title: The skin  transcriptome analysis of yellow catfish  (Tachysurus fulvidraco♀ × P. vachellii♂) under transport stress

city: WuXi

first: Tao

last: Zheng

address: No. 69, Xue Jiali, Nanquan Town

institute: NanJing Agricutural university

summary: The skin transcriptomes were examined by high-throughput sequencing at control group and 16 h transport group. A total of 1577 genes were differentially expressed, including 892 up-regulated and 685 down-regulated. It is interesting to note that the qPCR analysis further confirmed that the skin's immune response to transport stress was activated via Toll-like receptors (TLRs) and NOD-like receptors (NLRs) in skin: the tlr9, mfn2 and ikbke were significantly up-regulated and nfkbia,  map3k7cl were significantly down-regulated. Overall results suggested that transport stress. The overall results suggest that the skin responds to transport stress by regulating mucus secretion and activating the immune signal pathway. This study will help to optimize the transport conditions for cultured hybrid yellow catfish.

sample_organism: Tachysurus fulvidraco x Tachysurus vachelli

overall_design: The skin transcriptomes were examined  at control group and 16 h transport group.

first: Jun

last: Qiang

first: Yifan

last: Tao

first: Junhao

last: Zhu


title: T cell impact rituximab-mediated NK cell transcriptomics

status: Public on Jul 13 2021

city: Iowa City

first: Michael

middle: S

last: Chimenti

state: IA

address: 431 Newton Road

department: Iowa Institute of Human Genetics

country: USA

institute: University of Iowa

type: Expression profiling by high throughput sequencing

summary: We found that T cells impacted rituximab-mediated NK cell viability, ability to mediate antibody dependent cellular cytotoxicity, and phenotypical changes in vitro. To understand the effects of T cells on ritxuimab-mediated NK cell responses at the transcriptional lvel, we performed bulk mRNA sequencing of NK cells in different experimental settings.

overall_design: Raji lymphoma cells were cocultured with unfractionated peripheral blood mononuclear cells (PBMC) or T cell-depleted PBMC for 7 days. NK cells were isolated from the coculture on day 7. mRNA was isolated from NK cells for bulk mRNA sequencing.

first: Zhaoming

last: Wang

first: George

middle: J

last: Weiner


title: Activating NOTCH1 mutations increase T-ALL cells’ chemosensitivity by altering PREX2-AKT pathway

status: Public on Jul 07 2021

city: Zhengzhou

first: Hui

last: Yu

address: 100 Kexue Road

country: China

institute: Zhengzhou University

summary: Mutations on NOTCH1 gene are the most commonly found mutations in T-cell acute lymphoblastic leukemia (T-ALL) and they are reported to be favorable indicators for T-ALL patients' prognosis. However, the effects of activating NOTCH1 mutations on T-ALL's chemosensitivity have not been studied. We reported that NOTCH1 inhibition by gamma-secretase inhibitors or shRNA knockdown in MOLT-3 cells could reduce the T-ALL cells' sensitivity to chemotherapeutic drugs. However, this effect was absent in Jurkat and CUTLL1 cells. We further demonstrated that NOTCH1 inhibition could activate the PI3K-AKT pathway in a cell specific pattern similar as their effects on chemosensitivity. RNA-seq revealed that Phosphatidylinositol-3,4,5-Trisphosphate Dependent Rac Exchange Factor 2 (PREX2) is a target gene of NOTCH1 and may mediate the effects of activating NOTCH1 mutations on chemosensitivity. Consistently, we proved that overexpression of PREX2 could mimic the effects of NOTCH1 inhibition on chemosensitivity. Our study has highlighted the effects of activating NOTCH1 mutations on T-ALL's chemosensitivity by altering PREX2-AKT pathway, which may explain the favorable effects of NOTCH1 mutations on T-ALL patients' prognosis, as well as provided potential targets to sensitize T-ALL cells to chemotherapy.

overall_design: To search for NOTCH1 regulated genes which may contribute to the effects of NOTCH1 on T-ALL cells' chemosensitivity, the transcriptomes of compound E and DMSO treated MOLT-3 cells were analyzed by RNA-seq.

first: Yuxin

last: Du

first: Mingzhi

last: Zhang


title: Integrated transcriptomic and proteomic analysis reveals up regulation of apoptosis and small heat shock proteins in lens of rats under low temperature

city: Hangzhou

first: Jiayue

last: Zhou

state: Zhejiang

address: Number 88 Jiefang Road

department: The Eye Center, Second Affiliated Hospital of School of Medicine

institute: Zhejiang University

summary: Cold cataract is the reversible opacification of the lens when the temperature decreases. However, we observed that when temperature of the rats lens was maintained at a lower temperature for a prolonged time, the opacification of lens was only partly reversible. To review the potential molecular mechanism of the irreversible part of opacification under cold stimulation, we applied comparative transcriptomic and proteomic analysis to systematically investigate the molecular changes that occurred in the lens capsules of rats under low temperature treatments. The RNA sequencing based transcriptomic analysis showed a significant up-regulation of genes related to the lens structure and development in the Hypothermia Group. Hub genes were small heat shock proteins (sHSPs). Besides the same findings as the transcriptomic results, the liquid chromatography-tandem mass spectrometry based proteomic analysis also revealed the up-regulation of the apoptotic process. To further analyze the regulatory mechanism in this process, we subsequently performed integrated analysis and identified the down-regulation of Notch3/Hes1 and PI3K/Akt/Xiap signaling axis. Our research revealed the activation of the apoptotic process in rats lens under cold stimulation, and the sHSP related heat shock response as a potential protective factor through our transcriptomic and proteomic data.

overall_design: Lens capsule mRNA profiles of Hypothermia Group (treat at 4degC for 8h) rat (Group E) and Normal Control Group (Group F)

first: Jing

last: Wu

first: Sifan

first: Xiangjun

last: Chen

first: Daizhan

first: Xingchao

last: Shentu


title: Microarray Expression Analysis of Circular RNAs in papillary thyroid carcinoma.

city: Ghuangzhou

first: Yushuang

last: Sun

address: NO.2 Zhongshan Road

department: Institute of Precision Medicine

institute: The First Affiliated Hospital of Sun Yat-sen University

summary: CircRNA deregulation could be a crucial event in thyroid carcinoma. To investigate circRNA signatures present in several papillary thyroid carcinoma (PTC) patients to complement our understanding of PTC pathogenesis. Using microarray technology, we screened the circRNA profiles in 3 pairs of PTC tumors and matching adjacent normal tissues. This study evaluated circRNAs expression profiles and their ability to serve as reliable biomarkers and new potential diagnostic and therapeutic targets for PTC

overall_design: Three pairs of papillary thyroid carcinoma samples and matching adjacent normal tissues were collected, and total RNA was extracted. Subsequently, RNA was labeled and hybridized. Agilent Feature Extraction software (version 11.0.1.1) was used to analyze acquired array images. Quantile normalization and subsequent data processing were performed using the R software package.

first: M

last: Guo

first: Y

first: S

last: Li


title: Bulk RNA-sequencing of fibroblasts isolated by FACS from normal human prostate

city: Dallas

first: Gervaise

middle: H.

last: Henry

state: Texas

address: 5323 Harry Hines Blvd, Mail Code:9110

department: Urology

institute: UT Southwestern Medical Center

summary: Differential expression of prostatic fibroblasts were determined using RNA-sequencing of FACS sorted fibroblasts from normal human prostate transition and peripheral.

overall_design: Fresh human prostate specimens were digested into single-cell suspensions, and cryopreserved. Thawed samples were subject to FACS to isolate fibroblast populations of cells , and then subject to bulk RNA-sequencing.

first: Douglas

middle: W

last: Strand

middle: H


title: Single-cell RNA-sequencing of adult mouse urethra v2

summary: Single-cell RNA-sequencing was conducted on heterogeneous mouse urethra on the 10x Genomics platform.

overall_design: Fresh mouse urethral specimens were digested into single-cell suspensions, cells were subject to single-cell RNA-sequencing using the 10x Genomics platform.


title: Single-cell RNA-sequencing of adult mouse prostates v2

summary: Single-cell RNA-sequencing was conducted on heterogeneous mouse prostates on the 10x Genomics platform.

overall_design: Fresh mouse prostate specimens were digested into single-cell suspensions, cells were subject to single-cell RNA-sequencing using the 10x Genomics platform.


title: Gilteritinib-induced upregulation of S100A9 is mediated through BCL6 in Acute Myeloid Leukemia

city: WEST HOLLYWOOD

first: Moray

last: Campbell

state: CA

address: 8687 Melrose Avenue, Office B227.5G

institute: Cedars-Sinai Medical Center

type: Genome binding/occupancy profiling by high throughput sequencing

summary:
Purpose: Compare transcriptional changes between drug treated (gilteritinib, TP-0903) and vehicle in acute myeloid leukemia xenografts.
Methods: FLT3-ITD+ MOLM13-RES-Luc+ (MOLM13 cells with a D835Y mutation generating a resistant phenotype) AML cells were xenografted into NSG mice. Mice were randomized according to bioluminescence imaging, and treatment of FLT3 tyrosine kinase inhibitor (gilteritinib, 30 mg/kg, once daily for 5 days/week) was started on day 13 post-tail vein injection. At study end point, mice were humanely euthanized and bone marrow was collected. AML cells (human CD45+) were isolated, and ATAC-seq was performed on HiSeq 4000, total RNA. Sequencing reads were aligned and analyzed for differential gene expression of treatment vs vehicle cohorts.
Results: The analysis revealed the chromatin accessibility changes induced by gilteritinib in MOLM13-RES AML xenograft model.

overall_design: RNA-seq and ATAC-seq analyses were generated in FLT3-ITD+ AML cell lines from xenograft models treated with FLT3 tyrosine kinase inhibitors vs vehicle.

middle: E

last: Zavorka Thomas

first: J

middle: Y

last: Jeon

first: D

middle: R

last: Buelow

middle: D

last: Baker


title: Single-cell RNA-sequencing of adult human normal and BPH (glandular and stroma) prostates and urethra

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

overall_design: Refer to individual Series


title: Single-cell RNA-sequencing of adult human prostates from organ donors v2

summary: Single-cell RNA-sequencing was conducted on heterogeneous human prostates FACS sorted for viability from organ donors (with no known prostatic diseases) on the 10x Genomics platform.

overall_design:
Fresh human prostate specimens were digested into single-cell suspensions, cells were subject to single-cell RNA-sequencing using the 10x Genomics platform.

