deficient Oligodendrocyte Progenitor Cells (OPCs) proliferate properly, but fail to differentiate into mature oligodendrocytes, which impairs myelin production and remyelination after demyelinating injury. Genome-wide analyses show that Seh1 regulates a core myelinogenic regulatory network and depletion of Seh1 alters open chromatin configurations at its target genes. Mechanistically, Seh1 regulates OPCs differentiation by assembling Olig2 and Brd7 into a transcription complex at nuclear pores. Together, our results reveal that Seh1 is required for oligodendrocyte differentiation and myelination by promoting assembly of an Olig2-dependent transcription complex and expose nucleoporins as key players in the CNS.

overall_design: RNA-seq was performed on mouse control or Seh1cKO immature oligodendrocytes(T3 D2).

first: Liang

last: Zhang

first: Zhixiong

last: Liu


title: RNA-Seq Analysis of Wild Type and LGMN-/- Peritoneal Macrophage Transcriptomes.

status: Public on Sep 04 2018

city: Tianjin

first: Long

last: Shen

address: 22 Qixiangtai Road

institute: School of Basic Medical Sciences, Tianjin Medical University

summary: Research on the interaction between tumour-associated macrophages (TAMs) and tumour cells has generated great interest in the potential use of macrophages as a therapeutic strategy against tumour cells. Here, we show that deletion of legumain, a conversed proteolytic enzyme in macrophages, promotes senescence of macrophages and tumour cells. Peritoneal macrophages isolated from wide type and lgmn-/- mice were co-cultured with EO771 breast cancer cells for 4 days. Total RNA was extracted for RNA-Seq analysis, cDNA library construction and sequencing were performed using BGISEQ-500 platform.

overall_design: Examination of differential expressive genes in peritoneal macrophages extracted from wide type and lgmn-/- mice after co-cultured with EO771 cells for 4 days.

first: Xiaoyue

last: Tan


title: Expression data from mouse crypt

status: Public on Sep 03 2018

city: Louisville

first: Zhong-bin

last: Deng

address: 505 s Hancock street

department: Medicine

institute: University of Louisville

summary:
Paneth cells originate in the stem cell region near the bottom of the gland and release a large number of secretory granules containing antimicrobials. The antimicrobial-rich granules are discharged into the crypt lumen and prevent microbial invasion of the crypt  and defend the gland stem cells from microbial damage.
We  examined the global gene expression profiles in crypt IECs using the Clariom S sDNA array. We analyzed mRNA panels of antimicrobial peptides (AMPs)  produced in CSN8ΔIEC and CSN8fl/fl mice.

overall_design: To test whether CSN8 deficiency triggers dysbiosis via a defect in the production of AMPs, Small intestinal crypts  from CSN8ΔIEC and CSN8fl/fl mice were isolated for RNA extraction and hybridization on Affymetrix microarrays. In brief, the small intestine was removed. Using a microscope cover slide, the gut lumen was firmly scraped to remove villi and mucus. Intestines were cut into 5 mm pieces and shaken in Hank's balanced salt solution (HBSS) two times and then placed in HBSS containing 10 mM EDTA on ice for 30 min.  Tissue pieces were shaken and the collected contents were filtered twice through a 70µm strainer to remove villous material. At this point, the suspension was mainly composed of crypts

first: Huang-ge


title: Development of Trypanosoma brucei EATRO 1125 and Trypanosoma congolense IL3000 in the host bloodstream

status: Public on Oct 01 2018

city: Edinburgh

first: Alasdair

last: Ivens

address: Kings Buildings

institute: Centre for Immunity, Infection and Evolution

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

sample_organism:
Trypanosoma congolense
Trypanosoma brucei brucei

overall_design: Refer to individual Series


title: Identification of genes differentially regulated in Corynebacterium diphtheriae by iron and DtxR

