title: Differential expression analysis of a Vibrio parahaemolyticus ∆rpoN mutant compared to wild-type in minimal media supplemented with glucose or mouse intestinal mucus

city: Newark

first: E Fidelma

last: Boyd

state: DE

address: 118 Wolf Hall

institute: University of Delaware

summary: Vibrio parahaemolyticus is the leading bacterial cause for seafood-related gastroenteritis worldwide. As an intestinal pathogen, V. parahaemolyticus competes with other commensal bacteria for the same pool of nutrients. The major source of nutrition for intestinal bacteria is intestinal mucus. We wanted to determine the expression profile of wild-type V. parahaemolyticus in mouse intestinal mucus and then perform a differential expression analysis in a ∆rpoN deletion mutant.

overall_design: RNA-Seq analysis was performed on RNA isolated from two biological replicates of wild-type Vibrio parahaemolyticus strain RIMD2210633 and two biological replicates of the ∆rpoN mutant strain, grown in M9 minimal media supplemented with glucose or mouse intestinal mucus.

first: Sai

last: Kalburge

first: Ethna

middle: F


title: Single cell RNA-Seq of I2A rhabdoid cell line

status: Public on Feb 14 2020

city: Paris

first: Olivier

last: Delattre

address: 26 rue d'Ulm

country: France

institute: Institut Curie

type: Expression profiling by high throughput sequencing

summary:
We report the application of single-molecule-based sequencing technology for high-throughput profiling of I2A cell line
Examination of gene expression in I2A rhabdoid cell line, as a negative control

overall_design: Study of transcriptomic heterogeneity of Ewing Sarcoma models and comparison with control cell models

first: M

middle: M

last: Aynaud

first: O

last: Mirabeau

first: N

last: Gruel

first: S

last: Grossetête

first: A

last: Zinovyev


title: Transcriptional programs define intratumoral heterogeneity of Ewing sarcoma at single cell resolution

type: Genome binding/occupancy profiling by high throughput sequencing

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

overall_design: Refer to individual Series


title: Genome-wide analysis of colorectal cancer gene expression by using primary tumors, normal colon and lymph nodes

status: Public on Feb 13 2020

city: Umeå

first: Marie-Louise

last: Hammarström

address: Peter Lestadius väg

department: Clinical Microbiology

country: Sweden

institute: Umeå universitet

summary: Analysis of the difference in gene expression between colorectal cancer samples and control samples

overall_design: Total RNA was extracted from colorectal cancer primary tumors and lymph nodes metastasis and compared to RNA extracted from lymph nodes and  colon tissue of control patients

first: Sten

first: Lina

last: Olsson


title: Chordoma and osteosarcoma cell lines Illumina Infinium MethylationEPIC array

city: London

first: Adrienne

last: Flanagan

state: Middlesex

address: Huntley Street

country: United Kingdom

institute: University College London

summary: We report the DNA methylation profile of 4 chordoma cell lines (UCH1, UCH7, UM-Chor and MUG-Chor) and 1 ostesarcoma cell line (U2OS) using Illumina Infinium MethylationEPIC array

overall_design: Bisulphite converted DNA from the 5 samples were hybridised to the Illumina Infinium MethylationEPIC array

first: Lucia

last: Cottone


title: Head and neck cancer neural reprogramming

city: Houston

first: MORAN

last: AMIT

state: Texas

address: 1881 East Road

country: USA

institute: UT MD Anderson CC

summary: We investigated the route of neurotrophic cue delivery to the nerves

platform_organism:
Homo sapiens
Mus musculus

overall_design: In the study presented here, ncRNA expression levels in p53-isogenic cells were analyzed.

first: George

middle: A

last: Calin

first: Moran

last: Amit


title: Head and neck cancer neural reprogramming [ClariomSMouse]

overall_design: We compared the transcriptional profile of TG neurons transfected with miR-21, miR-34a, or miR-324 with that of TG neurons transfected with scramble miRNAs.


title: The human gene FOXM1 promotes cortical folding and improves learning and memory ability in mice [E15]

city: Beijing

first: Jianwei

last: Jiao

state: Beijing

address: 1 Beichen West Road

department: State Key Laboratory of Reproductive Biology

country: China

institute: Institute of Zoology, Chinese Academy of Sciences

summary:
Purpose: To gain futher insight into how FOXM1 regulates the proliferative of neural progenitors ,RNA-seq was used to analyze the genome-wide changes resulting from the cerebral cortices of E15 FOXM1 conditional knock in mice and littermate wild-type.
Methods: Total RNA from E15 telencephalic tissue of wild-type(WT) and FOXM1f/+;Nestin-Cre mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, total RNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics
Results: Approximately one thousand transcripts showed differential expression between the wild-type(WT) and FOXM1f/+;Nestin-Cre mice brain cortex, with a fold change ≥1.5 and p value <0.05.Geneontology analysis of the up-regulated genes showed obvious enrichment of biological processes related to development and proliferation.The down-regulated genes exhibited enrichment of biological processes related to the negative regulation of cell proliferation and developmental process. These results reflected human FOXM1 plays a role in cortex development.
Conclusions: RNA-seq based transcriptome characterization would provide a overall understanding how FOXM1 gene contribute to brain cortical development.

overall_design: Total mRNA profiles of E15 wild type (WT) and FOXM1f/+;Nestin-Cre mice were generated by deep sequencing, in triplicate, using Illumina HiSeq 2500.

first: Wenwen

last: Wang


title: Gene expression analysis of cell populations derived from skeletal muscle of young and aged mice

city: Kamakura

first: Satoshi

last: Kondo

state: Kanagawa

address: 10-1 tebiro 6-chome

country: Japan

institute: Toray Industries,Inc.

summary: Comprehensive analyses of mRNA expression were performed using three different cell populations isolated from skeletal muscle of young and aged mice to investigate age-related changes of each cell population.

overall_design: PDGFRa+ mesenchymal progenitors, satellite cells, and mixed population of endothelial or hematopoietic cells were FACS purified from hind limb muscles of young (8-10 w old) and aged (24-28 mo old) mice. Freshly sorted cells were pooled and cell sorting was performed multiple times until pooled cell number reached 0.4-1 x 10e6. Gene expression of freshly sorted cell populations were analyzed to identify genes that were specifically expressed in each cell population and altered by aging.

first: Akiyoshi

last: Uezumi


title: A stem cell-driven lymphoangiogenic switch (ChIP-seq)

status: Public on Feb 19 2020

city: New York

first: Hanseul

last: Yang

state: NY

address: 1230 York Avenue

institute: Rockefeller University

summary: Tissues rely on stem cells (SCs) for homeostasis and wound-repair. SCs reside in specialized microenvironments (niches) whose complexities and roles in orchestrating tissue growth are still unfolding. Here, we identify lymphatic capillaries as critical SC niche components. In skin, lymphatics form intimate networks around the SCs of each hair follicle (HF) during their non-regenerative phase, and remodel upon regeneration. Seeking understanding, we unravel a secretome switch within SCs that controls lymphatic behavior. Resting SCs express Angiopoietin-like 7 (Angptl7), promoting lymphatic drainage. Upon activation, SCs trigger an anti-lympho-angiogenic program, transiently sparking lymphatic dilation and dampened drainage. In mammals, this dynamic aria between SCs and lymphatics is essential for coordinating HFSC behavior and hair regeneration: Upon either depleting lymphatics, silencing Angptl7 or super-activating anti-lympho-angiogenesis, SCs precociously proliferate and HF regeneration becomes asynchronous. In unearthing lymphatic capillaries as a hitherto under-appreciated SC-niche element, we’ve learned how SCs coordinate their activity across a tissue.

overall_design: Mouse bulge hair follicle stem cells at the early hair cycle were FACS-purified for ChIP-seq analysis.

first: Shiri

last: Gur-Cohen

first: Elaine

last: Fuchs


title: A role of the CTCF binding site at enhancer Ea in Tcra rearrangement

city: Guangzhou

first: Hao

last: bingtao

address: ShataiNan Road, Baiyun District, Guangzhou, Guangdong Province

institute: Southern Medical University

summary: We found that the CTCF binding site (named as EACBE) at the enhancer Eα of Tcra is essential for normal Tcra rearrangement.The EACBE deletion impaired the TAD structure of the 3’ region of the Tcra/d locus and the interactions between the proximal Vα genes and the Jα genes without changing the accessibility of the Jα array.

overall_design: Histone modification, repertoire and chromatin conformation profiles of 4-8 weeks old wild type (WT) and EACBE-/- mice  were generated by deep sequencing, in duplicate, using Illumina Hiseq.

last: Zhao

first: Zhaoqiang

last: Li


title: Defining the adult hippocampal neural stem cell secretome: in vivo versus in vitro transcriptomic differences and their correlation to secreted protein levels.

city: Columbus

first: Elizabeth

middle: Diana

last: Kirby

state: OH

address: 1835 Neil Ave, 55 Psycholgy

department: Psychology

institute: The Ohio State University

summary: Recent evidence shows that adult hippocampal neural stem and progenitor cells (NSPCs) secrete a variety of proteins that affect tissue function. Though several individual NSPC-derived proteins have been shown to impact cellular processes like neuronal maturation and stem cell maintenance, a broad characterization of NSPC-secreted factors is lacking. Secretome profiling of low abundance stem cell populations is typically achieved via proteomic characterization of in vitro, isolated cells. Here, we analyzed the in vitro NSPC secretome using conditioned media from cultured adult mouse hippocampal NSPCs and detected over 200 different bioactive proteins with an antibody array. We next assessed the NSPC secretome on a transcriptional level with RNA sequencing (RNAseq) of cultured NSPCs. This comparison revealed that quantification of gene expression did not accurately predict relative protein abundance for several factors. Furthermore, comparing our transcriptional data with previously published single cell RNA sequencing datasets of freshly isolated hippocampal NSPCs, we found key differences in gene expression of secreted proteins between cultured and acutely isolated NSPCs. Understanding the components and functions of the NSPC secretome is essential to understanding how these cells may modulate the hippocampal neurogenic niche, as well as how they can be applied therapeutically. Cumulatively, our data emphasize the importance of using proteomic analysis in conjunction with transcriptomic studies and highlights the need for better methods of global unbiased secretome profiling.

overall_design:
4 separate primary cultures of neural stem cells isolated from adult C57/Bl6 mouse (aged 6-9 weeks) dentate gyrus (2 male, 2 female); 2 whole dentate gyri (1 female, 1 male) from adult C57Bl6 mice are also provided for comparison/normalization

Single cell analysis performed with 3 separate primary cultures of neural stem cells isolated from adult C57/Bl6 mouse (aged 6-9 weeks) Cells were pooled before sequencing.

first: Jiyeon

middle: K

last: Denninger

first: Xi

last: Chen

first: Altan

last: Turkoglu

first: Patricia

last: Sarchet

first: Abigail

last: Volk

first: Pearlly

last: Yan

middle: D


title: Knock down of FTO in cervical cancer cells

city: DUARTE

first: Lei

last: Dong

state: CA

address: 1500 DUARTE RD

institute: City of Hope

summary: FTO, an N6-methyladenosine (m6A) demethylase, can promote cervical cancer cell proliferation and migration. RNA-sequencing of SiHa cells with FTO knockdown was conducted to dissect the differentially expressed genes and the potential mechanism of FTO in cervical cancer.

overall_design: Cervical cancer cells SiHa were infected with lentivirus carrying the shRNA control and FTO shRNAs in duplicates. Cells were collected after lentivirus infection 48h for total RNA extraction.