Raw data files previously uploaded under GSE145843.


title: A functional map of genomic HIF1α-DNA complexes in the eye lens revealed through multiomics analysis [RNA-seq]

city: Boca Raton

first: Marc

last: Kantorow

state: FL

address: 777 Glades Road

institute: Florida Atlantic University

summary:
Background:
During eye lens development the fetal vasculature regresses leaving the lens without a direct oxygen source. Both embryonically and throughout adult life, the lens contains a decreasing oxygen gradient from the surface to the core that parallels the natural differentiation of immature surface epithelial cells into mature core transparent fiber cells. These properties of the lens suggest a potential role for hypoxia in the regulation of genes required for mature lens structure and function. Since HIF1α is a master regulator of the hypoxic response, these lens properties also implicate HIF1α as a potential requirement for lens formation and homeostasis.  Here, we employed a multiomics approach combining CUT&RUN, RNAseq and ATACseq analysis to establish the genomic complement of lens HIF1α binding sites, genes activated or repressed by HIF1α and the chromatin states of HIF1α-regulated genes.
Results:
CUT&RUN analysis revealed 8,375 HIF1α-DNA binding complexes in the chick lens genome. 1,190 HIF1α-DNA binding complexes were significantly clustered within chromatin accessible regions (χ2 test p < 1x10-55) identified by ATACseq. Formation of the identified HIF1α-DNA complexes paralleled the activation or repression of 526 genes, 116 of which contained HIF1α binding sites within 10kB of the transcription start sites. Some of the identified HIF1α genes have previously established lens functions while others have novel functions never before examined in the lens. GO and pathway analysis of these genes implicate HIF1α in the control of a wide-variety of cellular pathways potentially critical for lens formation, structure and function including glycolysis, cell cycle regulation, chromatin remodeling, Notch and Wnt signaling, differentiation, development, and transparency.
Conclusions:
These data establish the first functional map of genomic HIF1α-DNA complexes in the eye lens. They identify HIF1α as an important regulator of a wide-variety of genes previously shown to be critical for lens formation and function and they reveal a requirement for HIF1α in the regulation of a wide-variety of genes not yet examined for lens function. They support a requirement for HIF1α in lens development, structure and function and they provide a basis for understanding the potential roles and requirements for HIF1α in the development, structure and function of more complex tissues.

overall_design: RNA-seq of six samples

first: Joshua

last: Disatham

first: Lisa

last: Brennan

first: Daniel

last: Chauss

first: Jason

first: Behdad

last: Afzali


title: A functional map of genomic HIF1α-DNA complexes in the eye lens revealed through multiomics analysis


title: A functional map of genomic HIF1α-DNA complexes in the eye lens revealed through multiomics analysis [CUT&RUN]

overall_design: Examination of HIF1a binding and IgG in duplicate samples of primary lens cells via CUT&RUN


title: Single-cell RNA-sequencing of adult human prostates from BPH patients (glandular and stromal phenothpes)

summary: Single-cell RNA-sequencing was conducted on heterogeneous human prostates from BPH patients on the 10x Genomics platform.

overall_design: Fresh human prostate specimens were digested into single-cell suspensions, cells were subject to single-cell RNA-sequencing using the 10x Genomics platform.


title: Transcriptome analysis of Barley flag leaf during senescence

city: Rehovot

first: Robert

last: Fluhr

address: hertzl 234, 17

department: Plant and environmental sciences

country: Israel

institute: Weizmann institute of science

summary: Transcriptome analysis of Barley flag leaf at several stages of senescence. The experiment includes transcriptomic data of the cv.Karl and its early-senescing near-isogenic line '10_11'(jukanti et al.2008)

first: Andreas

last: Fisher

first: Maja

last: Cohen

first: Kendra

last: Hertweck


title: Single-cell RNA-sequencing of adult mouse lower urinary tracts v2


title: Diverging principles of selective sex chromosome regulation during evolution of Drosophila

city: Martinsried

first: Tobias

last: Straub

address: Großhadener Str. 9

department: Biomedical Center, Bioinformatics

country: Germany

institute: LMU Munich

summary: The dosage compensation complex (DCC) of Drosophila identifies its X chromosomal binding sites with exquisite selectivity. The principles that assure this vital targeting are known from the D. melanogaster model: DCC-intrinsic specificity of DNA binding, cooperativity with the CLAMP protein, and non-coding roX2 RNA transcribed from the X chromosome. We found that in D. virilis, a species separated from melanogaster by 40 million years of evolution, all principles are active, but contribute differently to X-specificity. In melanogaster, the DCC subunit MSL2 evolved intrinsic DNA-binding selectivity for rare PionX sites, which mark the X chromosome. In virilis, PionX sites are abundant and not X-enriched. Accordingly, MSL2 lacks specific recognition. Here, roX2 RNA plays a more instructive role, counteracting a non-productive interaction of CLAMP and modulating DCC binding selectivity. Remarkably, roX2 triggers a low-diffusion chromatin binding mode characteristic of DCC. Evidently, X-specific regulation is achieved by divergent evolution of similar components.

sample_organism:
Drosophila melanogaster
Drosophila virilis

overall_design: ChIP and DIP experiments with different target proteins and addition of accessory factors.

first: Raffaella

last: Villa

first: Pravin

middle: K

last: Jagtap

last: Thomae

first: Aline

middle: C

last: Sparr

first: Ignasi

last: Forné

first: Janosch

last: Hennig

first: Peter

middle: B

last: Becker


title: RNA sequencing data from MCF7 luminal breast cancer cells expressing STAT5a phospho-point mutants

city: RICHMOND

first: Alicia

middle: Eileen

last: Woock

state: VA

address: 1101 E Marshall St

department: Pathology

institute: Virginia Commonwealth University

summary:
Purpose: The goal of this study was to generate mRNA profiles for MCF7 breast cancer cells expressing phospho-deficient STAT5a point mutants with treatment of prolactin (PRL) to determine differential global genomic effects in breast cancer. This data was compared to in vitro studies using the same cells to determine phenotypic outcomes of the STAT5a point mutations.
Methods: mRNA profiles of prolactin (PRL) treated or untreated MCF7 cells expressing wild type (WT)-STAT5a, or phospho-deficient point mutants Y694F-, S726A-, or S780A-STAT5a were generated in triplicate by sequencing on the S4 flow cell platform of the Illumina NovaSEQ 6000 System (Illumina, Inc), generating ≥50 million 150 bp paired-end (PE) reads per sample. All libraries were prepared and sequenced in a single batch/flow cell lane.
Results: RNA-sequencing and subsequent Ingenuity Pathway Analysis predicted that loss of each phospho-site differentially affected both prolactin-induced gene expression as well as functional pathways of breast cancer (e.g. cell survival, proliferation, and colony formation). Gene set analysis for transcription factor activity (using ENCODE project ChIP-sequencing and the web platform Enrichr), illustrated multiple transcription factors at work in MCF7 cells expressing each phospho-deficient STAT5a point mutant, indicating that these point mutants have roles regulating STAT5a activity at various enhancer/promoters in a enhancer/promoter specific context.
Conclusion:

overall_design: mRNA profiling of MCF7 cells containing either WT-STAT5a, or point mutants Y694F-, S726A-, or S780A-STAT5a treated or untreated for 2 hours with prolactin (PRL).

first: Woock

last: Alicia E

first: Olex

last: Amy L


title: Circulating microRNA as potential diagnostic biomarkers for sleep disorder

city: Daejeon

first: Su-Jin

last: Baek

address: 1672, Yuseong-daero

country: South Korea

institute: KOREA INSTITUTE of ORIENTAL MEDICINE

type: Non-coding RNA profiling by high throughput sequencing

summary: Next Generation Sequencing (NGS) was carried out on subjects who visited an oriental medicine clinic due to recurrent sleep disturbance, and 40 individuals (17 male and 23 female) were set as the sleep diorder (SD) group based on their scores on the sleep distrurbance questionnaire of Pittsburgh sleep quality index (PSQI). The control group consisted of 40 healthy individuals (20 males and females each), as assessed by both subjective diagnosis and test for metabolic syndrome factors.Ten individuals (five males and females each) from the SD and the control group, respectively, were allocated for NGS analysis.

overall_design: Circulating miRNA profile in patient serum samples for identifcation of potential biomarkers in sleep disorder (sleep control: n=10, sleep disorder: n=10)

first: Seongwon

last: Cha

first: Hyo-Jeong

last: Ban


title: Next Generation Sequencing Facilitates Quantitative Analysis of Honey Bee Brain Transcriptomes Treated by Dinotefuran

first: Minjie

last: Huang

address: No. 145 Shiqiao Road

department: Institute of Animal Husbandry and Veterinary Science

institute: Zhejiang Academy of Agricultural Sciences

summary:
Purpose：The goals of this study are to obtain NGS-derived honey bee brain transcriptome profiling  (RNA-seq) after dinotefuran treatment in honey bee
Methods：Through deep sequencing in triplicate, using Illumina Hiseq2500,a comprehensive analysis of lncRNAs and mRNAs was performed following persistent exposure to 0.01 mg/L dinotefuran for 1, 5, and 10 d.
Results： In total, 312 lncRNAs and 1341 mRNAs, 347 lncRNAs and 1458 mRNAs, 345 lncRNAs and 1155 mRNAs were found to be differentially expressed (DE) on days 1, 5 and 10 respectively.
Conlusions：This study characterized the expression profile of lncRNAs upon exposure to neonicotinoid insecticides in young adult honey bees.

overall_design: Honey bee brain lncRNA profiles of 1-day old, 5-day-old and 10-day-old dinotefuran treated groups and control groups

first: Jie

last: Dong

first: Haikun

last: Guo

first: Deqian

last: wang


title: Chickpea shows genotype-specific nodulation responses across soil nitrogen environment and root disease resistance categories

city: Penrith

first: Krista

last: Plett

state: NSW

address: Locked Bag 1797

department: Hawkesbury Institute for the Environment

country: Australia

institute: Western Sydney University

summary: The ability of chickpea to obtain sufficient nitrogen via its symbiotic relationship with Mesorhizobium ciceri is of critical importance in supporting growth and grain production. A number of factors can affect this symbiotic relationship including abiotic conditions, plant genotype, and disruptions to host signalling/perception networks.  In order to support improved nodule formation in chickpea, we investigated how plant genotype and soil nutrient availability affect chickpea nodule formation and nitrogen fixation. Further, using transcriptomic profiling, we sought to identify gene expression patterns that characterize highly nodulated genotypes.

overall_design: RNA-sequencing of six chickpea genotypes three days post-inoculation with Mesorhizobium ciceri or a mock inoculated control

middle: L

first: Sean

last: Bithell

first: Adrian

last: Dando

first: Jonthan

middle: M


title: DNA hydroxymethylation analysis for target regions in human smooth muscle cells.

