title: Transcriptome profiling of murine aortic endothelium with combined deletion for three MEF2 transcription factors: Mef2a, Mef2c and Mef2d

city: Albany

first: John

last: Schwarz

state: NY

address: 47 New Scotland Ave.

department: Department of Molecular and Cellular Physiology

institute: Albany Medical College

summary:
Atherosclerosis predominantly forms in regions of oscillatory shear stress while regions of laminar shear stress are protected. This protection is partly through the endothelium in laminar flow regions expressing an anti-inflammatory and anti-thrombotic gene expression program. Several molecular pathways transmitting these distinct flow patterns to the endothelium have been defined. Our objective is to define the role of the MEF2 family of transcription factors in promoting an atheroprotective endothelium.
Endothelial-specific Mef2a -c and -d deficiency results in systemic inflammation, hemorrhage, thrombocytopenia, leukocytosis, and rapid lethality at 11 days post-injection. We collected RNA from the aortic endothelium at day 7 and process for transcriptome analysis in order to understand the phenotype and mechanism.

overall_design: Endothelial-specific, inducible-deletion of Mef2a, Mef2c and Mef2d was mediated by Cdh5-CreERT2 through 5 daily tamoxifen injections in 10 weeks old mice (ACDiEKO). Control animals were tamoxifen injected Cre-negative littermates. Thoracic aortas from these mice were harvest 7 days after the first injection of tamoxifen. Endothelial RNA from individual aortas was isolated by flushing TRIzol through the aortic lumen and processed for Clariom D Mouse assay (formally Mouse Transcriptome Array 1.0) (Affymetrix). Each sample was from a single aorta.

first: Yao

middle: W

last: Lu


title: RNA-sequencing reveals signaling pathways associated with tumor invasion and epithelial–mesenchymal transition in HIPK2-attenuated cells

status: Public on Jan 11 2021

city: Wuhan

first: Xueqing

last: Zheng

address: Luoyu Road

country: China

institute: Wuhan University

type: Expression profiling by high throughput sequencing

summary: Homeodomain-interacting protein kinase 2 (HIPK2), a well-known tumor suppressor, exhibits contradictory expression patterns in different cancers. This study was performed to reveal the potential mechanism of HIPK2 involvement in oral squamous cell carcinoma (OSCC) metastasis.  High throughput RNA-sequencing was used to detect the dysregulated signaling pathways in HIPK2 deficiency OSCC cells. Transwell assay and lymphatic metastatic orthotopic mouse model assay were performed to identify the effect of HIPK2 on tumor invasion. Western blotting and luciferase reporter assay were performed to examine the HIPK2/P53/E-Cadherin axis in OSCC. We observed that depletion of HIPK2 promoted tumor cell invasion in vitro and facilitated cervical lymph node metastasis in vivo. According to mRNA-sequencing, pathways closely related to tumor invasion were notably activated. HIPK2 was found to trigger E-Cadherin expression by mediating P53, which directly targets the CDH1 (coding E-Cadherin) promoter. Restoring P53 expression rescued the E-Cadherin suppression induced by HIPK2 deficiency. Together, the depletion of HIPK2 expression promoted OSCC metastasis by suppressing the P53/E-Cadherin axis, which might be a promising target for anti-cancer therapies.

overall_design: RNA-seq in the Cal-27 cell line before and after knockdown of HIPK2

first: Jiali

last: Zhang


title: Remodeling of white fat during browning involves YBX1 to drive thermogenic commitment

city: Copenhagen

first: Ali

last: Altintas

address: Blegdamsvej 3B

department: NNF Center for Basic Metabolic Research

country: Denmark

institute: Copenhagen University

summary: Effects of YBX1 activation in PPARγ-indcuded C3H/10T1/2-SAM pre-adipocytes on the transcriptome of cells during early differentation stages

overall_design: C3H/10T1/2-SAM pre-adipocytes containing dCas9-VP64 and MS2-P65-HSF1 were transfected with guide RNA taregting PPARγ or a combination of guides taregting PPARγ and YBX1 two days before differentiation start to model gain of funtion in pre-adipocytes. Transcriptome was analysed for day 0, day 2 and day 4 of differentiation.

first: Kaja

last: Plucińska

first: Galal

middle: N

last: Chehabi

first: Romain

last: Barrès

first: Brice

last: Emanuelli


title: Complete in vivo SHAPE-MaP structure of the SARS-CoV-2 genome

city: New Haven

first: Nicholas

last: Huston

state: Connecticut

address: 260 Whitney Avenue, YSB 308

country: USA

institute: Yale University

summary: SHAPE-MaP structure probing experiment was performed on SARS-CoV-2 infected Vero cells at 4 days post infection with two biological replicates. For each replciate, SHAPE-MaP includes a sample treated with 2-methylnicotinic acid imidazolide acid (modified) or a minue reagent (unmodified). NAI preferentially reacts with unpaired bases in RNA, forming acylated bases. These modifications are encoded as mutation during reverse transcripatse and library preparation. After sequencing and alignment, the reactivity profiles of 'modified' and 'unmodified' samples are used to calculate SHAPE reactivity of each base

sample_organism: Severe acute respiratory syndrome coronavirus 2

overall_design: SHAPE-MaP on SARS-CoV-2 genomic RNA growing in Vero cells

middle: C

first: Han

last: Wan

first: Craig

last: Wilen

first: Anna

last: Pyle


title: Type 2 Diabetes Mellitus is Associated with Transcriptome Alterations in Cortical Neurones and Associated Neurovascular Unit Cells in the Ageing Brain

city: Sheffield

first: Paul

middle: Roy

last: Heath

state: S. Yorks

address: SITraN, 385a Glossop Road

department: Academic Neurology Unit

country: United Kingdom

institute: University of Sheffield

summary: Type 2 diabetes mellitus (T2D), characterised by peripheral insulin resistance, is a risk factor for dementia. In addition to its contribution to small and large vessel disease, T2D may directly damage cells of the brain neurovascular unit. In this study, we investigated the transcriptomic changes in cortical neurones, and associated astrocytes and endothelial cells of the neurovascular unit, in the ageing brain

overall_design:
Neurone, astrocyte, and endothelial cell-enriched RNA, obtained by immuno-laser capture microdissection of temporal cortex (Brodmann area 21/22) from 6 cases with self-reported T2D in the Cognitive Function and Ageing Study neuropathology cohort, and 5 age and sex-matched controls, was hybridised onto Affymetrix GeneChip® HG-U133 Plus 2.0 arrays.
Expression profiling of Human brain Neurone, astrocyte, and endothelial cell-enriched RNA, obtained by immuno-laser capture microdissection of temporal cortex

first: Joanna

middle: J

last: Bury

first: Annabelle

last: Chambers

middle: R

middle: G

last: Ince

first: Pamela

last: Shaw

first: Fiona

middle: E

last: Matthews

first: Carol

last: Brayne

first: Julie

last: Simpson

first: Stephen

middle: B

last: Wharton


title: Mouse mutant phenotyping at scale reveals novel genes controlling bone mineral density

status: Public on Jan 12 2021

city: Strasbourg

first: maria

middle: del mar

last: muñiz moreno

state: Alsace

address: 1 Rue Laurent Fries

department: Translational medicine and neurogenetics

country: France

institute: IGBMC

type:
Expression profiling by array
Third-party reanalysis

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

relation:
SuperSeries of: GSE158146
SuperSeries of: GSE158147
SuperSeries of: GSE158148
SuperSeries of: GSE158149
SuperSeries of: GSE158150
Reanalysis of: GSM43225
Reanalysis of: GSM43216
Reanalysis of: GSM43195
Reanalysis of: GSM43188
Reanalysis of: GSM43202
Reanalysis of: GSM43209
Reanalysis of: GSM43184
Reanalysis of: GSM43205
Reanalysis of: GSM43198
Reanalysis of: GSM43191
Reanalysis of: GSM43212
Reanalysis of: GSM43219
Reanalysis of: GSM925429
Reanalysis of: GSM925430
Reanalysis of: GSM925431
Reanalysis of: GSM925432
Reanalysis of: GSM925433
Reanalysis of: GSM925434
Reanalysis of: GSM1071626
Reanalysis of: GSM1071627
Reanalysis of: GSM1071628
Reanalysis of: GSM1071629
Reanalysis of: GSM1071630
Reanalysis of: GSM1071631
Reanalysis of: GSM1383260
Reanalysis of: GSM1383261
Reanalysis of: GSM1383262
Reanalysis of: GSM1383263

overall_design: Refer to individual Series

first: Maria

middle: M

last: Muñiz Moreno

first: Yann

last: Herault

first: Philipp

last: Mayer-Kuckuk

first: Martin

last: Hrabe de Angelis


title: Single cell RNA-seq mapping of nasal and tracheobronchial airways in human healthy volunteers.

city: Valbonne - Sophia-Antipolis

first: Kevin

last: Lebrigand

address: 660 route des lucioles

institute: IPMC/CNRS

summary: We have explored cellular heterogeneity of human airways in 10 healthy volunteers by single-cell RNA profiling. 77,969 cells were collected by bronchoscopy at 35 distinct locations, from the nose to the 12th division of the airway tree, either by forceps (46,791 cells), or brush biopsies (31,178 cells). Use of cold-active proteases allowed dissociation of a high percentage of epithelial cells (89.1%, 15 distinct surface cell types and 2 glandular cell types), but also immune (6.2%, 7 cell types) and stromal (4.7%, 4 cell types) cells. Raw data has been submitted to EGA web portal under accession number EGAS00001004082 (https://ega-archive.org/studies/EGAS00001004082).

overall_design: Profiling of 35 brushings or biopsies of human airways samples in 10 healthy volunteers by single-cell RNA profiling

first: M

last: Deprez

first: L

last: Zaragosi

first: K

first: P

last: Barbry


title: Insulin-regulated periovulatory gene expression in superovulated mice

city: Carbondale

first: James

middle: Arthur

last: MacLean

state: Illinois

address: 1135 Lincoln Dr, Life Science III, Room 2071

department: Physiology

institute: Southern Illinois University

summary: Because mice with Pgr-Cre mediated double ablation of Insr and Igf1r are infertile and possess trapped oocytes in their corpora lutea, we performed RNA-seq to identify candidate pathways that contribute to ovulation failure.

overall_design: A direct comparison of conditional Insr/Igf1r double knockout mice with littermate controls (n=4 per group).

first: Kanako

last: Hayashi


title: DNA methylation dynamics in Atlantic salmon (Salmo salar) challenged with high temperature and moderate hypoxia

city: St. John's

first: Anne

last: Beemelmanns

address: 0 Marine Drive

department: Ocean Science

country: Canada

institute: Memorial University

type: Methylation profiling by high throughput sequencing

summary: In this study, we employed Multiplex Bisulfite Sequencing (MBS) to measure CpG methylation within a ~500 bp region around the transcription start of six thermal/hypoxia biomarker genes (cirbp, jund, pdk3, prdx6, serpinh, ucp2) in the liver of post-smolt Atlantic salmon following short-term (3 days) and prolonged (4 weeks) exposure to i) high temperature (20°C) and normoxia (~100% air saturation) (Warm & Normoxic - WN); or ii) high temperature (20°C) and moderate hypoxia (~70% air saturation) (Warm & Hypoxic - WH) as compared to iii) control conditions (12°C, ~100% air saturation) (Control - CT).We found distinct CpG methylation profiles for each treatment group based on responsive CpG sites that were strongly dependent on the duration of the exposure (i.e., 3 days vs. 4 weeks at 20°C) and also differed between regulatory genomic regions (i.e., 5’upstream region, 5’UTR, first exon, and first intron). Several of these changes in CpG methylation were highly correlated with changes in gene expression, and can be considered as potential epigenetic marks (epimarkers).