first: Dongling

last: Zou

first: Tao

last: Liu


title: Expression data from a staygreen mutant of citrus and its wild type [RNA-Seq]

city: Wuhan

first: Feng

last: Zhu

address: No.1,Shizishan Street

department: College of Horticulture & Forestry Sciences

institute: Huazhong Agricultural University

summary: The fruits color is one of the most important appearance qualities of citrus fruits. To illuminate the potential regulation of the color formation process of citrus fruits, the present study compared the different genes expression pattern between a spontaneous stay-green mutant and its wild type.

overall_design: The flavode of the citrus were collected at 210 days after flowering and 30 days after storage for RNA extraction and analysis.

first: Yunjiang

last: Cheng


title: ChIA-PET from HepG2 (ENCSR146FPM)

status: Public on Feb 12 2020

city: Stanford

first: ENCODE

last: DCC

address: 300 Pasteur Dr

institute: ENCODE DCC

summary:
RAD21 ChIA-PET in human HepG2 cells

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


title: Hepatocypte-specific Caveolin-1 knockout livers

city: Mannheim

first: Carsten

last: Sticht

address: Theodor-Kutzer-Ufer

department: ZMF

country: Germany

institute: University Heidelberg

summary:
mRNA expression was compared between wild type and hepatocyte-specific caveolin-1 knockout livers in healthy and non-alcoholic fatty liver disease (NAFLD) mice
mRNA expression was compared between gender

overall_design: RNA was isolated from livers of 12 weeks old male and female mice after 4 weeks control/MCD diet

first: Mei

last: Han

first: Christoph

last: Meyer


title: Sex differences in LCWE-induced model of Kawasaki Disease vascultitis and response to Anakinra treatment

city: Los Angeles

first: Rebecca

middle: Amelia

last: Porritt

address: 8700 Beverly Blvd

department: Pediatrics

institute: Cedars Sinai

summary: Analysis of abdominal aorta gene expression in the LCWE-induced Kawasaki Disease vasculitis model and responisveness to Anakinra treatment in male and female 5 wk. old mice

overall_design: 4-5 mice were analyzed per group


title: Transcriptome profiling of WM3248 melanoma cells following PGC1-alpha knockdown

first: Iman

last: Osman

address: 522 1st Avenue, Smilow 403

institute: NYU School of Medicine

summary: PGC1-alpha is a transcriptional coactivator that controls diverse cellular processes, including metabolism. PGC1-alpha expression is increased in invasive primary melanoma. To understand the role of PGC1-alpha in the invasive growth of primary melanoma, we generated transcriptional (RNA-Seq) profiles of WM3248 primary melanoma cells that were transfected with either negative control or PGC1-alpha siRNA.

overall_design: Cells were transfected with validated siRNAs: AllStars (negative control) or PGC1-alpha. RNA was harvested 48h later and used for RNA-Seq.

first: Keith

last: Giles


title: The expression of mRNAs after H19 overexpression in periodontal ligament cells

city: beijing

first: guo

last: runzhi

address: 205 chengfu road, haidian district, Beijing

institute: Peking university

summary: RNA (4 μg) extracted from PDLCs was treated with DNase. After removing the ribosomal RNA, the RNA library was prepared. RNA sequencing was performed on a HiSeq 2000 System (Illumina, San Diego, CA, USA). After the raw data were trimmed and filtered, the remaining data were then mapped to the human genome (hg19) using HISAT2. Differential gene expression was evaluated using the EBSeq package of the Bioconductor R program as previously described.  To preliminarily study the mechanism of H19 in the regulation of autophagy, RNA sequencing after transfection with the H19 vector was performed. The RNA sequencing data showed that 1120 mRNAs, including 431 upregulated and 689 downregulated mRNAs, were differentially expressed in the H19 overexpression group compared to the control group. The differential expression levels of mRNAs were visually expressed with a volcano plot. To evaluate the function of differentially expressed genes, KEGG pathway analyses were performed. The data showed that the differentially expressed mRNAs were enriched in the PI3K/AKT signaling pathway, which is relevant to autophagy regulation.

overall_design: examin the expression of mRNAs after H19 overexpression in periodontal ligament cells

first: Runzhi

last: Guo

first: Yiping

last: Huang


title: Analysis of apoptosis- and TGFB1-associated transcriptome changes in peripheral blood leukocytes during anti-EBV therapy

status: Public on Feb 11 2020

city: Nizhny Novgorod

first: Dmitry

last: Knyazev

address: Malaya Yamskaya, 71

country: Russia

institute: I.N. Blokhina Nizhny Novgorod Research Institute of Epidemiology and Microbiology

summary: Refer to the SuperSeries

overall_design: The splicing-sensitive microarray covers 450 genes including 12 EBV genes, each microarray encompasses 4 identical probe-containing areas. Blood samples from 6 EBV patients in acute phase of infection, 5 EBV patients after convalescence and 17 age-matched healthy donors were included in the experiment.

first: Nikolay

last: Sakharnov

first: Elena

last: Filatova

first: Leonid

last: Solntsev

first: Oleg

last: Utkin


title: Transcriptional profiling of germ-free and conventionalized mouse liver

city: Atlanta

first: Bejan

last: Saeedi

state: GA

address: 615 Michaels St

department: Pathology

institute: Emory University

summary: The microbiome has been shown to have significant effects on susceptibility to liver disease. How the microbiome affects hepatic signaling pathways to mechanistically mediate these responses is unknown. Utilizing germ-free and conventionalized (microbiome-replete) mice, we characterized the effects of having a microbiome on the hepatic transcriptome.

overall_design: Germ-free C57BL/6 mouse littermates were separated at weaning (approx. 21 days). Half were maintained in sterile isolators, the other half were moved out of the isolators and housed in cages containing dirty bedding derived from elsewhere in the animal facility. After 3 weeks, the mice were sacrificed and liver was harvested and utilized for RNAsequencing by Illumina HiSeq 3000 system. 3 male and 3 female mice were analyzed for each condition (a total of 12 mice).

middle: J

first: Andrew

middle: S

last: Neish


title: Infection of SC-beta cells with coxsackievirus B4 (CVB)

city: Worcester

first: Pranitha

last: Vangala

state: MA

address: 55 Lake Avenue North

institute: University of Massachussets Medical School

summary: SC-beta cells were infected with CVB and collected over a time course.

overall_design: Cells were infected with virus at a multiplicity of infection of 10 (or were mock-infected) and collected at 24, 48, and 72 hours for total RNA. RNA-Seq libraries were prepared using SMART-Seq. Pooled libraries were sequenced for 2 x 75 cycles to obtain paired end reads using a NextSeq 500 (Illumina).

first: Jennifer

last: Wang


title: Determining transcriptome changes in whole spinal cord of GarsdelETAQ/+ adult onset mice [18-burgess-006]

city: Bar Harbor

first: Abigail

last: Tadenev

state: ME

address: 600 Main St

institute: The Jackson Laboratory

summary:
To determine transcriptome changes in spinal cord induced by the GarsdelETAQ mutation.
How mutations in broadly expressed housekeeping genes lead to neurodegeneration in specific cell types remains unclear. Mutations in ubiquitously expressed tRNA synthetase genes cause axonal peripheral neuropathy, accounting for at least six forms of Charcot-Marie-Tooth disease. Genetic evidence in mouse and Drosophila models suggests a neomorphic gain-of-function mechanism. Here, we use in vivo, cell-type-specific transcriptional and translational profiling of affected peripheral neurons to show that mutant tRNA synthetases impair translation and activate the integrated stress response (ISR) through the sensor kinase, GCN2. The chronic activation of the ISR contributes to the pathophysiology, and genetic deletion of Gcn2 alleviates the peripheral neuropathy. The activation of GCN2 by tRNA synthetase mutations indicates their neomorphic activity is still related to translation and suggests inhibiting GCN2 or the ISR as a therapeutic strategy.

overall_design: Whole spinal cord RNA sequencing was performed on WT and GarsdelETAQ 8 week-old mice and differential expression analysis was run.

first: Emily

middle: L

last: Spaulding

first: Robert

middle: W

last: Burgess


title: Determining transcriptome changes in whole spinal cord of YarsE196K mice [19-burgess-002]

summary:
To determine transcriptome changes in adult spinal cord induced by the YarsE196K mutation.
How mutations in broadly expressed housekeeping genes lead to neurodegeneration in specific cell types remains unclear. Mutations in ubiquitously expressed tRNA synthetase genes cause axonal peripheral neuropathy, accounting for at least six forms of Charcot-Marie-Tooth disease. Genetic evidence in mouse and Drosophila models suggests a neomorphic gain-of-function mechanism. Here, we use in vivo, cell-type-specific transcriptional and translational profiling of affected peripheral neurons to show that mutant tRNA synthetases impair translation and activate the integrated stress response (ISR) through the sensor kinase, GCN2. The chronic activation of the ISR contributes to the pathophysiology, and genetic deletion of Gcn2 alleviates the peripheral neuropathy. The activation of GCN2 by tRNA synthetase mutations indicates their neomorphic activity is still related to translation and suggests inhibiting GCN2 or the ISR as a therapeutic strategy.

overall_design: Whole spinal cord RNA sequencing was performed on WT, YarsE196K heterozygous, and YarsE196K homozygous 7 month-old mice and differential expression analysis was run.


title: Determining transcriptome changes in whole spinal cord of GarsP278KY/+ pre-disease onset mice [18-burgess-001]

summary:
To determine transcriptome changes in pre-disease onset spinal cord induced by the GarsP278KY mutation.
How mutations in broadly expressed housekeeping genes lead to neurodegeneration in specific cell types remains unclear. Mutations in ubiquitously expressed tRNA synthetase genes cause axonal peripheral neuropathy, accounting for at least six forms of Charcot-Marie-Tooth disease. Genetic evidence in mouse and Drosophila models suggests a neomorphic gain-of-function mechanism. Here, we use in vivo, cell-type-specific transcriptional and translational profiling of affected peripheral neurons to show that mutant tRNA synthetases impair translation and activate the integrated stress response (ISR) through the sensor kinase, GCN2. The chronic activation of the ISR contributes to the pathophysiology, and genetic deletion of Gcn2 alleviates the peripheral neuropathy. The activation of GCN2 by tRNA synthetase mutations indicates their neomorphic activity is still related to translation and suggests inhibiting GCN2 or the ISR as a therapeutic strategy.

overall_design: Whole spinal cord RNA sequencing was performed on WT and GarsP278KY 1 week-old mice and differential expression analysis was run.


title: Determining ribosome-associated mRNA in motor neurons in pre-disease onset GarsC201R mice

summary:
To determine transcriptome changes in pre-disease onset motor neurons induced by the GarsC201R mutation.
How mutations in broadly expressed housekeeping genes lead to neurodegeneration in specific cell types remains unclear. Mutations in ubiquitously expressed tRNA synthetase genes cause axonal peripheral neuropathy, accounting for at least six forms of Charcot-Marie-Tooth disease. Genetic evidence in mouse and Drosophila models suggests a neomorphic gain-of-function mechanism. Here, we use in vivo, cell-type-specific transcriptional and translational profiling of affected peripheral neurons to show that mutant tRNA synthetases impair translation and activate the integrated stress response (ISR) through the sensor kinase, GCN2. The chronic activation of the ISR contributes to the pathophysiology, and genetic deletion of Gcn2 alleviates the peripheral neuropathy. The activation of GCN2 by tRNA synthetase mutations indicates their neomorphic activity is still related to translation and suggests inhibiting GCN2 or the ISR as a therapeutic strategy.