city: Fukuoka

first: Hiromitsu

last: Araki

address: 744 Motooka Nishi-Ku

country: Japan

institute: Kyushu University

type: Methylation profiling by high throughput sequencing

summary: Macrophage-like cells derived from vascular smooth muscle cells (SMCs) play critical roles in atherogenesis, and TET2-mediated DNA hydroxymethylation was implicated to regulate the transdifferentiation. We examined transcriptomes and (hydroxy)methylomes of human coronary artery SMCs during cholesterol-induced transdifferentiation. A unique approach of gene ontology (GO)-centric clustering of differentially expressed genes exhaustively identified through all possible pairwise comparisons (pan-DEGs) revealed dynamic and multifaceted modulations of genes involved in extracellular matrix organization, angiogenesis, cell migration, hypoxia response, and cholesterol biosynthesis. Intriguingly, transient activation was observed for an immuno-metabolic circuit consisting of type I interferon response and cholesterol metabolism. We found neither global nor DEG-proximal change in (hydroxy)methylation. These datasets would serve as a unique resource to address the mechanisms underlying cholesterol-induced transdifferentiation of SMCs. Moreover, GO-centric clustering of pan-DEGs may provide a useful approach to interpret multifaceted transcriptomic alterations.

overall_design: We conducted a series of genome and epigenome analysis, including RNA-sequencing and  DNA methylation and hydroxymethylation status in human smooth muscle cells.

first: Kentaro

last: Inoue

first: Fumihito

last: Miura

first: Takashi

last: Ito


title: DNA methylation analysis for target regions in human smooth muscle cells.


title: Expression profiles in the progression of the gastric cancer (mRNA+lncRNA+circRNA)

city: wuxi

first: fangmei

last: an

state: jiangsu

address: NO 299,QingYang Road

institute: Wuxi Public Hospital

overall_design: We report the mRNA, lncRNA, and cricRNA expression profiles in gastric mucosa with chronic superficial gastritis, chronic atrophic gastritis + intestinal metaplasia, dysplasia and gastric cancer

first: Qiang

last: Zhan

first: Fangmei

last: An


title: Transcriptome profiling of dendritic cells during JEV infection

city: Faridabad

first: Manjula

last: Kalia

state: Haryana

address: NCR Biotech Science cluster Gurugram-Faridabad Expressway

department: Virology

country: India

institute: Regional Centre for Biotechnology

summary: Characterization of transcriptional signature of innate immune response and metabolic pathways in monocytes derived dendritic cells (MoDCs) of healthy donors during JEV infection.

overall_design: mRNA profiling of monocytes derived dendritic cells from three different donors with Mock and JEV infection.

first: Shailendra

last: Chauhan


title: Single-Cell Chromatin Accessibility Landscape of Human Umbilical Cord Blood in Trisomy 18 Syndrome

city: guilin

first: qiu

last: fxiaofen

state: sz

address: Guangxi Normal University, Guilin, Guangxi

institute: Guangxi Normal University

summary: Trisomy 18 syndrome (Edwards Syndrome, ES) is a type of aneuploidy caused by the presence of an extra chromosome 18, and just the second most common autosomal trisomy syndrome after trisomy 21 (known as Down syndrome). Aneuploidy is the leading cause of early pregnancy loss, mental retardation, and multiple congenital anomalies. We used the commercial system Chromium platform (10x Genomics) to performed scATAC-seq to measure chromatin accessibility in 11,611 single umbilical cord blood cells, derived from 2 samples, respectively one Trisomy 18 Syndrome and one healthy donor. We obtain 13 distinct major clusters of cells, identified as 6 human umbilical cord blood mononuclear cell types marker-free and characterized the driving regulatory factors and differentially accessible loci that define each cluster. We set out to generate a single-cell atlas of chromatin accessibility among health and the 18 trisomy syndrome human umbilical cord blood. Finally, the cell-type-specific gene regulatory networks analysis at a single-cell resolution of this differential accessibility-related loci genes was carried out and disease-related transcription factors (TFs) and corresponding genes are predicted. These screened disease-related transcription factors (TFs) and corresponding genes provide a basis for further research and understanding of trisomy 18 syndrome. Finally, a cell-type-specific gene regulatory network analysis of these differentially accessible related locus genes was performed at single-cell resolution and predicted disease-related transcription factors (TFs) and corresponding genes. In detail, CCBN2 and MCM3 may be essential for the development of trisomy 18 and disease differential genes are enriched in the human T-cell leukemia virus 1 infection pathway.

overall_design: Single-cell chromatin accessibility (scATAC) profiles of Human Umbilical Cord Blood in Trisomy 18 Syndrome

first: Xaofen

last: Qiu

first: Yong

last: Dai


title: TRB sequences targeting ORF1ab are associated with disease severity in hospitalized COVID-19 patients

city: Rotterdam

first: Anton

last: Langerak

state: Zuid Holland

address: Dr. Molewaterplein 40

department: Immunology

country: Netherlands

institute: ErasmusMC

summary: The potential protective or pathogenic role of the adaptive immune response to SARS-CoV-2 infection has been vigorously debated. While COVID-19 patients consistently generate a T cell response to SARS-CoV-2 antigens, evidence of significant immune dysregulation in these patients continues to accumulate. In this study, next generation sequencing of the T cell receptor Beta chain (TRB) repertoire was conducted in hospitalized COVID-19 patients to determine if immunogenetic differences of the TRB repertoire contribute to the severity of the disease course. Clustering of highly similar TRB CDR3 amino acid sequences across COVID-19 patients yielded 785 shared TRB sequences. The TRB sequences were then filtered for known associations with common diseases such as EBV and CMV. The remaining sequences were cross-referenced to a publicly accessible dataset that mapped COVID-19 specific TCRs to the SARS-CoV-2 genome. We identified 140 SARS-CoV-2 specific TRB sequences belonging to 119 clusters in our COVID-19 patients. Next, we investigated 92 SARS-CoV-2 specific clusters binding only one peptide target in relation to disease course. Distinct skewing of SARS-CoV-2 specific TRB sequences towards the nonstructural proteins (NSPs) of ORF1a/b of the SARS-CoV-2 genome was observed in clusters with critical disease course when compared to COVID-19 clusters with a severe disease course. These data imply that T-lymphocyte reactivity towards peptides from nonstructural proteins of SARS-CoV-2 may not constitute an effective adaptive immune response and thus may negatively affect disease severity.

overall_design: T-cell receptor Beta chain sequencing of COVID-19 patients with severe and critical disease

first: A

first: J

last: Assmann

first: P

last: Kolijn


title: The VviNAC33 acts as a molecular switch by activating leaf degreening and repressing vegetative growth during the immature-to-mature phase transition in grapevine

city: Verona

first: Sara

last: Zenoni

address: Strada Le Grazie 15

country: Italy

institute: Università degli Studi di Verona

summary: In this study, we demonstrated that the grapevine NAC transcription factor VviNAC33 is directly involved in leaf degreening and organ growth. Through the application of DAP-seq approach we identified several putative targets of VviNAC33, among which the SGR1 involved in the breakdown of chlorophyll. Stable VviNAC33 overexpressing transgenic plants displayed an obvious degreening effect on leaves and an inhibition of leaf growth. Consistently, transgenic plant expressing a chimeric repressor of the VviNAC33 showed the opposite phenotypic alterations. Our results evidenced that VviNAC33 is a direct player of leaf senescence program and propose a blueprint of the complex transcriptional regulatory network that govern organ phase transition in grapevine.

overall_design: Transcriptomic changes caused by the VviNAC33 overexpression were inspected by a microarray analysis performed on leaf RNA of selected transgenic lines and control plants. Three biological replicates of young leaves were collected at the onset of phenotypic manifestation.

first: Erica

last: D’Incà

first: Stefano

last: Cazzaniga

first: Chiara

last: Foresti

first: Edoardo

last: Bertini

first: Nicola

last: Vitulo

first: Andrea

last: Gallavotti

first: Mary

last: Galli

first: Mario

last: Pezzotti

first: Giovanni

last: Tornielli


title: The VviNAC33 acts a molecular switch by activating leaf degreening and repressing vegetative growth during the immature-to-mature phase transition in grapevine

state: Verona

address: Ca' Vignal 1, Strada Le Grazie 15

department: Department Biotechnology

institute: University of Verona

summary: In this study we functionally characterized the grapevine VviNAC33 by its transient and stable overexpression in grapevine homologous system and the creation of its chimeric repressor. Through the application of DAP-seq approach we identified putative direct targets of VviNAC33, among which the SGR1 involved in the breakdown of chlorophyll. Stable VviNAC33 overexpressing transgenic plants displayed an obvious degreening effect on leaves and an inhibition of leaf growth. Consistently, transgenic plant expressing a chimeric repressor of the VviNAC33 showed the opposite phenotypic alterations. Our results evidenced that VviNAC33 is a direct player of leaf senescence program and propose a blueprint of the complex transcriptional regulatory network that govern organ phase transition in grapevine. transcription factor VviNAC33 is directly involved in leaf degreening and organ growth.

overall_design: Through the application of DAP-seq approach we identified putative direct targets of VviNAC33.


title: Ketogenesis restrains aging-induced exacerbation of COVID in a mouse model (scRNA-seq)

city: St. Louis

first: Maxim

last: Artyomov

state: MO

address: 425 S Euclid Ave

department: Pathology and Immunology

institute: Washington University in St. Louis

summary: Impaired immunometabolic response in the elderly regulates inflammation-driven COVID-19 severity which confers the greatest risk of mortality. To investigate how aging compromises defense against COVID-19, we developed a model of natural murine beta coronavirus (mCoV) infection with mouse hepatitis virus strain A59 (mCoV-A59) that recapitulated majority of hallmarks of COVID-19. Aged mCoV-A59-infected mice have increased mortality and higher systemic inflammation in the heart, adipose tissue and hypothalamus, including neutrophilia and loss of γδ T cells in lungs. Ketogenic diet increases beta-hydroxybutyrate, expands tissue protective γδ T cells, deactivates the inflammasome and decreases pathogenic monocytes in lungs during aging. These data underscore the value of mCoV-A59 model to test mechanism and establishes harnessing of ketogenic immunometabolic checkpoint as potential treatment against COVID-19 in the elderly.

overall_design: 1. Aged mice (20-21 months old) were fed a KD or chow diet for 5 days and then intranasally infected with mCoV-A59. 2. Chow diet fed aged (21 months old) or young mice (4 months old) were intranasally infected with mCoV-A59. In both experiments whole lung tissue was subjected to scRNAseq.

first: Seungjin

last: Ryu

first: Irina

last: Shchukina

first: Yun-Hee

last: Youm

first: Hua

last: Qing

first: Brandon

last: Hilliard

first: Tamara

last: Dlugos

first: Xinbo

last: Zhang

first: Yuki

last: Yasumoto

first: Carmen

last: Booth

first: Carlos

last: Fernández-Hernando

first: Yajaira

last: Suárez

first: Kamal

last: Khanna

first: Tamas

last: Horvath

first: Marcelo

middle: O

last: Dietrich

middle: N

first: Andrew

last: Wang

first: Vishwa

last: Deep Dixit


title: Ketogenesis restrains aging-induced exacerbation of COVID in a mouse model (bulk RNA-seq)

first: Maxim

last: Artyomov

overall_design: Aged mice (20-21 months old) were fed a KD or chow diet for 5 days and then intranasally infected with mCoV-A59. gdT cells were sorted from lungs.