overall_design: Atlantic salmon were exposed to following treatments: (1) Control (CT) constant temperature of 12°C and 100 % air saturation; (2) Warm&Normoxic (WN) incremental temperature increase (1°C per week from 12 - 20°C)  at 100% air saturation; and (3) Warm&Hypoxic (WH) decrease in oxygen content of 70% air saturation over one week, followed by two weeks of acclimation to this oxygen level, and then incremental temperature increase (1°C per week from 12 - 20°C) at 70% air saturation.

first: Laia

last: Ribas

first: Dafni

last: Anastasiadi

first: Javier

last: Moraleda-Prados

first: Fabio

middle: S

last: Zanuzzo

first: Matthew

middle: L

last: Rise

first: Anthony

middle: K

last: Gamperl


title: RNASeq of undifferentated and two types of differentiated 50B11 cells

city: Adelaide

first: Dusan

last: Matusica

state: South Australia

address: Sturt Road, Bedford Park

department: College of Medicine and Public Health

country: Australia

institute: FLINDERS UNIVERSITY OF SOUTH AUSTRALIA

summary: RNASeq of 50B11 cells before and after differentiation with forskolin and nerve growth factor or with forskolin and glial-derived neurotrophic factor

overall_design: Examination of differences in RNA expression profiles between different growth conditions in 50B11 cells

first: Matusica

last: Dusan

first: Letitia

last: Pimlott


title: The TGF-β superfamily cytokine Activin-A is induced during autoimmune neuroinflammation and drives pathogenic Th17 cell differentiation

city: Chapel Hill

first: Yisong

last: Wan

state: NC

address: 125 Mason Farm Road

department: Lineberger Comprehensive Cancer Center

institute: University of North Carolina-Chapel Hill

summary: Th17 cells are known to exert pathogenic and non-pathogenic functions. Although the cytokine transforming growth factor β1 (TGF-β1) is instrumental for Th17 cell differentiation, it is dispensable for generation of pathogenic Th17 cells. Here, we examined the T cell-intrinsic role of Activin-A, a TGF-β superfamily member closely related to TGF-β1, in pathogenic Th17 cell differentiation. Activin-A expression was increased in individuals with relapsing-remitting multiple sclerosis and in mice with experimental autoimmune encephalomyelitis. Stimulation with interleukin-6 and Activin-A induced a molecular program that mirrored that of pathogenic Th17 cells and was inhibited by blocking Activin-A signaling. Genetic disruption of Activin-A and its receptor ALK4 in T cells impaired pathogenic Th17 cell differentiation in vitro and in vivo. Mechanistically, extracellular-signal-regulated kinase (ERK) phosphorylation, which was essential for pathogenic Th17 cell differentiation, was suppressed by TGF-β1-ALK5 but not Activin-A-ALK4 signaling. Thus, Activin-A drives pathogenic Th17 cell differentiation, implicating the Activin-A-ALK4-ERK axis as a therapeutic target for Th17 cell-related diseases.

overall_design:
A: mRNA profiles of CA-ALK4 and CA-ALK5 transduced Th17 cells in the presence of IL-6 were generated by deep sequencing, in triplicate, using BGI’s unique DNBseq™.
B: mRNA profiles of Th17 cells differentiated by IL-1b+IL-6+IL-23, TGFb1+IL-6 and Activin A+IL-6 were generated by deep sequencing, in triplicate, using BGI’s unique DNBseq™.
C: mRNA profiles of Th17 cells differentiated by IL-1b+IL-6+IL-23, IL-1b+IL-6+IL-23+anti-Activin-A were generated by deep sequencing, in triplicate, using BGI?s unique DNBseq.
D: mRNA profiles of T cells differentiated by IL-6, IL-6+ Activin-A were generated by deep sequencing, in triplicate, using BGI?s unique DNBseq.

first: Bing

last: Wu

first: Ping

last: Li

first: Xiaojiang

last: Xu

first: Jian


title: Preservation of MYBBP1A at the chromatin in MYBBP1A hemizygous cells

city: Philadelphia

first: Gregory

last: Donahue

state: PA

address: 3400 Civic Center Blvd, Bldg 421

department: Cell & Developmental Biology

institute: The University of Pennsylvania

type: Genome binding/occupancy profiling by high throughput sequencing

summary: MYB Binding:    Protein 1 A (MYBBP1A) is hemizygous in a majority of PDAC due to chromosome 17p deletion  which also affects TP53. We generated isogenic homozygous and hemizygous MYBBP1A  knockout cell lines to elucidate MYBBP1A function in cancer. As the function of MYBBP1A at the chromatin is unclear, we performed MYBBP1A ChIPseq in MYBBP1A wild-type and hemizygous cells. Surprisingly, despite the hemizygous cells expressing decreased MYBBP1A expression, the whole genome binding profile is largely similar compared to MYBBP1A wild-type cells.

overall_design: ChIPseq of MYBBP1A was performed on CRISPR modified pancreatic cancer cell line HS766T

first: Antony

last: Hsieh

first: Jason

last: Pitarressi

first: Jonathan

last: Lerner

first: Greg

first: David

last: Hsiehchen

first: Anil

last: Rustgi

first: Kenneth

last: Zaret


title: Regulation of the circadian clock by the metabolic enzyme AHCY

city: Irvine

first: Christophe

middle: Nicolas

last: Magnan

state: CA

address: Institute for Genomics and Bioinformatics 236, Info & Computer Science Building 2

institute: University of California, Irvine

summary: Mammalian circadian rhythms are based on coupled transcriptional-translational feedback loops driven by the transcription factors CLOCK and BMAL1. Chromatin remodeling mechanisms are essential for the proper timing and extent of circadian gene expression. We report that the S-adenosylhomocysteine (SAH) hydrolysing enzyme AHCY binds to CLOCK-BMAL1 at chromatin and drives circadian transcription by promoting  cyclic H3K4 trimethylation and recruitment of BMAL1 to chromatin.

overall_design: To study how AHCY affects circadian gene expression we generated AHCY knock out MEF cell lines by performing CRISPR-Cas9 mediated gene editing or treated MEF with a specific inhibitor for AHCY (Dznep). MEF cells were synchronized with dexamethasone and RNA extracted at specific circadian time points (CT).  To study the role of AHCY for circadian physiology in vivo, we delivered DZnep or saline into the hypothalamus of mice by direct infusion and extracted RNA from the suprachiasmatic nucleus (SCN) at specific CT.

first: Carolina

last: Greco

first: Paolo

last: Sassone-Corsi

first: Pierre

last: Baldi

first: Nicholas

last: Ceglia

first: Muntaha

last: Samad


title: Protein-coding and non-coding RNA expression in whole blood leukocytes during experimental human endotoxemia.

city: Msida

first: Brendon

last: Scicluna

address: Msida campus

country: Malta

institute: University of Malta

summary: Genome-wide gene expression profiling of whole blood leukocytes during experimental human endotoxemia has been used extensively to model acute systemic host responses. Through technological advances in genomics it has become clear that transcription is not limited to protein-coding regions of the genome. Here, we describe a comprehensive analysis of RNA expression of blood leukocytes in healthy volunteers during experimental human endotoxemia.

overall_design: Whole-blood transcriptional patterns of protein-coding and non-coding RNA molecules were generated by means of the human transcriptome array 2.0 (HTA 2.0) chip. Whole blood of healthy male participants was collected before and 2, 4, 6 and 24 hours after intravenous administration of 2ng/kg Escherichia coli lipopolysaccharide (LPS). The Dutch Central Committee on Research Involving Human Subjects (CCMO) and the Medical Ethics Committee of the Academic Medical Center (AMC), Amsterdam, the Netherlands, approved the study. Title legend: endo_0h, healthy subjects before LPS administration; endo_2h, endo_4h, endo_6h, endo_24h, healthy subjects after 2, 4, 6 and 24 hours LPS administration, respectively; endo_dup_0h, duplicate samples of healthy subjects before LPS administration.

middle: P

first: Tom

last: van der Poll


title: m6A alterations through FTO in breast cancer [RNA-seq]

city: Gosselies

first: Martin

last: Bizet

address: Rue Adrienne Bolland, 8

country: Belgium

institute: Université Libre de Bruxelles

summary: Our understanding of posttranscriptional modifications that decorate RNA, a regulatory layer positioned between DNA and proteins, is in its infancy. N6-methyladenosine (m6A) is the most prevalent internal modification in messenger RNAs that is installed and erased by m6A methyltransferases and demethylases. The importance of these enzymes in cancer is rapidly emerging, yet information of their specific mode of actions during disease progression remain largely unknown. In the present study, we report that the m6A RNA demethylase FTO controls EMT and invasion in cancer through regulation of the Wnt pathway. We find that loss of FTO, in contrast to acute myeloid leukemia, is frequent in many cancer types, including breast and prostate cancers. Knockdown of FTO promotes tumor progression – specifically migration and invasion – in breast and prostate cancer cells. Furthermore, implantation of these cells accelerates tumor progression in recipient mice in vivo. In these tumors, FTO depletion leads to m6A-dependent activation of Wnt signaling, which drives an enhanced EMT program and invasion, thus leading to poor clinical outcome. However, loss of FTO also sensitizes cancers cells to Wnt inhibition, offering a rationale for the therapeutic targeting of Wnt for cancer patients with low FTO levels. Together, our work reveals FTO as a novel regulator of EMT and an unexpected mechanism by which Wnt signals are dysregulated in tumors, providing a rationale to stratify cancer patients treated with Wnt inhibitor. These data uncover a previously unrecognized relationship between RNA modification and EMT in cancer.

overall_design: Transcriptome sequencing in RNAi-depleted FTO (5 samples) and control (5 samples) SK-BR-3 cells.

first: Jana

last: Jeschke

first: Evelyne

last: Collignon

first: Clémence

last: Al Wardi

first: Mohammad

last: Krayem

first: Yan

last: Jia

first: Emilie

last: Calonne

first: Bouchra

last: Hassabi

first: Zena

last: Wimana

first: Renato

last: Morandini

first: Rachel

last: Deplus

first: Pascale

last: Putmans

first: Gaurav

last: Dube

first: Nitesh

last: Singh

first: Alexander

last: Koch

first: Kateryna

last: Shostak

first: Lara

last: Rizzotto

first: Robert

last: Ross

first: Soizic

last: Garaud

first: Christine

last: Desmedt

first: Yaccine

last: Bareche

first: Françoise

last: Rothe

first: Jacqueline

last: Lehmann-Che

first: Martine

last: Duterque-Coquillaud

first: Xavier

last: Leroy

first: Gerben

last: Menschaert

first: Luis

last: Teixeira

first: Mingzhou

last: Guo

first: Patrick

middle: A

last: Limbach

last: Close

first: Alain

last: Chariot

first: Eleonora

last: Leucci

first: Ghanem

last: Ghanem

first: Bi-Feng

last: Yuan

first: Christos

last: Sotiriou

first: Jean-Christophe

last: Marine

first: François

last: Fuks


title: MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with Host Cell Factor-1

city: Nashville

first: Jing

last: Wang

state: TN

address: 2220 Pierce Avenue

institute: Vanderbilt University Medical Center

summary: MYC is an oncoprotein transcription factor that is overexpressed in the majority cancers. Although MYC itself is considered undruggable, it may be possible to inhibit MYC by targeting the co-factors it uses to drive oncogenic gene expression patterns. Here, we use loss- and gain- of function approaches to interrogate how one MYC co-factor—Host Cell Factor (HCF)-1—contributes to MYC activity in a Burkitt lymphoma setting. We identify high-confidence direct targets of the MYC–HCF-1 interaction that are regulated through a recruitment-independent mechanism, including genes that control mitochondrial function and rate-limiting steps for ribosome biogenesis and translation. We describe how these gene expression events impact cell growth and metabolism, and demonstrate that the MYC–HCF-1 interaction is essential for tumor maintenance in vivo. This work highlights the MYC–HCF-1 interaction as a focal point for development of novel anti-cancer therapies.