overall_design: RiboTagging was performed on spinal cords from 2 week old HARPL22;ChAT-Cre;Gars+/+ or GarsC201R/+ and corresponding negative controls (no Cre) and differential expression analyis was run.


title: RT2 PCR Assay profiling analysis of lncRNAs expression in colon cancer cells

city: Shenyang

first: Yong

last: Zhou

state: Liaoning

address: 4 Chongshan Road

institute: the Fourth Affiliated Hospital of China Medical University

summary:
An increasing number of studies have shown that long noncoding RNA (lncRNA) dysregulation plays an important role in development of various cancers, including colon cancer. Nonetheless, the potential mechanisms of lncRNA in regorafenib-resistance remain unclear. Our research revealed the lncRNA AC069513.3 (MIR570MG) increased in regorafenib-resistant colon cancer cells compared to the regorafenib-sensitive cells. Furthermore, lncRNA AC069513.3 (MIR570MG) sponged miR-145, which declined in regorafenib-resistant colon cancer cell lines. More importantly, overexpression of miR-145 hampered cell proliferation and retrieved colon cancer regorafenib-sensitivity, contrary to the function of lncRNA AC069513.3 (MIR570MG). Dual luciferase reporter assay confirmed that miR-145 bound to 3’-UTR of SMAD3, a transcriptional modulator activated by TGFβ, resulting in blockage of TGFβ /SMAD3-mediated cell growth and cycle progression. Furthermore, ectopic expression of miR-145 inhibitor in the parental cells endowed resistance to regorafenib. Conversely, knockdown of AC069513.3 (MIR570MG) impoverished resistance against regorafenib. In summary, our findings suggested that lncRNA AC069513.3 (MIR570MG) promoted regorafenib resistance via releasing SMAD3 from miR-145, leading to activation of SMAD3-mediated signaling pathways.
Long noncoding RNA  profiling by RT-PCR

overall_design: Three SW480 clones and three SW480 regorafenib-resistant clones were collected in the present study. RT-PCR based LncRNA expression profiles were obtained with Qiagen custom RT2 PCR Arrays.


title: Determining transcriptome changes in whole spinal cord of GarsC201R/+ adult mice [17-burgess-001]

summary:
To determine transcriptome changes in adult spinal cord induced by the GarsC201R mutation.
How mutations in broadly expressed housekeeping genes lead to neurodegeneration in specific cell types remains unclear. Mutations in ubiquitously expressed tRNA synthetase genes cause axonal peripheral neuropathy, accounting for at least six forms of Charcot-Marie-Tooth disease. Genetic evidence in mouse and Drosophila models suggests a neomorphic gain-of-function mechanism. Here, we use in vivo, cell-type-specific transcriptional and translational profiling of affected peripheral neurons to show that mutant tRNA synthetases impair translation and activate the integrated stress response (ISR) through the sensor kinase, GCN2. The chronic activation of the ISR contributes to the pathophysiology, and genetic deletion of Gcn2 alleviates the peripheral neuropathy. The activation of GCN2 by tRNA synthetase mutations indicates their neomorphic activity is still related to translation and suggests inhibiting GCN2 or the ISR as a therapeutic strategy.

overall_design: Whole spinal cord RNA sequencing was performed on WT and GarsC201R 8 week-old mice and differential expression analysis was run.


title: Determining ribosome-associated mRNA in motor neurons in adult GarsP278KY/+ mice [17-burgess-004]

summary:
To determine transcriptome changes in motor neurons induced by the GarsP278KY mutation.
How mutations in broadly expressed housekeeping genes lead to neurodegeneration in specific cell types remains unclear. Mutations in ubiquitously expressed tRNA synthetase genes cause axonal peripheral neuropathy, accounting for at least six forms of Charcot-Marie-Tooth disease. Genetic evidence in mouse and Drosophila models suggests a neomorphic gain-of-function mechanism. Here, we use in vivo, cell-type-specific transcriptional and translational profiling of affected peripheral neurons to show that mutant tRNA synthetases impair translation and activate the integrated stress response (ISR) through the sensor kinase, GCN2. The chronic activation of the ISR contributes to the pathophysiology, and genetic deletion of Gcn2 alleviates the peripheral neuropathy. The activation of GCN2 by tRNA synthetase mutations indicates their neomorphic activity is still related to translation and suggests inhibiting GCN2 or the ISR as a therapeutic strategy.

overall_design: RiboTagging was performed on spinal cords from HARPL22;ChAT-Cre;Gars+/+ or GarsP278KY/+ and corresponding negative controls (no Cre) and differential expression analyis was run.


title: Determining ribosome-associated mRNA in motor neurons in adult GarsC201R/+ mice [16NGS-002-burgess]

summary:
To determine transcriptome changes in motor neurons induced by the GarsC201R mutation.
How mutations in broadly expressed housekeeping genes lead to neurodegeneration in specific cell types remains unclear. Mutations in ubiquitously expressed tRNA synthetase genes cause axonal peripheral neuropathy, accounting for at least six forms of Charcot-Marie-Tooth disease. Genetic evidence in mouse and Drosophila models suggests a neomorphic gain-of-function mechanism. Here, we use in vivo, cell-type-specific transcriptional and translational profiling of affected peripheral neurons to show that mutant tRNA synthetases impair translation and activate the integrated stress response (ISR) through the sensor kinase, GCN2. The chronic activation of the ISR contributes to the pathophysiology, and genetic deletion of Gcn2 alleviates the peripheral neuropathy. The activation of GCN2 by tRNA synthetase mutations indicates their neomorphic activity is still related to translation and suggests inhibiting GCN2 or the ISR as a therapeutic strategy.

overall_design: RiboTagging was performed on spinal cords from HARPL22;ChAT-Cre;Gars+/+ or GarsC201R/+ and corresponding negative controls (no Cre) and differential expression analyis was run.


title: Determining ribosome-associated mRNA in motor neurons after nerve crush [15NGS-001-rwb]

summary:
Determining ribosome-associated mRNA in motor neurons of wild-type adult mice 4 days after unilateral sciatic nerve crush
How mutations in broadly expressed housekeeping genes lead to neurodegeneration in specific cell types remains unclear. Mutations in ubiquitously expressed tRNA synthetase genes cause axonal peripheral neuropathy, accounting for at least six forms of Charcot-Marie-Tooth disease. Genetic evidence in mouse and Drosophila models suggests a neomorphic gain-of-function mechanism. Here, we use in vivo, cell-type-specific transcriptional and translational profiling of affected peripheral neurons to show that mutant tRNA synthetases impair translation and activate the integrated stress response (ISR) through the sensor kinase, GCN2. The chronic activation of the ISR contributes to the pathophysiology, and genetic deletion of Gcn2 alleviates the peripheral neuropathy. The activation of GCN2 by tRNA synthetase mutations indicates their neomorphic activity is still related to translation and suggests inhibiting GCN2 or the ISR as a therapeutic strategy.

overall_design: RiboTagging was performed on spinal cords from HARPL22;ChAT-Cre;Gars+/+ crushed or uncrushed and corresponding negative controls (no Cre) and differential expression analyis was run.


title: Determining transcriptome changes in whole spinal cord of GarsP278KY/+ adult mice [16NGS-003-burgess]

summary:
To determine transcriptome changes in adult spinal cord induced by the GarsP278KY mutation.
How mutations in broadly expressed housekeeping genes lead to neurodegeneration in specific cell types remains unclear. Mutations in ubiquitously expressed tRNA synthetase genes cause axonal peripheral neuropathy, accounting for at least six forms of Charcot-Marie-Tooth disease. Genetic evidence in mouse and Drosophila models suggests a neomorphic gain-of-function mechanism. Here, we use in vivo, cell-type-specific transcriptional and translational profiling of affected peripheral neurons to show that mutant tRNA synthetases impair translation and activate the integrated stress response (ISR) through the sensor kinase, GCN2. The chronic activation of the ISR contributes to the pathophysiology, and genetic deletion of Gcn2 alleviates the peripheral neuropathy. The activation of GCN2 by tRNA synthetase mutations indicates their neomorphic activity is still related to translation and suggests inhibiting GCN2 or the ISR as a therapeutic strategy.

overall_design: Whole spinal cord RNA sequencing was performed on WT and GarsP278KY 8 week-old mice and differential expression analysis was run.


title: Mutations in tRNA synthetases impair translation and activate the integrated stress response in inherited peripheral neuropathie

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

overall_design: Refer to individual Series


title: 450K analysis of pediatric histiocytic sarcomas and anteceding hematologic malignancies

city: Heidelberg

first: Pascal

middle: David

last: Johann

address: Im Neuenheimer Feld 580

department: Pediatric Neurooncology

institute: German Cancer Research Center

summary: The dataset contains 450K array data on 3 cases of histiocytc sarcomas and corresponding leukemias

overall_design: Histiocytic sarcoma and leukemia of the same patient

first: Matthias

last: Bleeke


title: Dissociating fibrosis from inflammation in systemic sclerosis – the case of interleukin-17A

city: Geneva

first: Sylvain

last: LEMEILLE

address: 1 rue Michel-Servet

department: Department of Pathology and Immunology

country: Switzerland

institute: University of Geneva Medical School

summary:
Objectives. Interleukin-17A (IL-17A) levels are increased in SSc skin and other organs but its role in fibrosis development is highly debated. Since epithelial cells are preferential targets of IL-17A, we aimed at investigating the role of IL-17A in the interactions between epidermis and dermis.
Methods. Organotypic cultures of HD full human skin were challenged with IL-17A,TNF and TGF-β. Inflammatory mediators and type I collagen (col-I) levels were quantified. IL-17A- and TGF-β-induced changes in gene expression in full human skin were analysed by RNA sequencing.
Results.  In full human skin, TGF-β induced pro-fibrotic gene signature dominated by Wnt signalling. While IL-17A strongly promoted expression of many pro-inflammatory genes, it did not affect collagen gene levels but decreased Wnt signalling. At the protein level, IL-17A showed direct anti-fibrotic effects, as well as decreased by 2-fold TGF-β-triggered col-I production.
Conclusions. We report here firstly, a novel model of fibrotic skin and secondly, that IL-17A acts as a potent anti-fibrotic factor in the full human skin. Furthermore, we show that IL-17A not only decreased ECM deposition by itself, but also counteracted TGF-β pro-fibrotic activities. Thus, IL-17A seems to play a dual role in SSc skin – strongly pro-inflammatory but anti-fibrotic, being an example that fibrosis and inflammation, although closely related, are two different processes. These data may help in directing and interpreting therapeutic approaches in SSc, since both, IL-17A and TGF-β, are target candidates in clinical trials.

overall_design: mRNA profiles of IL-17A, TNF and/or TGF-β- treated skin were generated by deep sequencing, in triplicate, using Illumina HiSeq 4000 sequencer.

first: Aleksandra

last: Dufour

first: Carlo

last: Chizzolini


title: c-Maf restrains T-bet-driven programming of CCR6-negative group 3 innate lymphoid cells

city: Berlin

first: Pawel

last: Durek

address: Charitéplatz 1

institute: Deutsches Rheuma-Forschungszentrum

summary: We performed RNA-Seq analysis of small intestinal lamina propria ILC3s of Rorc.Cre Maf.flox and Maf.flox control mice.

overall_design: NKp46+ CCR6- and NKp46- CCR6+ ILC3s were isolated from the small intestinal lamina propria of Rorc.Cre Maf.flox and Maf.flox control mice and subjected to RNA-Seq.