title: Ketogenesis restrains aging-induced exacerbation of COVID in a mouse model

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

overall_design: Refer to individual Series


title: Microarray-based gene expression analysis of DMBA and high fat diet-induced hepatocellular carcinoma in mice

city: Kamakura

first: Satoshi

last: Kondo

state: Kanagawa

address: Tebiro 6-10-1

department: New Projects Development Division

institute: Toray Industries,Inc.

summary: The gene expression in the liver tumor tissues or non-tumor tissues of DMBA-treated, high fat diet-fed mouse livers compared with those of  DMBA-treated, normal diet-fed mouse liver tissues were successfully analyzed through the expression profiling of a total of 23473 genes in mouse livers (three tumor bearing livers vs two normal mouse livers).

overall_design: In this study, mRNA samples from three tumor bearing high fat diet-fed livers and two normal diet-fed livers were induvially used to acquire gene expression.

first: Naoko

last: Ohtani

first: Eiji

last: Hara


title: Polyamine metabolism regulates the T cell epigenome through hypusination [ATAC-seq]

city: Baltimore

first: Immunometabolism

last: Department

state: Maryland

address: 1650 Orleans Street

department: Immunometabolism

institute: Johns Hopkins University

summary: We report here a central role for polyamines in T cell differentiation and function. Deficiency in ornithine decarboxylase (ODC), a critical enzyme for polyamine synthesis, resulted in a profound failure of CD4+ T cells to adopt correct subset specification, underscored by ectopic expression of multiple cytokines and lineage- defining transcription factors across TH1, TH2, TH17, and Treg polarizing conditions, and enhanced colitogenic potential. T cells deficient in deoxyhypusine synthase (DHPS) or deoxyhypusine hydroxylase (DOHH), which sequentially utilize polyamines to generate hypusine, phenocopied Odc-deficient T cells, and mice in which T cells lacked Dhps or Dohh developed colitis. Polyamine-hypusine pathway enzyme deficiency caused widespread chromatin and transcriptional dysregulation accompanied by alterations in histone methylation, histone acetylation, and TCA cycle metabolites. Epigenetic modulation by 2-hydroxyglutarate, or histone acetyltransferase inhibition, restored CD4+ T cell subset specification. Thus, polyamine synthesis via hypusine is critical for maintaining the epigenome to focus TH cell subset fidelity.

overall_design: Mice expressing Cre recombinase (CD4Cre) under the control of the CD4 promoter were crossed with Dohh flox/flox and Odc flox/flox mice. CD4 T cells were isolated from the spleen and lymph node of these animals and cultured in T helper subset polarizing conditions. The transcriptome and chromatin accessibility of 3-4 biological replicates per T cell subset in Cre- (WT) or Cre+ (KO) were analysed.

first: Daniel

last: Puleston

first: Francesc

last: Baixauli

first: David

last: Sanin

first: Matteo

last: Villa

first: Agnieska

last: Kabat

first: Marcin

last: Kaminski

first: Hauke

last: Weiss

first: Katarzyna

last: Grzes

first: Lea

last: Flachsmann

first: Cameron

middle: S

last: Field

first: Michal

last: Stanczak

first: Lena

last: Schimmelpfennig

first: Fabian

last: Hassler

first: Chao

first: Nir

last: Yosef

first: Vijay

last: Kuchroo

first: Yaarub

last: Musa

first: Gerhard

last: Mittler

first: Joerg

last: Buesscher

first: Stefan

last: Balabanov

first: Edward

last: Pearce

first: Douglas

last: Green

first: Erika


title: The VviNAC33 acts a molecular switch by activating leaf degreening and repressing vegetative growth during the immature-to-mature phase transition in grapevine

first: Sara

last: Zenoni

summary: In this study we demonstrated that the grapevine NAC transcription factor VviNAC33 is directly involved in leaf degreening and organ growth. Through the application of DAP-seq approach we identified several putative targets of VviNAC33, among which the SGR1 involved in the breakdown of chlorophyll. Stable VviNAC33 overexpressing transgenic plants displayed an obvious degreening effect on leaves and an inhibition of leaf growth. Consistently, transgenic plant expressing a chimeric repressor of the VviNAC33 showed the opposite phenotypic alterations. Our results evidenced that VviNAC33 is a direct player of leaf senescence program and propose a blueprint of the complex transcriptional regulatory network that govern organ phase transition in grapevine.

overall_design: For transient transformation of Vitis vinifera cv. Sultana, the 35S:VviNAC33 construct was transferred to Agrobacterium tumefaciens strain C58C1 by electroporation. As control, Agrobacterium was also transformed with an empty pK7WG2 containing a non-coding sequence. Eight in vitro six-week-old plants of grapevine cv. Sultana for overexpression and seven for the control were immersed in each bacterial suspension and vacuum infiltrated (2 X 2 min at 90kPa). After agroinfiltration, plantlets were allowed to recover in vitro for seven days before collecting material for RNA extraction and transcriptomic analysis.

first: Erica

last: D’Incà

first: Stefano

last: Cazzaniga

first: Chiara

last: Foresti

first: Edoardo

last: Bertini

first: Nicola

last: Vitulo

first: Andrea

last: Gallavotti

first: Mary

last: Galli

first: Mario

last: Pezzotti

first: Giovanni

last: Tornielli


title: Differential miRNA and mRNA Expression in Immortalized Human Keratinocytes (HaCaT) after Low Arsenic Exposure [miRNA-seq]

city: Louisville

first: J.

middle: Christopher

last: States

state: KY

address: 505 S. Hancock St., Rm 304

department: Department of Pharmacology & Toxicology

institute: University of Louisville

summary: Determining the miRNA and mRNA expression profiles in HaCaT cells at early and late stages of arsenite exposure to reveal early and late changes in the HaCaT cells transformation process.

overall_design: 4 biological rereplicates of HaCaT cells exposed to 100 nM sodium arsenite and unexposed HaCaT cells (Control)

first: Laila

last: Al-Eryani

first: Samantha

last: Jenkins

first: Elizabeth

last: Hudson

first: Theodore

last: Kalbfleisch

first: J


title: Polyamine metabolism regulates the T cell epigenome through hypusination [RNA-seq]

first: Immunometabolism

last: Department

overall_design: Mice expressing Cre recombinase (CD4Cre) under the control of the CD4 promoter were crossed with Dohh flox/flox and Odc flox/flox mice. CD4 T cells were isolated from the spleen and lymphnode of these animals and cultured in T helper subset polarizing conditions. The transcriptome and chromatin accessibility of 3-4 biological replicates per T cell subset in Cre- (WT) or Cre+ (KO) were analysed.

first: Daniel

middle: J

last: Puleston

first: Francesc

last: Baixauli

first: David

last: Sanin

first: Matteo

last: Villa

first: Agnieska

last: Kabat

first: Marcin

last: Kaminski

first: Hauke

last: Weiss

first: Katarzyna

last: Grzes

first: Lea

last: Flachsmann

first: Cameron

last: Field

first: Michal

last: Stanczak

first: Lena

last: Schimmelpfennig

first: Fabian

last: Hassler

first: Chao

last: Wang

first: Nir

last: Yosef

first: Vijay

last: Kuchroo

first: Yaarub

last: Musa

first: Gerhard

last: Mittler

first: Joerg

last: Buesscher

first: Stefan

last: Balabanov

first: Edward

last: Pearce

first: Douglas

first: Erika


title: Polyamine metabolism regulates the T cell epigenome through hypusination

first: Immunometabolism

last: Department


title: Characterizing epigenetic effects of HISTONE DEACETYLASE 6 on DNA methylation, siRNA biogenesis and nucleosome positioning using two hda6 alleles in ros1 background

city: HONG KONG

first: Huan

last: ZHONG

state: HONG KONG

address: T1012 CHA CHI-MING SCIENCE TOWER

department: BIOLOGY

country: Hong Kong

institute: HKBU

summary: DNA cytosine methylation is a hallmark of epigenetic gene silencing. DNA demethylation requires ROS1, a bifunctional DNA glycosylase/lyases and open chromatin status mediated by IDM1. HDA6 is a RDP3-like histone deacetylase and was confirmed to mediate DNA methylation. In previous screening for ros1 suppressor, we identified two hda6 mutants reverting ros1-caused hypermethylation at RD29A and 35S promoters respectively, indicating the antagonization of DNA methylation between HDA6 and ROS1. To learn antagonized effects between HDA6 and ROS1 at DNA cytosine methylation genome-wide, we performed whole genome bisulfite sequencing to search antagonized targets of HDA6 and ROS1 and their specific targets to evaluate their roles on DNA methylation. To evaluate HDA6’s roles in sRNA biogenesis and nucleosome positioning, we also performed small RNA sequencing and genome-wide mapping of nucleosome positioning of C24, ros1, hda6-9 and hda6-10.  Our results indicate that around 43% ros1-caused CG hypermethylation, 74.5% and 84.5% ros1-caused CHG and CHH hypermethylation were reverted by the two hda6 alleles in the ros1 background respectively. These results indicate that most of ROS1-demethylated targets are also HDA6-mediated DNA methylated targets. In addition, we observed that HDA6-affected DNA methylation targets are far more than ROS1-demethylation targets at CHG and CHH context, but not at CG context. sRNA analysis showed that HDA6 inhibits LTR/Gypsy and TE gene 24nt siRNA accumulation, while promotes RC/Helitron 24nt siRNA accumulation. Our Mono-nucleosome positioning data further showed that the two hda6 alleles have striking difference on nucleosome positioning, hda6-10 obviously have different nucleosome positioning patterns with hda6-9. Our results indicate HDA6 not only mediates overall DNA methylation at CG, CHG and CHH context, and antagonizes with ROS1 mediated DNA demethylation, but also regulates nucleosome positioning and small RNA accumulation at some genome specific regions.

overall_design: DNA methylone, nucleosome positioning and small RNA sequencing of C24, ros1, ros1hda6-9 and ros1hda6-10 mutants

first: Shoudong

last: Zhang

last: Zhong

first: Qianwen


title: An RNA-centric global view of Clostridioides difficile reveals broad activity of Hfq in a clinically important Gram-positive bacterium

city: Würzburg

first: Falk

last: Ponath

address: Josef-Schneider-Straße 2

institute: Helmholtz Institute for RNA-based Infection Research (HIRI)

summary: The Gram-positive bacterium Clostridium difficile, a leading cause of antibiotic-associated pseudomembranous colitis, has received increasing attention due to a rising incidence of clinical C. difficile infections (CDI). Despite progress understanding bacterial factors that promote CDI-associated morbidity and mortality, many fundamental aspects of C. difficile biology remain to be explored. Compared to other Gram-positive pathogens, little is known about the bacterium’s transcriptome architecture and in particular mechanisms of post-transcriptional control. To close this knowledge gap, we have applied a suite of transcriptome-focused techniques, including transcription start site mapping (dRNA-seq), transcription termination mapping, and Hfq RIP-seq, resulting in a single-nucleotide resolution RNA map of C. difficile strain 630.