overall_design: The Burkitt lymphoma line Ramos cells was modified using CRISPR/Cas9-triggered homologous recombination to create either MYC switchable allele (MYC-WT, MYC-4A, MYC-VP16 HBM) or FKBP12FV N-terminally tagged HCF-1 cell lines. These cells were used for RNA-seq and ChIP-seq.

first: William

last: Tansey

first: Tessa

last: Popay

first: Qi

last: Liu


title: Stimulation of functional neuronal regeneration from Müller glia in adult mice

status: Public on Jan 10 2021

city: SEATTLE

first: THOMAS

last: REH

state: WA

address: 1959 NE PACIFIC STREET

department: BIOLOGICAL STRUCTURE

institute: UNIVERSITY OF WASHINGTON

summary: Many retinal diseases lead to the loss of retinal neurons and cause visual impairment. The adult mammalian retina has little capacity for regeneration. By contrast, teleost fish functionally regenerate their retina following injury, and Müller glia (MG) are the source of regenerated neurons. The proneural transcription factor Ascl1 is upregulated in MG after retinal damage in zebrafish and is necessary for regeneration. Although Ascl1 is not expressed in mammalian MG after injury, forced expression of Ascl1 in mouse MG induces a neurogenic state in vitro and in vivo after NMDA (N-methyl-d-aspartate) damage in young mice. However, by postnatal day 16, mouse MG lose neurogenic capacity, despite Ascl1 overexpression. Loss of neurogenic capacity in mature MG is accompanied by reduced chromatin accessibility, suggesting that epigenetic factors limit regeneration. Here we show that MG-specific overexpression of Ascl1, together with a histone deacetylase inhibitor, enables adult mice to generate neurons from MG after retinal injury. The MG-derived neurons express markers of inner retinal neurons, synapse with host retinal neurons, and respond to light. Using an assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq), we show that the histone deacetylase inhibitor promotes accessibility at key gene loci in the MG, and allows more effective reprogramming. Our results thus provide a new approach for the treatment of blinding retinal diseases.

overall_design: Three ANT-treated Glast-CreER animals had their retinas pooled and were dissociated for FACS purification. Live purified cells were then pelleted at 300 g for 10 minutes at 4 şC and resuspended in 0.04% BSA in PBS at a concentration of 2,000 cells per uL. Cells were then loaded onto the Single Cell 3 Chip with a targeted cell recovery of 4000 cells. For control animals, two Rlbp-CreER: tdTomato animals had their retinas pooled and were run in parallel at equal cell concentrations. GEM generation and barcoding, RT, cleanup, cDNA amplification, and library construction were performed according to the Chromium Single Cell 3 Reagent Kits User Guide. Library QC was determined by TapeStation (Agilent Technologies, Inc., Santa Clara, CA). Single Cell libraries were sequenced on the Illumina NextSeq 500/550 v2 kit. Reads were processed in Cell Ranger (10x Genomics) and aligned to mm10.

first: Nikolas

last: Jorstad

first: Matthew

last: Wilken

middle: N

last: Grimes

first: Stefanie

last: Wohl

first: Leah

last: VandenBosch

first: Takeshi

last: Yoshimatsu

first: Rachel

middle: O

last: Wong

first: Fred

last: Rieke

first: Thomas

last: Reh


title: Small non-coding RNA expression in whole blood leukocytes of healthy subjects, critically-ill patients with sepsis or non-infectious etiology and human endotoxemia

first: Brendon

last: Scicluna

summary: Genome-wide gene expression profiling of whole blood leukocytes in critically ill patients with sepsis or non-infectious disease has been used extensively in search of diagnostic biomarkers, as well as prognostic signatures reflecting diseases severity and outcome. Through technological advances in genomics it has become clear that transcription is not limited to protein-coding regions of the genome. Here, we describe a comprehensive analysis of small non-coding RNA expression in blood leukocytes of critically ill patients with sepsis, a non-infectious condition, healthy subjects and experimental human endotoxemia

overall_design: Whole-blood transcriptional patterns of small non-coding RNA molecules in healthy subjects, critically-ill patients with sepsis or non-infectious conditions and experimental human endotoxemia (2ng/kg Escherichia coli lipopolysaccharide (LPS)) were generated by means of the Affymetrix Multispecies miRNA-4_1 Array. Whole-blood from patients was collected within 24 hours of intensive care unit (ICU) admission. Whole blood of healthy male volunteers who participated in a human endotoxemia study was collected before and 2, 4, 6 and 24 hours after intravenous LPS administration. The Dutch Central Committee on Research Involving Human Subjects (CCMO) and the Medical Ethics Committee of the Academic Medical Center (AMC), Amsterdam, the Netherlands, approved the study. Title legend: healthy, healthy subjects; sepsis, ICU patients with sepsis; noninfectious, ICU patients with non-infectious condition; endo_0h, healthy subjects before LPS administration; endo_2h, endo_4h, endo_6h, endo_24h, healthy subjects after 2, 4, 6 and 24 hours LPS administration, respectively.

first: Tom

last: van der Poll


city: RTP

first: NIEHS

last: Microarray Core

address: 111 T.W. Alexander Drive

department: DIR

institute: NIEHS

summary: Glucocorticoids and estrogen antagonism in cardiomyocytes negatively influences cell survival in the female heart after MI by a mechanism involving GR inhibition of ERalpha-dependent transcriptional regulation.

overall_design: RNA was isolated from HL-1 cells treated with vehicle, dexamethasone (Dex), estradiol (E2), and combination of Dex+E2 for 6 hours. Four independent experiments were performed.

first: Diana

last: Cruz-Topete

first: John

last: Cidlowski


title: PTBP1 is necessary for dendritic cells to regulate T cells homeostasis and antitumor immunity

city: TianJin

first: Changlu

last: Xu

state: TianJin

address: 288 Nanjing Rd, Heping

department: State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Institute of Hematology & Blood Diseases Hospital

institute: Chinese Academy of Medical Sciences & Peking Union Medical College

summary: Dendritic cells (DCs) play an important role in innate and adaptive immunity. DCs could sense environment pathogens and tumors, presenting those antigens to T cells. PTBP1, an RNA-binding protein, the function in DCs is unknown. Here, we found PTBP1 specific deficiency in DCs could impair T cell homeostasis. PTBP1 deletion in DCs could enhance antitumor immunity and increase asthma exacerbation. Further studies demonstrate that PTBP1 negatively regulates the induction of a subset of IFN-response genes. These findings revealed the novel functions of PTBP1 in DCs and might be a potential therapeutic target for tumors.

overall_design: Here, we performed RNA-seq of Dendritic cells(DCs) from Ptbp1 deficient mouses and WT to further study the molecular changed between KO and WT.

first: Guangfeng

last: Geng

first: Yushan

last: Zhu

first: Lihong

last: Shi


title: Two super-enhancers regulate Nanog expression through distinct mechanisms [45del]

city: Milwaukee

first: Sridhar

last: Rao

state: WI

address: 8727 Watertown Plank Road

department: Blood Research Institute

institute: BloodCenter of Wisconsin

summary: Enhancers are critical regulators of gene expression which are historically defined using plasmid-based approaches. Recent work has emphasized that enhancers operate by alleviating promoter-proximal pause release, implying that a single enhancer operates on a gene at any given moment. By contrast, our previous work postulated that two super-enhancers (SEs) may simultaneously operate on a single gene. To address this discrepancy we employed genomic editing, single cell analyses, and genome-wide approaches to assess how two SEs regulate Nanog expression in embryonic stem cells. We first demonstrate both distance and orientation independence in native chromatin, eliminating the issues raised with plasmid-based approaches. We also demonstrate that two SEs simultaneously operate on Nanog by regulating different phases of transcription, with one SE operating by recruiting and/or initiating RNA Polymerase II, and the second promoting transcriptional elongation after promoter-proximal pause release. These findings imply SEs can use different mechanisms to regulate expression.

overall_design: RNA-seq of 2 conditions, 3 replicates of each

first: Puja

last: Agrawal


title: The negative elongation factor NELF promotes active transcription of Drosophila ecdysone-dependent genes

city: Moscow

first: Nadezhda

last: Vorobyeva

address: Vavilova 34/5

country: Russia

institute: Institute of Gene Biology RAS

summary: The current work describes molecular mechanism used by the Negative elongation complex (NELF) to control the Pol II pause at genes whose transcription is induced by 20-hydroxyecdysone (20E). According to our data NELF complex is recruited to the promoters and enhancers of 20E-dependent genes. Its presence at the regulatory sites of 20E-dependent genes correlates with the described interaction of its NELF-A subunit with EcR receptor. The NELF complex, consisting of at least three subunits, is formed at the 20E-dependent promoters and participates in their active transcription and maintenance of their repressed state. NELF depletion causes a significant decrease in transcription induced by 20E. We associate this effect with the disruption of Pol II elongation complexes formation. A considerable reduction in the promoter-bound level of Spt5 subunit of DSIF was observed at the 20E-dependent genes upon NELF depletion. We presume that participation in stabilization of the Pol II-DSIF complex can be an important function of NELF with a big impact on transcription of its target genes. Part of our study was to directly link NELF to regulation of 20E-dependent genes in development. We showed presence of NELF at the promoters of 20E-dependent genes during their active transcription both in embryogenesis and metamorphosis. We also demonstrate that 20E-dependent promoters remain in a Pol II paused state at the larva stage, where they are temporarily repressed.

overall_design:
ChIP-Seqs by anti-NELF-A, anti-NELF-B, Rpb3, Pol II S2P, Pol II S5P, Spt5 antibodies were performed after 1 hour treatment with 20-hydroxyecdysone (20E 1h)  and in DMSO (Control) treated S2 Schneider cells (both states was treated by dsRNA against NELF-A/NELF-B or mock treated by dsRNA to GFP). ChIP-Seq by anti-NELF-A, Rpb3, Pol II S2P  antibodies were performed on embryos of various stages (2-4h, 6-8h, 10-12h after egg laying AEL) and on larvae L3 PS 1-3 (full gut) and prepupae 0-1h after puparium formation APF (Oregon-Modencode). ChIP-Seqs by anti CBP/Neijre and NELF-E antibodies were performed after 1 hour treatment with 20E (20E 1h) and in DMSO (Control) treated S2 Schenider cells. RNA-Seq were performed after 1 hour treatment with 20-hydroxyecdysone (20E 1h)  and in DMSO (Control) treated S2 Schneider cells.
RNA-Seq were performed after 1 hour treatment with 20-hydroxyecdysone (20E 1h)  and in DMSO (Control) treated S2 Schneider cells.

first: N


title: Genetic variants associated with coronary artery disease in Indians

city: Mumbai

first: TESTER

middle: F

last: ASHAVAID

state: Maharashtra

address: Lalita Girdhar bldg,3rd floor,Biochemistry Dept.,, V.S.Marg, Mahim

department: Lab Medicine

country: India

institute: P.D. HINDUJA HOSPITAL & MRC

summary:
Genetic variations were successfully associated among patients with coronary artery disease using Illumina Cardiometabochip containing 1,96,725 SNPs
Illumina Cardio-metabochip is a custom designed SNP microarray containing 1,96,725 SNPs designed by several GWAS and consortia

overall_design: In the study conducted at Hinduja Hospital, genetic variants were associated among a cohort of 150 angiographically proven coronary artery disease patients versus 150 angiographically verified negative controls using Illumina's Cardiometabochip containing 1,96,725 SNPs

first: Tester

last: Ashavaid

first: Sarosh

last: Fatakia

first: Sripriya

last: Natrajan

first: Prerna

last: Chawla

first: Ashley

last: Stanley

first: Prajakta

last: Kadam

first: Basuthkar

first: Chandrashekhar

last: Ponde

first: Rajesh

last: Rajani


title: Loss of Rab22a prevents Angiotensin II-induced Hypertension and vascular dysfunction by inhibiting AT1R recyling

city: Fuzhou

first: Jun

last: Peng

state: Fujian

address: 1 Qiuyang Road, Minhou Shangjie

department: Academy of Integrative Medicine

institute: Fujian University of Traditional Chinese Medicine

summary: The goals of this study is to compare the differently expressed genes in abdominal aorta of Rab22a KO mice and Rab22a WT mice with or without Angiotensin II treatment for 14 days at the concentration of 500ng/kg/min.The mice (n=20) were randomly divided into 4 groups:WT+AngII,WT+NS,KO+AngII,KO+NS (n = 5 for each group). Mice in WT+NS and KO+NS groups were infused with saline or 500 ng/kg/min of WT+AngII and KO+AngII respectively. Then the abdominal aorta were used to identify differentially expressed genes among different groups.