city: Silver Spring

first: Michael

last: Schmitt

state: MD

address: 10903 New Hampshire Ave

institute: US Food and Drug Administration

summary:
We assessed changes in gene expression in response to iron availability for the human pathogen Corynebacterium diphtheriae. Expression profiles of wild-type C. diphtheriae strain 1737 grown in semi-defined metal-poor media (mPGT) in iron-limiting (0.5 µM iron chloride supplementation) and iron-replete (10 µM supplementation) conditions were compared; the expression profiles of wild-type C. diphtheriae strain 1737 during growth in iron-replete conditions was also compared against an isogenic ΔdtxR mutant grown in iron-replete conditions. Three biological replicates were prepared by isolating total RNA from mid-logarithmic growth cultures and ten genes (dip0169, dip0415, dip1061, dip1062, dip2330, dip1486, dip0173, dip1252, dip1866, and dip0281) were quantified by real-time PCR to validate the array results.

Corynebacterium diphtheriae is the causative agent of the severe respiratory disease, diphtheria. Diphtheria Toxin (DT), encoded by the tox gene, is the potent exotoxin secreted by C. diphtheriae responsible for much of the morbidity and mortality of diphtheria. Expression of the tox gene is regulated by the Diphtheria Toxin Repressor (DtxR) and iron. In addition to the regulation of toxin expression, DtxR functions as a global iron-dependent regulatory factor that mediates iron homeostasis in C. diphtheriae. While numerous genes regulated by DtxR and iron are known, a genome-wide study of both the iron and DtxR regulons is lacking in C. diphtheriae. Here, we report novel iron- and DtxR-regulated genes revealed by a comprehensive transcriptomic analysis. Not all identified genes appear to be repressed by iron and DtxR; some genes were found to be induced by iron in a DtxR-dependent manner, a mechanism of regulation not previously described in C. diphtheriae. Using a prediction algorithm (MEME) and electrophoretic mobility shift assays, we verified DtxR binding to sequences upstream of several newly identified genes. Furthermore, we characterized expression of ferritin (ftn) and catalase (cat), which are both induced by iron, but differentially affected by DtxR. We identified three DtxR binding sites in the ftn promoter, while analysis of the cat promoter establishes a role for DtxR in cat expression and suggests complex regulation by additional regulators. Collectively, these results expand our knowledge on the function of DtxR and the diverse roles of this regulatory protein in controlling gene expression.

overall_design: Total RNA harvested from mid-logarithmic cultures of Corynebacterium diphtheriae strain 1737 (wild type and an isogenic dtxR mutant) with low-iron (wild type only) and high-iron (both strains) was assessed for differences. Three separate cultures were used per strain and condition for a total of nine samples.

first: Eric

last: Peng

middle: P


title: A Deiodinase Polymorphism Causes ER-Stress And Hypothyroidism In The Brain

status: Public on Sep 01 2018

city: Chicago

first: Gustavo

middle: Werpel

last: Fernandes

state: IL

address: 5841 South Maryland Av.

department: Endocrinology

institute: University of Chicago

summary:
Expression data from different brain regions of mice
Discrete brain areas were studied using an unbiased whole-transcript microarray approach (Ala92-Dio2 homozygotes vs Thr92-Dio2 homozygotes)

overall_design: Thr92-Dio2 and Ala92-Dio2 mice were selected  for RNA extraction and hybridization on Affymetrix microarrays. Here, we sought to characterize the genetic profile of the different areas of brain and how it differs between mice.

middle: W

first: Barbara

last: Bocco

first: Antonio

middle: C

last: Bianco


title: Human AK2 links intracellular bioenergetic redistribution to the fate of hematopoietic progenioptors

city: Kyoto

first: Megumu

last: Saito

address: 53, Shogoin-Kawahara

institute: Kyoto University

summary: Recent studies have linked bioenergetic regulation to cellular differentiation. However, the contribution of metabolic communication among subcellular components to the fate of progenitor cells remains unclear. Adenylate kinase 2 (AK2) is an adenylate phosphotransferase localized in the mitochondrial intermembrane space. Although AK2 mutations in human can cause a severe combined immunodeficiency with neutropenia, named reticular dysgenesis (RD), underlying mechanisms have not yet been elucidated. To address these questions, we established induced pluripotent stem cells (iPSCs) from two RD patients. Metabolic flux analysis revealed that AK2 mediates the distribution of glycolytic metabolites into the tricarbon acid cycle in mitochondria. Hematopoietic differentiation from RD-iPSCs was profoundly impaired. Intriguingly, RD-iPSC-derived hematopoietic progenitors exhibited an immature mitochondrial morphology, discordant ATP distribution among the mitochondria and nucleus, and alteration of global transcriptional profiles. These results highlight the importance of stage-specific intracellular energy communication for controlling the fate of multipotential progenitors.

