title: ABT263 treated Mice post RUUO

city: Edinburgh

first: Eoin

last: O'Sullivan

address: 47 Little France Crescent

department: Centre for Inflammation Research

institute: University of Edinburgh

summary: Mice treated with ABT263 to deplete senescent cells during recovery following R-UUO injury model

overall_design: 10 Bulk RNA-SEQ libraries. A PolyA library was constructed and run on an Illumina Novaseq using 5x150bp paired-end sequencing at a depth of 50M reads per library

first: David

last: Ferenbach


title: RNA-seq analysis of FACS-isolated distinct cell lineages in adult mouse prostates

status: Public on Jan 06 2023

city: Houston

first: Chad

last: Creighton

state: TX

address: One Baylor Plaza, Mail Stop: BCM305

department: Biostatistics, Ducan Cancer Center

country: USA

institute: Baylor College of Medicine

type: Expression profiling by high throughput sequencing

summary: To further characterize the molecular and biological features of the Sca-1+ luminal cells, we performed an RNA-seq analysis using FACS-isolated distinct cell lineages in adult mouse prostates, including the Lin-CD24lowCD49fhigh basal cells, Lin-CD24-CD49f- stromal cells, Lin-CD24highCD49flowSca-1- luminal cells, and Lin-CD24highCD49flowSca-1+ luminal cells.

overall_design: multiple group comparison

first: Yiqun

last: Zhang

first: Li

last: Xin


title: Single cell sequencing of ovarian organoids

city: Shanghai

first: Ji

last: Wu

address: No.800, Dongchuan Road, Minhang District

country: China

institute: Shanghai Jiao Tong University

summary: Revealed the cell types of ovarian organoids for the first time by single cell sequencing

overall_design: We  performed and analyzed 10 × Genomics single cell RNA sequencing (scRNA-Seq) to reveal gene expression signatures of individual cell types of ovarian organoids.

first: Xiaoyong

last: Li


title: The effects of Human Bocavirus I VLPs on peripheral blood mononuclear cells

city: Zurich

first: Hubert

last: Rehrauer

address: Winterthurerstr. 190

department: FGCZ

country: Switzerland

institute: ETH Zurich / University of Zurich

summary: Human bocavirus (HBoV) is a newly discovered parvovirus identified from pooled nasopharyngeal aspirate specimens. Human bocavirus 1 (HBoV1) is a respiratory virus observed in respiratory samples from small children presenting bronchiolitis, wheezing, cough, fever, and rhinorrhea. It is the fourth most common virus detected in respiratory infections. DNA of HBoV1 was detected in up to 18% of nasal or nasopharyngeal samples and another study has been shown that over than 85% of children in the United States have antibodies to this virus. HBoV1 is a small DNA virus with a nonenveloped icosahedral capsid. This virus previously has been associated with wheezing, acute otitis media, severe pneumonia and respiratory failure.  HBoV 1 has been also detected in the blood of acute respiratory patients and the selected group of immunocompromised children and also determined in healthy blood donors. The role of HBoV1 in the inflammatory process is poorly known.   The aim of this project is to clarify the role of HBOV1 in the immunoregulatory mechanisms.

overall_design: PBMCs were isolated from seven healthy individuals. Isolated cells were stimulated with 2.4 µg/ml HBoV1-VLPs for two different time points (6h and 24h). Total RNA isolation was performed from unstimulated and stimulated cultured PBMCs.

first: Cezmi

last: Akdis

first: Cagatay

last: Karaaslan


title: RNA-seq profiling of mouse prostate luminal cells with forced over-expression of CSF1

summary: We generated a transgenic mouse harboring mouse Csf-1 transgene driven by the rat probasin promoter. Luminal cells from the 4 month old transgenic mice and WT littermate controls were FACS isolated and RNA-seq analysis was performed to compare the gene expression profiles between the two groups.

overall_design: Two group comparison


title: CPI-0610, a potent and selective BET bromodomain inhibitor optimized for clinical development

city: Cambridge

first: Barbara

middle: M

last: Bryant

state: MA

address: 215 First Street

institute: Constellation Pharmaceuticals

type: Genome binding/occupancy profiling by high throughput sequencing

summary: SUDHL5 cells were treated with DMSO or 2.5 μM CPI203 for 4 hours, then processed for ChIP-Seq to obtain genome-wide binding changes for BRD4 upon treatment with a BET inhibitor.

overall_design: Examination of BRD4 binding in the absence or presence of a BET inhibitor in SUDHL5 DLBCL cell line using ChIP-Seq

first: Nicole

middle: E

last: Follmer

first: Charlie

last: Hatton

first: Robert

middle: J

last: Sims III


title: Transcriptome analysis of human glioblastoma tumor cells driven by PIK3CA mutation variants

summary: The RTK/RAS/PI3K pathway is a key driver of tumorigenesis across all cancers, with 90% of Glioblastoma (GBM) tumors exhibiting alterations in this pathway. Among the specific genes in this pathway mutations in PI3K’s catalytic subunit, PIK3CA, are found in 11% of GBM tumors. Sequencing of GBM samples has revealed several known hotspot mutations that drive tumorigenesis in several cancers (E545K, H1047R), as well as a series of 63 in frame mutations (as indexed in COSMIC) that remain largely unclassified. Cells from patient-derived primary GBM cell lines were lentivirally infected with different PIK3CA mutants (or a mCherry control reporter), and implanted in mice. The resulting tumors were then profiled for gene expression.

overall_design: We examined the global transcriptional effects of PIK3CA variants in our model system via RNA-Sequencing on end-stage tumors driven by the variants.

first: Fengju

last: Chen

first: Benjamin

last: Deneen


title: mRNA-seq analysis of Caenorhabditis elegans N2, daf-2(e1370), irld-39(duk1);irld-52(duk17), and daf-2(e1370); irld-39(duk1); irld-52(duk17) starved L1 larvae

city: Eugene

first: Amy

middle: K

last: Webster

state: Oregon

address: Institute of Ecology and Evolution

institute: University of Oregon

summary: Whole starved L1 larvae from four genotypes (N2, daf-2(e1370), irld-39(duk1);irld-52(duk17), and daf-2(e1370); irld-39(duk1); irld-52(duk17)) were collected after 12 hours of starvation

overall_design: 4 biological replicates of each of four genotypes at 12 hours of starvation during L1 arrest

first: Rojin

last: Chitrakar

first: L

middle: R

last: Baugh


title: mRNA-seq analysis of Caenorhabditis elegans N2 and irld-39(duk1); irld-52(duk17) throughout L1 starvation

summary: Whole starved L1 larvae were collected at 5 time points between 6 and 72 hours from two strain backgrounds, N2 and LRB444

overall_design: N2 and LRB444 [irld-39(duk1); irld-52(duk17)] were each collected after 6, 12, 24, 48, and 72 hr of L1 arrest. 3 biological replicates were collected for each time point and strain.

first: Jingxian


title: Integrated multiomic analysis reveals comprehensive tumor heterogeneity in primary and recurrent hepatocellular carcinomas

city: Chengdu

first: Wei

state: Sichuan

address: Department of Liver Surgery and Liver Transplantation Centre, West China Hospital, Sichuan University

summary: The tumor heterogeneity between the primary and recurrent hepatocellular carcinoma (HCC) has rarely been explored. The present study aims to illustrate the heterogeneity between the primary and recurrent tumors by integrating multiomic analyses.

overall_design: This study included 18 HCC patients with matched initial-relapsed tumors. We performed whole exome sequencing (WES), RNA sequencing and DIA-based proteomics analyses of all tumor and adjacent liver tissues. All recurrent tumors were divided into intrahepatic metastasis (IM) group and multi-centric (MC) tumor occurrence group. We explored the difference between IM and MC groups in the tumor mutation, tumor evolution, CNV, transcriptomic and proteomic levels. Additionally, we analyzed the KEGG pathways associated with tumor recurrence in the IM group. Lastly, the Sorafenib-targeted alterations were explored and linked to the clinical responses rate to Sorafenib treatment.

last: Wei

first: Yuan

last: Kefei

first: Wu

last: Hong

first: Zeng

last: Yong


title: irld genes modify insulin signaling to influence natural variation of starvation resistance

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

overall_design: Refer to individual Series


title: EZH2 suppresses the interferon-stimulated gene response in non-Hodgkin Lymphoma


title: EZH2 suppresses the interferon-stimulated gene response in non-Hodgkin Lymphoma [ChIP-seq]

summary: Pharmacological inhibition of the histone lysine methyltransferase EZH2 has emerged as a therapeutic strategy for the treatment of non-Hodgkin Lymphoma (NHL), in particular for cases with mono-allelic mutations in the EZH2 catalytic domain. Potent, selective EZH2 small molecule inhibitors have achieved tumor regression in mutant EZH2-containing preclinical lymphoma models and several of these inhibitors are currently engaged in cancer-focused clinical trials. Here, we show that the presence of EZH2 mutations do not always confer EZH2 inhibitor sensitivity. We discovered that EZH2 is usurped by lymphoma cells to attenuate JAK/STAT signaling and to repress pro-apoptotic interferon response genes. EZH2 inhibition results in the broad induction of interferon-stimulated genes (ISGs) in several phenotypically sensitive NHL cell models. In mutant EZH2-containing insensitive models, EZH2 inhibitors synergize specifically with type I interferons (IFNs) in vitro and in vivo to induce ISGs and apoptosis. The profound combinatorial activity of EZH2 inhibitors and type I IFNs is not restricted to NHL models with mutant EZH2 and, is preferentially observed in models that are not affected by either single agent. Molecular consequences of EZH2 inhibitor and type I IFN combinatorial treatment include STAT1 activation, binding of STAT transcription factor complexes to ISGs, reduction of H3K27me3 levels and increase of H3K4me3 levels at ISG transcriptional start sites, and ISG transcriptional activation. The molecular and anti-proliferative effects of the combination can be suppressed by inactivation of the JAK/STAT signaling pathway, by using the JAK inhibitor ruxolitinib. We suggest that EZH2 inhibitors can be therapeutically combined with type I IFNs for the treatment of NHL.

overall_design: To elucidate the genome-wide distribution patterns of H3K27me3 in RL cells. Two samples each of input chromatin, H3K27me3 IPs were analyzed.

first: William

middle: D

last: Bradley

first: Chih-Chi

last: Yuan

first: Patrick

last: Trojer


title: EZH2 suppresses the interferon-stimulated gene response in non-Hodgkin Lymphoma [RNA-seq]

first: Barbara

overall_design: 3 GCB-DLBCL cell lines harboring an activating mutation in the SET domain of EZH2 were analyzed.  2 phenotypically responsive cell lines (KARPAS-422 and Pfeiffer) were treated with DMSO or EZH2 inhibitor for 4 days to measure differential expression of transcripts following inhibition of EZH2 catalytic function, and 1 non-responsive cell line (RL) treated with DMSO only to measure baseline transcript expression levels.


title: BRD4 loading at the transcription start site mediates pause-release and underlies the disproportionate transcriptional response to BET bromodomain inhibition [RNA-Seq]

summary: BET bromodomain inhibition (BETi) abrogates cancer cell growth by disrupting oncogenic gene expression. BRD4 loading at enhancers has been suggested to mediate pause-release and underlie the selective transcriptional response to BETi. Here, we utilized GRO-seq coupled with ChIP-seq to assess the association between gene control elements and the transcriptional response to BETi. Genes immediately down-regulated by BETi display a marked pause-release defect with a minimal impact on transcript elongation within the gene body. Surprisingly, we find that BRD4 at super-enhancers does not render its associated genes or enhancer RNAs preferentially sensitive to BETi. In contrast, disproportionate loading of BRD4 at transcription start sites (TSS) correlates with the transcriptional response to BETi. Moreover, BRD4 loading at TSSs, but not enhancers, is associated with enhanced promoter-proximal pausing following BETi. Our findings stress a mechanistic role of promoter-associated BRD4 in pause-release and suggest that BRD4 loading at the TSS drives the selective transcriptional response to BETi.