first: Caroline

last: Tizian

first: Annette

last: Lahmann

first: Oliver

last: Hölsken

first: Michael

last: Kofoed-Branzk

first: Frederik

last: Heinrich

first: Mir-Farzin

last: Mashreghi

first: Andrey

last: Kruglov

first: Andreas

last: Diefenbach

first: Christian

last: Neumann


title: Determining transcriptome changes in whole spinal cord of Gcn2-/-;GarsP278KY/+ adult mice [18-burgess-011]

first: Abigail

last: Tadenev

summary:
To determine transcriptome changes in adult spinal cord induced by the combined effect of having the GarsP278KY mutation while lacking GCN2 kinase .
How mutations in broadly expressed housekeeping genes lead to neurodegeneration in specific cell types remains unclear. Mutations in ubiquitously expressed tRNA synthetase genes cause axonal peripheral neuropathy, accounting for at least six forms of Charcot-Marie-Tooth disease. Genetic evidence in mouse and Drosophila models suggests a neomorphic gain-of-function mechanism. Here, we use in vivo, cell-type-specific transcriptional and translational profiling of affected peripheral neurons to show that mutant tRNA synthetases impair translation and activate the integrated stress response (ISR) through the sensor kinase, GCN2. The chronic activation of the ISR contributes to the pathophysiology, and genetic deletion of Gcn2 alleviates the peripheral neuropathy. The activation of GCN2 by tRNA synthetase mutations indicates their neomorphic activity is still related to translation and suggests inhibiting GCN2 or the ISR as a therapeutic strategy.

overall_design: Whole spinal cord RNA sequencing was performed on (1)Gcn2+/+;Gars+/+, (2)Gcn2-/-;Gars+/+, (3)Gcn2+/+;GarsP278KY/+, and (4)Gcn2-/-;GarsP278KY/+ 8 week-old mice and differential expression analysis was run.

first: Emily

last: Spaulding

first: Robert

last: Burgess


title: Symmetric arginine dimethylation is selectively required for mRNA splicing and the initiation of type I and type III interferon signaling

city: San Diego

first: Patrick

last: Metz

address: 10777 Science Center Dr.

institute: Pfizer, Oncology Research, Development, & Medical

summary: The goal of this study was to assess the extent of symmetric arginine dimethylation-dependent splicing and its associated signaling outcomes by using human T lymphocyte activation as a model system with a high rate of de novo transcription. Naïve human T lymphocytes were activated and treated with a selective inhibitor of PRMT5, PF-06829927, and investigated for changes in gene expression, alternative splicing, and chromatin accessibility.

overall_design: Human naïve CD3+ (ATAC), CD4+ or CD8+ (expression and splicing) T lymphocytes were activated for 72 (expression and splicing) or 96 (ATAC) hours with platebound anti-CD3, anti-CD28, IL-2, and either DMSO or PF-06829927

first: Keith

last: Ching

first: Tao

last: Xie


title: Sox2-dependent fibronectin fibrillogenesis controls directional collective migration  of Schwann cells

city: Neuherberg

first: Dietrich

last: Trümbach

address: Ingolstädter Landstraße 1

department: Institute for Developmental Genetics

institute: Helmholtz Zentrum München German Research Center for Environmental Health

summary: The extracellular matrix is essential for tissue formation and regeneration through the control of cellular behavior. Deregulation of extracellular matrix components is associated to disease, including neurodegeneration. After peripheral nerve injury, Schwann cells guide regrowing axons to their targets. These glial cells migrate collectively and provide an extracellular environment to enable neural repair. How this occurs remains poorly understood. Here, we show that Sox2 controls fibronectin fibrillogenesis in Schwann cells to provide a highly oriented extracellular matrix, which supports their rapid collective migration with a continuous cellular flow. Sox2 directly activates fibronectin expression in Schwann cells, leading to an increase in fibrillogenesis and cellular huddling. Accordingly, loss of fibrillogenesis leads to glial disassembly and disorganized axon regrowth. In vivo, 7 days post nerve injury, we found that pro-regenerative Schwann cells co-express Sox2 and the EIIIA-containing fibronectin splicing isoform. This mechanism is conserved in mammals, including humans, but absent in zebrafish. Taken together, our results demonstrate that Sox2 directly controls fibrillogenesis and provide a novel mechanism for the modification of the environmental architecture by glial cells during neuronal repair.

overall_design: To identify Sox2 target genes and pathways with a focus on extracellular matrix (ECM) we measured expression arrays of two different clones of Sox2-positive Schwann cells (i.e. three replicates of RSC96_Sox2+ cells for each clone) and control cells (i.e. three replicates of RSC96 cells)

first: Elen

middle: T

last: Mejia

first: Charlotte

last: Keeberger

first: Ulf

last: Dornseifer

first: Tanja

last: Orschmann

first: Jara

last: Brenke

first: Kamyar

last: Hadian

first: Wolfgang

last: Wurst

first: Hernan

last: Lopez-Schier

first: Sabrina

last: Desbordes


title: Shoot-to-root mobile CEPD-like 2 integrates shoot nitrogen status to systemically regulate nitrate uptake in Arabidopsis

status: Public on Feb 10 2020

city: Nagoya

first: Yoshikatsu

last: Matsubayashi

state: Aichi

address: Chikusa

department: Graduate School of Science

institute: Nagoya University

summary: Plants modulate the efficiency of root nitrogen (N) acquisition in response to shoot N demand. However, molecular components directly involved in this shoot-to-root communication remain to be identified. Here, we show that phloem-mobile CEPD-like 2 (CEPDL2) polypeptide is upregulated in the leaf vasculature in response to decreased shoot N status and, after translocation to the roots, promotes high-affinity uptake and root-to-shoot transport of nitrate by activating nitrate transporter genes such as NRT2.1, NRT3.1 and NRT1.5. Loss of CEPDL2 decreases nitrate uptake and root-to-shoot transport activity in roots, leading to a reduction in shoot nitrate content and plant biomass. CEPDL2 contributes to N acquisition cooperatively with CEPD1 and CEPD2 that mediate root N status, and their complete loss severely impairs N homeostasis in plants. Reciprocal grafting analysis provided conclusive evidence that the shoot CEPDL2/CEPD genotype defines the root high-affinity uptake activity of nitrate. Our results indicate that plants integrate shoot N status and root N status in leaves and systemically regulate the efficiency of root N acquisition.

overall_design: Genome wide transcriptome analysis of roots of WT and CEPDL2ox plants grown under 10 mM nitrate condition

first: Ryosuke

last: Ota

first: Yuri

last: Ohkubo

first: Yasuko

last: Yamashita

first: Mari

last: Ogawa-Ohnishi


title: Genome-wide analysis reveals a switch in the translational program upon oocyte meiotic resumption

city: San Francisco

first: Xuan

last: Luong

address: 505 Parnassus Ave

institute: UCSF

summary: Examination of ribosome-bound mRNA at five timepoints (in duplicates) during oocyte meiosis (prophase I (0 hrs), early pro-metaphase I (2 hrs), pro-metaphase I (4 hrs), late pro-metaphase I (6 hrs), and late metaphase I (8 hrs)).

overall_design: Mouse oocytes were isolated and cultured in vitro. 200 oocytes were collected at various time points during meiotic resumption (prophase I (0 hrs), early pro-metaphase I (2 hrs), mid pro-metaphase I (4 hrs), late pro-metaphase I (6 hrs), metaphase I (8 hrs)). RiboTag-IP was performed and ribosome-bound mRNA was extracted along with total RNA. cDNA libraries were constructed and RNA-Seq was performed. Experiment was performed in duplicates.

middle: G

first: Enrico Maria

last: Daldello

first: Marco

last: Conti


title: Transcriptome analysis of CHI3L1 knockdown NP cells

city: Shanghai

first: Chen

last: Xu

address: No, 800, Rd. Xiangyin

institute: The Second Military Medical University

summary: Intervertebral disc degeneration is the main cause of low back pain and the mechanism of which is far from fully revealed. Although multiple factors are related to the intervertebral disc degeneration, inflammation and matrix metabolism dysregulation are the two key factors that play an important role in degeneration. Here, we found that inflammation-related factor CHI3L1 is highly regulated in the nucleus pulposus during degeneration in both RNA and protein level. Immunohistochemical analysis show that the expression of CHI3L1 are NP tissue specific, and increased significantly in the degenerated nucleus pulposus cells. The mechanism of CHI3L1 is thus studied in this experiment.

overall_design: MRNA profiles were done using primary culture cells of normal human intervertebral disc nucleus pulposus (NP) tissue. Each sample were treated with IL-1b, TNF-a, IL-1b+CHI3L1 (100ug/ml) or TNF-a+CHI3L1 (100ug/ml) for 48h.

first: Ruizhe

last: Wang

first: Wen

last: Yuan


title: Expression data from glioma cells

city: Tianjin

first: Rong

last: Fan

address: 1st Huizhihuan Road

institute: Logistic University of Chinese People’s Armed Police Force

summary:
As a member of the polycomb group, PCGF1 play a vital role in  the development of embryo nervus system. But our recent studies suggested PCGF1 may involved in the development, progression and relapse of glioma.
We used microarrays to detail the different expression of gene following the knockdown of PCGF1 expression in U87 cells.

overall_design: The expression of PCGF1 gene was knockdown in U87 cells for RNA extraction and hybridization on Affymetrix microarrays. Then we screen and analyze the differential expression genes between PCGF1 knockdown U87 cells and negative control U87 cells.

first: Rui

last: Yan


title: The RNA N6-methyladenosine regulates chromatin remodeling and transcription [HEC-1-A_seq_RNA_nascent]

first: Xiaoyang

last: Dou

address: 320 Yue Yang Road

institute: CAS Center for Excellence in Molecular Cell Science, CAS

summary: The N6-methyladenosine (m6A) has been shown to regulate stability and translation of messenger RNA (mRNA) in various biological processes. Here, we show that the knockout of the m6A writer Mettl3 or a nuclear reader Ythdc1 in mouse embryonic stem cells (mESCs) induces chromatin openness and transcription activation in an m6A-dependent manner. We identified extensive m6A modifications on caRNAs (chromosome-associated RNAs, including promoter-associated RNAs, enhancer RNAs and repeats) that are installed by METTL3. YTHDC1 can bind to a portion of these m6A-modified RNAs and facilitate their decay through the NEXT-mediated nuclear degradation. Therefore, the m6A methylation of these caRNAs reduces their abundances. The knockout of Mettl3 elevates levels of caRNAs and promote open chromatin state and downstream transcription. Collectively, our results reveal that m6A on caRNAs can globally tune chromatin state and transcription.

overall_design: Examine transcription rate in control and METTL3 knockdown HEC-1-A cells

first: Jun

last: Liu

first: Chuan

last: He


title: The RNA N6-methyladenosine regulates chromatin remodeling and transcription [HEC-1-A_seq_ChIP_histone]

overall_design: Examination of H3K27ac and H3K4me3 modifications in two HEC-1-A stable cell lines


title: Transcriptome analysis of human pancreatic cancer cell lines and gemcitabine-resistant pancreatic cancer cell lines

city: Hangzhou

first: Jiarong

last: Zhou

state: Zhejiang

address: No. 88 Jiefang Road

department: Department of Hepatobiliary and Pancreatic Surgery

institute: The Second Affiliated Hospital, Zhejiang University School of Medicine

summary: Gemcitabine (GEM) alone and GEM-based chemotherapy are the preferred regimens for treating advanced unresectable and metastatic pancreatic cancer (PC). However, these treatments have limited efficacy due to acquired resistance of cancer cells to chemotherapy, the mechanisms of which are not fully understood. In this study, we established two GEM-resistant cell lines (BxPC-3-GR and CFPAC-1-GR) and compared the expression profiles of mRNAs between parental (BxPC-3 and CFPAC-1) and GEM-resistant cells by high-throughput RNA sequencing, and to identify potential targets for GEM response in PC patients.