overall_design: RNA sequencing was performed with abdominal aorta of  mice in 4 groups (WT+AngII,WT+NS,KO+AngII,KO+NS,n = 5 for each group) to identify the differently expressed genes and related pathway.

first: Aling

last: Shen

first: Xiangyan

last: Wu

first: Zhiqing

first: Ying

last: Cheng


title: Identification of Genes Promoting Resistance to Enzalutamide

city: Salisbury

first: Philip

middle: D

last: Anderson

state: Maryland

address: 1101 Camden Avenue

department: Biological Sciences

institute: Salisbury University

summary: In 2012, the US Food and Drug Administration approved enzalutamide (Xtandi) for the treatment of patients with metastatic castration-resistant prostate cancer who have previously received docetaxel. In most patients, enzalutamide halts progression of the disease for a short period of time, but patients usually relapse, which is associated with poor prognosis. Identifying the genes and pathways that the cancer cells use to overcome enzalutamide are of interest, because new interventions aimed at preventing relapse after enzalutamide therapy would have therapeutic value to late-stage prostate cancer patients. In this study, we took advantage of RNA interference techniques and an in vitro model of castration-resistant prostate cancer cells to identify genes that drive resistance to enzalutamide.

overall_design: We transduced one-third of a commercially-available barcoded lentiviral shRNA library (DECIPHER Module 1 from Cellecta) into C4-2B cells. The shRNA library contained shRNA clones targeting approximately 5045 human genes. The shRNA integrated into the chromosomal DNA of the transduced C4-2B cells and stably knocked down messenger RNA transcripts. Our methodology called for the establishment of three populations of transduced C4-2B cells, which were maintained for six days before the cells were harvested and genomic DNA extracted. The first population (hereafter, "Initial") is a control that was maintained in the absence of enzalutamide and DMSO, which is the solvent for enzalutamide. The second population ("EnzNeg") was maintained in the presence of DMSO, but not enzalutamide, to control for the effects of the solvent. The third population ("EnzPos") was a test population maintained in the presence of both DMSO and enzalutamide. Genomic DNA from two replicates from Initial and three replicates from each of EnzNeg and EnzPos were subjected to targeted deep sequencing on an Illumina HiSeq 2500, for a total of eight samples. The targeting protocol specifically promoted the sequencing of the bar-coded shRNA in the genome. In this analysis, we count the number of times each shRNA bar-code was sequenced in the eight samples, and calculate the ratio of the abundance of each shRNA in EnzPos versus both control groups. Our hypothesis is that if a shRNA-targeted gene helps cancer cells to achieve resistance  when selected by enzalutamide, we will observe fewer bar-codes for those genes relative to both controls (which translates into more mRNA for the gene in EnzPos than both controls). A given shRNA was considered a “hit” if it showed at least two-fold abundance decrease in enzalutamide-positive relative to both enzalutamide-negative control and initial samples.

first: Wisam

last: Awadallah

first: Robert

last: Phillips

first: Thomas

middle: C

last: Case

first: Renjie

last: Jin

first: Jagpreet

last: Nanda

first: Xiuping

last: Yu

first: Peter

last: Clark

first: Yajun

last: Yi

middle: J

last: Matusik

first: Magdalena

last: Grabowska


title: The study of EF4 mediated gene expression under tetracycline stress in two Escherichia coli strains

status: Public on Jan 09 2021

city: Beijing

first: Bin

last: Liu

state: Beijing

address: Hai Dian

department: School of Life Sciences

institute: Tsinghua University

summary:
Purpose: We use the gene expression data to estimate the effects of tetracycline on gene expression and average ribosome density.
Methods: The mRNAs were extracted with TRIzol reagent.  The mRNAs were fragmented into 280 bp and the sequencing process was conducted on HiSeq 2500 platform.  We use cutadapt, bowtie2, Plastid and DEseq2 software to analyze the expression levels of genes in two Escherichia coli strains.
Results: The gene expression in EF4 knockout Escherichia coli strain was similar with BW25113 strain under normal condition. Under tetracycline treatment, many genes' expression were differentially regulated. Interestingly, we found that the gene expression of ribosomal proteins was up-regulated in WT strain comparing with EF4 knockout E. coli strain.
Conclusions: Our results suggest that EF4 affects the average ribosome density and global gene expression in two Escherichia coli strain under tetracycline treatment.

overall_design: mRNA from WT and ΔEF4 strains and the two strains treated with tetracycline were fragmented and sequenced, in two replicates, using Illumina HiSeq 2500.

first: Chunlai

last: Chen


title: Forkhead box E1 (FOXE1) RNAis vs control RNAi in HEKa cells

city: Xi'an

first: Yan

last: Zheng

state: China

address: Xi'an Jiaotong University, No. 28 Xianning West Road, Beilin District, Xi'an, Shaanxi Province

institute: the second affiliated hospital of Xi'an Jiaotong University

summary: Analysis of HEKa cells depleted of Forkhead box E1 (FOXE1). FOXE1  is induced in psoriasis lesions and promotes keratinocytes. Results provide insight into the downstream targets of FOXE1 function in psoriasis.

overall_design: HEKa cells were transfected with 2 kinds of FOXE1-specific RNAis or control RNAi. After 48 hours, cell were harvested and lysed with TRIzol reagent. A total amount of 1 μg RNA per sample was uesd as input material for the RNA sample preparations.

first: Yongping

last: Shao

first: Meng

first: Guanfei

last: Zhang


title: Loss of m6A RNA methylation during glioma stem cell differentiation is regulated by miRNAs and promotes translation efficiency

city: Providence

first: Nikos

last: Tapinos

state: RHODE ISLAND

address: 593 Eddy street

department: Neurosurgery

institute: Brown University

summary: This study highlights a critical role of m6A RNA methylation in regulation of translation in human cancer cells and identifies regulatory miRNAs that functionally influence the epitranscriptome during glioma stem cell differentiation.

overall_design: RNA-seq, MeRIP-seq, Ribo-seq

first: Eduardo

last: Fajardo


title: Gene expression in the brain of sporadic Creutzfeldt-Jakob disease patients (CJD), and normal controls (CT)

status: Public on Jan 08 2021

city: Copenhagen N

last: Litman

state: Outside the US or Canada

address: Blegdamsvej 3C

department: ISIM

institute: University of Copenhagen

summary:
Neuroinflammation is an essential part of neurodegeneration. Yet, current understanding of neuroinflamma-tion associated molecular events in distinct brain regions of prion disease patients is insufficient to lay the ground for effective treatment strategies targeting this complex neuropathological process. To address this problem, we analyzed expression of 800 neuroinflammation associated genes to create a profile of biological processes taking place in frontal cortex and cerebellum of patients, who suffered from sporadic Creutzfeldt-Jakob disease. The analysis was performed using NanoString nCounter technology, human neuroinflamma-tion panel+. The observed gene expression patterns indicate regionally, and sub-regionally common and dis-tinct molecular pathways associated with sporadic Creutzfeldt-Jakob disease pathogenesis. Moreover, the data show that the neuroinflammatory response in samples from the same brain region is variable.
Based on the gene expression profiles from FC and CB, regional, neuroinflammatory patterns were observed.

overall_design: Frexh frozen brain samples were collected from frontal cortex (FC) and cerebellum (CB) from 14 CJD patients and 10 brain donors. In total, 27 CJD and 20 normal controls (CT) were profiled by NanoString gene expression analysis

first: Ausrine

last: Areskeviciute

first: Jens

last: Eriksen


title: A forward genetic screen for regulators of muscle morphogenesis in Drosophila

city: St. Louis

first: Aaron

last: Johnson

state: MO

address: 600 S Euclid

institute: Washington University School of Medicine in St. Louis

summary: We performed a forward genetic screen and used RNAseq to identify potential variants in 6 independent strains. This approach successfully identified causative variants.

overall_design: Variant calling by RNAseq of 6 Drosophila lines, with two technical replicates per line.

first: Paul

last: Gontarz


title: In vivo chemical reprogramming of astrocytes into neurons

first: Yan-Tao

last: Ma

address: No. 5 Yiheyuan Road

institute: Peking University

summary: We established a chemical cocktail that converts astrocytes into neuronal-like cells in vitro.

overall_design: mRNA profiles of chemical-induced neurons at different time-points in vitro.

first: Yantao

first: Longteng

last: Wang

first: Handan

last: Xie

first: Xiaomin

last: Du

first: Hongkui

last: Deng


title: Serotonin receptor 4 in the hippocampus modulates mood and anxiety

city: New York

first: Eric

last: Schmidt

state: NY

address: 1230 York Avenue

institute: The Rockefeller University

summary: Serotonin receptor 4 (5‑HT4R) plays an important role in regulating mood, anxiety, and cognition, and drugs that activate this receptor have fast-acting antidepressant (AD)-like effects in preclinical models. However, 5‑HT4R is widely expressed throughout the central nervous system (CNS) and periphery, making it difficult to pinpoint the cell types and circuits underlying its effects. Therefore, we generated a Cre-dependent 5‑HT4R knockout mouse line to dissect the function of 5‑HT4R in specific brain regions and cell types. We show that the loss of functional 5‑HT4R specifically from excitatory neurons of hippocampus led to robust AD-like behavioral responses and an elevation in baseline anxiety. 5‑HT4R was necessary to maintain the proper excitability of dentate gyrus (DG) granule cells and cell type specific molecular profiling revealed a dysregulation of genes necessary for normal neural function and plasticity in cells lacking 5‑HT4R. These adaptations were accompanied by an increase in the number of immature neurons in ventral, but not dorsal, dentate gyrus, indicating a broad impact of 5‑HT4R loss on the local cellular environment. This study is the first to use conditional genetic targeting to demonstrate a direct role for hippocampal 5‑HT4R signaling in modulating mood and anxiety. Our findings also underscore the need for cell type-based approaches to elucidate the complex action of neuromodulatory systems on distinct neural circuits.

overall_design: Polysome-bound mRNAs from TRAP IPs were compared to whole tissue mRNAs (input) or TRAP IP mRNAs were compared between wildtype (WT) and conditional Htr4 knockouts (cKO). Data was collected from neurons in the ventral dentate gyrus using TRAP. We collected three replicates for WT IP and inputs, while cKO data was collected in duplicate.

first: Nathaniel

last: Heintz


title: Induction of spontaneous human neocentromere formation and long-term maturation (NativeCA ChIP-Seq)

city: Oxford

first: Marina

last: Murillo-Pineda

address: South Parks Road

department: Department of Biochemistry

institute: University of Oxford

summary: We report a chromosome engineering system for human neocentromere formation and characterize the first experimentally generated human neocentromere. Neocentromere formation promotes local H3K9me3 eviction and cohesin and RNA polymerase II recruitment. Long-term culture results in gradual maturation of the inner centromere.

overall_design: CENP-A occupancy in survivor clone after endogenous centromere deletion containing a neocentromere to detect the exact genomic position of this neocentromere formation event.