overall_design: LP-1 multiple myeloma cell line was treated with DMSO or 0.5 μM JQ1 for 4 hours and then analyzed by RNA-Seq

first: Nicole

first: Jennifer

middle: A

last: Mertz

first: Hon-Ren

last: Huang

first: Minho

last: Chae

first: W

middle: L

last: Kraus


title: BRD4 loading at the transcription start site mediates pause-release and underlies the disproportionate transcriptional response to BET bromodomain inhibition

last: Bryant

last: Follmer

first: Charlie

last: Hatton

first: Robert

last: Sims III


title: BRD4 loading at the transcription start site mediates pause-release and underlies the disproportionate transcriptional response to BET bromodomain inhibition [ChIP-Seq]

overall_design: LP-1 multiple myeloma cell line was treated with DMSO or 0.5 μM JQ1 for 4 hours and then analyzed by ChIP-Seq


title: Liver-specific FGFR4 knockdown in mice on a HFD increases bile acid synthesis and improves hepatic steatosis

status: Public on Jan 05 2023

city: Boston

first: Hui

last: Pan

address: 1 Joslin Place

department: Bioinformatics and Biostatistics Core

institute: Joslin Diabetes Center

summary: Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease with increased risk in patients with metabolic syndrome. There are no FDA approved treatments, but farnesoid X receptor (FXR) agonists have shown promising results in clinical studies for NAFLD management. In addition to FXR, fibroblast growth factor receptor FGFR4 is a key mediator of hepatic bile acid synthesis. Using N-acetylgalactosamine-conjugated siRNA, we knocked down FGFR4 specifically in the liver of mice on chow or high-fat diet (HFD) and in mouse primary hepatocytes to determine the role of FGFR4 in metabolic processes and hepatic steatosis. Liver-specific FGFR4 silencing increased bile acid production and lowered serum cholesterol. Additionally, we found that HFD-induced liver steatosis and insulin resistance improved following FGFR4 knockdown. These improvements were associated with activation of the FXR-FGF15 axis in intestinal cells, but not in hepatocytes. We conclude that targeting FGFR4 in the liver to activate the intestinal FXR-FGF15 axis may be a promising strategy for the treatment of NAFLD and metabolic dysfunction.

overall_design: C57BL6/J male mice were placed on Chow (Mouse Diet 9F, PharmaServ) or 60% HFD (Research diets, D12492) for 12 weeks. The mice were injected subcutaneously with 3 mg/kg of GalNAc conjugated siRNA targeting FGFR4 or a sterile 0.9% sodium chloride solution (control) every two weeks while on the diets. Total RNA was isolated from the liver.

first: Softic

last: Samir


title: Particulate Matter10-induced airway inflammation and fibrosis can be regulated by chitinase-1 suppression

city: Seoul

first: YONG JUN

last: CHOI

state: Seoul

address: Gangnam Severance Hospital 211 Eonjuro, Gangnam-gu Korea

department: Internal Medicine

country: South Korea

institute: Yonsei University College of Medicine

summary: Particulate matter10 (PM10) can induce airway inflammation and fibrosis. Chitinase-1 is recently known to have key roles in inflammation and fibrosis. We aimed to investigate the effects of chitinase-1 inhibitor in PM10-treated murine models. PM10 and/or OVA-induced airway inflammation and fibrosis murine models were well established. CPX and dexamethasone ameliorated PM10 or PM10/OVA-induced airway hyper-responsiveness, airway inflammation, and fibrosis. CPX and dexamethasone also reduced levels of various inflammatory markers including chitinase-1 in lung homogenates. PM10 and OVA also induced extreme changes of mRNA expression. CPX and dexamethasone decreased levels of mRNA expression especially associated with inflammation and immune regulation. They also significantly regulated asthma and asthma related pathway including JACK-STAT signaling pathway.Chitinase-1 suppression by CPX can regulate PM10-induced and aggravated airway inflammation and fibrosis via various signaling pathway.

overall_design: In female BALB/c mice, PM10 was intranasally administered four times over 2 weeks, and ovalbumin (OVA) was intraperitoneally injected and then intranasally administered. Chitinase-1 inhibitor (CPX) 6 times over 3 weeks or dexamethasone 3 times in last week were treated intraperitoneally. After 2 days from the last challenges, mice were sacrificed. Full RNA sequencing using lung homogenates was conducted to evaluate signaling pathway.

first: Heejae

last: Han

first: Yong Jun

last: Choi

first: Hye Jung

last: Park


title: BRD4 loading at the transcription start site mediates pause-release and underlies the disproportionate transcriptional response to BET bromodomain inhibition [GRO-Seq]

overall_design: LP-1 multiple myeloma cell line was treated with DMSO or 0.5 μM JQ1 for 10 min, or with 0.5 μM JQ1 for 30 min and then anyzed by GRO-Seq


title: miRNA expression in epididymal adipose tissue of mice fed a normal or high-fat diet

city: Kamakura

first: Satoshi

last: Kondo

state: Kanagawa

address: 10-1 tebiro 6-chome

country: Japan

institute: Toray Industries,Inc.

summary: Individualized outcome prediction classifiers were successfully constructed through expression profiling of a total of 1,900 miRNAs.

overall_design: In the study presented here, epididymal adipose tissue of mice fed a normal or high-fat diet, were used to acquire expression profiles of a total of 1,900 unique miRNAs.

first: Tomomi

last: Sano


title: single-nucleus RNA-seq of microvessel-enriched vascular cells and corresponding parenchyma from frontal cortex samples

city: Cardiff

first: Frank

last: Wessely

address: Maindy Road

department: UK DRI

country: United Kingdom

institute: Cardiff University

summary: Vascular cell types are under-represented in standard single-nucleus RNA-Seq studies of human frozen post-mortem brain tissue. Using a novel microvessel-enrichment procedure allows to obtain highly purified fractions of vascular cell types and their corresponding parenchymal fraction of the same post-mortem brain tissue sample.

overall_design: Vascular and parenchymal fractions of post-mortem frontal cortex samples were obtained from 10 control and 10 Alzheimer's disease patients, resulting in a total of 40 samples subjected to single-nucleus RNA-seq (10X Genomics)

first: Hannah

last: Sleven

first: Zameel

last: Cader

first: Caleb

last: Webber

first: Olaf

last: Ansorge


title: High level and nature of transcriptional noise in yeast cells [RNA-seq]

first: Zlata

last: Gvozdenov

address: 240 Longwood Ave

department: BCMP

institute: Harvard Medical School

summary: “Biological noise” is defined as functionally insignificant events that occur in living cells due to imperfect fidelity of biological processes.  Distinguishing between biological function and biological noise is often difficult, and experiments to measure biological noise have not been performed.  Here, we measure biological noise in yeast cells by analyzing chromatin structure and transcription of an 18 kb region of DNA whose sequence was randomly generated and hence is functionally irrelevant.  Nucleosome occupancy on random-sequence DNA is comparable to that on yeast genomic DNA.  However, nucleosome-depleted regions are much less frequent, and there are fewer well-positioned nucleosomes and shorter nucleosome arrays.  Steady-state levels of RNAs expressed from random-sequence DNA are comparable to those of yeast mRNAs, although transcription and mRNA decay rates are at higher levels.  Transcriptional initiation (5’ ends) from random-sequence DNA occurs at numerous sites at low levels, indicating very low intrinsic specificity of the Pol II machinery.  In contrast, poly(A) profiles (relative levels and clustering of 3’ isoforms) of random-sequence RNAs are roughly comparable to those of endogenous yeast RNAs, which are restricted to 3’ untranslated regions.   RNAs expressed from random-sequence DNA show higher cell-to-cell variability than RNAs expressed from yeast genomic DNA, suggesting that functional elements limit the variability among individual cells within a population.  These observations indicate that transcriptional noise occurs at high levels in yeast, and they provide insight into how chromatin and transcription patterns arise from the evolved yeast genome.

overall_design: RNase-Seq of the strain harboring random-sequence artificial chromosome (ChrXVII).

first: Kevin

last: Struhl


title: PD-1highCXCR5–CD4+ Peripheral Helper T (Tph) cells Promote CXCR3+ Plasmablasts in the early phase of COVID-19

city: New Haven

first: Hiromitsu

last: Asashima

state: CT

address: 300George St

institute: Yele School of Medicine

summary: T cell–B cell interaction is the key immune response to protect host from severe viral infection. We used COVID-19 as a model of acute viral infections and analyzed CD4+ T cell subsets associated with plasmablasts expansion and clinical outcome. Peripheral helper T cells (Tph, denoted as PD-1highCXCR5–CD4+ T cells) were significantly increased, as were plasmablasts. Tph cells exhibited “B-cell help” signatures and induced plasmablasts differentiation in vitro. Expanded plasmablasts showed increased CXCR3 expression, which is positively correlated with higher frequency of activated Tph cells and better clinical outcome. These results elucidate a critical role for Tph cells in regulating protective B cell response during acute viral infection.

overall_design: sorted 6 subsets of CD4+CD45RA- T cells based on PD-1 and CXCR5 expressions from 3 patients with COVID-19

first: Subhasis

last: Mohanty

first: David

last: Hafler


title: High level and nature of transcriptional noise in yeast cells [3'READS]

overall_design: 3'READS of the strain harboring random-sequence artificial chromosome (ChrXVII).


title: High level and nature of transcriptional noise in yeast cells [4tU-Seq]

overall_design: 4tU-Seq of the strain harboring random-sequence artificial chromosome (ChrXVII).


title: Meta-analysis of glioblastoma tissue RNA-seq datasets points to ferroptosis pathway dysregulation

city: Mol

first: Mohamed

last: Mysara

state: Belgium

address: Boeretang 200

country: Belgium

institute: Belgian nuclear research center (SCK-CEN)

type: Non-coding RNA profiling by high throughput sequencing

summary: Glioblastoma is a grade IV glioma of heterogeneous nature which complicates disease pathophysiology and biomarker research. Thus, the aim of our meta-analysis is to identify long noncoding RNAs (lncRNAs) and protein coding genes (PCGs) that are differentially expressed over different glioblastoma tissue datasets. Small RNA-seq of glioblastoma tissues was also performed to identify differentially expressed microRNAs (miRNAs) relative to paired controls.

overall_design: Fresh frozen brain tissue samples from patients with glioblastoma (n = 17) and normal controls from tumor-adjacent normal tissue (n = 3) were collected from Biobank Antwerp (University Hospital of Antwerp (UZA), Antwerp, Belgium; ID: BE 71030031000). The tissues then underwent small RNA-seq to identify differentially expressed microRNA relative to paired controls.

first: M

last: Sallam


title: Small RNA sequencing in wild type and GCH1-knockdown (KD) BV2 microglial cells

first: Zheyu

last: Zhang

address: Yueyang Road

institute: CAS

summary: We conducted small RNA sequencing and bioinformatics analysis of GCH1-KD BV2 microglial cells treated with adenovirus. Their RNA was extracted and analyzed, and the results were verified by quantitative real-time polymerase chain reaction (qRT-PCR). This study explored the miRNAs and mRNAs regulated by GCH1 and revealed a possible mechanism of GCH1 in microglial activation.

overall_design: Small RNA expression profiles of wild type and GCH1-KD BV2 microglial cells were generated by high-throughput sequencing, in triplicate, using Illumina NextSeq 500 sequencer.

first: Chunyang

last: Meng

first: Shu

last: Jia


title: High level and nature of transcriptional noise in yeast cells [5'-Seq]

overall_design: 5'-Seq (5' isoforms or transcription start sites) of the strain harboring random-sequence artificial chromosome (ChrXVII).