overall_design: Examing 4 conditions, each with 3 replicates

first: Linshi

last: Zhang


title: Tumor-promoting functions of UHRF1 in retinoblastoma

city: Guangzhou

first: Chunsik

last: Lee

state: Guangdong

address: NO.7 Jinsui Rd.

institute: Sun Yat-Sen University

summary: UHRF1 (ubiquitin-like with PHD and ring finger domains 1) is an epigenetic regulator that is involved in the regulation of DNA and histone methylation and many other cellular events. The UHRF1 is frequently found to be overexpressed in various human cancers including retinoblastoma, and its overexpression has been associated with tumor-promoting effects such as inhibition of apoptosis and high metastatic potential. However, the detailed mechanisms underlying these tumor-promoting functions of UHRF1 in retinoblastoma still remain unclear. In this study, we uncovered that UHRF1 depletion in retinoblastoma cells sensitizes the cells to histone deacetylase (HDAC) inhibitors, augmenting apoptotic cell death. To understand the molecular mechanisms underlying the enhanced sensitivity to HDAC inhibitors in the UHRF1-depleted retinoblastoma cells, we performed the gene expression profiling in UHRF1-knockdown Y79 cells in comparison with control-knockdown cells by RNA-sequencing to identify differentially expressed genes. Our RNA-seq results revealed that UHRF1 depletion downregulates redox-responsive genes such as GSTA4 and TXN2, leading to increased intracellular oxidative stress and higher susceptibility to HDAC inhibitor treatment.

overall_design: Gene expression profiling of control-knockdown (YT) and UHRF1-knockdown (YS) Y79 retinoblastoma cell line by RNA-seq; Identification of differentially expressed genes between control and UHRF-knockdown Y79 cells using two independent biological replicates

first: JongKyong

last: Kim


title: Goto-Kakizaki rats with Roux-en-Y gastric bypass surgery

first: Meiyi

last: Li

address: No.320 Yueyang Road

institute: Institute of Biochemistry and Cell Biology

summary:
Metabolic surgery has been increasingly recommended for obese diabetic patients, but questions remain as to its effectiveness for nonobese diabetic patients and its mechanism that leads to glucose homeostasis independently of weight loss.
Roux-en-Y gastric bypass (RYGB), as one of the most effective metabolic operations, excludes a portion of stomach with the proximal intestine (biliopancreatic limb, BL) and rearranges the distal end of the intestine into a Y-configuration, in which food can flow from the upper stomach pouch through the Roux limb (RL). To address the above questions to RYGB surgery,  we designed a series of surgical procedures in Goto-Kakizaki （GK） rats to assess the relationship between glycemic control independent of weight loss and RL length in the RYGB procedure and studied the molecular mechanism of the RL from a systematic and comprehensive view.

overall_design: In total, 10 male 16-wk-old GK rats were randomly grouped to take RYGB surgery or sham surgery. After 14 wk postoperation, all GK rats and 5 Wistar rats under the same feeding condition were sacrificed for measuring whole-genome expression.

first: Zhiyuan

first: Bangguo

last: Qian

first: Weixin

first: Katsuhisa

last: Horimoto

first: Huarong

first: Luonan

last: Chen


title: Transcriptomic profile of amiR-bpm and Col-0

status: Public on Feb 09 2020

city: Madrid

first: Jose M.

last: Franco-Zorrilla

state: Madrid

address: Darwin, 3

department: Plant Molecular Genetics

country: Spain

institute: Centro Nacinal de Biotecnologia-CSIC

summary: The Jasmonate pathway regulators MYC2, MYC3 and MYC4 are central nodes in plant signaling networks integrating environmental and developmental signals to fine-tune jasmonate defenses and plant growth. Hence, their activity needs to be tightly regulated in order to optimize plant fitness. Among the increasing number of mechanisms regulating MYCs activity, protein stability is arising as a major player. However, how the levels of MYCs proteins are modulated is still poorly understood. Here, we report that MYC2, MYC3 and MYC4 are targets of BPM proteins, which act as substrate adaptors of CUL3-based E3 ubiquitin ligases. Reduction-of-function of CUL3BPM in amiR-bpm lines, bpm235 triple mutants and cul3ab double mutants enhances MYC2 and MYC3 stability and accumulation, and potentiates plant responses to JA such as root-growth inhibition, and MYC-regulated gene expression. BPM3 protein is stabilized by JA, suggesting a new negative feed-back regulatory mechanism to control MYCs activity. Our results uncover a new layer for JA-pathway regulation by CUL3BPM–mediated degradation of MYC TFs.

overall_design: Comparison of gene expression of amiR-bpm versus Col-0

first: Jose

last: Chico

first: Gemma

last: Fernandez-Barbero

first: Gloria

last: García-Casado

first: Roberto

last: Solano


title: The RNA N6-methyladenosine regulates chromatin remodeling and transcription [HEC-1-A_seq_RNA_nuclear]

first: Xiaoyang

overall_design: Examine gene expression in control and METTL3 knockdown HEC-1-A cells

first: Jun

first: Chuan


title: RNA-binding protein IGF2BP1 maintains leukemia stem cell properties by regulating HOXB4, MYB, and ALDH1A1.

city: Hershey

first: Irina

last: Elcheva

state: PA

address: 500 Univeristy Drive

institute: PennState College of Medicine

summary: • IGF2BP1 promotes leukemia stem cell phenotype by regulating HOXB4, MYB and ALDH1A1.• Inhibition of IGF2BP1 reduces leukemia tumorigenicity, and enhances leukemia cell death and differentiation.

overall_design: RNA sequencing analysis of 697 (EU3) ALDH+ subpopulations with and without IGF2BP1 knockdown was performed from four biological replicates (n=4). Each biological replicate represents de novo selection of ALDH+ cells and independent doxycycline treatments.

first: Vladimir

last: Spiegelman

first: Zhenqiu

first: Yuka

last: Imamura


title: Transcriptional signature of human mesoangioblasts from different fetal tissues.

first: Sylvain

last: LEMEILLE

summary:
Purpose: We performed comparative transcriptome analysis of mesoangioblasts (MABs) derived from different cardiovascular or skeletal muscle tissues  to determine possible gene signatures underlying their specific differentation capacities and define future appropriate cell therapy applications.
Methods: RNA was extracted from human fetal mesoangioblasts  derived from Aorta, Atrium, Ventricle and Skeletal muscle (Ao, A, V and Sk) in proliferative conditions.  Deep sequencing was used to determine quantitative gene expression between the different cell populations.
Results: MABs derived from different tissues show differences in their transcriptome profile, despite their common ebryologic origin and isolation using common caracterization markers.  The expression by Sk MABs of key cardiogenic genes (i.e. Isl1, TBX2) and the identification of active signaling pathways will serve for future skeletal to cardiac differentiation protocols.
Conclusion: Cardiogenic Sk MABs may thus represent a easily accessible cell source for cardiac regeneration.

overall_design: Mesoangioblast mRNA profiles were determined by deep sequencing using 8 independent cell lines of human fetal origin.

first: Flavio

last: Ronzoni

last: Lemeille

first: Rostyslav

last: Kuziakiv

first: Maurilio

last: Sampaolesi

first: Marisa

last: Jaconi


title: The RNA N6-methyladenosine regulates chromatin remodeling and transcription [HEC-1-A_seq_RNA_MeRIP]

last: Dou

type: Methylation profiling by high throughput sequencing

overall_design: chromatin-associated RNA m6A profiles of METTL3 knockdown HEC-1-A and its control  were generated by deep sequencing, in diplicate, using Illumina NovaSeq.

last: Liu

last: He


title: Role of the mRNA-binding protein HuR in the global transcriptomic status of cells stimulated with electrophiles and oxidants

city: Boston

first: Jesse

last: Poganik

address: 77 Avenue Louis Pasteur

department: Medicine/Genetics

institute: Brigham and Women's Hospital, Harvard Medical School

summary: HuR has been implicated as a stress-responsive protein: cytoplasmic translocation of HuR is promoted by several small-molecule stressors, e.g., H2O2, arsenite, and the cyclopentenone prostaglandin A2 (PGA2), a Michael acceptor RES (Wang et al., 2000; Yang et al., 2004). Treatment with PGA2 also increases the affinity of HuR for p21 mRNA (Wang et al., 2000). Intrigued by these reports, we launched HuR-dependent gene-expression profiling studies in the presence and absence of small-molecule stress signals. HNE—a native RES with a reactive core chemically similar to that of PGA2—was selected as a representative bioactive RES (Jacobs and Marnett, 2009; Schopfer et al., 2011) and H2O2 was selected as a representative ROS. shHuR and shControl HEK293T cells were first generated and then treated with HNE or H2O2 under the conditions where cell viability is largely unaffected. We subsequently sequenced their RNA post ribosomal RNA (rRNA) depletion (see details below). Significant differential expression was evaluated with CuffDiff (Trapnell et al., 2013).

overall_design: 12 samples were analyzed (see below). Two biological replicates were included per cell line/treatment condition. Negative controls: shControl cell line; non-treated cells

middle: R

first: Marcus

last: Long

first: Michael

last: Disare

first: Xuyu

first: Sung-Hee

last: Chang

first: Timothy

last: Hla

first: Yimon

last: Aye


title: Epigenome analysis of placental DNA methylation and added sugar intake during pregnancy

city: New York

first: Seonjoo

last: Lee

address: 1051 Riverside Drive Unit 48

department: Psychiatry and Biostatistics

institute: NYSPI/Columbia University

summary: Genome wide DNA methylation profiling of placenta at birth. A 1 cm3 sample of the placenta was collected (using scissor, midway between the umbilical cord and the outer edge of the placenta) and genomic DNA was extracted. DNA integrity was assessed by agarose gel electrophoresis with ethidium bromide staining and PicoGreen (Life Technologies, Carlsbad, Calif.). Starting with 500 ng of genomic DNA, bisulfite conversion and methylation profiling was performed according to the manufacturer’s instructions for Illumina Human Methylation 450K BeadChips. All assays were performed at the Roswell Park Cancer Institute Genomics Shared Resource. After background correction and normalization to internal controls, Genome Studio software was used to calculate the fractional methylation (AVG_Beta) at each CpG (N= 453,144 CpG sites). Samples includes XX placenta.

overall_design: Bisulphite converted DNA from the 89 samples were hybridised to Illumina Human Methylation 450K BeadChips with at least one sugar intake variable and non-missing at covariates of interest.

first: Catherine

last: Monk

first: Benjamin

last: Tycko


title: The RNA N6-methyladenosine regulates chromatin remodeling and transcription [HEC-1-A_seq]

first: Xiaoyang

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

overall_design: Refer to individual Series


title: Global exploration of the metabolic requirements of gallid alphaherpesvirus 1

city: Xi'an

first: Hai

last: Li

address: No.76 Yanta West Road

department: Department of Pathogenic Microbiology and Immunology

institute: Xi'an Jiaotong University

summary: We sequenced mRNA from ILTV uninfected or infected DF-1 cells and LMH cells at 3 hpi.

overall_design: Examination of mRNA levels in individual condition were compared. Four independent experiments were performed.