first: Lars

middle: T

last: Jansen


title: Expression data from Human liver biopsy

status: Public on Jan 07 2021

city: Toronto

first: Marc

last: Angeli

state: Ontario

address: 101 College street

department: Multi Organ Transplant

institute: University Health Network

summary: Liver transplantation (LT) for Hepatocellular carcinoma (HCC) can be offered to patients beyond Milan criteria. However, there are currently no molecular markers that can be used on HCC explant histology to predict recurrence, which arises in up to 20% of LT recipients . The goal of our study was to identify proteins on HCC explant predictive of recurrence post-transplant, thereby guiding surveillance strategies and identifying patients beyond Milan criteria who would fare well following LT.

overall_design: Patients having received a LT for HCC beyond Milan criteria in the context of hepatitis B cirrhosis were identified. Tumor explants from patients with recurrence (N=6) versus those without recurrence (N=3) were analyzed by mass spectrometry and gene expression array

first: Mamatha

last: Bhat


title: Induction of spontaneous human neocentromere formation and long-term maturation (QuantChIP-Seq)

overall_design: Examination of the indicated proteins occupancy before  (parental cell line,S40-RPE) and after neocentromere formation (neocentromere cell line,Neo4p13) . Same analysis in Neo4p13 after long-term continuous culture (Neo4p13_100d and 200d). All samples were spiked-in 1% crosslinked immortalized mouse embrionic fibroblats (MEFs) for quantitative analysis.


title: RNA-seq of Microcystis aeruginosa PCC7806: on hydrogen peroxide

city: Seoul

first: Minkyung

last: Kim

address: Anam-ro 145, Seongbuk-gu

department: Laboratory of molecular environmental microbiology

country: South Korea

institute: Korea University

summary: Comparison for gene expression of Microcystis aeruginosa PCC7806 after hydrogen peroxide treatment

overall_design: 1 control (no treatment) and 1 sample (140 µM H2O2), 1h at 25 °C with light condition


title: Transcriptome analysis of intellectual disability patients with mutation in transcription factor genes

city: Tehran

first: kolsoum

last: InanlooRahatloo

address: velenjak

country: Iran

institute: University of social welfare and rehabilitation sciences

summary: In the current study, we applied whole transcriptome analysis using RNA-seq to identify biological and molecular pathways underling ID disease in families with mutation in CCNT2, CDK9, and TAF2 transcription factors. The transcriptional profile showed significant deregulation of gene expression patterns with an emphasis on genes related to neuronal and skeletal functions.

overall_design: 12 blood samples were analyzed, 6 patients and 6 controls

first: Kolsoum

first: Hossein

last: Najmabadi


title: Expressions of MicroRNA in Mouse Kidney with Unilateral Ureteral Obstruction

city: Saitama

first: Shohei

last: Kaneko

state: Saitama

address: 1-847 Amanuma-cho, Omiya-ku

country: Japan

institute: Saitama Medical Center, Jichi Medical University

summary: Renal fibrosis is the final common pathway for chronic kidney disease. However, the detailed mechanisms and therapeutic strategies for renal fibrosis have not been established. MicroRNAs (miRNAs) are small, non coding RNAs that regulate various pathological conditions and diseases. Previous studies reported that miRNAs play a pivotal role in renal fibrosis. However, the role of miRNAs in renal fibrosis has not been completely elucidated. Therefore, in this study, miRNAs on renal fibrosis was investigated in a renal fibrosis mouse model generated by unilateral ureteral obstruction. MiRNA microarray analysis revealed 109 miRNAs that were upregulated more than 2 fold and 113 miRNAs that were downregulated less than 0.5 fold in the kidney of UUO mice compared with control mice.

overall_design: Kidney tissue obtained 7 days after unilateral ureteral obstruction surgery or sham surgery was used for microarray analyses (n = 4, each group ).


title: RNA-seq analysis of primarily cultured neurospheres from FGF13Aoe and control mice

city: Shanghai

first: Qiaoqiao

last: Yang

address: 320 Yue Yang Road

department: Institute of Neuroscience

institute: Chinese Academy of Sciences

summary: To reveal the mechanisms of FGF13A in regulation of neural progenitor development, we carried out RNA-seq gene expression profiling analysis in primarily cultured neurospheres from neonatal FGF13Aoe mice.  2 biological independent sample from FGF13oe (hGAFPCre+;ROSA26FGF13A LSL/+) mice mice were compared with 2 independentlitermate control(hGAFPCre+, ROSA26FGF13A +/+) samples.

overall_design: RNAseq from Primarily cultured neurospheres from FGF13Aoe and litermate control mice, 2 samples in each group,  using Illumina2000.


title: ATAC-seq from primarily cultured neurospheres from FGF13cko and control mice

summary: To identify the changes of chromatin structure in neural progenitors upon Fgf13 depletion, we compared the chromatin accessibility of primarily cultured hippocampal neurosphere from neonatal FGF13cko (hGAFPCre+;Fgf13 flox/y) mice and litermate control (hGAFPCre+;Fgf13 +/y) mice by ATAC-seq analysis.

overall_design: We compared the chromatin accessibility of primarily cultured hippocampal neurosphere from neonatal FGF13cko mice and litermate control mice by ATAC-seq, 2 samples in each group.


title: RNA-seq analysis of primarily cultured neurospheres from ARID1B haploinsufficient and control mice

summary: To identify ARID1B associated  genes in development of neural progenitor , we carried out RNA-seq gene expression profiling analysis in primarily cultured neurospheres from ARID1B haploinsufficient and control mice.  3 biological independent sample from ARID1B hi (hGAFPCre+;ARID1B flox/+) mice were compared with 2 independent litermate control (hGAFPCre+; ARID1B +/+) samples.

overall_design: RNAseq from Primarily cultured neurospheres from ARID1B haploinsufficient  and control mice, 3 samples in ARID1B hi group and 2 samples in litermate control group , using Illumina HiSeq Xten.


title: The identification of plasma exosomal miR-423-3p as a potential predictive biomarker for prostate cancer castration-resistance development by plasma exosomal miRNA sequencing

city: LONDON

first: YONG-JIE

last: LU

address: Charterhouse Square

department: Barts Cancer Institute

institute: BLSMD, Queen Mary University of London

type: Non-coding RNA profiling by high throughput sequencing

summary:
Exosomal miRNAs play important roles in cancer progression and therapeutic resistance and have shown great potential as liquid biopsy biomarkers for cancer diagnosis/prognosis. We investigated for the first time plasma exosomal miRNAs for their association with and early detection potential of castration-resistant prostate cancer (CRPC).
RNA-sequencing was performed to identify candidate exosomal miRNAs associated with development of CRPC in 24 treatment-naive prostate cancer (PCa) and 24 CRPC patients.

overall_design: Examine differentially expressed plasma exosomal miRNAs between 24 treatment-naïve prostate cancer patients and 24 castration-resistant prostate cancer patients.

first: Tianyu

last: Guo

first: Yang

first: Jing

last: Jia

first: Xueying

last: Mao

first: Elzbieta

last: Stankiewicz

first: Glenda

last: Scandura

first: Edwina

last: Burke

first: Lei

last: Xu

first: Jacek

last: Marzec

first: Caitlin

middle: R

last: Davies

first: Jiaying

last: Lu

first: Prabhakar

last: Rajan

first: Alistair

last: Grey

first: Karen

last: Tipples

first: John

last: Hines

first: Sakunthala

last: Kudahetti

first: Tim

last: Oliver

first: Thomas

last: Powles

first: Constantine

last: Alifrangis

first: Manish

last: Kohli

first: Greg

last: Shaw

first: Wen

first: Ninghan

last: Feng

first: Jonathan

last: Shamash

first: Daniel

last: Berney

first: Liang

first: Yong-jie


title: Comparison of mitochondrial tRNA abundance profiling in wild type and mutant mitochondrial RNA polymerase overexpression flies.

status: Public on Jan 06 2021

city: Bethesda

first: Mehdi

last: Pirooznia

state: MD

address: 12 SOUTH DR

institute: National Institutes of Health

summary: To investigate differential mitochondrial tRNA gene expression in wild type (WT) and mutant (E423P) mitochondrial RNA polymerase (POLRMT) overexpression flies, we performed Drsophila mitochondrial tRNA-seq according to the Hydro-tRNAseq method. tRNA-seq reads were subjected to 3' - adapter filtering , 3' - adapter trimming and quality control. The tRNAs expression levels were measured by tag count. For each tRNA sequence-based profile, the mapped reads number used to estimate the expression level of each tRNA. The tRNAs expression profiling was calculated based on uniquely mapped reads and including mapped reads, respectively. We found no difference in the relative abundance of mitochondrial individual tRNAs between WT and E423P overexpression flies.

overall_design: Examination of mitochondrial tRNA expression profile in two overexpression files.

first: Yi

last: Liu

first: Hong

last: Xu


title: Comparative transcriptomic analyses in mice treated with Fructus chebulae and water group

city: Harbin

first: Jian

last: Wang

address: 600 Changjiang Road

institute: Northeast Agricultural University

summary: Transcriptome sequencing of mice treated with Chebulae Fructus hydrosoluble extract ethyl acetate fraction and water were performed, and the gene expression profiles were compared.

overall_design: Specific pathogen-free (SPF) mice were administered Chebulae Fructus hydrosoluble extract ethyl acetate fraction (1g/kg/day) by gastric irrigation for 1 week. Control mice were given the same volume of water alone. The mice were then killed by cervical dislocation, and the liver was quickly picked and numbered in liquid nitrogen for gene expression analysis.

first: Wanjun

last: Hu

first: Zunlai

last: Sheng


title: Prematurity alters the progenitor cell program of the upper respiratory tract of neonates

first: Wellington

middle: V

last: Cardoso

state: New York

address: 650 West 168th Street

department: Department of Medicine

institute: Columbia University Medical Center

summary: The impact of prematurity in human development and neonatal diseases, such as bronchopulmonary dysplasia, have been widely reported. However, little is known about the effects of prematurity on the programs of stem cell self-renewal and differentiation of the upper respiratory epithelium, key for adaptation to neonatal life. Here we developed a minimally invasive methodology for isolation and functional analysis of basal cells from nasopharyngeal (NP) aspirates of newborn infants in organotypic cultures to address this issue.  We show that pre-term NP progenitors have a markedly distinct molecular signature of a prematurity-associated abnormal program of proliferation and mitochondria quality control compared to term cells. Prematurity differentially inhibited mitochondria respiration and, although it did not prevent cell differentiation  it was later associated with differences in mitochondrial and innate immunity-related genes. Together these differences suggested increased sensitivity  of pre-term progenitors to  environmental stressors compared to term under non-homeostatic conditions.

overall_design: Basal cells from nasopharyngeal (NP) were cultured and subjected to ALI (Air liquid interface) culture. Transcriptome profiling between PreTerm and Term NP progenitors at ALI day0 and day21 was investigated.

first: Shui

middle: E

last: Jessica

first: Liu

last: Helu

first: Qian

last: Jun

first: Stepanova

last: Anna

first: Liao

last: Grace

first: Wang

last: Wei

first: Ai

last: Xingbin

first: Ten

last: Vadim

first: Lu

last: Jining

first: Cardoso

last: Wellington


title: RNA-seq analysis of primarily cultured neurospheres from FGF13cko and control mice

first: Qiaoqiao

last: Yang

summary: To reveal the mechanisms of FGF13 in regulation of neural progenitor development, we carried out RNA-seq gene expression profiling analysis in primarily cultured hippocampal neurospheres from FGF13cko mice.  3 biological independent samples from FGF13cko (hGAFPCre+;Fgf13 flox/y) mice  were compared with 3 independent litermate control (hGAFPCre+;Fgf13 +/y) samples.

overall_design: RNAseq from Primarily cultured neurospheres from FGF13cko and litermate control mice, in triplicate, using Illumina HiSeq Xten.