title: CBX5 loss drives EGFR inhibitor resistance and results in therapeutically actionable vulnerabilities in lung cancer

city: Birmingham

first: Narendra

last: Wajapeyee

state: AL

address: 720 20th Street South, Kaul 540A

department: Department of Biochemistry and Molecular Genetics

institute: University of Alabama at Birmingham

summary: The study evaluated the differential gene expression in CBX5 knockdown cells compared to control shRNA expressed HCC827 cells. Briefly, human lung cancer HCC827 cells stably expressing either CBX5 shRNAs or control shRNA were analysed for gene expression.

overall_design: Total RNA was extracted from all the 3 transformed cells, followed by poly-A selection and RNA-sequencing using Illumina Hi-Seq 2500 platform, with three biological replicates for each transformed sample.

first: Suresh

last: Bugide


title: Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and knock-in TrkAC lumbar dorsal roots ganglia transcriptomes in a context of arthritis induced by intra-articular injection of complete Freund's adjuvant

city: Clermont-Ferrand

first: Fabien

last: Marchand

address: 28 Place Henri Dunant

department: Fundamental and clinical pharmacology of pain

country: France

institute: Université Clermont Auvergne, Inserm U1107 NEURO-DOL

summary: Our aim was to better understand the involvement of the specific intracellular signalling pathways activated by NGF through its specific tyrosine kinase type A (TrkA) receptor in the pathophysiology of rheumatoid arthritis using knock-in TrkA/C mice. This mice expresses the native extracellular part of TrkA able to bind NGF but the functional transmembrane and intracellular parts of TrkA were replaced by those of the specific receptor of neurotrophin 3 (NT3): the tyrosine kinase type C  receptor (TrkC). RNA sequencing analysis was performed  on lumbar (L4-L5-L6) dorsal roots ganglia of Wild Type littermates and knock-in TrkA/C mice  14 days after intraarticular injection in the ankle joint of complete freund adjuvant (CFA) or vehicle (n=4 biological samples per group).

overall_design: Lumbar dorsal roots ganglia RNA profiles of 10-12 weeks old wild-type and TrkA/C knock-in mice 14 days after injection in the ankle of vehicle or complete Freund's adjuvant (CFA)

first: Emeric

last: Dubois

first: Celia

last: Barrachina

first: Youssef

last: Aissouni

first: Lauriane

last: Delay


title: Influenza vaccination reveals sex dimorphic imprints of prior mild COVID-19

status: Public on Jan 04 2023

city: Bethesda

first: William

middle: W

last: Lau

state: MD

address: 4 Memorial Drive

department: Laboratory of Immune System Biology

institute: National Institute of Allergy and Infectious Diseases

overall_design: Refer to individual Series


title: Gene expression profiles of hiPSCs, hiPSC-drived neuroepithelial cells (NECs), and hiPSC-derived neural crest cells (NCCs).

city: Shinjuku-ku

first: Tsukasa

last: Sanosaka

state: Tokyo

address: 35 Shinanomachi

department: Department of Physiology

institute: Keio University School of Medicine

summary: We performed gene expression profiling analysis using data obtained from RNA-seq of 3 different cells types.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for iPSCs, iPSC-drived NECs, and iPSC-drived NCCs.


title: High level and nature of transcriptional noise in yeast cells

first: Zlata

last: Gvozdenov

type: Methylation profiling by high throughput sequencing


title: AKT1-FOXO4 Axis Regulates Hemochorial Placentation [Foxo4-KO-JZ]

city: Stillwater,

first: Khursheed

last: Iqbal

state: OK

address: 310 N Monroe St,

institute: Oklahoma state university

summary: AKT1 is a serine/threonine kinase implicated in fetal, placental, and postnatal growth. In this study, we investigated roles for AKT1 in placental development using a genome-edited/loss-of-function rat model. Both heterozygous and homozygous Akt1 mutant rats were viable and fertile. Disruption of AKT1 resulted in placental, fetal, and postnatal growth restriction. Akt1 null placentas showed deficits in both junctional zone and labyrinth zone size and their ability to adapt to a physiological stressor. Robust differences in the transcriptome of wild type versus Akt1 null junctional zones were identified. Among the differentially expressed junctional zone transcripts was forkhead box O4 (Foxo4), which encodes a transcription factor and known AKT substrate. FOXO4 expression was prominent in the junctional zone and invasive trophoblast cells of the rat placentation site and enhanced following rat TS cell differentiation. Foxo4 gene disruption using genome-editing resulted in placentomegaly, including an enlarged junctional zone. AKT1 and FOXO4 regulate the expression of many of the same transcripts expressed by trophoblast cells; however, in opposite directions. In summary, we have identified AKT1 and FOXO4 as part of a regulatory network controlling hemochorial placenta development.

overall_design: 1) Rat placentation site compartments were dissected on gd18.5. Dissected junctional zone tissues from wild type, Akt1 null, and Foxo4Xm- fetuses were snap-frozen in liquid nitrogen and stored at -80°C until processing for RNA isolation. 2) Foxo4 was knocked down in rat trophoblast stem cells using lentiviral delivery of shRNA. Following selection by puromycin, cells were differentiated for fifteen days. On day fifteen of differentiation, cells treated with either control shRNA or Foxo4-specific shRNA were collected and RNA was isolated.

first: Keisuke

last: Kozai

first: Michael

last: Soares


title: Cancer-associated SMARCAL1 loss-of-function mutations promote alternative lengthening of telomeres and tumorigenesis in telomerase-negative glioblastoma cells

city: Durham

first: Matthew

last: Waitkus

state: NC

address: 203 Research Drive, Medical Science Research Building 1, Room 181A

institute: Duke University

summary:
In this study, we used a patient-derived ALT-positive GBM cell line with native SMARCAL1 deficiency to investigate the role of SMARCAL1 in ALT-mediated telomere synthesis and gliomagenesis in vitro and in vivo.
Differential gene expression programs associated with tumorigenesis in D06MG xenografts.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for Patient derived cells, subcutaneous tumor cells and the initial NSC medium-maintained cells

first: Heng

last: Liu

first: Cheng

last: Xu

first: Bill

middle: H

last: Diplas

first: Alexandrea

last: Brown

first: Laura

last: Strickland

first: Jinjie

last: Ling

first: Roger

last: McLendon

first: Stephen

middle: T

last: Keir

first: David

last: Ashley

first: Yiping

last: He

middle: S


title: A neural substrate for negative affect dictates female parental behaviour

city: Lausanne

first: Ludovic

last: Telley

address: Department of Biomedical Sciences University of Lausanne Rue du Bugnon 9

institute: UNIL

summary: Parental behaviours are essential to secure survival and wellbeing of newborns. Concomitantly, parenting also limits negative affective states in adults, which emerge when the coping with neonatal distress becomes a challenge. Whether neural circuits that process negative affect orchestrate components of parental behaviours remains, however, unknown. Here, we identify functional and transcriptional signatures of parental behaviours in neurons of the negative emotion center lateral habenula receiving bed nucleus of the stria terminalis innervation (BNSTLHb). Calcium imaging and optogenetic manipulations reveal that LHb neurons of virgin female mice increase their activity in response to pup distress vocalization and are necessary for pup calls-driven aversive behaviours. Accordingly, LHb activity rises during the retrieval of a pup to a nest, a behaviour worsened by optogenetic LHb inactivation. Intersectional cell identification and transcriptional profiling associates the BNSTLHb neuronal population to parental behaviours and outlines gene expression in female virgins that is similar to mothers but divergent from non-parental virgin male mice. Accordingly, optogenetic activation and inactivation of the BNST-LHb pathway maximizes and suppresses, respectively, the parental behaviour. Finally, tracking and manipulating single BNSTLHb cell activity demonstrates specificity of this neuronal subset for encoding negative affect and pup retrieval, but not sociability amongst conspecifics. Thus, BNSTLHb cells are operational for female parenting, demonstrating that a negative affect neural circuit processes newborn distress signals and limits them through female parenting.

overall_design: Single cell RNA sequencing (scRNA-seq) on sorted  KASH-GFP+ BNSTLHb from three categories, namely virgin females, sexually-experienced females (mothers) and  virgin male mice.

first: Salvatore

last: Lecca

first: Mauro

last: Congiu

first: Lea

last: Royon

first: Leonardo

last: Restivo

first: Benoit

last: Girard

first: Noemie

last: Mazaré

first: Camilla

last: Bellone

first: Manuel

last: Mameli


title: The whole transcriptome analysis for seminal plasma extracellular vesicles (SPEVs) of Yorkshire boars

city: Beijing

first: yu

last: zhang

state: China

address: Yuan Mingyuan west road

institute: China Agricultural University

summary: The seminal plasma contains large quantities of extracellular vesicles (EVs). However, the role of these EVs and their interactions with sperms are not clear. To identify the important molecules affecting sperm motility in EVs, we sequenced the EVs in the seminal plasma of Yorkshire boars with different sperm motility using whole RNA sequence.

overall_design: We evaluated the sperm motility phenotypic data of 230 boars by using a computer-assisted sperm analysis from a national boar station. Twelve Yorkshire boars with high sperm motility and twelve Yorkshire boars with low sperm motility were selected for SPEV extraction. All the individuals were sexually mature, aged between 14 and 36 months old. The average total sperm motility of H group was 0.94, while that of L group was 0.40. For each boar, 60 mL of semen plasma was used to extract EVs. Deep RNA sequencing was performed to gain insight into the types of RNA in SPEVs, including mRNAs, miRNAs, lncRNAs and circRNAs.

first: Ning

last: Ding

first: Yu

last: Zhang

first: Mengna

last: Huang

first: Jianfeng

last: Liu

first: Chonglong

last: Wang

first: Chun

first: Jinkang

last: Cao

first: Qin

first: Li

last: Jiang


title: Loss of KDM5B ameliorates pathological cardiac fibrosis and dysfunction by epigenetically enhancing ATF3 expression

city: Shanghai

first: Zhenzhen

last: Zhan

address: Jimo Road 150

department: Research Center for Translational Medicine

institute: Shanghai East Hospital, Tongji University School of Medicine,

summary: Myocardial fibrosis is the most common pathological feather of adverse ventricular remodeling, and persistent fibrotic extension decreases myocardial compliance, promotes the development of heart failure. Epigenetics has been considered to play a potent regulatory role in the development of excessive myocardial fibrosis. Although, the explicit mechanism of epigenetic regulation in myocardial fibrosis still needs to be fully elucidated.RNA-seq analysis was used to screen differentially expressed genes in cardiac fibroblasts isolated from  KDM5B KO and littermate control WT mice hearts at day 7 after MI operation.

overall_design: 8-10-week-old male KDM5B KO mice and their corresponding WT mice were subjected to myocardial infarction by ligation of the left anterior descending coronary artery. At 7 days after myocardial infarction, cardiac fibroblasts  were isolated  for RNA-seq analysis. Each group contain with 3 replicates

first: Bo

first: Xingguang


title: Analysis of long non-coding RNAs expression in sarcoma

city: Linhai

first: BINXIANG

last: CHU

address: XINMEN street

summary: We report on sarcoma resected from human patients that the tumours express long non-coding RNA.

overall_design: Expression profiling of sarcoma (n=12) samples.