first: Shengwang


title: DLX3 binding sites in rat enamel organ

city: Bethesda

first: Hong-wei

last: Sun

state: MD

address: 9000 Rockville Pile

department: Office of Science & Technology

institute: NIAMS

summary: DLX3 is a homeodomain transcription factor involved in amelogenesis. Mutations in DLX3 in human lead to Tricho-Dento-Osseous syndrome featuring enamel hypoplasia and hypomineralization. Here we investigated the distribution of DLX3 DNA binding sites in rat enamel organ using ChIP-seq.

overall_design: Enamel organs were dissected from continuously growing rat mandibular incisors and used for ChIP-seq analysis using anti-DLX3 and anti-H3K4me3 antibodies.

first: Olivier

last: Duverger

first: Takahiro

last: Ohara

first: Paul

last: Bible

first: Gustavo

last: Gutierrez-Cruz

first: Stephen

last: Brooks

first: Hong-Wei

first: Maria

middle: I

last: Morasso


title: Photoactivatable-Ribonucleotide-Enhanced Crosslinking and Immunoprecipitation (PAR-CLIP) of RNA-binding proteins (RBPs), IGF2BP1 and IGF2BP3 in the K562 CML-derived cell line

first: Stefan

last: Muljo

address: 10 CENTER DR RM 11N306

institute: NIH/NIAID

summary: Transcriptome-wide profiling of RNA-binding by IGF2BP1 and IGF2BP3 in the K562 cell line. Binding sites are characterized by T-to-C cross-linking mutations, depth and location on transcript

overall_design: Two biological replicates of PAR-CLIP are provided each for IGF2BP1 and IGF2BP3

first: Madeline

last: Wong

first: Bryan

last: Chim

first: Markus

last: Hafner


title: Active DNA Demethylation Regulates Plant Gamete and Zygote Genome Reprogramming

status: Public on Feb 08 2020

city: Wuhan

first: shaoli

last: zhou

state: Hubei

address: shizishan street

department: National Key Laboratory of Crop Genetic Improvement

institute: Huazhong Agricultural University

summary: Fertilization constitutes a critical step in the plant life cycle during which the gamete genomes undergo reprogramming in preparation for embryogenesis. However, it is unclear whether and how DNA methylation that epigenetically regulates gene expression is reprogramed during fertilization. Here, we characterized DNA methylation patterns and investigated the function of DNA glycosylases in rice eggs, sperms and unicellular zygotes. We found that DNA methylation is extensively reprogramed at non-CG sites in euchromatin regions upon fertilization, which intensifies during early embryogenesis. Genetic and genomic analysis revealed that rice DNA glycosylase genes DNG702, DNG701 and DNG704 demethylate at distinct and complementary loci in egg, sperm, and zygote genomes and are required for zygotic gene expression and development. The results indicate that active demethylation takes place in the gametes and the zygote to reprogram DNA methylation and zygotic genome activation in plant.

overall_design: BS-seq and RNA-seq of gametes and unicellular zygote of wild type, dng702, dng701/4 knock out mutant

first: S

last: Zhou

first: X

first: D

middle: X


title: Sickle Cell Disease mouse lung

first: Youqiong

last: Ye

address: 280 Chongqing south road

institute: Shanghai Jiao Tong University School of Medicine

summary: To determine gene expression in humanized SCD Berkeley lung compared to WT control lung

overall_design: 2 mouse lung per genetic group was processed for RNA extraction, RNA quality was assessed and ran on Affymetrix platform

first: Morayo

last: Adebiyi

first: Yang

last: Xia


title: Next Generation Sequencing Facilitated Differential Transcriptome Study of melanocytes treated with UVB radiation compared to matched fibroblasts and keratinocytes

city: MADISON

first: Vijayasaradhi

last: Setaluri

address: 1300 University Avenue

department: Dermatology

institute: University of Wisconsin-Madison

type: Non-coding RNA profiling by high throughput sequencing

summary: Transcriptome profiling (mRNA-seq) of Fibroblasts, keratinocytes, melanocytes and melanocytes irradiated with UVB

overall_design: mRNA profiles are generated for firbroblasts, keratinocytes, melanocytes and melanocytes irradiated with UVB in triplicates using Illumina’s HiSeq 2500 platform


title: Nuclear receptors and coregulators in triple negative breast cancer

city: Chicago

first: Geoffrey

last: Greene

state: IL

address: 929 East 57th Street

department: Ben May Department for Cancer Research

institute: University of Chicago

summary: The underlying mechanisms of how NCOA3 and SHC1 regulate drug response and metastasis of triple negative breast cancer

overall_design:
Performed RNAseq after gene knockdown with siRNA
Artificial Intelligene (AI, www.artificialintelligene.com)

first: Ya-Fang

last: Chang


title: Transcriptomic profile of bpm2,3,5 triple mutant and Col-0

first: Jose M.

last: Franco-Zorrilla

overall_design: Comparison of gene expression of bpm2,3,5 triple mutant versus Col-0

first: Jose

last: Chico

first: Gemma

last: Fernandez-Barbero

first: Gloria

last: García-Casado

first: Roberto

last: Solano


title: Global gene expression profile of hIAPP-Tg mice

city: Barcelona

first: Gema

last: Alcarraz-Vizán

address: Rossello 149

department: Diabetes & Obesity Laboratory

institute: IDIBAPS

summary:
10-12 weeks old wild type and hIAPP transgenic mice were taken for the study. Pancreatic islets were isolated at sacrifice. RNA was extracted and hybridized on Affymetrix microarrays.
We used microarrays to determine gene expression changes in pancreatic islets from mice overexepressing hIAPP and wild type mice.

first: Montse

last: Visa

first: Joan-Marc

last: Servitja

first: Anna

last: Novials


title: First Clinical Study Targeting ROR1, A Cancer Stem Cell Antigen Involved In Rho-GTPase Activation

city: La Jolla

first: Emanuela

middle: Maria

last: Ghia

address: 9310 Athena Circle

department: Center For Novel Therapeutics

institute: University of California San Diego

summary: Cirmtuzumab is a humanized monoclonal antibody that selectively targets ROR1, which is expressed on cancer stem cells (CSCs). Patients experienced reversal of the stemness gene expression signature associated with oncogenic dedifferentiation, inhibition of leukemia-cell activation of Rho-GTPases and  HS1, reductions in leukemia cell counts, and prolonged time-to-next-treatment (TTNT) following only 4 biweekly infusions of cirmtuzumab.

overall_design: Peripheral Blood Mononuclear Cells (PBMC) of 3 CLL samples were collected at day 0 (Pre) and at day 28 of cirmtuzumab treatment (Post). Negative  isolation of CLL cells to ≥95% purity was performed prior to RNA isolation. Data were analyzed  by Rosalind (https://rosalind.onramp.bio/), with a HyperScale architecture developed by OnRamp BioInformatics, Inc. (San Diego, CA).

first: Michael

middle: Y

last: Choi

first: George

middle: F

last: Widhopf II

first: Reilly

last: Kidwell

first: Md

last: Hasan

first: Jian

last: Yu

first: Laura

middle: Z

last: Rassenti

first: Liguan

last: Chen

first: Yun

first: Emily

last: Pittman

first: Minya

last: Pu

first: Karen

last: Messer

first: Charles

last: Prussak

first: Januario

middle: E

last: Castro

first: Catriona

last: Jamieson

first: Thomas

last: Kipps


title: Deregulation of ribosomal protein expression and translation promotes breast cancer metastasis [rna-Seq BRx142]

status: Public on Feb 07 2020

first: Ben

middle: S.

last: Wittner

address: 149 13th Street

department: Center for Cancer Research

institute: Massachusetts General Hospital

summary: We conducted an in vivo genome-wide CRISPR activation screen to identify genes that accelerate distal metastasis by breast cancer patient-derived circulating tumor cells (CTCs) following direct intravascular inoculation in mice. Regulators of translation and ribosomal proteins were prominent among these, and expression of RPL15, a component of the large ribosome subunit, was sufficient to increase metastatic growth in multiple organs. RPL15 overexpression selectively increases translation of other ribosomal proteins and cell cycle regulators. Unsupervised analysis of single-cell RNA sequencing of freshly-isolated CTCs from breast cancer patients identifies a subset with strong ribosomal and protein translation signatures, correlated with increased proliferative markers, epithelial markers and poor clinical outcome. Thus, ribosome protein expression identifies an aggressive subset of CTCs, whose therapeutic targeting may suppress metastatic progression.

overall_design: We performed mRNA profiling in control and RPL15 overexpressing circulating tumor cell-derived cell lines to determine the translational efficiency for any given transcript (i.e., the ratio of ribosome-bound mRNA to all poly-A mRNA). Two control specimens and two RPL15 overexpressing specimens were profiled.

first: Richard

last: Ebright

first: Sooncheol

last: Lee

first: Kira

last: Niederhoffer

first: Benjamin

last: Nicholson

first: Aditya

last: Bardia

first: Samuel

last: Truesdell

first: Devon

last: Wiley

last: Wesley

first: Selena

last: Li

first: Andy

last: Mai

first: Nicola

last: Aceto

first: Nicole

last: Vincent-Jordan

first: Annamaria

last: Szabolcs

first: Brian

last: Chirn

first: Johannes

last: Kreuzer

first: Valentine

last: Comaills

first: Mark

last: Kalinich

first: Wilhelm

last: Haas

first: David

last: Ting

first: Mehmet

last: Toner

first: Shobha

last: Vasudevan

first: Daniel

middle: A

last: Haber

first: Shyamala

last: Maheswaran

first: Douglas

last: Micalizzi


title: LT-HSC from young and middle-age mice stimulated with IGF1 RNA-seq

city: Bar Harbor

first: Jennifer

last: Trowbridge

state: Maine

address: 600 Main Street

department: Research

institute: The Jackson Laboratory

summary: Long-term hematopoietic stem cells (LT-HSCs) are responsible for lifelong maintenance and regeneration of the blood system. Loss of LT-HSC function is a major contributor to decline in hematopoietic function with aging, leading to increased rate of infection, poor vaccination response, and increased risk of hematologic malignancies. While cellular and molecular hallmarks of LT-HSC aging have been defined1-3, a barrier to achieving the goal of extending healthy hematopoietic function into older age is the lack of understanding of the nature and timing of the initiating events that cause LT-HSC aging. Here we show that hallmarks of LT-HSC aging and decline in hematopoietic function accumulate by middle age in mice, and that the hematopoietic cell-extrinsic bone marrow (BM) microenvironment at middle age is necessary and sufficient to cause LT-HSC aging. Using unbiased transcriptome-based approaches, we identify decreased production of IGF1 by mesenchymal stromal cells (MSC) in the local middle-aged BM microenvironment as a factor causing LT-HSC aging and show that direct stimulation of middle-aged LT-HSCs with IGF1 rescues hallmarks of aging. Together, our study demonstrates that the initiating events causing LT-HSC and hematopoietic aging emerge by middle age and are caused by hematopoietic cell-extrinsic changes in the BM microenvironment. Declining IGF1 in the BM microenvironment at middle age represents a compelling target for intervention using prophylactic therapies to effectively extend healthspan and prevent decline in hematopoietic function during aging.

overall_design: 3 replicates of each condition, young (control), middle-aged (control) and middle-aged stimulated with IGF1 (experimental) LT-HSCs, young stimulated with IGF1 is not included in this dataset

first: Kira

last: Young


title: Expression data from Arabidopsis seedling during plastid development

city: Hannover

first: Thomas

last: Pflannschmidt

address: Herrenhäuser Straße 2

institute: Leibniz-Universität Hannover

summary:
For establishing the photosynthetic apparatus plant cells must orchestrate the expression of genes encoded in both nucleus and chloroplast. Therefore a crosstalk between the two compartments is necessary.
We employed a gene expression profiling approach in order to elucidate the changes in gene expression that occur at different stages of plastid development.