overall_design: Differential RNA-seq (dRNA-seq) was performed for C. difficile strain 630 in either different media and different growth stages to identify transcriptional start sites, 5'UTRs and sRNAs. The RNAtag-seq protocol was used to determine 3'UTRs of transcripts. RIP-seq was carried out to identify RNAs bound by Hfq in C. difficile.

first: Manuela

last: Fuchs

first: Vanessa

last: Lamm-Schmidt

first: Johannes

last: Sulzer

first: Laura

last: Jenniches

first: Joseph

middle: A

last: Kirk

first: Robert

middle: P

last: Fagan

first: Lars

last: Barquist

first: Jörg

last: Vogel

first: Franziska

last: Faber


title: The molecular basis of coupling between poly(A)-tail length and translational efficiency

city: Cambridge

first: David

last: Bartel

address: 455 Main Street

institute: Whitehead Institute

summary: In animal oocytes and early embryos, mRNA poly(A)-tail length strongly influences translational efficiency (TE), but later in development this coupling between tail length and TE disappears. Here, we elucidate how this coupling is first established and why it disappears. Overexpressing cytoplasmic poly(A)-binding protein (PABPC) in frog oocytes specifically improved translation of short-tailed mRNAs, thereby diminishing coupling between tail length and TE. Thus, coupling requires limiting PABPC, implying that in coupled systems longer-tail mRNAs better compete for limiting PABPC. In addition to expressing excess PABPC, post-embryonic cells had two other properties that prevented strong coupling: terminal-uridylation-dependent destabilization of mRNAs lacking bound PABPC, and a regulatory regime wherein PABPC contributes minimally to TE. Thus, these results revealed three fundamental mechanistic requirements for coupling and defined the context-dependent functions for PABPC, in which this protein promotes TE but not mRNA stability in coupled systems and mRNA stability but not TE in uncoupled systems.

sample_organism:
Xenopus laevis
Homo sapiens
Mus musculus

overall_design: RNA-seq, Ribo-seq TAIL-seq, PAL-seq

first: Kehui

last: Xiang


title: An epithelial Nfkb2 pathway exacerbates intestinal inflammation by supplementing latent RelA complexes to the canonical NF-kB module

city: New Delhi

first: Soumen

last: Basak

state: Delhi

address: Aruna Asaf Ali Marg

institute: National Institute of Immunology

summary: The canonical NF-kB module induces nuclear translocation of RelA heterodimers from the latent cytoplasmic complexes. RelA directs inflammatory immune responses against microbial entities. However, aberrant RelA activity also triggers destructive inflammation, including those associated with inflammatory bowel disease (IBD). What provokes this pathological RelA activity remains unclear. As such, the noncanonical NF-kB pathway activates RelB heterodimers and mediates immune organogenesis. Because NF-kB-activating pathways are interlinked, we asked if noncanonical NF-kB signaling exacerbated intestinal inflammation. Our investigation revealed recurrent engagement of the noncanonical pathway in human IBD. In a mouse model of chemical colitis, the noncanonical NF-kB signaling gene Nfkb2 aggravated inflammation by amplifying the RelA activity induced in intestinal epithelial cells. Our mechanistic studies clarified that noncanonical signaling augmented the abundance of latent RelA complexes leading to hyperactive canonical NF-kB response in the colitogenic gut. In sum, latent dimer homeostasis appears to link noncanonical NF-kB signaling to RelA-driven inflammatory pathologies.

overall_design: IECs were obtained from WT and Nfkb2-/- mice, either left untreated or treated with DSS for 48h. mRNA levels in all four samples with 3 biological replicates were generated via next generation sequencing.

first: Subhra

last: Biswas

first: Meenakshi

last: Chawla

first: Budhaditya

last: Chatterjee


title: Androgene Receptor (AR) splice variant ARv567es mediated transcriptome in LNCaP cells

city: Houston

first: Nancy

last: Weigel

state: TX

address: One Baylor Plaza

institute: Baylor College of Medicine

summary: Purpose of the study was to identify unique transcriptomic changes mediated by Androgen Receptor (AR) splice variant ARv567es in LNCaP cells

overall_design: LNCaP cells with doxycycline (dox) inducible expression of Androgen Receptor (AR) splice variant ARv567es were developed through lentiviral infection. This cell line is labeled LNCaP-ARv567es. RNA Sequencing was performed using two independent biological replicates collected at different time points in order to identify the transcriptomic changes mediated by ARv567es. The vehicle or control group consisted of LNCaP-ARv567es cells treated with 0.1% ethanol and test or experimental group consisted of LNCaP-ARv567es cells treated with 30 ng/ml dox. Treatment with vehicle or dox was for 24 hours, after which mRNA was extracted and submitted for RNA Sequencing

first: Cristian

last: Coarfa


title: Identification of the PRC1-interacting protein, L3mbtl3 as a novel gatekeeper of neocortical neurogenesis and proneural gene function  [ATAC-seq]

status: Public on Jul 06 2021

city: Lethbridge

first: Yaroslav

last: Ilnytskyy

state: AB

address: 4401, University Drive W

department: Biology

country: Canada

institute: University of Lethbridge

summary: The neocortex is comprised of six neuronal layers that are derived in an inside-out sequence. Neurog2, a proneural gene encoding a basic-helix-loop-helix transcription factor, is required and sufficient to specify the fate of only early-born, deep-layer neurons, despite being expressed throughout the cortical neurogenic period. To identify potential inhibitors of Neurog2 function, we used a TAP-tagging screen, identifying L3mbtl3, a histone methyl-lysine binding protein that interacts with Rnf2 in Polycomb Repressive Complex 1 (PRC1), as a novel Neurog2 interactor. We found that L3mbtl3 is co-expressed with Neurog2 and other PRC1 genes in cortical progenitors. In L3mbtl3 knock-out (KO)  cortices, upper-layer neurons are generated in reduced numbers, and instead, the cortical progenitor pool is expanded. Transcriptomic analyses of L3mbtl3 KO cortices at early and mid neurogenesis revealed a striking upregulation of negative regulators of transcription, including Rest, a repressor of many neurogenic genes, and an associated downregulation of neuronal differentiation and maturation genes. Notably, transcriptomic changes occur in the absence of any changes to chromatin structure, suggesting that L3mbtl3 influences gene transcription directly and not via changes to the chromatin. Instead, L3mbtl3 represses Neurog2 transcriptional activity in vitro and blocks cortical progenitor cell maturation and neuronal migration in vivo by altering the expression of scaffold genes. L3mbtl3 is thus an essential negative regulator of cortical neurogenesis.

overall_design: CD15+ E14.5 dorsal telencephalon NPCs ATACseq libararies from 3 control and 4 L3mbtl3 KO samples.

first: Sisu

last: Han

first: Grey

last: Wilkinson


title: RNA Sequencing data of gene expression chenges induced by NGPF2 treatment in primary neuronal culture

city: Shanghai

first: Xiaoyun

last: Zhang

address: 555 Zuchongzhi Road

institute: Shanghai Institute of Materia Medica, Chinese Academy of Sciences

summary: Mouse cortical primary neuronal cultures (DIV12-13) were treated with NGPF2 (1.5 ng/ml)  for 2 hours and then fixed for RNA sequencing.

overall_design: 3 separate pairs of control (vehicle) and treatment (NGPF2) groups from 3 independet experiments.

first: Zikai

last: Zhou

first: Guiqin

last: He


title: RNA-seq of granulocytes derived from control and AK2 depleted human HSPCs

city: Stanford

first: Wenqing

last: Wang

state: CA

address: 2500 BMI, 1291 Welch Rd

department: Department of Pediatrics

institute: Stanford University School of Medicine

summary: Reticular Dysgenesis (RD) is a rare but devastating form of severe combined immunodeficiency, characterized by a maturation arrest of the myeloid and lymphoid lineages paired with sensorineural hearing loss. RD is caused by biallelic loss-of-function mutations in the mitochondrial enzyme adenylate kinase 2 (AK2). To study the effect of AK2 depletion on HSPC differentiation, we developed a biallelic AK2 CRISPR knock-out model using human HSPCs. AK2 depleted HSPCs display severe proliferation and myeloid differentiation defects, recapitulating RD patient phenotype.

overall_design: AK2 and AAVS1 (safe harbor control) knock-out HSPCs were differentiated along the granulocytic lineage and cells at different maturation stages were FACS sorted

first: Katja

middle: G

last: Weinacht


title: Targeting lncRNA HUMT attenuates chemoresistance of LUAD via impairing glycolysis signaling

city: harbin

first: shoubin

last: sun

address: baojian road 157

institute: harbin medical university

summary: gefitinib-resistant lung adenocarcinoma cell lines（PC9/GR）transfect HUMT-specific shHUMT to knockdown HUMT1 and analysis differential gefitinib-resistant lung adenocarcinoma cell lines（PC9/GR）transfect HUMT-specific shHUMT to knockdown HUMT1 and analysis differential

overall_design: carboplatin resistance retinoblastoma cell lines (Weri-RB1/CRP) transfect SNHG1-specific shSNHG1 to knockdown SNHG1 and analysis differential gene in Weri-RB1/CRP

first: K


title: BCLIN25 / miRNA-125b axis regulates chemotherapeutic resistance and epithelial-mesenchymal transition

summary: paclitaxel-resistant triple-negative breast cancer cell lines (MDA-MB-231/PTX）transfect BCLIN25-specific si-BCLIN25 to knockdown BCLIN25 and analysis differential paclitaxel-resistantlung adenocarcinoma cell lines（PC9/GR）transfect HUMT-specific shHUMT to knockdown HUMT1 and analysis differential

overall_design: paclitaxel-resistant triple-negative breast cancer cell lines (MDA-MB-231/PTX）transfect BCLIN25-specific si-BCLIN25 to knockdown BCLIN25 and analysis differential paclitaxel-resistantRB1/CRP

first: Wan

last: Lin


title: Next Generation Sequencing samples from mouse liver tumor

first: yang

last: xu

state: Shanghai

address: 180 Fenglin road shanghai

institute: Zhongshan Hospital, Fudan University

summary: We report the application of next generation sequencing technology for high-throughput profiling of transcriptome in HCC murine cells treated by anti-PD-1 or IFN-α or anti-PD-1 combined with IFN-α

overall_design: Examination of HCC murine cells treated by different methods

first: Bo

last: Hu

first: Mincheng

last: Yu

first: Xiaolu

last: Ma

first: Jialei

last: Sun

first: Chenglong

last: Liu

first: Peiyao

last: Fu

first: Zhen

last: Yang

first: Yungang

first: Cheng

last: Huang

first: Xinrong

first: Yinghong

last: Shi

first: Shuangjian

last: Qiu

first: Huichuan

first: Andrew

middle: X

last: Zhu

first: Jian

first: Yang

last: Xu

first: Di

first: Jia

last: Fan


title: Identification of the PRC1-interacting protein, L3mbtl3 as a novel gatekeeper of neocortical neurogenesis and proneural gene function

first: Yaroslav

last: Ilnytskyy

overall_design: 1) GFP+ cells isolated by FACS in utero electroporation of 3 pCIG2 and 3 pCIG2-L3mbtl3 in dorsal telencephalon from E12.5 to E15.5  2) E12.5 dorsal telencephalon mRNA from 3 control and 2 L3mbtl3 KO samples.  3) CD15+ E14.5 dorsal telencephalon NPCs mRNA from 3 control and 3 L3mbtl3 KO samples.