first: BIN

middle: X


title: Single-cell transcriptomic profiling of the zebrafish inner ear reveals molecularly distinct hair cell and supporting cell subtypes

city: Los Angeles

first: Tuo

last: Shi

state: California

address: 1425 San Pablo St BCC 403

institute: University of Southern California

summary: A major cause of human deafness and vestibular dysfunction is permanent loss of the mechanosensory hair cells of the inner ear. In non-mammalian vertebrates such as zebrafish, regeneration of missing hair cells can occur throughout life. While a comparative approach has the potential to reveal the basis of such differential regenerative ability, the degree to which the inner ears of fish and mammals share common hair and supporting cell types remains unresolved. Here we perform single-cell RNA sequencing of the zebrafish inner ear at embryonic through adult stages to catalog the diversity of hair and non-sensory supporting cells. We identify a putative progenitor population for hair and supporting cells, as well as distinct hair and supporting cell types in the maculae versus cristae. The hair and supporting cell types differ from those described for the lateral line, a distributed mechanosensory organ in zebrafish in which most studies of hair cell regeneration have been conducted. In the maculae, we identify two subtypes of hair cells that share gene expression with mammalian striolar or extrastriolar hair cells. In situ hybridization reveals that these hair cell subtypes occupy distinct spatial domains within the two major macular organs, the utricle and saccule, consistent with the reported distinct electrophysiological properties of hair cells within these domains. These findings suggest that primitive specialization of spatially distinct striolar and extrastriolar hair cells likely arose in the last common ancestor of fish and mammals. The similarities of inner ear cell type composition between fish and mammals also support using zebrafish as a relevant model for understanding inner ear-specific hair cell function and regeneration.

overall_design: Inner ears were dissected from the Sox10Cre;UbiSwitch zebrafish at 14dpf (n=35) and 12mpf (n=6). Converted cells were isolated by Fluorescence-activated cell sorting (FACS) according to the presence or absence of mCherry signal and analyzed using 10x genomics based scRNAseq. Reads were aligned to danRer11 using the Cellranger pipeline

first: Marielle

middle: O

last: Beaulieu

first: Lauren

last: Saunders

first: Peter

last: Fabian

first: Cole

last: Trapnell

first: Neil

last: Segil

first: J

middle: G

last: Crump

first: David

last: Raible


title: CEP120 Promotes Centrosome Amplification And Progression Of Gastric Cancer Via USP54-Mediated Deubiquitination Of PLK4

city: wuhan

first: Chenggang

state: hubei

address: No. 1277 Jiefang Avenue

institute: Union Hospital, Tongji Medical College, Huazhong University of Science and Technology

summary: Centrosomal protein 120 (CEP120) is a 120kD centrosome protein that plays an important role in centrosome replication. Overexpression of CEP120 can lead to centrosome amplification, which is closely associated with tumorigenesis and development. However, there are no reports on the relationship between CEP120 and tumors. In our study, overexpression of CEP120 promoted centrosome amplification in gastric cancer (GC), and the role of CEP120 in promoting GC progression was demonstrated in vitro and in vivo. We demonstrated that CEP120 promotes centrosome amplification and GC progression by promoting the expression and centrosome aggregation of the deubiquitinating enzyme USP54, maintaining the stability of PLK4 and reducing its ubiquitination degradation. In conclusion, the CEP120-USP54-PLK4 axis may play an important role in promoting centrosome amplification and GC progression, thus providing a potential therapeutic target for GC.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for SGC7901 cells and its CEP120-overexpressed derivatives (SGC7901-vector, SGC7901-CEP120).

first: Xianxiong

last: Ma

first: Xiuxian

last: Zhu

first: Guanxin

last: Wei


title: mRNA expression data from livers of wild-type (WT) mice, mice that lack ribosomal protein S6 (Rps6) (DS6), mice that overexpress c-Myc (Myc) and livers that lack Rps6 and also overexpress c-Myc (DS6 Myc)

city: San Antonio

first: Yidong

last: Chen

state: Texas

address: 8403 Floyd Curl Drive, MSC 7784

department: Population Health Sciences

institute: UT Health Science Center at San Antonio

summary:
Targeted depletion of ribosomal protein S6 (Rps6) from hepatoblasts of the developing liver results in neonatal sub-lethal hepatic failure due to inhibition of bile duct development and widespread induction of hepatocyte death triggering regeneration.  Overexpression of c-Myc is hepatoprotective in the context of Rps6-deficiency and eliminates the need for DS6 livers to regenerate by preventing hepatocyte death.
Microarrays were used to identify the transcriptional program associated with loss of hepatic Rps6 and to identify mRNAs associated with c-Myc's hepatoprotective effect in DS6 livers

overall_design: Total RNA was prepared from livers of young adult (5 week-old) WT, DS6, Myc and DS6 Myc mice (3/group)

first: Sarah

last: Comerford

first: Robert

last: Hammer

first: Elizabeth

last: Hinnant


title: Sequential treatment with activin and hepatocyte growth factor(HGF) induces FOXM1 to promote colorectal cancer liver metastasis

city: Bishan

first: Hong

last: Peng

state: ChongQing

address: Shuangxing avenue 9

institute: AffiliatedBishan hospital of Chongqing Medical  University

summary:
To investigate the effect of sequential treatment with activin and/or HGF on HCT116 cells,
we performed gene expression profiling analysis using data obtained from RNA-seq of 3 groups(NC, Activin, Activin+HGF).

overall_design: Comparative gene expression profiling analysis of RNA-seq data for HCT116 cells treated with NC, Activin or Activin+HGF.

first: Jinjun

last: Guo


title: Dysregulation of intercellular communication indicates cellular processes controlled by transcription factors involved in doxorubicin-induced long-term cardiotoxicity in cancer survivors

city: Krakow

first: Paweł

last: Wołkow

address: Kopernika 7c

department: Centre for Medical Genomics - OMICRON

country: Poland

institute: Jagiellonian University Medical College

summary: Long-term side effects of doxorubicin include cardiotoxicity. Because studying transcriptional network alterations in human heart at early stages of cardiac dysfunction development is not feasible, in the present study, we used circulating microRNAs (miRNAs) to obtain insight into cellular processes in acute lymphoblastic leukemia (ALL) survivors with a history of doxorubicin treatment. We showed that altered miRNA profiles in plasma and circulating extracellular vesicles (EVs) and particularly the distribution of miRNAs between the two compartments in ALL survivors are linked to cellular transcriptomic processes controlled by transcription factors involved in epigenetic regulation, oxidative stress response, senescence, fibrosis, or epithelial-mesenchymal transition (EMT)—a phenomenon involved in organ injury, repair, and remodeling. These alterations could also be linked to cardiac complications and interindividual variability in cardiomyocyte response to doxorubicin. Thus, circulating miRNAs can indicate the possible molecular mechanisms of cardiotoxicity in patients previously exposed to anthracyclines even when there are no apparent clinical signs of heart dysfunction.

overall_design: Study was designed to compare non-coding RNA circulating in extracellular vesicles and plasma in 61 ALL survivors and 59 healthy controls.

first: Justyna

last: Totoń-Żurańska

first: Michał

last: Seweryn


title: Effect of depletion of USP36 on gene expression of ECA109 cells, esophageal squamous cell carcinoma cell line.

city: jinan

first: Wenhao

last: Zhang

address: Beiyuan Street 247

institute: The Second Hospital of Shandong University

summary: To investigate the function of USP36 in the regulation of cell proliferation and escc progression, we established eca109 cell lines in which each target gene has been knocked down by siRNA.We then performed gene expression profiling analysis using data obtained from RNA-seq of 6 different cells at same time points.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for depletion USP36 of ECA109 cells.

first: Xiaogang

last: Zhao

first: Jian


title: RNA-seq in human keratinocytes HaCaT cell line

city: Guangzhou

first: Yi

last: Jin

address: Department of Toxicology, School of Public Health, Southern Medical University, Shatai Road, Baiyun, Guangzhou, China

institute: Southern Medical University

summary: To figure out the expression level of genes in normal human keratinocytes, we performed RNA-seq analysis in HaCaT cells. Here, we used 4 HaCaT cells as parallel samples.

overall_design: Performed RNA-seq analysis in HaCaT cells.

first: Xingyuan

last: Liu

first: Xiaoting

last: Liang

first: Jieyu

first: Liang

last: Zhou


title: Iron treatment induces resistance against the rice blast fungus Magnaporthe oryzae through potentiation of immune responses

city: Bellaterra

first: Blanca

last: San Segundo

address: Edifici CRAG. Campus UAB. Carrer de la Vall Moronta s/n

country: Spain

institute: Center for Research in Agricultural Genomics (CRAG)

summary: To investigate the role of iron excess in rice immune responses to Magnaporthe oryzae infection. Gene expression profiling analysis were performed using data obtained from RNA-seq of rice plants grown in differential iron supply and challenged with Magnaporthe oryzae spores.

overall_design: Comparative gene expression profiling analysis of RNA-seq data of rice plants treated either with an control Fe or high Fe nutrient solution and infected or not with Magnaporthe oryza

first: Ferran

last: Sanchez Sanuy

first: Roberto

last: Mateluna Cuadra

first: Keisuke

last: Tomita

first: Kazunori

last: Okada

first: Gian

last: Sacchi

first: Sonia

last: Campo


title: High-temperature adaptation of an OsNRT2.3 allele is thermoregulated by small RNAs

city: Nanjing

first: Xiaorong

last: Fan

address: Nanjing city Wei Tong Road 6

department: 1State Key Laboratory of Crop Genetics and Germplasm Enhancement

institute: Nanjing Agricultural University

summary: OsNRT2.3 impacts NUE and yield by a temperature dependent mechanism of post-transcriptional and translation regulation by a sRNA

overall_design: Use target-specific DMS-MaPseq to probe in vivo OsNRT2.3a and OsNRT2.3b RNA structure.

first: Yong

first: Hisae

last: Tateishi-Karimata

first: Tamaki

last: Endoh

first: Qiongli

first: Kexin

last: Li

first: Xiaoru

first: Yingjun

last: Ma

first: Limin

last: Gao

first: Haiyan

last: Lu

first: Zhiye

last: Wang

first: Art

last: Cho

first: Xuefeng

last: Yao

first: Chunming

first: Naoki

last: Sugimoto

first: Shiwei

last: Guo

first: Xiangdong

last: Fu

first: Guohua

last: Xu

first: Qirong

last: Shen

first: Luis

last: Herrera-Estrella


title: Transcriptional changes in Wnt antagonism- and TGFβ agonism-induced MSC chondrogenesis.

city: Zhunan

first: B. LINJU

last: Yen

address: 35 Keyan Road

country: Taiwan

institute: National Health Research Institutes

summary: Wnt/β-catenin signaling is important in skeletal related-tissue development. We have found that Wnt/β-catenin antagonist XAV could replace traditionally used TGFβ3 as chondrogenic inducer. Here we applied gene expression array to characterize transcriptomic changes between XAV- and TGFβ-induced chondrogenic differentiation in human bone marrow (BM) and induced pluripotent stem cell (iPSC) derived MSCs.

overall_design: RNA samples were collected from human MSC pellets (1 BMMSC and 2 iPSC-MSC) with XAV- or TGFβ-based chondrogenic induction for 3 days.

first: Chen-Chan

last: Hsieh

first: B


title: Probing the role of tsukushi in  the transcriptional regulation of lateral ventricular GFAP expressing neural stem/progenitor cell

city: Fukuoka

first: kunimasa

last: Ohta

address: Department of Stem Cell Biology, Faculty of Arts and Science , Kyushu University. 744, Motooka, Nishi-ku,

department: Stem Cell Biology

institute: Kyushu University

summary: To investigate the role of  proteoglygacn tsukushi  in the transcriptional regulation of GFAP expressing lateral ventricular stem/progenitor cell, we generated a tsukushi knockout mouse that express GFP at the GFAP positive cell by mating TSK-KO with GFAP-GFP mouse. GFAP positive cells were collected from the lateral ventricle slices and then RNA -seq was performed. RNA-seq data revealed that the tsukushi is involved with the post transcriptional regulation and critical for developmental signaling process.