overall_design: The four conditions compared were: Arabidopsis thaliana mutant rpoTmp and wildtype Col-0 grown in dark for 4 days after germination. Arabidopsis thaliana mutant pap7 and wildtype col-0 for 5 days in light. Plants were grown separately on MS medium in Petri dish per condition. around 50 seedlings per petridish.

first: Björn

last: Grübler

first: Livia

last: Merendino

last: Pfannschmidt


title: Deregulation of ribosomal protein expression and translation promotes breast cancer metastasis [rna-uArray MCF10A]

first: Ben

last: Wittner

overall_design: To explore the link between epithelial-to-mesenchymal transition (EMT) and protein translation, we assessed translational changes in the canonical EMT model of TGF-beta breast epithelial cells, MCF10A cells [PUBMED ID 18593909].

first: Richard

last: Ebright

first: Sooncheol

last: Lee

last: Niederhoffer

first: Benjamin

last: Nicholson

first: Aditya

last: Bardia

first: Samuel

last: Truesdell

first: Devon

last: Wiley

last: Wesley

first: Selena

last: Li

first: Andy

last: Mai

first: Nicola

last: Aceto

first: Nicole

last: Vincent-Jordan

first: Annamaria

last: Szabolcs

last: Chirn


title: LT-HSC re-isolated from tranplants altering the age (young and middle age) of the donor LT-HSC, support cells and recipient mice

first: Jennifer

last: Trowbridge

overall_design: 2-4 replicates of re-isolated LT-HSC from each transplant condition (YYY, MMM and MMY), the MYM transplant condition was not included in this dataset

last: Young


title: Deregulation of ribosomal protein expression and translation promotes breast cancer metastasis [rna-Seq CTCs 2]

last: Wittner

overall_design: The CTC-iChip microfluidic device [PMID: 23552373 ] enables isolation of rare viable circulating tumor cells (CTCs) directly from whole blood specimens of patients with cancer, with RNA quality compatible with single-cell RNA sequencing (RNA-seq). We generated RNA-seq profiles of 195 freshly isolated single candidate CTCs or CTC-clusters from 41 women with metastatic breast cancer. Fifty-four candidate CTCs had fewer than 100,000 uniquely mapped reads and therefore were dropped from further consideration. Of the remaining candidate CTCs, 32 expressed PTPRC at a level higher than 10 reads-per-million, so were deemed potential white blood cells and therefore dropped from further consideration. This resulted in profiles of 109 CTCs or CTC-clusters from 33 patients.

first: Kira

first: Brian

first: Johannes

last: Kreuzer

first: Valentine

last: Comaills

first: Mark

last: Kalinich

first: Wilhelm

last: Haas

first: David

last: Ting

first: Mehmet

last: Toner

first: Shobha

last: Vasudevan

first: Daniel

last: Haber

first: Shyamala

last: Maheswaran

first: Douglas

last: Micalizzi


title: ChIP-seq analysis of Fezf2 in mTECs

city: bunkyo

first: Yoshihiko

last: Tomofuji

state: Tokyo

address: hongo 7-3-1

department: Immunology

institute: University of Tokyo

summary: To investigate the genome-wide binding pattern of Fezf2, we performed ChIP-seq analysis for Fezf2. ChIP-seq of transcription factor in mTECs is difficult because of small number of mTECs or difficulty in gaining ChIP grade antibodies. Then, we generated Fezf2-3Flag knock in mice and performed ChIP-seq analysis by using anti-Flag antibody.

overall_design: ChIP-seq in mTECs from Fezf2-3Flag KI mice.

first: Cristian

middle: D

last: Peña Martinez

first: Akashi

last: Taguchi

first: Hiroyuki

last: Takaba


title: Gene expression in spinal cord microglia during demyelination and remyelination following neuroattenuated JHMV infection

city: Coralville

first: Alan

middle: Jacob

last: Sariol

state: IA

address: 2868 Coral Ct., Apt 201

department: Microbiology and Immunology

institute: University of Iowa

summary: Microglia are considered both pathogenic and protective during recovery from demyelination, but their precise role remains ill-defined. Here, using an inhibitor of colony stimulating factor 1 receptor (CSF1R), PLX5622, and mice infected with a neurotropic coronavirus (mouse hepatitis virus, strain JHMV), we show that depletion of microglia after clearance of virus infection resulted in impaired myelin repair and prolonged clinical disease. Microglia were required only during the early stages of remyelination. Notably, large deposits of extracellular vesiculated myelin and cellular debris were detected in the spinal cords of PLX5622-treated and not control mice, which correlated with decreased numbers of oligodendrocytes in demyelinating lesions in drug-treated mice. Further, gene expression analyses demonstrated differential expression of genes involved in myelin debris clearance, lipid and cholesterol recycling, and promotion of oligodendrocyte function. The results also demonstrate that microglial function could not be compensated by infiltrating macrophages. Together, these results demonstrate key roles for microglia in debris clearance and the initiation of remyelination following infection with a neurotropic coronavirus but are not necessary during later stages of remyelination.

overall_design: We used RNA-seq to analyze FACS-sorted microglia from the spinal cords of mock-infected, as well as 14 and 21 day post-JHMV infection mice, n=4 mice per group.

first: Stanley

last: Perlman


title: Deregulation of ribosomal protein expression and translation promotes breast cancer metastasis [ribo-Seq BRx142]

first: Ben

last: Wittner

overall_design: We performed ribosomal profiling in control and RPL15 overexpressing circulating tumor cell-derived cell lines to determine the global ribosome occupancy of mRNA transcripts, identify changes in translational preference, and calculate the translational efficiency for any given transcript (i.e., the ratio of ribosome-bound mRNA to all polyA-mRNA). One control specimen and one RPL15 overexpressing specimen was profiled in each of two batches.

first: Richard

last: Ebright

first: Sooncheol

last: Lee

middle: S

first: Kira

middle: L

last: Niederhoffer

first: Benjamin

last: Nicholson

first: Aditya

last: Bardia

first: Samuel

last: Truesdell

first: Devon

last: Wiley

last: Wesley

first: Selena

last: Li

first: Andy

last: Mai

first: Nicola

last: Aceto

first: Nicole

last: Vincent-Jordan

first: Annamaria

last: Szabolcs

first: Brian

last: Chirn


title: Seven-lncRNA signature in esophageal squamous cell carcinoma

first: Nuoqing

last: Weng

address: 651，Dongfengdong road

institute: State Key Laboratory of Oncology in South China,Sun Yat-sen University

summary: A seven-lncRNA signature was identified in the training set, which is significantly associated with overall survival (OS) (Hazard Ratio [HR]: 3.535, 95% confidence interval [CI]: 2.113-5.915, P < 0.001) and disease-free survival (DFS) (Hazard Ratio [HR]: 2.413, 95% confidence interval [CI]: 1.573-3.703, P < 0.001). Patients in high-risk group have shorter overall survival (HR: 3.555, 95% CI: 2.195-5.757, p < 0.001) and disease-free survival (HR: 2.537, 95% CI: 1.646-3.909, p < 0.001) in the training set, and we found the same conclusion in the independent set for OS (HR 2.665, p < 0.001) and DFS (HR 2.360, p = 0.001). Combination of the signature and TNM staging system was more powerful than TNM staging system alone in predicting outcomes in both the training set (AUC: 0.772 vs 0.681, p = 0.002) and in the independent set (AUC: 0.772 vs 0.660, p = 0.003).

overall_design: Using a 2520 probe microarray, we retrospectively analyzed lncRNA expression profiles in 141 samples of ESCC and 81 paired non-cancer specimens from SUN YAT-SEN University Cancer Center (Guangzhou, China), which were served as the training set to identify a signature associated with clinical outcomes. We randomly selected 40 paired tumor tissues and paired adjacent normal tissues from the above samples for the quantitative RT-PCR to confirm the credibility of microarray data. Then we conducted the quantitative RT-PCR in another 103 samples of ESCC as an independent set to verify the signature.

first: Jun

last: Chi

first: Huiyun

last: Wang


title: EphrinB1 Modulates Glutamatergic Inputs into POMC Neurons and Controls Glucose Homeostasis

city: Lausanne

first: sophie

last: croizier

address: Genopode building

department: CIG

institute: University of Lausanne

summary: We aim at identifying genes enriched in POMC neurons versus NPY neurons that were involved in glutamatergic synapse formation

overall_design: We used Pomc-Cre;tdTomato reporter mice crossed with Npy-hrGFP mice, to specifically sort POMC (Tom, red), NPY (GFP, green) and POMC becoming NPY (yellow, double positive=DP) neuronal populations and perform RNA-sequencing

first: Manon

last: Gervais

first: Alexandre

last: Picard

first: Bernard

last: Thorens

first: Sophie

last: Croizier


title: Effects of FTY720 on B cells in experimental autoimmune encephalomyelitis (EAE)

city: Würzburg

first: Claus

middle: Juergen

last: Scholz

address: Josef-Schneider-Str. 2

department: Core Unit SysMed

institute: University Hospital Würzburg

summary: MP4-induced experimental autoimmune encephalomyelitis (EAE) is a B cell-dependent mouse model of multiple sclerosis (MS), which enables targeted research on B cells, currently much discussed protagonists in MS pathogenesis. Here, we used this model to study the impact of the S1P1 receptor modulator FTY720 (fingolimod) on the autoreactive B cell and antibody response both in the periphery and central nervous system (CNS) itself.

overall_design: Expression profiling of S1P1 receptor modulator FTY720- and vehicle-treated B cells from EAE mice.

first: Quirin

last: Notz

middle: J

first: Stefanie

last: Kuerten


title: Transient postnatal lung changes on alveolar development after in utero and lactation exposure to nicotine

city: Geneva

first: Sylvain

last: LEMEILLE

address: 1 rue Michel-Servet

department: Department of Pathology and Immunology

institute: University of Geneva Medical School

summary:
Purpose: The goal of this study is to address the consequences of in utero and early life nicotine exposure on alveolar phase of lung development in mice
Methods:  A mouse model of gestational and early life nicotine exposure was used in this study. Briefly, Nicotine (200 mg/L) was supplied immediately after mating and administered to the females in drinking water supplemented with 2% saccharin for the whole period of gestation and lactation (nicotine group). As a control, we used drinking water with 2% saccharin (saccharin group). Pups born from nicotine-exposed or control mothers were collected at different postnatal days (PNDs) and their lungs were subjected to RNAseq, western blot, histological and detailed stereological analysis.
Results: Among 13 827 genes tested, nicotine treatment induced an upregulation of 2098 and downregulation of 1859. Pathway analysis performed with MetaCore software (https://portal.genego.com/) (threshold of 2 and p<0.05) identified several different pathways as upregulated upon nicotine exposure, namely cell cycle, epithelial to mesenchymal transition, stem cell related pathway, WNT signaling pathway, stromal-epithelial interaction, cell adhesion and DNA damage. Furthermore, majority of downregulated genes were associated with the immune system.
Conclusions: Our results indicate that in utero and early life nicotine exposure induces extensive changes in gene expression following the birth of mice that reflects in accelerated kinetics of lung development. This effect, however, is transient, and not lomger detectable by pnd16. On the other hand, nicotine decreased proliferation and endothelial cell density detected at pnd16, thereby affecting on of two main cell lines involved in oxygen exchange. This results are important in the context of growing interest for nicotine patch replacement therapy and electronic cigarettes.