overall_design: We compared expression profiles of ES cells, AK2-deficient and AK2-supplemented  clones during four sequential developmental stages: undifferentiated pluripotent stem cells, day 6 CD34+KDR+ hemoangiogenic progenitors, day 13 CD34+CD45+ myeloid progenitor cells and day 22 neutrophils

first: Koichi

last: Oshima

first: Norikazu

last: Saiki

first: Michihiro

last: Tanaka

first: Hiromi

last: Imamura

first: Akira

last: Niwa

first: Akiyoshi

last: Hirayama

first: Ayako

last: Tanimura

first: Junko

last: Kuwabara

first: Keisuke

last: Okita

first: Akitsu

last: Hotta

first: Shuichi

last: Kitayama

first: Michiko

last: Yoshida

first: Yukari

last: Jindai

first: Saori

last: Nakamura

first: Mitsujiro

last: Osawa

first: Shin

last: Kaneko

last: Watanabe

first: Isao

last: Asaka

first: Wataru

last: Fujibuchi

first: Kohsuke

last: Imai

first: Hiromasa

last: Yabe

first: Yoshiro

last: Kamachi

first: Junichi

last: Hara

first: Seiji

last: Kojima

first: Masaru

last: Tomita

first: Tomoyoshi

last: Soga

first: Takafumi

last: Noma

first: Shigeaki

last: Nonoyama

first: Tatsutoshi

last: Nakahata


title: Gene expression in testes of 5 week old mice after PHF13 depletion

city: Erlangen

first: Soeren

last: Lukassen

address: Schwabachanlage 10

department: Institute of Human Genetics

institute: Friedrich-Alexander Universitaet Erlangen Nuernberg

summary: Expression changes in testes of 5 week old mice after knockout of Phf13 were analyzed using Affymetrix mouse genome 430 2.0 expression microarrays. Transcripts on the X- and Y-chromosome were significantly upregulated.

overall_design: RNA was isolated from the testes of 5 week old PHF13-knockout and wild type mice and analyzed using Affymetrix expression microarrays.

first: Andreas

last: Winterpacht

first: Sören


title: Hypoxia is NOT THE MAIN stress When M. tuberculosis is in a dormancy-LIKE FATTY ACID environment

status: Public on Aug 31 2018

city: Bogota

first: Juan

middle: Manuel

last: Anzola

state: Bogota

department: Bioinformatics

country: Colombia

institute: CorpoGen

summary: The capacity of Mycobacterium tuberculosis (Mtb) to sense, respond and adapt to variable and hostile environment within the host, has made it one of the most successful human pathogens. During different stages of infection, the bacillus is surrounding by a plethora of lipid rich molecules and current evidence points out the relevance of fatty acids during the Mtb infectious process. In this study, we have compared the transcriptional response of Mtb to hypoxia in cultures grown in both, a mix of even long-chain fatty acids and dextrose as carbon sources. Using RNA sequencing, we have identified the differential expressed genes in early and late hypoxia defined according to the in vitro Wayne model and compared the results with the exponential phase of growth in both carbon sources. Our results showed that, different to dextrose, the number of genes overexpressed in hypoxia in the lipid medium was quite low in both, early and late hypoxia in all functional categories describes for Mtb. The exception were the transcripts of stable and non-coding RNAs which were more expressed in the fatty acid medium. We found that SigB and SigE were overexpressed in the early phase of hypoxia, confirming their pivotal role in early adaptation to low oxygen concentration independently of the carbon source. A drastic contrast was found with the transcriptional regulatory factors at early hypoxia. Only 2 transcriptional factors were overexpressed in early hypoxia in the lipid medium compared to 37 that were overexpressed in the dextrose medium. Instead of Rv0081, known to be the central regulator of hypoxia in dextrose, Rv2745c, (ClgR), is playing a main role in hypoxia in the fatty acids medium. The low level of genes associated to stress-response, showed by Mtb during their adaptation to hypoxia in fatty acids, suggested that this lipid environment makes hypoxia a less stressful condition for the tubercle bacilli. Therefore, when the bacillus is surviving in that environment, its metabolism seemed to be already adapted to different stresses within the host, including hypoxia. This fact could explain the success of Mtb to establish long-term survival during latent infection.