overall_design: RNA-seq on wildtype (GFAP-GFP mouse) and Tsukushi knockout ( TSK-KO-GFAP-GFP) mouse brain lateral ventricular GFAP expressing cell

first: Arif

last: Istiaq

first: Teremusa

last: Umemoto

first: Naofumi

last: Ito

first: Kunimasa


title: Genome-wide identification of m6A-related transcriptional profiles in cortex of rats with cerebral ischemia-reperfusion and intervention of Buyang Huanwu Decoction

city: Changsha

first: Bo-wei

last: CHEN

address: No. 95 Shaoshan Middle Road

institute: Hunan University of Chinese Medicine

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

summary: To reveal the effect of Buyang Huanwu Decoction on m6A related transcriptional profiles of cortex in rats with cerebral ischemia-reperfusion injury

overall_design: Three-condition experiment: control group, model group and Buyang Huanwu Decoction(BHD) group.The middle cerebral artery embolization method was used to replicate thecerebral ischemia-reperfusion injury model in all groups except the control group. After 7 days of intervention, Arraystar Rat Epitranscriptomic microarray was used to screen m6A differentially methylated lncRNAs and mRNAs.

last: Chen

first: LE

last: Shao

first: Jian

last: Yi

first: Zhi-hua

first: Bai-yan

last: Liu


title: ChIP-seq in SUNE1 cells that overexpressed CBX1

first: Jun

last: Ma

address: 651 Dongfeng Road East

institute: Sun Yat-sen University Cancer Center

summary: ChIP experiment against anti-FLAG in SUNE1 cells trasfected with FLAG-CBX1 plasmid.

overall_design: ChIP experiment against anti-FLAG in SUNE1 cells trasfected with FLAG-CBX1 plasmid, then purified RNA are used to perferm RNA-seq.


title: TDP-43 safeguards the embryo genome from L1 retrotransposition

city: Shinjuku

first: Haruhiko

last: Siomi

address: 35 Shinanomachi

department: Department of Molecular Biology

institute: Keio University School of Medicine

summary: We report that TAR DNA binding protein 43 (TDP-43), mutations in which constitute a major risk factor for amyotrophic lateral sclerosis (ALS), inhibits L1 retrotransposition in mouse embryonic stem cells (mESCs) and preimplantation embryos. Knockdown of TDP-43 resulted in massive genomic L1 expansion and impaired cell growth in preimplantation embryos and ESCs. Functional analysis demonstrated that TDP-43 interacts with L1 open reading frame 1 protein (L1 ORF1p) to mediate genomic protection, and loss of this interaction led to de-repression of L1 retrotransposition. Our results identify TDP-43 as a guardian of the embryonic genome by protecting it from massive L1 retrotransposition.

overall_design: This accession includes RNA-seq data of mouse morula subjected to siScramble and siTardbp treatmen.

first: Ten

last: Li

first: Youjia

last: Guo


title: m6A-seq and RNA-seq of  4 pairs NPC tissues with or without metastasis

summary: Nasopharyngeal carcinoma (NPC), which arises from the nasopharyngeal pharynx, is a metastasis-prone malignancy highly prevalent in East and Southeast Asia, especially southern China. Despite progress in chemo-radiotherapeutic strategies, about 20% of NPC patients still suffer from distant metastasis, thus developing new therapeutic strategies for NPC is of vital importance. N6-methyladenosine (m6A) RNA modification, the most abundant epitranscriptomic modification in eukaryotic mRNA, has attracted great attention in cancer research because of its vital biological functions. However, little is known about the underlying molecular mechanisms between m6A modification and NPC progression. We aimed to identified differential m6A peaks by analyzing the m6A modification profile in NPC with paired tissues with or without metastasis using m6A-seq.  For RNA-seq and ChIP-seq, we aimed to identified the downstream targets of CBX1 in NPC.

overall_design:
Total RNA from 4 pairs NPC tissues with or without metastasis were extracted using Trizol reagent (Invitrogen, CA, USA) following the manufacturer's procedure. The total RNA quality and quantity were analysis of Bioanalyzer 2100 and RNA 6000 Nano LabChip Kit (Agilent, CA, USA) with RIN number >7.0. Approximately more than 25 ug of total RNA representing a specific adipose type was used to deplete ribosomal RNA according to the manuscript of the Epicentre Ribo-Zero Gold Kit (Illumina, San Diego, USA). Following purification, the ribosomal-depleted RNA is fragmented into ~100-nt-long oligonucleotides using divalent cations under elevated temperature. Then the cleaved RNA fragments were subjected to incubated for 2h at 4℃ with m6A-specific antibody (No. 202003, Synaptic Systems, Germany) in IP buffer (50 mM Tris-HCl, 750 mM NaCl and 0.5% Igepal CA-630) supplemented with BSA (0.5 μg μl−1). The mixture was then incubated with protein-A beads and eluted with elution buffer (1 × IP buffer and 6.7mM m6A). Eluted RNA was precipitated by 75% ethanol. Eluted m6A-containing fragments (IP) and untreated input control fragments are converted to final cDNA library in accordance with a strand-specific library preparation by dUTP method. The average insert size for the paired-end libraries was ~100±50 bp. And then we performed the paired-end 2×150bp sequencing on an Illumina Novaseq 6000 platform at the LC-BIO Bio-tech ltd (Hangzhou, China) following the vendor's recommended protocol.
m6A seq  and RNA seq of  4 pairs NPC tissues with or without metastasis


title: Effect of depletion of CBX1 on gene expression of SUNE1 cells [RNA-seq]

overall_design:
Comparative gene expression profiling analysis of RNA-seq data for SUNE1 cells (sgCBX1 and sgNC).
To investigate the CBX1 in the progression of nasopharyngeal carcinoma, we established SUNE1 cell lines in which CBX1 has been knocked out by sgRNA.
We then performed gene expression profiling analysis using data obtained from RNA-seq of sgNC and sgCBX1.


title: m6A-modified CBX1 regulates NPC progression.

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

overall_design: Refer to individual Series


title: Paternal diet induces transgenerational epigenetic inheritance of DNA methylation signatures and phenotypes in sheep model

city: Madison

first: Hasan

last: Khatib

state: Wisconsin

address: 1675 Observatory Dr.

department: Animal and Dairy Sciences

institute: University of Wisconsin-Madison

summary: We examined whether paternal diet from weaning to puberty induces sperm DNA methylation changes that can be transmitted to subsequent generations. Over 100 methylated cytosines environmentally altered in the F0 generation were inherited by the F1 and F2 generations. Furthermore, the F0 paternal diet was associated with growth and male fertility phenotypes in these generations. Differentially methylated genes also showed correlations with gene expression.

overall_design: Evaluation of the effect of paternal diet on DNA methylation and phenotypes of subsequent generations

first: Camila

middle: U

last: Braz

first: Todd

last: Taylor

first: Hadjer

last: Namous

first: Jessica

last: Townsend

first: Thomas

last: Crenshaw


title: CD137 (4-1BB) ligand mediates CD4 T-cell immuno-surveillance of pre-  lymphoma B cells in a lymphoma-prone mouse model

city: Melbourne

first: Zhoujie

last: Ding

state: VIC

address: 89 Commercial Road

country: Australia

institute: Monash University

summary: Aberrant expression of the proto-oncogene BCL6 is a driver of tumorigenesis in diffuse large B cell lymphoma (DLBCL). Mice overexpressing BCL6 from the B cell-specific immunoglobulin heavy chain μ intron promoter (Iμ-Bcl6 Tg/+ ) develop B cell lymphomas with features typical of human DLBCL. B cell lymphoma development in these mice is tightly controlled by T cells; however, the mechanisms of this immune surveillance are poorly understood. Here we show that CD4 T cells contribute to the control of lymphoproliferative disease in lymphoma-prone Iμ-Bcl6 Tg/+ mice. Furthermore, we reveal that this CD4 T-cell immuno-surveillance requires signaling by the co-stimulatory molecule, CD137 ligand (CD137L; also known as 4-1BBL), which promotes the transition of pre malignant B cells with an activated phenotype into the germinal center stage, preventing their hazardous accumulation. Thus, CD137L-mediated CD4 T cell immuno-surveillance adds another layer of protection against B-cell malignancy to that provided by CD8 T-cell cytotoxicity.

overall_design: 12 samples for T cell sufficient lymphoma and 11 samples for T cell deficient lymphoma. Samples were ran in two runs and the sample T cell sufficient lymphoma_1/76_S1 was used as a reference sample between the two runs/batches. Sample 76_S1 from both batches are included in this series.

first: Dimitra

last: Zotos

first: Feng

last: Yan

first: Wei

last: Shi

first: Axel

last: Kallies

first: Daivd

last: Tarlinton


title: Expression data for Sweet Syndrome patient and Healthy Controls

city: Philadelphia

first: Thomas H.

last: Leung

state: PA

address: 421 Curie Blvd.

department: Dermatology

institute: University of Pennsylvania

summary:
Acute febrile neutrophilic dermatosis (Sweet syndrome) is a potentially fatal multiorgan inflammatory disease characterized by fever, leukocytosis, and rash with a neutrophilic infiltrate. Disease pathophysiology remains elusive. Corticosteroids and steroid sparing agents remain mainstays of treatment, but refractory cases pose a clinical challenge. Transcriptomic profiling of a refractory Sweet syndrome patient will improve our understanding of pathophysiology of the disease and, ultimately wiil help us to find a guided therapy.
We used microarray to perform molecular characterization of a particular refractory Sweet Syndrome patient and to identify altered pathways that may be targeted via currently available small molecular inhibitors.

overall_design: Lesional skin samples of the refractory pateint, Healthy-Controls and other Sweet Syndrome pateint samples were obtained as per study protocol that was approved by the Institutional Review Board of the University of Pennsylvania School of Medicine. Dermis was specifically isolated by laser capture microdissection from Formalin-Fixed paraffin embedded tissue section. It was followed by RNA extraction from dermal tissue and hybridization on Affymetrix microarrays.

first: Shreya

last: Bhattacharya

first: Emily

last: Sheng

first: Misha

last: Rosenbach


title: Identification of differently expressed mRNAs in LNPPS overexpression bladder cancer cells

city: Jinan

first: chuanxin

last: wang

address: 247 Beiyuan Street, Jinan 250033, Shandong, China,

summary: In this study, we aimed to explore RNAs profiling regulated by LNPPS in bladder cancer. RNA-seq analysis of three pairs of LNPPS-overexpressing 5637 cells and control cells was completed in this project. A total of 17.6Gb raw data was obtained. In concluion, our data showed that the overexpression of LNPPS caused the significantly upregulation of 82 mRNAs, and the downregulation of 102 mRNAs (|Log2FC|>1.5, p<0.05). Further studies will focus on the potential regulatory mechanisms of these significantly differently expressed mRNAs in the LNPPS-mediated development of bladder cancer.

overall_design: RNA profiles of three paires of LNPPS-overexpressing and control 5637 cells by high throughput sequencing

first: Chuanxin

last: Wang

first: Lutao

last: Du

first: Peilong

last: Li

first: Juan


title: A novel intergenic enhancer that regulates Bdnf expression in developing cortical neurons

city: London

last: Brookes

state: London

address: Gower Street

department: MRC Laboratory for Molecular Cell Biology

institute: University College London

summary: Brain-derived Neurotrophic Factor (BDNF) promotes neuronal differentiation and survival and is implicated in the pathogenesis of many neurological disorders. Here, we identified a novel intergenic enhancer located 170 kb from the Bdnf gene, which promotes the expression of Bdnf transcript variants during mouse neuronal differentiation and activity. Following Bdnf activation, enhancer-promoter contacts increase, and the region moves away from the repressive nuclear periphery. Bdnf enhancer activity is necessary for neuronal clustering and dendritogenesis in vitro, and for cortical development in vivo. Our findings provide the first evidence of a regulatory mechanism whereby the activation of a distal enhancer promotes Bdnf expression during brain development.