first: Sisu

last: Han

first: Grey

last: Wilkinson


title: Single cell transcriptome profiling of Reticular Dysgenesis patient bone marrow

first: Wenqing

last: Wang

summary: Reticular Dysgenesis (RD) is a rare but devastating form of severe combined immunodeficiency, characterized by a maturation arrest of the myeloid and lymphoid lineages paired with sensorineural hearing loss. RD is caused by biallelic loss-of-function mutations in the mitochondrial enzyme adenylate kinase 2 (AK2). Understanding the gene expression impact of AK2 loss-of-function on a single cell level would not only allow us to  develop rational therapies for RD and other mitochondrial diseases but enable us to reconstruct metabolic changes that occur during development and how they impact cell fate decisions.

overall_design: Single cell RNA-seq of CD45+ bone marrow cells from RD patients and a healthy donor.

first: Katja

last: Weinacht


title: Active elimination of intestinal cells drives oncogenic growth in organoids

city: Amsterdam

first: Saskia

middle: JE

last: Suijkerbuijk

address: Plesmanlaan 121

institute: Netherlands Cancer Institute

summary: Competitive cell-interactions play a crucial role in quality control during development and homeostasis. Here we show that cancer cells use such interactions to actively eliminate wild-type intestine cells in enteroid monolayers and organoids. This apoptosis-dependent process boosts proliferation of intestinal cancer cells. The remaining wild-type population activates markers of primitive epithelia and transits to a fetal-like state. Prevention of this cell fate transition avoids elimination of wild-type cells and, importantly, limits the proliferation of cancer cells. JNK signaling is activated in competing cells and is required for cell fate change and elimination of wild-type cells. Thus, cell competition drives growth of cancer cells by active out-competition of wild-type cells through forced cell death and cell fate change in a JNK dependent manner.

overall_design: Bulk mRNA sequencing of sorted pure and mixed murine wild-type and cancer small intestine organoids

first: Ana

last: Krotenberg Garcia

first: Arianna

last: Fumagalli

first: Huy

last: Quang Le

first: Rene-Filip

last: Jackstadt

first: Tamsin

middle: R

last: Lannagan

first: Owen

last: Sansom

first: Jacco

last: van Rheenen


title: Single cell transcriptomic characterization of microtia reveals pathogenic dysregulation in previously unrecognized chondral stem/progenitor cell population

first: Yan

last: Zijun

address: Sohong Road2005

institute: Fudan university

summary: As one of most common birth defects worldwide, microtia results from auricular cartilage dysplasia and has unfortunate physical and psychological consequences for children. However, existing treatments have adverse outcomes and its pathogenesis is poorly understood. Since characterization of cell type composition and function in normal auricular cartilage can increase our understanding of microtia, we conducted single-cell transcriptomic profiling for 47,969 human auricular cartilage cells obtained from three microtia and six normal control (NC) samples. Comprehensive bioinformatic analysis identified seven cartilage-related cell subtypes belonging to the chondral and stromal lineages. We also found age-associated changes in gene expression shared across all subtypes in the chondral lineage of NC. Additionally, we revealed the previously unrecognized chondral stem/progenitor cells (CSPCs) that were mainly located in the chondrium and might have the potential for directed chondrogenic differentiation. Our results showed that dysregulation of SOX8 and EGR1 in CSPCs of microtia impaired cartilage development and enhanced oxidative stress response, respectively. These findings shed light on the potential mechanisms of microtia pathogenesis and offer novel avenues for the development of treatment strategies

overall_design: Single-cell mRNA sequencing of human auricular cartilage cells obtained from three microtia and six normal control (NC) samples.

first: Jing

last: Ma

first: Yu

last: Zhang

first: Zijun

last: Yan

first: Peixuan

last: Wu


title: DFMO effect on Th17 and iTreg cells (ATAC-Seq)

city: Berkeley

first: Allon

last: Wagner

address: 378 Stanley Hall

institute: UC Berkeley

summary: We studied the effects of polyamine pathway inhibitors on differentiation of nonpathogenic Th17 cellsin vitro. Here, we used difluoromethylornithine (DFMO), an irreversible inhibitor of ODC1, the enzyme that catalyzes the conversion of ornithine to putrescine.

overall_design: Non-pathogenic Th17 cells (Th17n), and induced T regulatory cells (iTreg) were differentiated in vitro from naïve cells isolated from WT mice. Cells were harvested at 68 hours and were performed in the presence or absence of 100µM DFMO (Sigma)

first: Chao

first: Kaminski

last: James

first: Pratiksha

last: Thakore

first: Christian

last: Elena


title: Mice kidney tissue: control vs. acute kidney injury

city: guangzhou

first: canming

last: li

state: guangdong

address: NO 600, Tianhe ave.

institute: The Third Affiliated Hospital of Sun Yat-sen University

type:
Expression profiling by array
Other

summary: Transcriptional profiling of mouse  kidney tissue comparing control untreated mice with mice treated with cisplatin. The latter makes kidney failure. Goal was to identify the alterations of N6-methyladenosine (m6A) RNA profiles in cisplatin-induced acute kidney injury (AKI) in mice.

overall_design: Two-condition experiment, control vs. AKI mice. Biological replicates: 4 control replicates, 4 AKI replicates.

first: Canming

last: Li

first: Ming

first: Wenbo

last: Zhao

first: Zengchun

last: Ye

first: Hui

last: Peng


title: Metabolic alterations mediated by STAT3 promotes drug persistence in CML [K562 bulk RNA-Seq]

city: Boston

first: Mahmoud

middle: Adel

last: Bassal

state: Massachusetts

address: 3 Blackfan Circle

department: Hematology and Oncology

institute: Beth Israel Deaconess Medical Center

summary: Leukemic stem cells (LSCs) can acquire non-mutational resistance following drug treatment leading to therapeutic failure and relapse. However, oncogene-independent mechanisms of drug persistence in LSCs are incompletely understood, which is the primary focus of this study. We integrated proteomics, transcriptomics, and metabolomics to determine the contribution of STAT3 in promoting metabolic changes in tyrosine kinase inhibitor (TKI) persistent chronic myeloid leukemia (CML) cells. Proteomic and transcriptional differences in TKI persistent CML cells revealed BCR-ABL-independent STAT3 activation in these cells. While knockout of STAT3 inhibited the CML cells from developing drug-persistence, inhibition of STAT3 using a small molecule inhibitor sensitized the persistent CML cells to TKI treatment. Interestingly, given the role of phosphorylated STAT3 as a transcription factor, it localized uniquely to genes regulating metabolic pathways in the TKI-persistent CML stem and progenitor cells. Subsequently, we observed that STAT3 dysregulated mitochondrial metabolism forcing the TKI-persistent CML cells to depend on glycolysis, unlike TKI-sensitive CML cells, which are more reliant on oxidative phosphorylation. Finally, targeting pyruvate kinase M2, a rate-limiting glycolytic enzyme, specifically eradicated the TKI-persistent CML cells. By exploring the role of STAT3 in altering metabolism, we provide critical insight into identifying potential therapeutic targets for eliminating TKI-persistent LSCs.

overall_design: Comparing drug-sensitive and resistant CML leukemic cells and murine stem progenitor cells

first: S

last: Patel

first: T

last: Nemkov

first: D

last: Stefanoni

first: G

last: Benavides

first: M

first: B

last: Crown

first: V

last: Matkins

last: Camacho

last: Kuznetsova

first: A

middle: T

last: Hoang

middle: E

last: Tenen

last: Wolock

first: J

last: Park

first: L

last: Ying

first: Z

last: Yue

middle: Y

last: JChen

first: Y

last: Henry

first: P

last: Ferrell

first: R

last: Lu

last: Darley-Usmar

last: D’Alessandro

last: Bhatia

last: Welner


title: Zfp57 inactivation illustrates the relationship between DNA methylation and imprinted gene expression in mouse neural precursor cells

city: Naples

first: Ankit

last: Verma

state: Naples

address: Via Pietro Castellino, 111

institute: Institute of Genetics and Biophysics "A. Buzzati Traverso" (IGB-ABT)

summary: ZFP57 interacts with the germline-derived differentially methylated regions (DMRs) of imprinted genes, and is required to maintain DMR methylation in mouse embryonic stem cells (ESCs). Although DNA methylation has a key role in maintaining genomic imprinting, several imprinted genes are controlled by different mechanisms, and a comprehensive study of the relationship between DMR methylation and imprinted gene expression is lacking. To address this issue, we differentiated wild-type and Zfp57 -/- hybrid mouse ESCs into neural precursor cells (NPCs) and evaluated allelic expression of imprinted genes. In Zfp57-mutant NPCs, we observed loss of allelic bias of all the 35 genes that were imprinted in wild-type cells, demonstrating that Zfp57-dependent methylation is required to globally maintain gene expression imprinting. Analysis of bulk expression showed that most of the genes expressed from the non-methylated chromosome were up-regulated, and most of those expressed from the methylated chromosome were down-regulated in mutant cells, but also that several other imprinted genes acquiring biallelic expression were not significantly affected, suggesting the existence of compensatory mechanisms that control their RNA level. Since neuronal differentiation was impaired in Zfp57-mutant cells, this study also indicates that deregulation of imprinted genes and/or other ZFP57-target non-imprinted genes is incompatible with proper neurogenesis.

overall_design: RNA-Seq profiles of Neuronal Progenitor Cells differentiated from WT hybrid JB1 cells ( mESCs)  and Zfp57-/- line  using Illumina HiSeq 2500 platform in two replicates.The presence of SNPs allowed the analysis of allele specific expression genome-wide.