overall_design: Examination of transcription profiles of M. tuberculosis H37Rv under hypoxic conditions

first: Patricia

middle: D

last: Portillo

first: Lazaro

last: Morales

first: Carmen

last: Menendez

last: Rodriguez

first: Cecilia

last: Helguera-Repetto

first: Miguel

last: Ares

first: Rafael

last: Prados-Rosales

first: Jorge

last: Gonzalez-y-Merchand

first: Maria

last: Garcia


title: PLSCR2 deficiency in the IFN-I-induced antiviral and inflammatory gene signature

city: Taipei

first: Ming-Hsun

last: Tsai

address: Rm513, No 1, Sec 1, Jen-Ai Rd

department: Graduate Institute of Immunology

country: Taiwan

institute: National Taiwan University

summary:
Phospholipid scramblase 2 (PLSCR2) plays an negative role in type I IFN responses.  PLSCR2 constitutively interacts with STAT3, and PLSCR2 deficiency enhances IFN-I-induced gene expression and antiviral activity in an STAT3-dependent manner.
We used microarrays to compare the overall difference of intrinsic and IFN-induced gene expression between wild-type and PLSCR2 deficient cells

overall_design: PLSCR2 knockout (PLS2KO) cells were generated from immortalized hepatocyte cell line ML-1. In this study, wild-type and PLS2KO ML-1 cells were treated with mouse IFN-α4 in 1000U/ml for 6 hours to compare their antiviral and inflammatory gene signature by  using the affymetrix Mouse Clariom S Array platform.

first: Chien-Kuo

last: Lee


title: Gene expression in testes of 15-20 week old mice after PHF13 depletion

summary: Expression changes in testes of 15-20 week old mice after knockout of Phf13 were analyzed using Affymetrix mouse genome 430 2.0 expression microarrays. Transcripts on the X- and Y-chromosome were significantly upregulated.

overall_design: RNA was isolated from the testes of 15-20 week old PHF13-knockout and wild type mice and analyzed using Affymetrix expression microarrays.


title: Nuclear miRNA-mediated gene silencing dependent on Argonaute proteins is required for embryonic stem cell differentiation [6_chr_seq]

city: Bethesda

first: Markus

last: Hafner

address: 50 South Drive

department: NIAMS

institute: NIH

summary: Here, we show that embryonic stem cells (ESCs) and muscle stem cells contain high levels of nuclear AGO proteins and that in ESCs nuclear AGO2 protein activity is sufficient to allow for differentiation. Transcriptome-wide mapping of binding sites at nucleotide resolution revealed that nuclear AGO2 expands its target sequence repertoire in a miRNA-dependent manner to include intronic sequences to induce post-transcriptional gene silencing

overall_design: RNA seq from the chromatin fraction

first: Aishe

last: Sarshad

first: Aster

middle: H

last: Juan

first: Ana

middle: I

last: Correa Muler

first: Dimitrios

last: Anastasakis

first: Xiantao

last: Wang

first: Pavol

last: Genzor

first: Xuesong

last: Feng

first: Pei-Fang

first: Hong-Wei

last: Sun

first: Astrid

last: Haase

first: Vittorio

last: Sartorelli


title: Nuclear miRNA-mediated gene silencing dependent on Argonaute proteins is required for embryonic stem cell differentiation


title: Nuclear miRNA-mediated gene silencing dependent on Argonaute proteins is required for embryonic stem cell differentiation [5_miRNA-seq]

overall_design: Argonaute immunoprecipitation and small RNA cloning in ESC from cytoplasmic and nuclear fractions