title: RNAseq and ATACseq Analysis CD4+ T cells response to isoalloLCA treatment in vitro

city: Boston

first: Huh

last: lab

state: MA

address: 77 Avenue Louis Pasteur

department: Department of Immunology

institute: Harvard Medical School

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

overall_design: Refer to individual Series


title: Smoothened-activating lipids drive resistance to CDK4/6 inhibition in Hedgehog-associated medulloblastoma cells and preclinical models

city: San Francsico

first: David

last: Raleigh

state: CA

address: 1450 3rd Street Rm 402

department: Department of Radiation Oncology

institute: University of California, San Francisco

summary: We report a novel resistance mechanism to CDK4/6 inhibition in Hedgehog-associated medulloblastoma where cell models and mouse models demonstrate that prolonged inhibition of CDK4/6 inhibits ribosome biogenesis, activates the unfolded protein response, and increases the amount of Smoothened-activating lipids. This RNA-Sequencing dataset represents genomically-engineered mouse medulloblastoma models that either have wild-type Cdk6 or genomic knockout of Cdk6. We find that tumors that grew despite genetic loss of Cdk6 have suppresed ribosome biogenesis.

overall_design: comparison of genetically engeinereed mouse medulloblastomas that have intact Cdk6 or genetic deleiton of Cdk6. Sequencing was performed on a Illumina HiSeq 4000 with 50bp single-end reads with at least 37 million reads per sample. Differential expression analysis was performed with DESeq2.

first: Vikas

last: Daggubati

first: Jordan

last: Hochstelter

first: Ani

last: Bommireddy

first: Abrar

last: Choudhury

first: Alexis

last: Krup

first: Pervinder

last: Kaur

first: Pakteema

last: Tong

first: Amy

last: Li

first: Libin

last: Xu

first: Jeremy

last: Reiter


title: Primarily cultured neurospheres


title: IL-17-producing γδT cells ameliorate intestinal acute graft-versus-host disease by recruitment of Gr-1+CD11b+ myeloid-derived suppressor cells

city: Hangzhou

first: Lin

address: 261 Huansha Road

department: Department of Hematology

institute: Affliated Hangzhou First People's Hospital, Zhejiang University School of Medicine

summary: We generated γδT17 cells from splenocytes and compared gene expression profiles of initial and induced γδT17 cells using RNA-seq to explore their biological functions.

overall_design: Explore mRNA profiles of initial and induced γδT17 cells.

first: He

last: Huang

first: Xue


title: ATACseq Analysis CD4+ T cells response to isoalloLCA treatment in vitro

summary: We examine the chromatin landscape of murine CD4+ T cell cultured under Th0 condition (anti-CD3; anti-CD28; IL-2), treated with DMSO,  isoalloLCA (20 uM) for 48 hrs,  We compare cells from wild-type control mice and Nr4a1-deficient mice

overall_design: Examination of isoalloLCA induced chromatin accessibility changes in CD4+ conventional T cells from wild-type control mice versus Nr4a1-deficient mice.

first: Saiyu

last: Hang

first: Yuan

last: Fang

first: Jun

last: Huh


title: Robust parameter design of human induced pluripotent stem cell differentiation protocols defines lineage‐specific induction of anterior‐posterior gut tube endodermal cells

city: Chuo-ku

first: Keisuke

last: Sekine

state: Tokyo

address: 5-1-1 Tsukiji

department: Graduate School of Medicine

institute: National Cancer Center Research Institute, Japan

summary: Tissues and cells derived from pluripotent stem cells (PSC) are likely to become widely used in disease modeling, drug screening, and regenerative medicine. For these applications, the in vitro PSC differentiation process must be elaborately investigated and controlled to reliably obtain the desired end products. However, because traditional experimental methods, such as one factor at a time (OFAT) or brute-force approaches, are impractical for detailed screening of complex PSC cultivation conditions, more strategic and effective screening based on statistical design of experiments (DOE) ought to be indispensable. Among various DOE approaches, we regard robust parameter design (RPD) as particularly suited for differentiation protocol optimization due to its suitability for multi-factorial screening. We confirmed the adaptability of RPD for investigating human induced PSC (hiPSC) lineage specification toward anterior–posterior gut tube endodermal cells and clarified the contribution of each cell signaling pathway and the effect of cell signaling condition alteration on marker RNA expression levels, while increasing the efficiency of the screening in 243-fold (18 vs 4374) compared to that of a brute-force approach. Specific induction of anterior foregut, hepatic, pancreatic, or mid-hindgut cells was achieved using seven iPSC strains with the optimal culture protocols established on the basis of RPD analysis. RPD has the potential to enable efficient construction and optimization of PSC differentiation protocols, and its use is recommended from fundamental research to mass production of PSC-derived products.

overall_design: mRNA expression profiles of iPSC-derived anterior foregut, pancreatic, hepatic, and mid-hindgut cells

first: Ryota

last: Yasui

first: Kiyoshi

last: Yamaguchi


title: Differential sex-dependent regulation of the alveolar macrophage miRNome of SP-A2 and co-ex (SP-A1/SP-A2) and sex differences attenuation after 18h of ozone exposure

city: hershey

first: Nithyananda

last: Thorenoor

state: PA

address: 500 University Drive

department: Pediatrics

institute: Penn State University College of Medicine

summary: BACKGROUND: Human SP-A1 and SP-A2, encoded by SFTPA1 and SFTPA2 and their genetic variants differentially impact alveolar macrophage (AM) functions and regulation, including the miRNome.  We investigated whether miRNome differences previously observed between AM from SP-A2 and SP-A1/SP-A2 mice are due to continued qualitative differences or a delayed response of mice carrying a single gene.    METHODS: Human transgenic (hTG) mice, carrying SP-A2 or both SP-A genes and SP-A-KO mice were exposed to filtered air (FA) or O3. AM miRNA levels, target gene expression and pathways determined 18 h after O3 exposure.    RESULTS: We found: (a) Differences in miRNome due to sex, SP-A genotype, and exposure; (b) miRNome of both sexes was largely downregulated by O3 ; co-ex had fewer changed (≥2X) miRNAs than either group.  (c) the number and direction of expression of genes with significant changes in males and females in co-ex is almost the opposite of those in SP-A2; (iv) The same pathways were found in the studied groups; (e) O3 exposure attenuated sex differences; a higher number of genotype-dependent and genotype-independent miRNAs was common in both sexes after O3 exposure.    CONCLUSION: Qualitative differences between SP-A2 and co-ex persist 18 h post-O3, and O3 attenuates sex differences.

overall_design: Twelve week old, humanized transgenic (hTG) mice carrying a single SP-A2 (1A0) variant, or both SP-A1/SP-A2 (6A2/1A0, co-ex) gene variants, as well as SP-A knockout (KO) mice, were used in this study.  The hTG mice were generated on the C57BL/6J SP-A (KO) background . The animals were exposed to FA or O3 in parallel.  A group of 4 animals/sex/condition (FA, O3, except for SP-A2 (1A0) and co-ex male, 3 animals/condition) for miRNA analysis  were exposed to FA or O3 for 3 h, and alveolar macrophages (AM) were isolated after 18 h of recovery as described . Total RNA extraction from AM cells, library construction, and sequencing were performed.  The differentially expressed miRNAs between FA and O3-exposed males and females were identified by using the edgeR and the TCC v1.14.0 R package with false discovery rate (FDR) adjusted P-value of 0.1 as a significance cutoff.

first: Joanna

last: Floros


title: NEUROD1 intrinsically initiates differentiation of induced pluripotent stem cells into neural progenitor cells

first: Young-Joon

last: Kim

address: Yonsei-ro 50

institute: Yonsei university

summary: We generated ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) data and Hi-C data for induced pluripotent stem cell (iPSC), neuronal progentior cell (NPC), and investigated cell type-specific open chromatin regions and related enhancers

overall_design: ATAC-seq for iPSC and NPC. Hi-C for iPSC and NPC. H3K27ac ChIP-seq for iPSC and NPC.

first: Won-Young

last: Choi


title: Characterizing an HSF1-dependent transcriptional program in metastatic lung adenocarcinoma

city: Durham

first: Ann Marie

last: Pendergast

state: North Carolina

address: 308 Research Drive LSRC

department: Pharmacology and Cancer Biology

institute: Duke University

summary: The purpose of this study was to identify gene targets differentially regulated by shRNA-mediated knockdown of the HSF1 transcription factor in the brain-metastatic lung adenocarcinoma cell line PC9-BrM3.

overall_design: Samples were analyzed for differential gene expression in PC9-BrM3 cells transduced with shRNAs against NTC (non-target control) versus HSF1. Additionally, differential expression analysis was performed on another set of samples comparing PC9 parental versus PC9-BrM3 cells to identify genes differentially expressed relevant to brain metastasis.

first: Jacob

last: Hoj

first: Ann

middle: M


title: RNA sequencing of CD11b+ mouse bone marrow cells in mice treated with exosomes with or without HDL mimicking nanoparticles

city: Chicago

first: Stephen

last: Henrich

state: IL

address: 540 West Briar Place, Apt 2M

department: Urology

institute: Northwestern Unversity

summary: We report the sequencing of total RNA from CD11b+ mouse bone marrow cells in three groups of C57BL/6 mice: 1) Mice treated with three systemic (tail vein) injections (Days 1, 3, and 5) of phosphate buffered saline (PBS) (pH = 7.4), 2) Mice treated with three tail vein injections (Days 1, 3, and 5) of exosomes derived from enzalutamide resistant CWR-R1 prostate cancer cells (EnzR exosomes), and 3) Mice treated with three tail vein injections of EnzR exosomes (Days 1, 3, and 5) and high-density lipoprotein mimetic nanoparticles (HDL NPs) (Days 0, 2, and 4). Mice were sacrificed on Day 6, when mouse bone marrow was harvested and RNA from CD11b+ cells was obtained. We find that mice treated with EnzR exosome exhibit alteration in the expression of the matricellular protein, thrombospondin-1. Moreover, we find that HDL NP pre-treatment prevented thrombospondin-1 downregulation in mice treated with EnzR exosomes. This is consistent with our published findings that HDL NPs inhibit the uptake of EnzR exosomes by CD11b+ mouse bone marrow cells.

overall_design: Identification of gene expression changes in mouse bone marrow cells induced by prostate cancer exosomes +/- high-density lipoprotein mimicking nanoparticles (HDL NPs).

first: C

middle: S

last: Thaxton

first: Matthew

last: Schipma


title: Genome-wide analysis of hypoxia-regulated long noncoding RNAs in lung cancer cells

city: Yongin

first: Young-Chul

state: Gyeonggi-do

address: 1 Seocheon-dong Giheung-gu

institute: Kyung Hee University

summary:
Analysis of changes in gene expression of long noncoding RNAs under hypoxia in lung cancer cells by using microarray-based profiling assay

Hypoxia plays important roles in cancer progression by inducing angiogenesis, metastasis, and drug resistance. However, the effects of hypoxia on long noncoding RNA (lncRNA) expression have not been clarified. In this study, we evaluated alterations in lncRNA expression in lung cancer cells under hypoxic conditions using lncRNA microarray analyses. Among 40,173 lncRNAs, 211 and 113 lncRNAs were up- and downregulated, respectively, in both A549 and NCI-H460 cells. Genome-wide profiling of lncRNA expression altered under hypoxia may provide a basis for understanding the role of hypoxia-regulated lncRNAs in cancer growth and metastasis under hypoxic conditions as well as the mechanism underlying hypoxia-induced expression of lncRNAs.

overall_design: Total RNA was obtained from A549 and NCI-H460 lung cancer cells grown under normoxia and hypoxia and gene expression  was compared using microarrays.