first: Basilia

last: Acurzio

first: Alessia

last: Polito

first: Carlo

last: Giaccari

first: Francesco

last: Cecere

first: Annalisa

last: Fico

first: Claudia

last: Angelini

first: Floriana

middle: D

last: Ragione

first: Salvatore

last: Fioriniello

first: Robert

last: Feil

first: Andrea

last: Riccio


title: Transcriptome analysis of B. pertussis-stimulated human monocyte-derived dendritic cells

city: Bilthoven

first: Alberto

last: Miranda-Bedate

state: Utrecht

address: Antonie van Leeuwenhoeklaan 9

department: Department of Immune Mechanisms (IMM)

institute: RIVM

summary: We analysed the transcriptome, using an illumina RNAseq platform, of human monocyte-derived dendritic cells after a 3 hour stimulation with 9 different naturally circulating B. pertussis strains that varied in their pertactin expression

overall_design: human monocyte-derived dendritic cells were stimulated for 3h with 9 different B. pertussis strains after which the transcriptome was analysed using RNAseq

first: Michiel

last: Kroes

first: Elena

last: Pinelli


title: The commensal bacterium Lactiplantibacillus plantarum imprints innate memory-like responses in mononuclear phagocytes

city: Derio

first: Ana

middle: Maria

last: Aransay

state: BIZKAIA

address: Parque tecnologico de Bizkaia, Building 801-A

department: Genome Analysis Platform

country: Spain

institute: CIC bioGUNE

summary: Gut microbiota is a constant source of antigens and stimuli to which the resident immune system has developed tolerance. However, the mechanisms by which mononuclear phagocytes, specifically monocytes/macrophages, cope with these usually pro-inflammatory signals is poorly understood. Here, we show that innate immune memory promotes anti-inflammatory homeostasis using as a model strains of the commensal bacterium, Lactiplantibacillus plantarum. Priming of monocytes/macrophages with bacteria, especially in its live form, enhances bacterial intracellular survival and decreases the release of pro-inflammatory signals to the environment, with lower production of TNF and higher levels of IL-10. Analysis of the transcriptomic landscape of these cells shows downregulation of pathways associated with the production of reactive oxygen species (ROS) and the release of cytokines, chemokines and antimicrobial peptides. Indeed, the induction of ROS prevents memory-induced bacterial survival. In addition, there is a dysregulation in gene expression of several metabolic pathways leading to decreased glycolytic and respiratory rates in memory cells. These data support commensal microbe-specific metabolic changes in innate immune memory cells that might contribute to homeostasis in the gut.

overall_design: Genome-wide changes in gene expression in human monocytes exposed to culture medium, live or heat-killed L. plantarum

first: Juan

last: Anguita

first: Aize

last: Pellon

first: Monika

last: Gonzalez

middle: M


title: Metabolic alterations mediated by STAT3 promotes drug persistence in CML [HSC Bulk RNA-seq]

first: Mahmoud

last: Bassal

first: S

middle: B

last: Patel

first: T

last: Nemkov

first: D

last: Stefanoni

first: G

last: Benavides

first: M

first: B

middle: L

last: Crown

first: V

last: Matkins

last: Camacho

last: Kuznetsova

first: A

last: Hoang

last: Tenen

last: Wolock

first: J

last: Park

first: L

last: Ying

first: Z

last: Yue

last: JChen

first: Y

last: Henry

first: P

last: Ferrell

first: R

last: Lu

last: Darley-Usmar

last: D'Alessandro

last: Bhatia

last: Welner


title: OLIG2 maintenance is not essentially required for diffuse intrinsic pontine glioma cell line growth but regulates tumor phenotypes

city: Cincinnati

first: Richard

state: OH

address: 3333 Burnet Ave

department: CBDI

institute: Cincinnati Children's Hospital Medical Center

summary: we found that CCHMC-DIPG1 cells express little OLIG2 and exhibit a mesenchymal phenotype, which raised a question regarding the role of OLIG2 in the growth of DIPG cells. Our results indicate that OLIG2 is dispensable for DIPG cell growth but is required for maintenance of the proneural tumor phenotype. Downregulation of OLIG2 leads to deregulation of adaptive YAP1 and EGFR signaling.

overall_design:
Examination of ATAC-seq and Chip-seq in 2 patient-derived DIPG cell lines
RNA-seq: 4 patient-derived DIPG cell line, human NSC cells and 2 olig2 KO DIPG cell lines; DNA Methylation: 4 patient-derived DIPG cell lines

first: Yunfei

last: Liao

first: Qing


title: Effects of oral-glucose load on the gene expression of peripheral blood mono-nuclear cells in Asian-Indian men.

city: Bangalore

first: madavan

last: vasudevan

state: Karnataka

address: Kasturi Nagar

institute: Theomics International Private Limited

summary: The objective of this study was to perform a global, non-targeted gene expression analysis by microarray, to understand the immune cell gene regulation at fasting and in response to oral glucose load and how this regulation is different in Asian-Indian men with normal glucose tolerance (NGT) and pre-diabetes (PD). Through observing real-time gene expression changes, this study highlights 1. the importance of acute metabolic challenges like oral glucose load in regulating the immune cell gene expression and function. 2. How insulin resistance and pre-diabetes causes severe perturbation of baseline gene expression and thus alters the response to oral glucose load as well.

overall_design: PBMCs were isolated from fasting (8-12 hours) and 2 hour-post 75 gm. oral glucose load blood samples of healthy (NGT) and pre-diabetic (PD) Asian-Indian men. RNA was isolated and after due quality check, was used to hybridize on the array. A total of 28 RNA samples were hybridized (6 NGT fasting samples, 6 NGT 2-hour samples, 9 PD fasting samples and 7 PD 2-hour samples). A total of three comparisons were carried out in this study, listed as follows : 1) 2-hour post glucose load versus fasting (control) in NGT subjects with fold change cut-off >1.5 and p value cut-off of < 0.05 in paired Student’s t-test, 2) 2-hour post glucose load versus fasting (control) for PD with fold change cut-off >1.5 and p value cut-off of < 0.05 in paired Student’s t-test and 3) fasting PD versus fasting NGT (control) with fold change cut-off >2.0 and p value cut-off of < 0.05 in un-paired Student’s t-test

first: Madhulika

last: Dixit

first: Abhiram

middle: C

last: Mallu

first: Madavan

last: Vasudevan


title: Metabolic alterations mediated by STAT3 promotes drug persistence in CML

first: Mahmoud

last: Bassal

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

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus

overall_design: Refer to individual Series


title: Regulation of Th17/Treg Balance by the Polyamine Pathway

first: Allon

last: Wagner


title: The chromatin regulator JMJD3 partially mediates the polyamine-dependent effect on Th17 cells

summary: We studied the effects of polyamine pathway inhibitors on differentiation of Th17 cells in vitro. Here, we used difluoromethylornithine (DFMO), an irreversible inhibitor of ODC1, the enzyme that catalyzes the conversion of ornithine to putrescine, against a genetic background of WT or Jmjd3-deficient cells.

overall_design: We analyzed the effect of DFMO on Th17 cells differentiated from naïve CD4 T cells isolated from control or JMJD3fl/flCD4cre mice

first: Chao

last: Wang

first: Elena

last: Christian

first: Fessler

last: Johannes

first: Regev

last: Aviv

first: Yosef

last: Nir

first: Kuchroo

middle: K

last: Vijay


title: DFMO effect on Th17 and iTreg cells (RNA-Seq)

summary: We studied the effects of polyamine pathway inhibitors on differentiation of pathogenic and nonpathogenic Th17 cells in vitro. Here, we used difluoromethylornithine (DFMO), an irreversible inhibitor of ODC1, the enzyme that catalyzes the conversion of ornithine to putrescine.

overall_design: Pathogenic Th17 cells (Th17p), non-pathogenic Th17 cells (Th17n), and induced T regulatory cells (iTreg) were differentiated in vitro from naïve cells isolated from WT mice. Each library was run on two separate Next-Seq runs on the same day.


title: MicroRNA-96 is required to prevent allodynia by repressing voltage-gated sodium channels in spinal cord

city: Yangpu

first: Changgeng

last: Peng

address: Siping Road 1239

department: School of Medicine

institute: Tongji University

summary: Voltage-gated sodium channels (Navs) 1.7, 1.8, and 1.9 are predominately expressed in peripheral sensory neurons and are critical for action potential propagation in nociceptors. Unexpectedly, we found that expression of SCN9A, SCN10A, SCN11A, and SCN2A, the alpha subunit of Nav1.7, Nav1.8, Nav1.9 and Nav1.2, respectively, are up-regulated in spinal dorsal horn (SDH) neurons of miR-96 knockout mice. These mice also have de-repression of CACNA2d1/2 in DRG and display heat and mechanical allodynia that could be attenuated by intrathecal or intraperitoneal injection of Nav1.7 or Nav1.8 inhibitors or Gabapentin. Moreover, Gad2::CreERT2 conditional miR-96 knockout mice phenocopied global knockout mice, implicating inhibitory neurons; nerve injury induced significant loss of miR-96 in SDH GABAergic and Glutamatergic neurons in mice which negative correlated to up-regulation of Nav1.7, Nav1.8, Nav1.9 and Scn2a, this dis-regulation of miR-96 and Navs in SDH neurons contributed to neuropathic pain which can be alleviated by intrathecal injection of Nav1.7 or Nav1.8 blockers. In conclusion, miR-96 is required to avoid allodynia through limiting the expression of VGCCs and Navs in DRG and Navs in SDH in naïve and nerve injury induced neuropathic pain mice. Our findings suggest that central nervous system penetrating Nav1.7 and Nav1.8 inhibitors may be efficacious for pain relief.

overall_design: Bulk RNA of spinal dorsal horn profiling data  from 4 wild type and 4 miR-96 knock-out mice.

first: Liting

last: Sun

first: Ruilong

last: Xia


title: Expression data from hela cells stable clones overexpressing TFEB-3xFLAG

city: Pozzuoli

first: Rossella

last: De Cegli

address: Via Campi Flegrei 34

institute: Tigem

summary:
In order to identify the effects of TFEB overexpression on the hela cells transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the hela TFEB stable clones
Transcriptome analysis of hela stable clones overexpressing TFEB-3xFLAG

overall_design: For the analysis on the hela stable clones overexpressing TFEB, total RNA was extracted from the cells of three biological replicates; RNA extracted from hela WT cells was used as control.


title: Metabolic alterations mediated by STAT3 promotes drug persistence in CML [ChIP-seq]

first: S

last: Patel

first: T

last: Nemkov

first: D

last: Stefanoni

first: G

middle: A

last: Benavides

first: M

first: B

last: Crown

first: V

last: Matkins

last: Camacho

last: Kuznetsova

first: A

last: Hoang

last: Tenen

last: Wolock

first: J

last: Park

first: L

last: Ying

first: Z

last: Yue

last: JChen

first: Y

last: Henry

first: P

last: Ferrell

first: R

last: Lu

last: Darley-Usmar

last: D'Alessandro

last: Bhatia

middle: S

last: Welner


title: Hepatitis B Virus Episome DNA Localizes To the Vicinity of Chromosome 19 In 3D Host Genome Upon Infection

city: Beijing

first: Wenhui

last: Li

address: 7 Science Park Road ZGC Life Science Park

institute: National Institute of Biological Sciences

summary: Hepatitis B virus (HBV) infects 240 million people worldwide. The infection requires establishment and persistence of a viral episome, the covalently closed circular (ccc) DNA, in the nucleus. Here we studied cccDNA spatial localization in the 3D host genome by using chromosome conformation capture based sequencing analysis and fluorescence in situ hybridization (FISH). We show cccDNA is not randomly distributed in host nucleus, rather, it is preferentially accumulated at specialized areas, particularly in regions close to chromosome 19 (chr.19). Activation of cccDNA appears to be associated with its re-localization from a heterochromatin hub pre-established by 5 regions of chr.19 to transcriptionally active regions formed by chromosomes in close proximity to chr.19 including chr. 16, 17, 20, 22. This active versus inactive positioning at discrete regions of host genome is primarily controlled by viral HBx protein and host factors including the structural maintenance of chromosomes protein 5/6 (SMC5/6) complex.