title: Nuclear miRNA-mediated gene silencing dependent on Argonaute proteins is required for embryonic stem cell differentiation [4_Cnot shRNA-seq]

overall_design: shRNA CNOT1 and CNOT7 and RNA-seq from nuclear fraction


title: Nuclear miRNA-mediated gene silencing dependent on Argonaute proteins is required for embryonic stem cell differentiation [3_RNA-seq]

overall_design: RNA-seq in ESC from total and nuclear fractions


title: Nuclear miRNA-mediated gene silencing dependent on Argonaute proteins is required for embryonic stem cell differentiation [1_Differentiation_rna_seq]

overall_design: LIF withdrawal and ESC differentiation for 6 days with WT ESC and ESC expressing NLS-AGO2


title: Nuclear miRNA-mediated gene silencing dependent on Argonaute proteins is required for embryonic stem cell differentiation [2_PAR-CLIP]

overall_design: Argonaute PAR-CLIP to identify binding targets in ESC from cytoplasmic and nuclear fractions


title: Epidermal fatty acid binding protein prevents chemical-induced skin tumorigenesis by inhibition of SOX2 expression in keratinocytes

status: Public on Aug 30 2018

first: Bing

last: Li

state: Kentucky

address: 505 S Hancock St

department: Microbiology and Immunology

summary: E-FABP expression in keratinocytes increase interferons, in particualur IFNlamda, expression, which activate P53, a critical tumor suppessor, to inhibit or prevent chemical-induced skin tumorigenesis.

overall_design: Wild type(WT) mice and E-FABP deficient(EKO) mice were treated with DMBA/TPA according to procotol for 5 months. Skin tumors from WT and E-FABP-deficient mice (n=3/group) were collected and digested to single cells. Total RNA was extracted from 1 millions of tumor cells using RNeasy mini Kit and subjected to mouse mRNA gene expression by affymetrix microarray

first: Jiaqing

last: Hao


title: Expression data from blood of rats

status: Public on Aug 29 2018

city: Pont-à-Celles

first: Marie

last: Dagonnier

state: Hainaut

address: Place du Fichaux, 38

department: Stroke

institute: The Florey Institutes for Neurosciences

summary:
Stroke evolution is a highly dynamic but variable disease which makes clinical decision making difficult. We have used gene array technology to determine blood mRNA expression
Changes over the first day after stroke in rats in order to identy a stroke time signature.

overall_design: Blood samples were collected from 8 male spontaneously hypertensive rats at 0, 1, 2, 3, 6 and 24h post stroke induction by middle cerebral artery occlusion. RNA was extracted from whole blood stabilized in PAXgene tubes and mRNA expression was detected by oligonucleotide Affymetrix microarray.

first: Willliam

middle: J

last: Wilson

first: Jenny

last: Favaloro

first: Sarah

middle: S

last: Rewell

first: Linda

last: Lockett

first: Stephen

last: Sastra

first: Amy

middle: L

last: Jeffreys

first: Helen

last: Dewey

first: Geoffrey

last: Donnan

first: David

last: Howells


title: TCPOBOP-induced hepatomegaly & hepatocyte proliferation is attenuated by combined disruption of MET & EGFR signaling in mice