overall_design: Examination of 4C-seq looping in NPC, PMN and cortical neurons from a Bdnf exon I viewpoint, and in cortical neurons from an enhancer viewpoint


title: RNA sequencing of SSTR2 overexpression or knockout in gastric cancer cell lines

city: Daejeon

first: Byoung-Ha

last: Yoon

address: Gwahak-ro, Yuseong-gu, Daejeon 34141, Korea

institute: KRIBB

summary: Gene expression signatures in SSTR2 overexpression or knockout and control gastric cancer cell lines using RNA sequencing

overall_design: mRNA profiles of SSTR2 overexpression (AGS, MKN45, and MKN74) or knockout (SNU638) and control gastric cancer cell lines were generated by deep sequencing, in triplicate, using Illumina Hiseq.

first: Yong

last: Kim

first: Hee-Jin


title: Noncoding RNA expression profiles in five pairs of bladder cancer tumor tissues and matched adjacent non-tumor tissues

summary: In this study, we aimed to seek out abnormal noncoding RNAs (lncRNAs and circRNAs) involved in the development of bladder cancer through RNA-seq analysis. Transcriptome analysis of five pairs of bladder cancer tumor tissues and matched adjacent non-tumor tissues was completed in this project.  A total of 68.18Gb clean data (sequencing data after quality control) was obtained. In conclusion, high-throughput sequencing analysis provided a distinctive landscape for the expression of noncoding RNAs and screened a series of significantly differently expressed lncRNAs and circRNAs, such as lncRNA LNPPS (ENST00000622374) and circSLC38A1. Further studies will focus on the potential function and intrinsic regulatory mechanisms of these significantly differently expressed lncRNAs and circRNAs in the development of bladder cancer.

overall_design: Noncoding RNA profiles of 5 bladder cancer tumor tissues and 5 matched adjacent non-timor tissue


title: An Unexpected Role for Acetyl Coenzyme A Carboxylase in Metabolic Control of the Macrophage Acute Inflammatory Response

city: Charlottesville

first: Scott

last: Yeudall

state: Virginia

address: 1340 Jefferson Park Avenue, Pinn Hall 5036

department: Pharmacology

institute: University of Virginia

summary: Macrophages must rapidly shift their cellular metabolism to facilitate the induction of the proinflammatory response, including activation of lipid synthesis pathways. However, the links between lipid metabolism and polarization in response to inflammatory signals remains unclear. Acetyl-CoA Carboxylase (ACC) is central to lipid synthesis, cellular energy utilization, and acetylation-dependent enzyme activation, but its role in macrophages remains unclear. To interrogate the role of ACC in the inflammatory response, we generated myeloid-specific LysMCre Acacafl/fl Acacbfl/fl ACC double knockout (ACCLysM) mice. Unexpectedly, myeloid-specific deletion or pharmacological inhibition of ACC attenuated lipopolysaccharide (LPS)-induced inflammation in mice, with decreased gene expression and protein levels of the proinflammatory cytokines IL-6 and IL-1. Using in vitro transcriptomics, lipidomics, and bioenergetics approaches we find that ACC deletion reestablishes the metabolic setpoint in macrophages and is required for metabolic rewiring in response to LPS- but not IL-4-dependent signaling. This translated to blunted phenotypic polarization to proinflammatory but not alternatively activating stimuli. Mechanistically, we identified that the metabolic rewiring that results from ACC deletion increased basal acetylation at histone H3 lysine 27 (H3K27Ac), a marker of active enhancers, which was reduced in response to LPS in ACC-deficient BMDMs. The failure of macrophages lacking ACC to adapt their glycolytic metabolism and polarize to inflammatory stimuli impaired macrophage proinflammatory effector functions. Taken together these data identify a novel role for ACC in metabolic and transcriptional regulation of the acute inflammatory response.

overall_design: Bone marrow-derived macrophages (BMDMs) from four male Acaca loxp/loxp Acacb loxp/loxp (flox control) and four male LysM-Cre Acaca loxp/loxp Acacb loxp/loxp (ACCLysM ACC1/ACC2 deficient) mice were stimulated with LPS (100ng/mL) for 6 hours and total RNA isolated for RNAseq

first: Clint

last: Upchurch

first: Philip

middle: V

last: Seegren

first: Caitlin

last: Pavelec

first: Bimal

middle: N

last: Desai

first: Kyle

last: Hoehn

first: Norbert

last: Leitinger


title: Integration of 3D genome architecture and local chromatin features uncovers enhancers underlying craniofacial-specific cartilage defects

city: Shanghai

first: Qian

last: Bian

address: Jinzun Road No.115

department: Shanghai Institute of Precision Medicine, Ninth People’s Hospital

institute: Shanghai Jiao Tong University School of Medicine

summary: Aberrations in tissue-specific enhancers underlie many developmental defects. Disrupting a distal noncoding region of the human SOX9 gene causes the Pierre Robin sequence (PRS) characterized by the undersized lower jaw. Such a craniofacial-specific defect has been previously linked to enhancers transiently active in cranial neural crest cells (CNCCs). We demonstrate the PRS region also strongly regulates Sox9 in CNCC-derived Meckel's cartilage (MC), but not in limb cartilages. The MC-specific regulatory function of the PRS region cannot be attributed to the CNCC enhancers that have been inactivated in cartilages, but correlates with its MC-specific interactions with the Sox9 gene. By integrating the enhancer signatures and chromatin topology, we uncovered ~20,000 enhancers that function differentially between MC and limb cartilages and demonstrated their association with human diseases. Our findings highlight the importance of lineage-dependent chromatin topology in instructing enhancer usage and provide critical insights for interpreting the genetic basis of craniofacial pathologies.

overall_design: In this study, we systematically identified the enhancer atlas in mouse mandibular Meckel's cartilage (MC) and forelimb cartilage with multiple high-throughput sequencing techiniques including ATAC-seq, H3K27Ac CUT & Tag and Hi-C. By integrating  local chromatin features and 3D genome architecture, our analyses uncovered several distal enhancers that specifically regulate Sox9 expression in MC, which could possibly contribute to the incidence of Pierre Robin sequence when disrupted.

first: Jiewen

last: Dai

first: Qiming

last: Chen


title: Non-adhesive alginate promotes further differentiation and models fibrosis of human lung organoids in vitro.

city: Ann Arbor

first: Joseph

last: Decker

state: Michigan

address: 1011 N University Avenue

department: Cariology, Restorative Sciences, and Endodontics

institute: University of Michigan

summary: Human lung organoids (HLOs) are enabling the study of human lung development and disease by modelling native organ tissue structure, cellular composition, and cellular organization. In this report, we demonstrate that human lung organoids (HLOs) derived from human pluripotent stem cells (hPSCs) cultured in alginate, a fully defined non-animal product substrate, exhibit enhanced cellular differentiation compared to HLOs cultured in the commercially available Matrigel. More specifically, we observed an earlier onset and increase in the number of multi-ciliated cells, along with mucus producing MUC5AC+ goblet-like cells that were not observed in HLOs cultured in Matrigel. The epithelium in alginate-grown HLOs was organized in a pseudostratified epithelium with airway basal cells lining the basal lamina, but with the apical surface of cells on the exterior of the organoid. We further observed that HLOs cultured in Matrigel exhibited mesenchymal overgrowth that was not present in alginate cultures. The containment of the mesenchyme within HLOs in alginate enabled modeling of key features of Idiopathic Pulmonary Fibrosis (IPF) by treatment with TGFb. TGFβ treatment resulted in morphological changes including an increase in mesenchymal growth, increased expression of IPF markers, and decreased numbers of alveolar-like cells. This culture system provides a model to study the interaction of the mesenchyme with the epithelium during lung development and diseased states such as IPF.

overall_design: Evaluation of human pluripotent stem cell-derived lung organoids grown in Matrigel versus alginate, and treated with TGFB as a fibrosis model

first: Briana

last: Dye

first: Renee

middle: F

last: Hein

first: Alyssa

last: Miller

first: Sha

last: Huang

first: Jason

last: Spence

first: Lonnie

last: Shea


title: MultiEditR: The first tool for detection and quantification of multiple RNA editing sites from Sanger sequencing demonstrates comparable fidelity to RNA-seq

city: Heidelberg

first: F. Nina

last: Papavasiliou

address: Im Neuenheimer Feld 280

department: Tumor Immunology Unit

country: Germany

institute: German Cancer Research Center (DKFZ)

summary: We present MultiEditR, the first algorithm specifically designed to detect and quantify RNA editing from Sanger sequencing (z.umn.edu/multieditr). Although RNA editing is routinely evaluated by measuring the heights of peaks from in Sanger sequencing traces, the accuracy and the precision of this approach has yet to be evaluated against gold-standards next-generation sequencing methods. Through a comprehensive comparison to RNA-seq and amplicon based deep sequencing, we show that MultiEditR is accurate, precise, and reliable for detecting endogenous and programmable RNA editing.

overall_design: MultiEditR reliably detects RNA editing from Sanger Sequencing data, as compared to NGS RNA-seq data from RAW 264.7 (WT, 3 replicates vs APOEBC1-KO, 3 replicates) mouse macrophages.

first: Mitchell

last: Kluesner

first: Rafail

last: Tasakis

first: Taga

last: Lerner

first: Annette

last: Arnold

first: Sandra

last: Wüst

first: Marco

last: Binder

first: Beau

last: Webber

first: Branden

last: Moriarity

first: Riccardo

last: Pecori


title: GGC repeat expansion within NOTCH2NLC causes behavioral deficits and neurodegeneration through misregulated alternative splicing

city: Houston

first: Ziyi

last: Li

state: TX

address: 1400 Pressler Street

institute: MD Anderson Cancer Center

summary: GGC repeat expansion within NOTCH2NLC gene has been identified as the genetic cause of neuronal intranuclear inclusion disease (NIID). To understand the molecular pathogenesis of NIID, here we have established both a transgenic mouse model and a human neural progenitor cell (hNPC) model. We show that the expression of the NOTCH2NLC gene with expanded GGC repeats produces multiple forms of polypeptides, including polyglycine (polyG), polyalanine (polyA) and polyarginine (polyR), and leads to widespread intranuclear inclusions, severe neurodegeneration, motor dysfunction and cognitive deficits, which faithfully mimics the clinical manifestations and pathological features associated with NIID. We further performed RNA-seq on the prefrontal cortex, cerebellum and hippocampus of the transgenic mice and on the hNPC model and identified a large proportion of conserved alternative splicing between the NIID mouse and hNPC cell models. Analyses of the conserved alternative splicing revealed the enrichment of the binding motif of hnRNPM. We found that hnRNPM could interact with and be sequestered by expanded NOTCH2NLC-polyG and -polyA. Functional expression of hnRNPM could ameliorate the cellular toxicity caused by expanded GGC repeats within NOTCH2NLC. These results together suggest that dysregulated alternative splicing could play a vital role in the molecular pathogenesis of NIID.