first: Kwanghee

last: Baek

first: Yuree

last: Byun


title: DNA methyation of intragenic CpG islands are required for differentiation from iPSC to NPC

summary: We generated whole genome bisulfite sequencing (WGBS) data with high sequencing depth in induced pluripotent stem cell (iPSC), neuronal progentior cell (NPC) and Early Neuron (EN), and investigated the relationship between DNA methylation changes in CpG islands (CGIs) and corresponding gene expression during NPC differentiation

overall_design: WGBS for iPSC, NPC and EN. mRNA-seq for iPSC and NPC. H3K4me3 ChIP-seq for iPSC and NPC. H3K27me3 ChIP-seq for iPSC and NPC


title: Stressed erythrophagocytosis weakens host immunity through heme-mediated STAT1 dysregulation

city: Pittsburgh

first: Zeyu

last: Xiong

state: Pennsylvania

address: 3459 5th Ave, MUH W631

department: Medicine

institute: University of Pittsburgh

summary: This file comprises RNA-Seq data from the livers of mice challenged with acute intrapulmonary Klebsiella pneumoniae infection followed 1 h later with either storage-damaged RBC (stressed RBC) or young RBC. The livers were harvested from mice in both groups 24 h post-infection.

overall_design: Liver mRNA profiles of 8 weeks old C57BL/6J mice at 24 hours after Klebsiella pneumoniae infection (at 10^3 CFU inoculum) and transfusion with storage-damaged RBC (stressed RBC) or young RBC were generated by paired sequencing with Illumina NextSeq 500 System

first: Janet

last: Lee


title: Induction of spontaneous human neocentromere formation and long-term maturation

city: Oxford

first: Marina

last: Murillo-Pineda

address: South Parks Road

institute: University of Oxford


title: Comparison of microRNA Expression Profile in Patients with Chronic Myeloid Leukemia Treated by Allogeneic Hematopoietic Stem Cell Transplantation and Chronic Myeloid Leukemia patients treated with imatinib mesylate.

city: Botucatu

first: Juliana

middle: Ravelli Baldassarre

last: Martins

state: SP

address: Rua Mansueto Lunardi, 37

country: Brazil

institute: Faculdade de Medicina de Botucatu

summary: Expression profile of 14 Chronic Myeloid Leukemia Philadelphia chromossome negative patients after allo haematopoietc stem cell transplantation and Chronic Myeloid Leukemia treated with imatinib mesylate. We tested 754 microRNAs by reverse transcription quantitative polymerase chain reaction (RT-qPCR) array for each patient.

overall_design: Expression profile of Chronic Myeloid Leukemia Philadelphia chromossome negative patients after allo haematopoietc stem cell tranplantation and 14 Chronic Myeloid Leukemia treated with imatinib mesylate.

first: Leonardo

last: de Moraes

first: Sarah

last: Cury

last: Dadalto

last: Capannacci

first: Robson

last: Carvalho

first: Regina

last: Nogueira

first: Newton

last: Hokama

first: Paula

last: de Oliveira Montandon Hokama


title: Methotrexate attenuates vascular inflammation through an adenosine-microRNA dependent pathway

city: Valencia

first: Daniel

last: Perez-Cremades

state: Valencia

address: 15 Blasco Ibañez Avenue

department: Physiology Department

country: Spain

institute: University of Valencia

summary: We report transcriptomic changes in white adipose tissue of systemic miR-181a2b2 KO mice in response to high fat diet and methotrexate.

overall_design: miR-181a2b2-/- (KO) and miR-181a2b2flox/flox (flox) mice were placed on a 60% high fat diet for 12 weeks. Each group of mice was weekly i.p. injected with vehicle control or methotrexate (1 mg/kg). White adipose tissue was harvested and RNA-Seq analysis was performed using Illumina HiSeq2500 V4 2x150 bp  (Genewiz, South Plainfield, NJ).

first: Dafeng

last: Yang

first: Stefan

last: Haemmig

first: Haoyang

last: Zhou

last: Pérez-Cremades

first: Xinghui

last: Sun

first: Lei

last: Chen

first: Jie

last: Li

first: Jorge

last: Haneo-Mejia

first: Tianlun

first: Ivana

last: Hollan

first: Mark

middle: W

last: Feinberg


title: LncRNA data in gastrocnemius muscles from mice that have undergone denervation of the right sciatic nerve or not

first: Jin

address: 99 Shangda Road

institute: Shanghai University

type:
Expression profiling by array
Non-coding RNA profiling by array

summary:
This study was to identify lncRNAs responsible for muscle atrophy
Muscle atrophy commonly occurs in aging, disuse, starvation, and many chronic diseases including heart failure and cancer. Muscle atrophy leads to muscular weakness and reduced quality of life, which also significantly increases morbidity and mortality. While progress has been made in understanding the molecular underpinnings of muscle atrophy, currently there are no effective approved drugs to combat muscle atrophy. Thus, novel therapies for muscle atrophy would address an important unmet clinical need. Long non-coding RNAs (LncRNAs) are transcribed RNAs longer than 200 nucleotides with little or no protein-coding capacity.  Several lncRNAs have been reported in myogenesis and few lncRNAs have been mechanistically linked to skeletal muscle diseases. Here we want to identify a lncRNA  as a common regulator of  multitypes of muscle atrophy.

overall_design: Total RNAs were extracted from gastrocnemius muscles from mice that have undergone denervation of the right sciatic nerve or not (n=4 per group), and then subjected to lncRNA array analysis (Agilent Mouse lncRNA（4*180K，Design ID：049801）).

first: Junjie

last: Xiao


title: Dysregulation of the IL-17A pathway in women with unexplained infertility affects pregnancy outcome following assisted reproductive therapy

city: Dublin

first: Bruce

last: Moran

address: Nutley Lane, Dublin 4

department: Dept. of Pathology

country: Ireland

institute: St. Vincent's University Hospital

summary: IL-17 signaling is an important candidate pathway that may contribute to dysregulated immune function in the endometrium of women with unexplained infertility after ART who are not pregnant

overall_design: Discovery set (n=20)

first: David

last: Crosby

first: Donal

last: Brennan

first: Cliona

last: O’Farrelly


title: Transcriptional down-regulation of metabolic genes by Gdown1 ablation induces quiescent cell re-entry into the cell cycle

city: New York

first: Miki

last: JIshage

address: 1230 York Avenue

institute: Rockefeller University


title: SUMOylation controls the neurodevelopmental function of the transcription factor Zbtb20

city: Goettingen

first: Gabriela

last: Salinas

state: Lower-Saxony

address: Kreuzbergring 57

department: Department of Pathology

country: Germany

institute: Universitaetsmedizin Goettingen

summary: SUMOylation is a dynamic post-translational protein modification that primarily takes place in cell nuclei, where it plays a key role in multiple DNA-related processes. In brain cells, and particularly in neurons, mostly nuclear proteins are SUMOylated, and the SUMOylation-dependent control of a subset of neuronal transcription factors is known to regulate various aspects of nerve cell differentiation, development, and function. In an unbiased screen for endogenous SUMOylation targets in the developing mouse brain, we previously identified the transcription factor Zbtb20 as a new SUMO1 conjugate. We show here that the three key SUMO paralogues SUMO1, SUMO2, and SUMO3 can all be conjugated to Zbtb20 in vitro, and we confirm the SUMOylation of Zbtb20 in vivo. Using primary hippocampal neurons as a model system, we then demonstrate that the expression of Zbtb20 is required for proper nerve cell development and neurite growth and branching. Furthermore, we show that the SUMOylation of Zbtb20 is essential for Zbtb20 function in this context, and provide evidence indicating that SUMOylation affects the Zbtb20-dependent transcriptional profile of neurons. Taken together, our data highlight the role of SUMOylation in the regulation of neuronal transcription factors that determine nerve cell development. Specifically, our data demonstrate that key functions of the transcription factor Zbtb20 in neuronal development and neurite growth are under the obligatory control of SUMOylation.

overall_design: primary neuron cultured were infected with various virus (see below) after 1 days in culture, and lyzed in Trizol after 5 days culture.

first: Silvia

last: Ripamonti

first: Marilyn

last: Tirard


title: Differentially expressed genes in Gdown1 KO liver [array]

summary: To investigate the biological role of Gdown1, we chose mouse liver and generated Gdown1 conditional knockout mice. Differentially expressed genes in Gdown1 KO liver were analyzed by microarrays.

overall_design: Gdown1 KO and control (FF) mice were maintained under controlled environmental conditions under a 12-h light /dark cycle and allowed ad libitum access to water and standard laboratory diet. At 8 weeks, mice were sacrificed from 11 am to 1 pm.

last: Jishage


title: Altered Innate Immunity Confers Staphylococcus aureus Resistance in O-glycosylation Deficient Caenorhabditis elegans bus Mutants

city: Bethesda

first: WeiPing

address: Bldg 8, Room 1A11, NIDDK/NIH

department: GCL

institute: NIDDK/NIH

summary: The Caenorhabditis elegans bus (bacterial unswollen) mutants were isolated by their altered response to the nematode pathogen Microbacterium nematophilum. The bus-2, bus-4 and bus-17 mutants are resistant to infection by this bacterium and to infection by human pathogens Yersinia pestis and Yersinia pseudotuberculosis. Here we extend that list to Staphylococcus aureus. The bus-2, bus-4 and bus-17 mutants each harbors a defect in a different glycosyltransferase involved in O-glycosylation. Glycomics analysis of these strains reveals significant O-glycosylation defects.  We further investigated the nature of bus mutant phenotypes in bus-2, bus-4 and bus-17 by gene expression analysis. Three distinct areas of altered expression were identified: 1) N- and O-glycosylation; 2) innate immune response; 3) protein folding and editing control.  As expected N- and O-glycosylation gene expression was altered at key enzymatic steps. Innate immune system expression patterns were altered in a way that significantly overlapped with expression patterns seen in wild-type upon exposure to Staphylococuss aureus. Upon infection with S. aureus markers of innate immune activity increased significantly compared to wild-type. The abu/pqn genes, active in the non-canonical unfolded protein response (UPR) pathway were dramatically upregulated in bus when these mutants were exposed to the pathogen. This work demonstrates a genetic link between O-glycosylation and expression of key components of the innate immune response.

overall_design: Identification of genes expressed in three groups with 5 groups three replications (N2D as control)

first: Salil

middle: K

last: Ghosh

first: Rhaman

last: Mizanur

first: Michelle

last: Bond

first: Ewa

last: Jankowska

first: John

last: Hanover

last: Cipollo


title: GVHD-mediated Vicious Cascade: Impaired Reconstitution of Immunosuppressive Donor Plasmacytoid Dendritic Cells

city: Philadelphia

first: Yi

last: Zhang

address: 3500 N Broad Street

department: Microbiology and Immunology

institute: Temple University

summary: In patients undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT), severe graft-versus-host disease (GVHD) is tied to failed donor plasmacytoid DC (pDC) reconstitution. The mechanism whereby GVHD causes donor pDC defects and the precise role donor pDCs play in GVHD remain poorly understood. pDCs develop from HSCs in successive stages through Flt3 signaling-dependent differentiation, beginning as multi-potent progenitors (MPPs) and later becoming common DC progenitors. We observed that MPPs were critical for sustaining pDCs and were severely depleted during GVHD. Loss of MPPs was associated with decreased amounts of MPP-producing HSCs and mTOR activation-induced cell death of proliferating MPPs. Additionally, GM-CSF derived from alloreactive T cells subverted MPP production of pDCs. Together, GVHD and alloreactive T cells caused donor pDC defects by impairing the generation, maintenance and differentiation of HSCs and MPPs. Importantly, pDCs suppressed the proliferation and expansion of activated autologous CD4+ T cells via a type I-IFN signaling-dependent mechanism. Transfer of donor pDCs early after transplantation repressed GVHD and preserved potent GVL effects, significantly improving the survival of leukemia mice undergoing allo-HSCT. Our findings identify novel strategies that improve the recovery of donor pDCs early after allo-HSCT and thus may represent an effective therapy to control GVHD. Our findings have broad implications for other diseases in which functional DC development is impaired, such as chronic infections, autoimmunity and cancer.