status: Public on Aug 28 2018

city: Pittsburgh

first: George

middle: K

last: Michalopoulos

state: Pennsylvania

address: 411 SBST, 200 Lothrop Street

institute: University of Pittsburgh

summary:
TCPOBOP (1,4-Bis [2-(3,5-Dichloropyridyloxy)] benzene) is a constitutive androstane receptor (CAR) agonist that induces robust hepatocyte proliferation and hepatomegaly without any liver injury or tissue loss. TCPOBOP-induced direct hyperplasia has been considered to be CAR-dependent with no evidence of involvement of cytokines or growth factor signaling. Receptor tyrosine kinases (RTKs), MET and EGFR, are known to play a critical role in liver regeneration after partial hepatectomy, but their role in TCPOBOP-induced direct hyperplasia, not yet explored, is investigated in the current study. Disruption of the RTK-mediated signaling was achieved utilizing MET KO mice along with Canertinib treatment for EGFR inhibition. Combined elimination of MET and EGFR signaling [MET KO + EGFRi], but not individual disruption, dramatically reduced TCPOBOP-induced hepatomegaly and hepatocyte proliferation. TCPOBOP-driven CAR activation was not altered in [MET KO + EGFRi] mice, as measured by nuclear CAR translocation and analysis of typical CAR target genes. However, TCPOBOP induced cell cycle activation was impaired in [MET KO + EGFRi] mice due to defective induction of cyclins, which regulate cell cycle initiation and progression. TCPOBOP-driven induction of FOXM1, a key transcriptional regulator of cell cycle progression during TCPOBOP-mediated hepatocyte proliferation, was greatly attenuated in [MET KO + EGFRi] mice. Interestingly, TCPOBOP treatment caused transient decline in HNF4α expression concomitant to proliferative response; this was not seen in [MET KO + EGFRi] mice. Transcriptomic profiling revealed vast majority (~40%) of TCPOBOP-dependent genes mainly related to proliferative response, but not to drug metabolism, were differentially expressed in [MET KO + EGFRi] mice. Conclusion: Taken together, combined disruption of EGFR and MET signaling lead to dramatic impairment of TCPOBOP-induced proliferative response without altering CAR activation.
We used microarrays to detail the global programme of gene expression in [METKO + EGFRi] mice liver  following TCPOBOP treatment

overall_design: Systemic inhibition MET-EGFR signaling pathway in mice was carried out by using a tamoxifen inducible system to systemically delete MET  and EGFR was inhibited by using Canertinib added to diet. TCPOBOP was administered at Day  0 and liver tissue harvested at defined time points and gene arrays carried out.

first: Bharat

last: Bhushan


title: Suppression of human T-cell activation by a novel anti-human CD3 antibody

city: Kobe

first: Sunao

last: Sugita

address: 2-2-3 Minatojima-minamimachi, Chuo-ku

department: The Laboratory for Retinal Regeneration

institute: RIKEN Center for Developmental Biology

summary: The agonistic anti-human CD3ε antibody , OKT-3, has been used to control acute transplant rejection. The in vivo administration of OKT-3 was previously shown to induce the partial depletion of T cells and anergy in the remaining CD4+ T cells. However, this therapy is also associated with the systemic release of several cytokines, which leads to a series of adverse side effects. We established a novel anti-human CD3ε Ab, 20-2b2 (#1 abs), which recognized a close, but different determinant on the CD3ε molecule from that recognized by OKT3. 20-2b2 was non-mitogenic for human CD4+ T cells, could inhibit the activation of T cells in vitro, and induced T cell anergy in in vivo experiments using humanized mice. Cytokine release in humanized mice induced by the administration of 20-2b2 was significantly less than that induced by OKT-3. Our results indicated that the CD3ε molecule is still an attractive, effective, and useful target for the modulation of T cell responses. The establishment of other Abs that recognize CD3ε, even though the determinant recognized by those Abs may be close to or different from that recognized by OKT-3, may represent a novel approach for the development of safer Ab therapies using anti-CD3 Abs, in addition to the modification of OKT-3 in terms of the induction of cytokine production.

overall_design: We examined whether a novel anti-human CD3 antibody (#1 abs: 20-2b2) could suppress T-cell activation in vitro, and we would liken to find which genes could suppress in the cells.  #1 abs was incubated with human peripheral blood mononuclear cells (PBMC) from a healthy volunteer in cell culture plate for 2 days (48 hr). In addition, we also used Rat IgG (a negative control) & OKT-3 abs (an experimental control) in the cultures. We then extracted total RNA of abs-treated PBMC (n=3).

first: Shota

last: Fujii

first: Masayo

last: Takahashi

first: Kenich

last: Makabe

first: Jun

last: Shimizu

first: Takeshi

last: Watanabe


title: SNP arrays  in matched colorectal cancer and normal colonic mucosa.

city: Catania

first: Daniele

middle: F

last: Condorelli

state: Italy

address: Via S. Sofia 64

department: Biomedical and Biotechnological Sciences

institute: University of Catania

summary: We analyzed, by last-generation high-resolution SNP arrays, colorectal adenocarcinoma samples and matched normal colonic tissues in order to determine the number of tumor-associated copy number abnormalities (CNAs) and copy neutral-loss of heterozygosity (CN-LOH) regions per patient and to identify possible recurring genomic abnormalities.