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: RNA-seq of human neural progenitor cells (ctrl and NIID), and mouse brain samples including cerebellum, cortex, and hippocampus (control, NOTCH2NLC (GGC)98 repeat mice).

first: Yunhee

last: Kang

first: Yangping


title: Transcriptomic changes induced by RGCC overexpression, stimulation with TGF-beta, and their combination in primary human lung fibroblasts

city: Baltimore

first: JP

last: Courneya

state: United States of America

address: 685 W Baltimore St., HSF2 Room 480

institute: University of Maryland, Baltimore

summary: RNA-Seq of normal adult human lung fibroblasts

overall_design: Normal human lung fibroblasts from an adult donor were electroporated with either RGCC-encoding or a control non-coding (NULL) plasmids, and, 24 h later, either stimulated or not with rhTGF-beta. Analyses were performed 24 h later.

first: Sergei

middle: P

last: Atamas

first: Irina

last: Luzina


title: Epigenome profiling in gastric carcinogenesis by whole genome bisulfite sequencing

first: Byoung-Ha

last: Yoon

summary: In this study, GC-specific DNA methylation profiling was investigated in nine fresh frozen tissues which included non-tumor, intestinal metaplasia, and gastric tumor using whole genome bisulfite sequencing to deeply understanding epigenome change during gastric carcinogenesis

overall_design: Examination of five GM, nine IM and GT tissues

first: Yong

last: Kim


title: White matter abnormalities in the Hdc knockout mouse, a model of  tic and OCD pathophysiology

city: St Louis

first: Joseph

last: Dougherty

state: Missouri

address: 4566 Scott Ave, box 8232

department: Genetics and Psychiatry

institute: Washington University

summary: An inactivating mutation in the histidine decarboxylase gene (Hdc) has been identified as a rare but high-penetrance genetic cause of Tourette syndrome (TS).  TS is a neurodevelopmental syndrome characterized by recurrent motor and vocal tics; it is accompanied by structural and functional abnormalities in the cortico-basal ganglia circuitry.  Hdc, which is expressed both in the posterior hypothalamus and peripherally, encodes an enzyme required for the biosynthesis of histamine.  Hdc knockout mice (Hdc-KO) recapitulate this mutation and exhibit behavioral and neurochemical abnormalities that parallel those seen in patients with TS.  Exploratory RNA-Seq analysis revealed, unexpectedly, that genes associated with oligodendrocytes and with myelin production are upregulated in the dorsal striatum of these mice.  This was confirmed by qPCR and immunoblotting.  These results suggest an abnormality in myelination in the striatum.  To test this in an intact brain, we performed whole-brain ex vivo diffusion tensor imaging (DTI), which revealed reduced fractional anisotropy (FA) in the mid-dorsal striatum.  While the DTI literature in individuals with TS is sparse, these results are consistent with findings of disrupted descending cortical projections in patients with tics.  The Hdc-KO model may represent a powerful system in which to examine the developmental mechanisms underlying this abnormality.

overall_design: 28 samples in total; 1-3 brain samples from 2-3 month old Hdc knockout, heterozygous, and wild-type mice.  Dissected tissues were ventral and dorsal striatum, hypothalamus, and motor cortex.

first: Kantiya

last: Jindachomthong

first: Fahmeed

last: Hyder

first: Chengran

last: Yang

first: Luciana

last: Frick

first: Christopher

last: Pittenger


title: TSG-6 supports fistulizing Crohn’s disease by a mechanoregulated activation of the epithelial-to-mesenchymal transition

city: Milano

first: Luca

last: Massimino

state: MI

address: Via Olgettina, 58

department: Gastroenterology

country: Italy

institute: Ospedale San Raffaele

summary:
BACKGROUND AND AIMS: Perianal fistula represents one of the most important complications in Crohn’s Disease (CD). Epithelial-to-mesenchymal transition (EMT) has been demonstrated to play a major role in the pathogenesis, however the mechanisms driving EMT need to be clarified. Significant alterations in the tissue structural composition occur in the fistula, but how these changes promote EMT was not addressed. We aim to explore the relevance of TSG-6, a stabilizer of extracellular matrix, in the fistula pathogenesis.
METHODS: Intestinal surgical specimens from perianal fistula tissue and surrounding region of fistulizing CD were analyzed histologically and by RNA sequencing (RNA-seq). Significantly modulated genes and TSG-6 expression were validated by RT-PCR, WB and immunofluorescence assays [N=20]. TSG-6 expression was reconstituted in Caco-2 cell line and primary perifistula-derived fibroblasts, and proliferative and migratory assays were performed.
RESULTS: A marked different organization of extracellular matrix was found across fistula and perifistula regions with an increased expression of integrins, hyaluronan synthases, TSG-6 and MMPs in the fistula. TSG-6 overexpression in Caco-2 cells reduced proliferation, promoted the EMT transcription factor SNAIL, and, in co-stimulation with TGFβ1, migration. The acquisition of TSG-6 increased SNAI1 and hyaluronan synthases levels, and led to activated phenotype of perifistula-derived fibroblasts. Positive Pearson correlation was observed between TSG-6 expression and mechanosensitive proteins in fistula tissue.
CONCLUSIONS: By mediating changes in the extracellular matrix organization, TSG-6 triggers the EMT transcription factor SNAIL through the activation of mechanosensitive proteins. These data point to TSG-6 as a new potential target for the treatment of perianal fistula.

overall_design: 6x Healthy with fistule, 6x Healthy with perifistule, 9x Crohn's with fistule, 9x Crohn's with perifistule.

first: Luigi

last: Lamparelli

first: Stefania

last: Vetrano

first: Silvio

last: Danese


title: The matricellular protein Connective Tissue Growth Factor promotes motor axon regeneration

city: Povo (TN)

first: Fabio

last: Lauria

address: Via alla Cascata 56

institute: Institute of Biophysics (Italian National Research Council)

summary: Regeneration of the neuromuscular junction (NMJ) is orchestrated by signals exchanged among its components. Neuronal hydrogen peroxide (H2O2), produced in response to injury, is a major Schwann cells (SC) activator. Genes differentially expressed by SCs exposed to H2O2 were used as a signature gene set for functional enrichment analysis of NMJ transcripts profiled during motor axon terminal degeneration and re-growth. We found that at the regenerating NMJ: i) the H2O2 signature is enriched in extracellular matrix terms; ii) the mRNA of Connective Tissue Growth Factor (Ctgf) is strongly up-regulated, iii) Ctgf is produced by terminal SCs, iv) Ctgf neutralization delays functional recovery upon nerve injury.   We show here compelling evidence of a pro-regenerative role of Ctgf in neurotransmission rescue, and that the transcriptome of the regenerating NMJ is a powerful source of candidates with pro-regenerative potential. A profound ECM remodeling occurs during nerve regeneration, and H2O2 is among the triggers.

overall_design: In this study, we performed RNA-Seq of neuromuscular junctions (NMJs) of soleus muscles from control and α-LTx treated mice (samples collected 4, 16, 72 and 168 hours after α-LTx injection) to investigate motor axon terminal degeneration and re-growth. Experiments were performed in biological triplicate (72h), quadruplicate (ctrl) and quintuplicate (4h, 16h, 168h).

first: Samuele

last: Negro

first: Marco

last: Stazi

first: Toma

last: Tebaldi

first: Giorgia

last: D’Este

last: Pirazzini

first: Aram

last: Megighian

first: Francesca

last: Lessi

first: Chiara

middle: M

last: Mazzanti

first: Gabriele

last: Sales

last: Romualdi

first: Silvia

last: Fillo

first: Florigio

last: Lista

first: Gabriella

last: Viero

first: Michela

last: Rigoni


title: ZFP462 safeguards neural lineage specification by targeting G9A/GLP mediated heterochromatin to silence enhancers

city: Vienna

first: Ramesh

last: Yelagandula

address: Dr.-Bohr-Gasse 3

country: Austria

institute: IMBA

summary: ZNF462 haploinsufficiency is linked to Weiss–Kruszka syndrome, a genetic disorder characterized by neurodevelopmental defects, including autism. Though conserved in vertebrates and essential for embryonic development, the molecular functions of ZNF462 remain unclear. We identified its murine homologue ZFP462 in a screen for mediators of epigenetic gene silencing. Here we show that ZFP462 safeguards neural lineage specification of mouse embryonic stem cells (ESCs) by targeting the H3K9-specific histone methyltransferase complex G9A/GLP to silence meso-endodermal genes. ZFP462 binds to transposable elements that are potential enhancers harbouring ESC-specific transcription factor binding sites. Recruiting G9A/GLP, ZFP462 seeds heterochromatin, restricting transcription factor binding. Loss of ZFP462 in ESCs results in increased chromatin accessibility at target sites and ectopic expression of meso-endodermal genes. Taken together, ZFP462 confers lineage and locus specificity to the broadly expressed epigenetic regulator G9A/GLP. Our results suggest that aberrant activation of lineage non-specific genes in the neuronal lineage underlies ZNF462-associated neurodevelopmental pathology.

overall_design:
RNA-seq
ChIP-seq
ATAC-seq

first: Oliver

last: Bell


title: Nucleoporin Seh1 Maintain Schwann Cell Homeostasis by Regulating Genome Stability and Necroptosis

status: Public on Jan 03 2023

city: shanghai

first: Ximing

last: Nian

state: Shanghai

address: Chongqing Nanlu 227

institute: Shanghai Jiao Tong University

summary: Schwann cells play critical roles in peripheral neuropathies, however, the regulatory mechanisms of their homeostasis remain largely unknown. Here we show that nucleoporin Seh1, a component of nuclear pore complex, is important for Schwann cell homeostasis and loss of Seh1 led to necroptosis of non-myelinating Schwann cell and degeneration of sensory neurons. While myelinogenesis, myelinating Schwann cell, and wrapped large fibers were not affected, mice with depletion of Seh1 in Schwann cell lineage developed progressive reduction of non-myelinating Schwann cells in sciatic nerves, followed by the degeneration of unmyelinated small sensory fibers and malfunction of the sensory system. Mechanistically, Seh1 safeguards genome stability by mediating the interaction between SETDB1 and KAP1. The disrupted interaction after ablation of Seh1 derepresses endogenous retroviruses, which triggers ZBP1-dependent necroptosis in non-myelinating Schwann cells. Collectively, our results reveal that Seh1 is required for homeostasis of Schwann cells and suggest that decrease of nucleoporins as aging may participate in the pathogenesis of periphery neuropathies.

overall_design: RNA-seq was performed on the sciatic nerves of control or Seh1cKO mice(P4, P14, P30, P60).

first: Liang

last: Zhang

first: Minbiao

last: Yan

first: Mei

last: Wu


title: Sequencing of Raw 264.7 macrophage cells treated with 1,5-Anhydroglucitol(1,5-AG).

first: Min

state: Shandong

address: Wenhua West Road

institute: Shandong University

summary: Our previous studies identified an increase in the levels of the metabolite 1,5-anhydroglucitol (1,5-AG) in the plasma of patients with newly diagnosed B-ALL by untargeted metabolomics detection.Except for the direct influence of 1,5-AG on leukemia cells, the effect on macrophages is still unclear.We reported the application of RNA sequencing to determine the transcriptional response of murine macrophage Raw 264.7 cells in response to stimulate with 1,5-AG conditions.

overall_design: 2 replicates for control; 2 replicates for treated

first: Xiuli

last: Ju


title: Multipotent Schwann cell precursors generate steroid-producing cells of the adrenal cortex and chromaffin cells of the adrenal medulla

city: Dresden

first: Charlotte

last: Steenblock

state: Saxony

address: Fetscherstraße 74

department: Medizinische Klinik und Poliklinik III

institute: Universitätsklinikum Carl Gustav Carus

summary: Multipotent stem cells are considered as promising biological tools for regenerative medicine, and transcriptome analysis of these cells is fundamental for identifying new factors controlling proliferation versus differentiation. To obtain a comprehensive characterization of adrenal progenitors, we have developed an analytical pipeline relying on flow cytometric sorting of living cells followed by RNA sequencing. This analysis showed that two distinct populations of Nestin-positive progenitors are located in the adrenal cortex and medulla, respectively. Though 1039 genes were differentially regulated, both populations showed Schwann cell precursor properties suggesting both populations to be neural crest-derived.

overall_design: mRNA profiles of FACS sorted Nestin-positive progenitor cells from the adrenal cortex and medulla.

first: Stefan

middle: R

last: Bornstein


title: Alterations of DNA Methylation Profile in Peripheral Blood of Children with Simple Obesity

city: Haikou

first: peng

last: Huang

address: Haikou, Hainan province

institute: Department of Pediatrics, Haikou Hospital of the Maternal and Child Health, Haikou. 570100, China.