overall_design: Normal vs. GVHD

first: Yuanyuan

last: Tian

first: Lijun

last: Meng

first: Ying

last: Wang

first: Bohan

last: Li

first: Hongshuang

last: Yu

first: Yan

last: Zhou

first: Tien

last: Bui

first: Alicia

first: Yongping

first: Jian

first: Shin

last: Mineishi

first: Hong

last: Zheng

first: Stefania

last: Gallucci

first: Yanyun

first: Shaoyan

last: Hu


title: Identification of Pol II(G) target genes in mouse liver [ChIP-seq]

first: Miki

last: JIshage

summary: To investigate the biological role of Pol II(G), we identified Pol II(G) target genes in normal mouse liver.

overall_design: To identify genes that are directly targeted by Pol II(G) in hepatocytes, we performed ChIP-seq analysis with non-crosslinked chromatin prepared from Gdown1 flox/flox (FF) or Gdown1flox/flox;Alb-Cre (KO) liver at 7W of age. We also analyzed Gdown1 target genes in p53KO hepatocytes. For the negative control, tamoxifen (TAM)-inducible Gdown1flox/floxKO mice carrying both the Alb-CreERT2 transgene and a p53 null mutation was used.

last: Jishage


title: Transcriptomic analysis of HCT116 cells cultured under different oxygen conditions

city: Tokyo

first: Masatoshi

last: Wakui

address: 35 Shinanomachi, Shinjuku-ku

department: Department of Laboratory Medicine

institute: Keio University School of Medicine

summary: To explore the molecular basis of hypoxic response, we analyzed gene expression profiles of HCT116 cells cultured under different oxygen conditions with or without inhibition of P53 signaling or fatty acid b oxidation (FAO).

overall_design: HCT116 cells were cultured normoxically or hypoxically with or without pharmacological inhibition of P53 signaling or fatty acid b oxidation (FAO) and then subjected to transcriptomic analysis.


title: Open chromatin and transcriptome analysis of iPSCs differentiated into lung epithelium at air-liquid interface reveals key transcriptional drivers and processes

city: Cleveland

first: Ann

last: Harris

state: Ohio

address: 2109 Adelbert Rd Building

department: Genetics and Genome Sciences

institute: Case Western Reserve University

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

overall_design: Refer to individual Series


title: RNAseq Analysis CD4+ T cells response to isoalloLCA treatment in vitro

city: Boston

first: Huh

last: lab

address: 77 Avenue Louis Pasteur

institute: Harvard Medical School

summary: We examine the transcription response of murine CD4+ T cell cultured under Th0 condition (anti-CD3; anti-CD28; IL-2), treated with DMSO,  isoalloLCA (20 uM) for 48 hrs, or in the presence of TGFbeta (0.25 ng/mL). We compare the differential genes regulated by isoalloLCA and TGFbeta.

overall_design: Examination of isoalloLCA induced transcriptional change compare to TGFbeta induced transcriptional change in CD4+ conventional T cells.

first: Saiyu

last: Hang

first: Yuan

last: Fang

first: Jun

last: Huh


title: Open chromatin and transcriptome analysis of iPSCs differentiated into lung epithelium at air-liquid interface reveals key transcriptional drivers and processes (RNA-seq data)

summary: The availability of robust protocols to differentiate induced pluripotent stem cells (iPSCs) into many human cell lineages has transformed research into the origins of human disease.  The efficacy of differentiating iPSCs into specific cellular models is influenced by many factors including both intrinsic and extrinsic features.  Among the most challenging models is the generation of human bronchial epithelium at air-liquid interface (HBE-ALI), which is the gold standard for many studies of respiratory diseases including cystic fibrosis.  Here we perform open chromatin mapping by ATAC-seq and transcriptomics by RNA-seq in parallel, to define the functional genomics of key stages of the iPSC to HBE-ALI differentiation. Within open chromatin peaks the overrepresented motifs include the architectural protein CTCF at all stages, while motifs for the FOXA and GATA pioneer factors families are only seen at early stages, and those regulating key airway epithelial functions, such as EHF, are limited to later stages.  The RNA-seq data illustrate dynamic pathways during the iPSC to HBE-ALI differentiation, and also the marked functional divergence of different iPSC lines at the ALI stages of differentiation.  Moreover, a comparison of iPSC-derived and lung donor-derived HBE-ALI cultures reveals substantial differences between these models.

overall_design: Examination of the transcriptome of each stage of differentiation from iPSC to ALI-HBE

first: Alekh

last: Paranjapye

first: Shih-Hsing

last: Leir


title: Role of KLF6 in shaping macrophage inflammatory response

first: Ernest

last: Chan

state: OH

address: 10900 Euclid Ave, Robbins E211

department: PQHS

institute: CWRU

summary: Kruppel-like transcription factor 6 (KLF6) is a member of zinc-finger family transcription factors that regulate critical cellular processes including development, differentiation, proliferation, and programmed cell death.  Alterations in KLF6 expression or function has been associated with the pathogenesis of numerous human ailments, including inflammatory bowel diseases, cancer, hepatic steatosis, and hepatic fibrosis.

overall_design: Here we isolated bone marrow of 3 mice per group (Lyz2cre and Lyz2cre:KLF6Fl/Fl) and differentiated into macrophages by culturing them in M-CSF containing media. These cells were stimulated with Heat-killed Candida albicans (HKCA) or 50 micrograms/ml Scleroglucan for 5 hours. Total RNA was isolated and subjected to RNAseq analyses.

first: Ganapati

middle: H

last: Mahabeleshwar

first: E


title: mRNA profiling of AGS Gastric Cancer cell line upon treatment with 5µM of Doxycycline

city: Madurai

first: Kumaresan

last: Ganesan

state: Tamil Nadu

address: School of Biological Sciences,

department: Genetics

institute: Madurai Kamaraj University

summary: Doxycycline, a tetracycline based antibiotic which has bacteriostatic activity against a broad range of both gram positive and gram negative bacteria was identified to inhibit the expression of ERK/MAPK signaling pathway in gastric cancer. ERK/MAPK pathway is one of the highly activated and a crucial player in gastric cancer progression. To delineate the complex transcription program associated with ERK/MAPK pathway and thus inhibited by doxycycline in gastric cancer cells, doxycycline was treated in AGS, one of the ERK/MAPK overexpressed gastric cancer cell line. The resulatant changes in genome-wide mRNA expression pattern between control and doxycycline treated was profiled using Human Transcriptome 2.0 arrays.

overall_design: Total RNA was isolated from AGS gastric cancer cell line treated with 5µM of doxycycline and 0.01% of DMSO as a control and profiled using GeneChip® Human Transcriptome Array 2.0 (HTA-2_0).

first: S

last: JAISHREE

first: G

last: KUMARESAN


title: Differentially expressed genes in Gdown1 knockout and Gdown1/p53 double-knockout mouse liver [RNA-seq]

state: NY

summary: To investigate the biological role of Gdown1, differentially expressed genes in Gdown1 knockout and p53/Gdown1 double-knockout mouse liver were analyzed by RNA-seq.

overall_design: To investigate differentially expressed genes in Gdown1 knockout (KO) hepatocytes in the presence or absence of p53, total RNA was isolated from liver tissues of the following genotypes: Gdown1 flox/flox (FF), Gdown1flox/flox;Alb-Cre (KO), Gdown1 flox/flox;p53-/- (p53KO), and Gdown1flox/flox;Alb-Cre;p53-/- (DKO). To investigate the immediate effects of the Gdown1 KO, we generated tamoxifen (TAM)-inducible Gdown1flox/floxKO mice carrying both the Alb-CreERT2 transgene and a p53 null mutation (DKOAlb-CreERT2mice). The liver tissues were collected from p53KO or DKOAlb-CreERT2 mice at 24 hours after tamoxifen injection.


title: WDR76 promotes MLL-rearranged leukemia via highly-selective binding of 5-hydroxymethylcytosine in DNA

first: Alexander

last: Ruthenburg

address: 920 E 58th St, CLSC 855

department: MGCB/BMB

institute: University of Chicago

summary: Although rare, the distribution of the 5-hydroxymethylcytosine (hmC) modification in mammalian DNA is tissue- and gene-specific, yet distinct from its repressive methylcytosine (mC) precursor, suggesting unique functions. To examine this possibility, we fractionated mammalian brain extracts to discover binding partners specific for oxidized states of mC. We demonstrate that one such factor, WDR76, is a highly hmC-specific binding protein that modulates gene expression within chromosomal regions enriched in hmC where it binds. In human cell lines and mouse models, WDR76 recruitment by hmC is critical for the initiation and maintenance of MLL-rearranged leukemias. Beyond its canonical role as an intermediate in mC remediation, we show that hmC can be an epigenetic mark whose recognition drives leukemogenesis, portending analogous signaling pathways for other rare DNA modifications.

overall_design: ChiP-seq of epitope tagged WDR76 and RNA-seq of Wdr76 knockout in mouse embyrionic stem cells

first: Kathryn

last: Malecek

first: Hengyou

last: Weng

first: Matthew

middle: A

last: Sullivan

first: Michael

last: Werner

first: Jianjun

last: Chen


title: Profound effect of histone methyltransferase (DIM5) on genomic expression of Beauveria bassiana

status: Public on Jan 05 2021

city: Zhejiang Province

first: kang

last: ren

address: Yuhangtang Road No.388

country: China

institute: Zhejiang University

summary:
Methods: Total RNAs were extracted from three 3-day-old hyphal cultures (replicates) of dim5 disruption and wild-type strains grown under normal culture conditions and and subjected to deep sequencing on Illumina Novaseq 6000 platform. The sequence reads that passed quality filters were mapped to the genome of Beauveria bassiana. All genes differentially expressed in the disruptant versus the wild-type strain were enriched to GO function classes and KEGG pathways.
Results: The resultant transcriptome comprises 10915 genes annotated or not annotated. Among those, 1201 genes (genomic 11.59%) were dysregulated in the absence of dim5, including 489 down-regulated and 712 up-regulated.
Conclusions: DIM5 has profound impact on the genomic expression of Beauveria bassiana.

overall_design: RNA profiles from 3-day-old hyphal cultures of dim5 disruption and wild-type strains.

first: Ren

last: Kang

first: Ming-Guang

last: Feng


title: Open chromatin and transcriptome analysis of iPSCs differentiated into lung epithelium at air-liquid interface reveals key transcriptional drivers and processes (ATAC-seq data)

first: Ann

last: Harris

country: USA

summary: The availability of robust protocols to differentiate induced pluripotent stem cells (iPSCs) into many human cell lineages has transformed research into the origins of human disease.  The efficacy of differentiating iPSCs into specific cellular models is influenced by many factors including both intrinsic and extrinsic features.  Among the most challenging models is the generation of human bronchial epithelium at air-liquid interface (HBE-ALI), which is the gold standard for many studies of respiratory diseases including cystic fibrosis.  Here we perform open chromatin mapping by ATAC-seq and transcriptomics by RNA-seq in parallel, to define the functional genomics of key stages of the definitive endoderm (DE) to HBE-ALI differentiation. Within open chromatin peaks the overrepresented motifs include the architectural protein CTCF at all stages, while motifs for the FOXA and GATA pioneer factors families are only seen at early stages, and those regulating key airway epithelial functions such as EHF are limited to later stages.  The RNA seq data illustrate dynamic pathways during the DE to HBE-ALI differentiation and also the marked functional divergence of different iPSC lines at the ALI stages of differentiation.  Moreover, a comparison of iPSC-derived and lung donor-derived HBE cultures reveals substantial differences in these culture models.

first: Shiyi

last: Yin

first: Jenny

middle: L

last: Kerschner