overall_design: Lung mRNA profiles of 2-days and 16-day old wild type (WT) C57BL/6J mice, control or nicotine exposed, were generated using single-end reads (50nt-long) with Illumina HiSeq2500

first: Sanja

last: Blaskovic

first: Yves

last: Donati

first: Filippo

last: Zanetti

first: Isabelle

last: Ruchonnet-Metrailler

last: Lemeille

first: Tiziana

middle: P

last: Cremona

first: Johannes

middle: C

last: Schittny

first: Constance

last: Barazzone-Argiroffo


title: Transcriptomic analysis of thymic epithelial cells and extra thymic epithelial cells

status: Public on Feb 06 2020

city: Montréal

first: Claude

last: Perreault

state: Québec

address: 2950, Chemin de Polytechnique

country: Canada

institute: Institute for Research in Immunology and Cancer

summary: Regulation of MHC I expression has been studied almost exclusively in hematolymphoid cells. We report that thymic epithelial cells (TECs), particularly in the medulla (mTECs), constitutively express up to 100-fold more cell surface MHC I proteins than epithelial cells (ECs) from the skin, colon and lung. Differential abundance of cell surface MHC I in primary ECs is regulated via transcription of MHC I and of genes implicated in the generation of MHC I-binding peptides. Superior MHC I expression in TECs is unaffected by deletion of Ifnar1 or Ifngr1, but is lessened by deletion of Aire, Ifnlr1, Stat1 or Nlrc5, and is driven mainly by type III IFN produced by mTECs. Ifnlr1−/− mice show impaired negative selection of CD8 thymocytes, and at 9 months of age, present autoimmune manifestations. Our study shows unanticipated variation in MHC I expression by ECs from various sites and provides compelling evidence that superior expression of MHC I in TECs is crucial for proper thymocyte education.

overall_design: We performed RNA-sequencing in triplicate from different types of primary epithelial cells (ECs) isolated from thymus, skin, lung and colon in order to identify the mechanisms involved in differential  expression level of MHC I molecules on these different sources of ECs. Each  replicate contained a pool of FACS-sorted ECs isolated from 5 mice.

first: Mohamed

last: Benhammadi

first: Justine

last: Mathé

first: Maude

last: Dumont-Lagacé

first: Koichi

last: Kobayashi

first: Louis

last: Gaboury

first: Sylvie

last: Brochu


title: Role of Hdac2 in pancreatic ductal adenocarcinoma

city: Berlin

first: Matthias

last: Wirth

address: Hindenburgdamm 30

institute: Charité Berlin

summary: Microarrays were used to determine transcriptional differences between Hdac2 knockout versus Hdac2 wildtype pancreatic cancer cells.

overall_design: RNA was extracted from a total of 6 KrasG12D driven primary pancreatic cancer cell lines with indicated Hdac2 status

first: Günter

last: Schneider


title: Expression data from cells in peritoneal cavity of CD-1 outbred mice infected with different Toxoplasma gondii strains

city: Knoxville

first: Chunlei

last: Su

state: TN

address: 1311 Cumberland Avenue

department: Microbiology

institute: University of Tennessee

summary: The findings in our study revealed dynamic differences of gene expression and different pathways of immune response in mice infected with three distinct strains of T. gondii.

overall_design: We conducted a time course study of gene expression in CD-1 outbred mice during acute infection (days 1 to 7) with the highly virulent type I (GT1 strain), intermediately virulent type II (PTG strain) and non-virulent type III (CTG strain) parasites. Mice were infected with 500 parasites by intraperitoneal injection. Three to 4 mice were euthanized on day 1, 2, 3, 4, 5 and 7 post infection, respectively. Peritoneal cells were collected for RNA extraction and gene expression study.

first: Li

last: Yu

first: Keats

last: Shwab

first: Rachel

last: Hill

first: Xing-Quan

last: Zhu

first: Julia

last: Gouffon

first: Jilong

last: Shen


title: Hydrolyzed Fat Formula Increases Brain White Matter in Small for Gestational Age and Appropriate for Gestational Age Neonatal Piglets

city: Urbana

first: Rodney

middle: W.

last: Johnson

address: 1207 W. Gregory Dr.

department: Animal Sciences

institute: Univ of Illinois in Urbana

summary: Intrauterine growth restriction is a common cause of small for gestational age (SGA) infants worldwide. SGA infants are deficient in digestive enzymes required for fat digestion and absorption compared to appropriate for gestational age (AGA), putting them at risk for impaired neurocognitive development. The objective was to determine if a hydrolyzed fat (HF) infant formula containing soy free fatty acids, 2-monoacylglycerolpalmitate, cholesterol, and soy lecithin could increase brain tissue incorporation of essential fatty acids or white matter to enhance brain development in SGA and AGA neonatal piglet models. Sex-matched, littermate pairs of SGA (0.5-0.9kg) and AGA (1.2-1.8kg) 2 day old piglets (N=60) were randomly assigned to control (CON) or HF formula diets in a 2 x 2 factorial design. On day 14, 24 piglets were used for hippocampal RNA-sequencing; the rest began a spatial learning task. On days 26-29, brain structure was assessed by magnetic resonance imaging (MRI). Cerebellum and hippocampus were analyzed for fatty acid content. SGA piglets grew more slowly than AGA piglets, with no effect of diet on daily weight gain or weight at MRI. HF diet did not affect brain weight. HF diet increased relative volumes of 7 brain regions and white matter (WM) volume in both SGA and AGA piglets. However, HF did not ameliorate SGA total WM integrity deficits. RNA sequencing revealed SGA piglets had increased gene expression of synapse and cell signaling pathways and decreased expression of ribosome pathways in the hippocampus compared to AGA. HF decreased expression of immune response related genes in the hippocampus of AGA and SGA piglets, but did not correct gene expression patterns in SGA piglets. Piglets learned the T-maze task at the same rate, but SGA HF, SGA CON, and AGA HF piglets had more accurate performance than AGA CON piglets on reversal day 2. HF increased arachidonic acid (ARA) percentage in the cerebellum and total ARA in the hippocampus. HF enhanced brain development in the neonatal piglet measured by brain volume and WM volume in specific brain regions; however, more studies are needed to assess long-term outcomes.

overall_design: An independent cohort of 14 day old neonatal piglets (n = 6/group) was used to analyze the effects of SGA and HF in a 2 x 2 factorial arrangement of size (SGA or AGA) and diet (CON or HF) on the hippocampal transcriptome.

first: Megan

last: Caputo

first: Jennifer

middle: N

last: Williams

first: Jenny

last: Drnevich

first: Emily

last: Radlowski

first: Ryan

last: Larsen

first: Bradley

last: Sutton

first: Brian

last: Leyshon

first: Jamal

last: Hussain

first: Manabu

middle: T

last: Nakamura

first: Matthew

last: Kuchan

first: Tapas

last: Das

middle: W


title: Gene Expression and Physiological Differences in Neo-Octoploid Switchgrass Subjected to Drought Stress

city: Albany

first: Christian

middle: M

last: Tobias

state: CA

address: USDA-ARS, 800 Buchanan Street Rm 2101

institute: USDA-ARS

summary: Switchgrass (Panicum virgatum L.) has been subject to breeding to improve its yield and composition for bioenergy, but improving its tolerance to environmental variability is just beginning. Different ploidy populations act as somewhat distinct gene pools which can only be bridged through whole genome reduction or duplication events. In order to document potential wide-ranging effects of whole genome duplication, we examined the effects of water stress on growth, physiology, and gene expression in individual tetraploid clones of the switchgrass cultivar ‘Liberty’ as well as neo-octoploid lines derived from it. The neo-octoploids behaved similarly to Liberty under water-stress and recovery conditions. Growth rates, photosynthesis, gas exchange, node numbers, and height were reduced in plants under water stress while proline levels were increased.  A total of 6134 differentially expressed genes (8% of the annotated genes with detectable expression in crown tissue) were detected under water deficit stress, while 3310 differentially expressed genes were detected in crown tissue after 1 week of recovery from water deficit stress relative to well-watered treatments. Only a small number of genes were identified as being differentially expressed between 4x Liberty and its 8x derivatives.

overall_design: mRNA profiles of crown tissue from related individuals and cultivars were sampled after water-stress and during a recovery period. Paired-end sequencing of mRNA was performed using Illumina.

first: Lisa

last: Chanbusarakum

last: Bragg

first: Prisca

middle: K

last: Cheng

first: Sheyla

last: Aucar

first: Gautam

last: Sarath

first: Nathan

last: Palmer

first: Serge

last: Edme


title: Transcriptomic and epigenetic profiling of genome control in the germline stem cell cycle in mice [ChIP-seq II]

city: Kyoto

first: Shinichiro

last: Chuma

state: Kyoto

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

department: Institute for Frontier Life and Medical Sciences

institute: Kyoto university

summary: The faithful transmission of genome information is fundamental to the germline stem cell cycle. One exception to this is meiosis when active recombination takes place. This study aims to understand how dna damage responses and meiotic recombination mechanisms are properly coordinated with developmental programs of germ cells by comparing transcriptomic and epigenetic profiles of germline competent pluripotent stem cells, germline stem cells and somatic cells etc. in mice.

overall_design: Control IgG ChIP and genome DNA (from whole cell extract) samples of mouse germline stem (GS) cells were analyzed by Illumina deep sequencing.

first: Mihoko

last: Hosokawa


title: Ribosome profiling in RPEI cells upon CDK1-inhibition

city: Mannheim

first: Johanna

middle: Daniela

last: Schott

address: Franz-Volhard-Straße 6

department: Mannheim Institute for Innate Immunoscience

institute: Heidelberg University

summary: Protein synthesis is the second most energy-intensive process in the cell. Therefore, cells tightly control mRNA translation rates in response to external stimuli (growth factors, differentiation signals) and the internal resources available (nutrients, energy). We set out to unravel new molecular mechanisms of global translation control required for cellular homeostasis. Using a siRNA screening approach to knock-down all human kinases and phosphatases, we analyzed the impact of protein phosphorylation on translation regulation in unstressed, proliferating cells. A visual screen was conducted to assess stress granule formation (as a consequence of translational shutdown) in the absence of 711 kinases and 256 phosphatases. Several candidates identified in the screen are linked, either directly or indirectly, to cell cycle regulation. We further identified a cyclin-dependent kinase (CDK), whose genetic downregulation or chemical inhibition results in global translation suppression. In order to assess CDK downstream signaling, we performed phosphoproteomics analysis and found the phosphorylation status of many ribosomal proteins to be altered upon CDK inhibition. Indeed, we could show that S6-kinase 1 partially contributes to CDK-dependent translational control. Ribosome profiling further revealed that the translation of 5’TOP mRNAs, including many mRNAs encoding for ribosomal proteins, is especially sensitive to CDK inhibition. While the translation regulatory function of this kinase is independent of the cell cycle phase, its activity is ideally suited to couple the overall proliferation rate of cells to the global rate of protein synthesis. Our results identify a pathway that enables cells to directly adapt protein homeostasis to proliferation and growth signals.

overall_design: RO-3306 or DMSO treated RPEI cells were subjected to ribosome profiling in three biological replicates. As a spike-in to detect global changes in translation efficiency, S. cerevisiae lysate was added to the RPEI lysates. To determine ribosome densities, both ribosome protected fragments and alkaline-fragmented input material were analyzed, amounting to 12 samples in total.

first: Katharina

last: Haneke

last: Schubert

first: Doris

last: Lindner

first: Georg

last: Stoecklin