type: Methylation profiling by genome tiling array

summary: Genome wide DNA methylation profiling of peripheral blood samples from 41 children with simple obesity and 31 normal controls. The Illumina Infinium MethylationEPIC BeadChip (Illumina 850k, San Diego, CA)  was used to obtain DNA methylation profiles across greater than 850,000 CpG sites across the genome. Samples included 31 normal and 41 obesity peripheral blood.

overall_design: Bisulphite converted DNA from the 72 samples were hybridised to the Illumina Infinium MethylationEPIC BeadChip (Illumina 850k, San Diego, CA).

first: Yi

last: Ren

first: Peng

first: Xiaojie

last: He

first: Wei

last: Xiang

first: Xiaoyan

first: Xuewei

last: Ding

first: Lu

first: Hong

last: Peng

first: Zhou

last: She

first: Senlin

last: Luo

first: Lingjuan

last: Liu

first: Jiang

last: Chen

first: Shanwen

first: Liqun


title: Sstr2 knockout mice

first: Byoung-Ha

last: Yoon

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

overall_design: Refer to individual Series


title: Fibro/Adipogenic Progenitors Are Key Effectors and Regulators of Skeletal Muscle Fibrosis in Muscular Dystrophy

city: New York

first: Gregory

middle: Robert

last: Smith

state: NY

address: 1 Gustave L. Levy Pl

department: Neurology

institute: Mount Sinai Hospital

summary: Fibrosis is a prominent pathological feature of skeletal muscle in Duchenne muscular dystrophy (DMD). The commonly used disease mouse model, mdx5cv, displays progressive fibrosis in diaphragm but not limb muscles. We use single-cell RNA sequencing to determine the cellular expression of the genes involved in extracellular matrix (ECM) production and degradation in mdx5cv diaphragm and quadriceps. We find that fibro/adipogenic progenitors (FAPs) are not only the primary source of ECM but also the predominant cells that express important ECM regulatory genes, including Ccn2, Ltbp4, Mmp2, Mmp14, Timp1, Timp2, and Loxs. The effector and regulatory functions are exerted by diverse FAP clusters which are different between diaphragm and quadriceps, indicating their activation by different tissue microenvironment. FAPs are more abundant in diaphragm than in quadriceps.

overall_design: Single cell suspensions were prepared from diaphragm and quadriceps of mdx5cv and WT mice at 14 weeks of age, and were then used for single cell-based RNA sequencing.

first: Xingyu

last: Wang

first: Jianming

first: Frederique

last: Ruf-Zamojski

first: Sachiko

last: Homma

first: Yinhang

first: Stuart

middle: C

last: Sealfon

first: Lan

last: Zhou


title: Single-cell RNA-sequencing (scRNA-seq) of GFP+cells isolated from Tg(Brn3c:mGFP) 6 days zebrafish with GFP expression in all hair cells.

city: Nantong

first: Wei

last: Guanyun

address: 9 of Seyuan Lu

institute: Nantong University

summary: Hair cells play key roles in hearing and balance, and hair cell loss would result in hearing loss or vestibular dysfunction. Zebrafsh, owing to their hair cell-enriched organs, have been widely applied in hair cell-related research worldwide. In this study, we analyzed the GFP+cells isolated from Tg(Brn3c:mGFP) larvae with GFP expression in all hair cells using single-cell RNA-sequencing (scRNA-seq). Three subtypes of hair cells, namely macula hair cell (MHC), crista hair cell (CHC), and neuromast hair cell (NHC), were characterized and validated by whole-mount in situ hybridization analysis of marker genes. The hair cell scRNA-seq data revealed hair cell-specifc genes, including hearing loss genes that have been identifed in humans and novel genes potentially involved in hair cell formation and function.

overall_design: Zebrafsh were maintained at 28.5 °C. The Tg(Brn3c:mGFP) transgenic zebrafsh larvae at 6 days post-fertilization (dpf) were anesthetized and then treated with 0.25% trypsin to dissociate into single cells, which were divided into GFP-positive and GFP-negative cells through the fuorescent activated cell sorter, and the RNA expressed in GFP-positive cells were then obtained and sequenced using the 10×Genomics platform

first: Qian

last: Fuping

first: Xie

last: Gangcai

first: Liu

last: Dong


title: Small RNA sequencing of mouse brain after middle cerebral artery occlusion

city: Kuopio

first: Nea

last: Korvenlaita

address: Neulaniementie 2

country: Finland

institute: University of Eastern Finland

summary: Here, we analyzed ischemic stroke induced changes in microRNA levels in mouse brain using permanent cerebral ischemia model. We performed enrichment of small RNAs from peri-ischemic brain region for RNA sequencing and present data set containing several small RNA species to facilitate the discovery of ischemia induced changes in non-coding RNAs.

overall_design: Small RNAs were enriched and sequenced from mice 3 days after permanent middle cerebral artery occlusion (n=5) or sham (n=6) surgery.

first: Benjamin

last: Huremagic

first: Rosalba

last: Giugno

first: Tarja

last: Malm


title: Discovering of microRNA target genes in N2A cells [HITS-CLIP]

summary: Here, we use HITS-CLIP sequencing to observe microRNA enrichment and microRNA target coverage under normal culture conditions in neuroblastoma cell line. We show abundance of several microRNAs and the presence of target genes for these microRNAs in the N2A cells.

overall_design: Samples from untreated N2A neuroblastoma cells were High throughput crosslinked and immunoprecipitated for sequencing (HITS-CLIP seq). Three replicates were included.

first: Luca

last: Giudice

first: Sanna

last: Loppi


title: Glutamate-induced transcriptional changes in embryonic mouse cortical neurons [GRO-seq]

summary: Glutamate is a major excitatory neurotransmitter in the nervous system. Increased and persistent release of glutamate is toxic to neurons and this excitotoxicity is a hallmark of several neurodegenerative diseases. Here, we use GRO-seq to screen for the acute transcriptional changes induced by glutamate exposure on embryonic mouse cortical neurons to reveal downstream molecules which could participate in glutamate-induced toxicity. We show that several miRNA genes, such as miR-21, have altered expression upon glutamate exposure.

overall_design: Primary cortical neurons from C57Bl/6J mouse embryos (E15) were cultured in vitro for 7 days and treated with 400 µM glutamate or vehicle for 6 hours before nuclei extraction. Experiment contained two biological replicates for both treatment groups.

first: Ana

last: de Sande

first: Merja

last: Heinäniemi

first: Minna

last: Kaikkonen


title: Transcriptional profiling of trimethylamine N-oxide (TMAO) stimulated human aortic endothelial cells (HAECs)

city: Philadelphia

first: Fatma

last: Saaoud

address: 3500 N. Broad St

institute: Temple University

summary: Purpose: The goals of this study were to identify preferential gene expression signatures that are unique to HAECs stimulated with the uremic toxin, TMAO, to accelerate vascular inflammation associated with chronic kidney diseases.  Methods and results: HAECs were treated with TMAO (600 µM) for 18 hours, and RNAs were collected to generate mRNA transcription profiles. Transcriptional profiling revealed a unique TMAO stimulated HAECs relative to a non-stimulated control HAECs.  Conclusion: Our study represents the first detailed analysis of TMAO treated HAECs transcriptome.

overall_design: HAECs were treated with or without TMAO (600 µM) for 18 hours

first: Xiaofeng

last: Yang


title: Multiplatform Analysis of Primary and Metastatic Breast Tumors from the AURORA US Network identifies microenvironment and epigenetics differences as drivers of metastasis [Methylation]

city: Pittsburgh

first: Uma

last: Chandran

address: 5150 Center Ave

department: BioMedical Informatics

institute: University of Pittsburgh

summary: Patients with metastatic breast cancer (MBC) typically have short survival times and their successful treatment represents one of the most challenging aspects of patient care. This poor prognostic behavior is in part due to molecular features including increased tumor cell clonal heterogeneity, multiple drug resistance mechanisms, and alterations of the tumor microenvironment. The AURORA US Metastasis Project was established with the goal to identify molecular features specifically associated with metastasis. We therefore collected and molecularly characterized specimens from 55 metastatic breast cancer (BC) patients representing 51 primary cancers and 102 metastases. The 153 unique tumors were assayed using RNAseq, tumor/germline DNA exomes and low pass whole genome sequencing, and global DNA methylation microarrays. We found intrinsic molecular subtype differences between primary tumors and their matched metastases to be rare in triple negative breast cancer (TNBC)/Basal-like subtype tumors. Conversely, tumor subtype changes were relatively frequent in estrogen receptor positive (ER+) cancers where ~30% of Luminal A cases switched to Luminal B or HER2-enriched (HER2E) subtypes. Clonal evolution studies identified changes in expression subtype coincident with DNA clonality shifts, especially involving HER2 amplification and/or the HER2E expression subtype. In contrast, we found remarkable conservation of cancer-associated DNA hypermethylation profiles within primary tumor-metastasis pairs. We further found evidence for ER-mediated downregulation of genes involved in cell-cell adhesion in metastases. Microenvironment differences varied according to tumor subtype where ER+/Luminal metastases had lower fibroblast and endothelial cell content, while TNBC/Basal-like metastases showed a dramatic decrease in B cells and T cells. In 17% of metastatic tumors, we identified DNA hypermethylation and/or focal DNA deletions near HLA-A that were associated with its significantly reduced expression, and with lower immune cell infiltrates. We also identified low immune cell features in brain and liver metastases when compared to other metastatic sites, even within the same patient. These findings have implications for the treatment of metastatic breast cancer patients with immune- and HER2-targeting therapies and suggest potential novel therapeutic avenues for the improvement of outcomes for some patients with MBC

overall_design: DNA methylation profiles in breast primary and matched metastatic tumors were analyzed using the Infinium MethylationEPIC Array

first: Susana

last: Garcia-Recio

first: Toshinori

last: Hinoue

first: Gregory

middle: L

last: Wheeler

middle: J

last: Kelly

last: Garrido-Castro

first: Tomas

last: Pascual

first: Aguirre

middle: A

last: De Cubas

first: Youli

last: Xia

first: Brooke

last: Felsheim

first: Marni

middle: B

last: McClure

first: Andrei

last: Rajkovic

first: Ezgi

last: Karaesmen

first: Markia

last: Smith

first: Cheng

last: Fan

first: Paula

middle: I

last: Gonzalez Ericsson

first: Melinda

middle: E

last: Sanders

first: Chad

last: Creighton

first: Jay

last: Bowen

first: Kristen

last: Leraas

first: Robyn

last: Burns

first: Sara

last: Coppens

first: Amy

last: Wheless

first: Salma

last: Rezk

last: Garrett

first: Joel

last: Parker

first: Kelly

middle: K

last: Foy

first: Hui

last: Shen

first: Ben

last: Park

first: Ian

last: Krop

first: Carey

last: Anders

first: Julie

last: Gastier-Foster

first: Mothaffar

last: Rimawi

first: Rita

last: Nanda

first: Nancy

last: Lin

first: Claudine

last: Isaacs

first: P

last: Marcom

first: Anna


title: MicroRNA expression data from skin samples of adult atopic dermatitis and psoriasis patients and healthy controls

city: Tartu

first: Ana

last: Rebane

address: Ravila 14B

department: Institute of Biomedicine and Translational Medicine

country: Estonia

institute: University of Tartu

summary:
Atopic dermatitis (AD) and psoriasis vulgaris (PV) affect up to 3-5% of adults in developed countries and severely impair their quality of life thorough adulthood. MicroRNAs contribute to either the development or regulation of several diseases and are present in tissue.
Although several miRNAs have been associated with AD or PV, to our knowledge, scarce studies have been published to date of miRNA profiling comparing AD and PV patients.

overall_design: We conducted a miRNA profiling analysis of skin samples from adult AD and PV patients and control individuals.

first: Gemma

last: Carreras-Badosa