overall_design: 69 tumoral bioptic samples, deriving from 51 patients, were collected directly after surgical resection. The mean age was 66.86 years (SD 14.29) for 29 male patients and 69.77 (SD 13.41) for 22 female patients. In 16 patients, two samples were taken at arbitrary positions in the tumor area, separated by at least 1 cm (double-sampling pairs, indicated as tumoral sample 1 or 2). In one patient a sample from a synchronous colorectal adenocarcinoma was also collected (tumoral sample 3). In 28 cases biopsies of adjacent normal mucosa (at distance of 3-6 cm from the tumor) were also collected (matched tumor/mucosa pairs).

first: Vincenza

last: Barresi


title: Circadian Clock Protein CRY Regulates Autoimmunity

status: Public on Aug 24 2018

city: La Jolla

first: Ruth

middle: T

last: Yu

state: CA

address: 10010 N Torrey Pines Rd

department: Gene Expression Lab

institute: Salk Institute

summary: The circadian system regulates numerous physiological processes including the adaptive immune system. Here we show that mice deficient for the circadian genes Cry1 and Cry2, (DKO) display an autoimmune phenotype including higher serum IgG concentration, presence of serum anti-nuclear antibodies, precipitation of IgG, IgM and complement 3 in glomeruli, and massive infiltrations of leukocytes into the lung and kidney. Activation of Cry DKO splenic B cells elicited markedly enhanced and prolonged tyrosine phosphorylation of cellular proteins compared to cells from control mice, suggesting that over activation of the BCR signaling pathway may contribute to autoimmunity in the Cry DKO mice. Expression of C1q, deficiency of which contributes to the pathogenesis of Systemic lupus erythematosus (SLE), was significantly downregulated in Cry DKO B cells. This suggests that B cell development, BCR signaling pathway and C1q expression may be under direct circadian control and dysregulation of which contributes to autoimmunity.

overall_design: Comparison of wild-type and Cry1/2 double KO BM cells

first: Qi

last: Cao


title: Expression data from FACS-isolated liver endothelial cells

status: Public on Aug 27 2018

city: Mannheim

first: Mahak

last: Singhal

address: Ludolf-Krehl-Straße 13-17

institute: European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University

summary:
Cellular sources of liver endothelial cells remain elusive. Here, we used irradiation-conditioned bone marrow chimeric mice to lineage trace the endothelial cells.
Bone marrow-derived (YFP+) and resident (YFP-) liver endothelial cells were isolated and total RNA were used for microarray analysis using Clariom S mouse assays (Applied Biosystems).

overall_design: We generated bone marrow chimeras by transplanted 5000 YFP-labeled LSK cells in wild-type C57BL\6N mice which were irradiated with 9 Gy (2 x 4.5 Gy) radiation. After one month, the successful bone marrow chimeric mice were sacrificed and liver endothelial cells were isolated by FACS. Further, liver EC were segregated into YFP+ (bone marrow-derived endothelial cells) and YFP- (resident liver endothelial cell). Total RNA was isolated with Arcturus PicoPure RNA isolation kit. cDNA libraries were prepared and analyzed by the DKFZ Genomics core facility, according to the standard operating protocols.

first: Singhal

last: Mahak

first: Augustin

middle: G

last: Hellmut


title: Gene expression data from mouse cerebellar tumor samples

city: Heidelberg

first: Marcel

last: Kool

address: Im Neuenheimer Feld 280

department: Pediatric Neurooncology

institute: German Cancer Research Center DKFZ

summary: Gene expression data from mouse cerebellar tumors generated using CRISPR/Cas9 technology to disrupt Ptch1 and Chd7 in the embryonic cerebellum of Chd7 fl/+ mice by in utero electroporation.

overall_design: RNA was isolated from four different mouse tumors and used to generate gene expression data using the Affymetrix Mouse Genome 430 2.0 arrays

first: Daisuke

last: Kawauchi