overall_design: HBV-4C was used to study HBV cccDNA spatial localization in the 3D host nucleus using de novo HBV infection model. Hi-C was used to analyze overall host chromatin organization. Transcriptional activity was analyzed by combing RNA-seq.

first: Dingbin

last: Tang

first: Hanqing

last: Zhao


title: Gene expression profiles of mutant ASXL1 knock-in HSPCs

status: Public on Jul 05 2021

city: Tokyo

first: Keita

last: Yamamoto

address: 4-6-1 Shirokanedai, Minato-ku

department: Division of Cellular Therapy

institute: The University of Tokyo

summary: To assess the effect of mutant ASXL1 (ASXL1-MT) on gene expression and RNA splicing in hematopoietic cells, we performed RNA-seq using HSPCs (bone marrow lineage-, c-Kit+ cells) derived from control or ASXL1-MT-KI mice.

overall_design: Total RNA extracted from bone marrow LK cells derived from 8- to 12-week-old littermate wild-type and ASXL1-MT-KI mice were subjected to RNA-Seq analysis. Three biologically independent experiments were perfomed for each sample.

first: Susumu

last: Goyama

first: Ayana

last: Kon

first: Yasuhito

last: Nannya

first: Seishi

last: Ogawa

first: Toshio

last: Kitamura


title: Polymerase II binding analysis during nutrient restriction using targeted DamID

city: Santiago

first: Esteban

middle: Gonzalo

last: Contreras Sepúlveda

address: Independencia 1027

country: Chile

institute: Universidad de Chile

summary: The adaptable transcriptional response to changes in food availability not only ensures animal survival, but also permits progressing with embryonic development. Interestingly, the central nervous system is preferentially protected to periods of malnutrition, a phenomenon known as ‘brain sparing’. However, the mechanisms that mediates this genetic response remains poorly understood. To get a better understanding of this, we used Drosophila melanogaster as a genetic model, analysing the transcriptional response of larval neural stem cells (neuroblasts) and glial cells of the blood-brain barrier during nutrient restriction using the targeted DamID technique.

overall_design: Polymerase II Targeted DamID using neuroblasts and blood-brain barrier glial drivers. Drosophila larvae were raised for 8 days at 18°C and transferred to 29°C in nutrient restriction or normal fed conditions.

middle: G

last: Contreras


title: Nascent RNA scaffolds contribute to chromosome territory architecture and counter chromatin compaction

city: Worcester

first: Kevin

last: Creamer

state: MA

address: 55 Lake Ave N

institute: UMMS

summary: Nuclear chromosomes transcribe far more RNA than required to code for protein. Here we investigate whether non-coding RNA broadly contributes to cytological-scale chromosome territory architecture. We develop a procedure that depletes soluble proteins, chromatin and most nuclear RNA from the nucleus, but does not delocalize XIST, a known architectural RNA, from an insoluble chromosome “scaffold.” RNA-seq analysis reveals most RNA in the nuclear scaffold is repeat-rich, non-coding, and predominantly derived from introns of nascent transcripts. This repeat-rich (C0T-1) RNA inversely correlates with chromatin compaction in normal and experimentally manipulated nuclei, demonstrating RNA physically antagonizes a propensity for chromatin to condense. C0T-1 hnRNA co-distributes on euchromatin with several known scaffold proteins including scaffold attachment factor A (SAF-A). We further show that RNA is required for SAF-A to interact with chromatin and to form structurally embedded scaffold-attachment regions (SARs) in the nuclear genome. Collectively, results indicate nascent transcripts serve a dynamic structural role in the open architecture of active chromosome territories

overall_design: RNA-sequencing and DNA-sequencing of TIG-1 cells after subnuclear fractionation

first: Heather

middle: J

last: Kolpa

first: Jeanne

last: Lawrence


title: mTORC1-mediated growth of kidney cysts is rapidly bypassed by other signaling pathways

city: Lübeck

first: Hauke

last: Busch

state: Schleswig-Holstein

address: Ratzeburger Allee 160

department: Lübeck Institute of Experimental Dermatology

institute: University of Lübeck

summary: Cystic kidney disease (CyKD) is the leading monogenetic cause of endstage renal disease. In both mice and humans CyKD has been consistently linked to the activation of the mTORC1 pathway. Yet, the utility of mTORC1 inhibitors in CyKD patients remains controversial despite promising preclinical data. To conclusively define the cell intrinsic role of mTORC1 for cyst development, mTORC1 was selectively inactivated in renal tubular cells of an aciliary mouse model of CyKD by deleting the decisive scaffolding protein RAPTOR. Initial preservation of renal function in CyKD∆RAP mice was followed by a steady decline in renal function coinciding with the development of renal cysts in these animals. While overall survival in CyKD∆RAP was considerably prolonged, in-depth transcriptomic analysis showed a rapid activation of other growth-promoting pathways, limiting the effects of mTORC1 deficiency to a relatively small therapeutic window. Future trials in patients with polycystic kidney disease need to acknowledge these findings, and might have to consider combinatorial or sequential therapies to improve efficacy.

overall_design: Raptor fl/fl or Kif fl/fl mice (used as Control), Raptor fl/fl*KspCre, Kif3a fl/fl*KspCre and Raptor fl/fl*Kif3a fl/fl*KspCre animals were sacrificed at 1 day, 1, 2 and 4 weeks (n>=7). Kidneys were split in half and immediately snap frozen in liquid nitrogen. RNA was purified using standard procedures and analyzed using Affimetrix Mouse Genome 430 2.0 gene chips.

first: Melanie

last: Boerries

first: Nurgazy

last: Sulaimanov

first: Tobias

last: Huber

first: Florian

last: Grahammer

first: Pierre

last: Moulin


title: IRS1 phosphorylation determines a heritable probability of cancer cells to persist during EGFR inhibition therapy [Mars-seq]

city: Rehovot

first: Zohar

last: Meir

state: Shfela

address: Herzl 234

department: Mathematics & CS

institute: Weizmann Institute of Science

summary: As part of a multi-omic pursuit for mechanisms of persistency of cancer cells to drug treatment, we generated pair-wise transcriptome analysis of nearly 200 single-cell-derived clonal populations, with and w/o drug treatment.

overall_design: Single PC-9 cancer cells were cultured and propagated to form hundreds of single-cell-derived clonal populations. Each clonal population was later split into parallel interrogation of its CTP (chance to persist drug treatment), population doubling time, and two transcriptome profiles – 24 hours post Gefitinib drug treatment or mock DMSO treatment. This dataset aimed to find clonally semi-stable molecular signatures that correlate with the observed inherited ability to persist drug treatment.

first: Adi

last: Jacob

first: Ravid

last: Straussman


title: Differential expression of miRNA in tissue microarray

city: Shanghai

first: yu

middle: zhi

last: long

address: NO.100 Haining Road

department: General Surgery

institute: Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University

summary: The expression of miRNA in cancer tissues of gastric cancer patients with different lymph node stages was compared. N0 indicated no lymph node metastasis, and N3 indicated 7 or more lymph node metastasis

overall_design: Total RNA was quantified by the NanoDrop ND-2000 (Thermo Scientific)and the RNA integrity was assessed using Agilent Bioanalyzer 2100 (Agilent Technologies).The sample labeling, microarray hybridization and washing were performed based on the manufacturer’s standard protocols. Briefly, total RNA were dephosphorylated, denaturated and then labeled with Cyanine-3-CTP. After purification the labeled RNAs were hybridized onto the microarray. After washing, the arrays were scanned with the Agilent Scanner G2505C(Agilent Technologies). 20 samples have been finished.

first: Zhilong

last: Yu

first: Chen

last: Huang


title: Essential requirement for polypyrimidine tract binding proteins 1 and 3 in the maturation and maintenance of mature B cells in mice

city: Cambridge

first: Louise

last: Matheson

address: Babraham Research Campus

department: Laboratory of Lymphocyte Signalling and Development

country: United Kingdom

institute: The Babraham Institute

summary: The maturation of immature B cells and the survival of mature B cells is stringently controlled to maintain a diverse repertoire of antibody specificities while avoiding self-reactivity. At the molecular level this is regulated by signalling from membrane immunoglobulin and the BAFF-receptor which sustain a pro-survival programme of gene expression. Whether and how posttranscriptional mechanisms contribute to B cell maturation and survival remains poorly understood. Here we show that the polypyrimidine tract binding proteins (PTBP) PTBP1 and PTBP3 bind to a large and overlapping set of transcripts in B cells. Both PTBP1 and PTBP3 bind to introns and exons where they are predicted to regulate alternative splicing. Moreover, they also show high density of binding in the 3’ untranslated regions suggesting they influence the transcriptome in diverse ways. We show that PTBP1 and PTBP3 are required in B cells beyond the immature cell stage to sustain transitional B cells and the B1, marginal zone and follicular B cell lineages. Therefore, PTBP1 and PTBP3 promote the survival of quiescent B cells by regulating gene expression at the post-transcriptional level.

overall_design: PTBP3 iCLIP from in vitro activated B cells (LPS 48h). Three libraries were prepared from the same iCLIP sample where the membrane containing the RNA-RBP complexes was cut at three different molecular weight ranges

first: Elisa

last: Monzon-Casanova

first: Christopher

middle: W

last: Smith

first: Martin

last: Turner


title: Effect of bromodomain inhibitors on dopamine D1R induced gene expression in striatal neurons

city: Montreal

first: Terence

last: Hébert

state: Quebec

address: 3655 Promenade Sir William Osler

department: Pharmacology and Therapeutics

institute: McGill University

summary: The dopamine D1R is Gs coupled GPCR which is expressed in striatal neurons and stimulates gene expression upon activation by dopamine or other agonists. In this work we investigated the role of the BET protein bromodomain containing protein 4 (Brd4) in mediating D1R-dependent gene expression in rat striatal neurons. Here we report the results of 3 RNA sequencing experiments. In Experiment 1 we treated primary striatal neurons with the D1R-selective agonist SKF-81297 alone or in combination with the non-selective BET inhibitor JQ1 for 60 minutes to assess the effect of BET inhibition on acute D1R-dependent gene expression. In Experiment 2, we treated primary striatal neurons with the D1R-selective agonist SKF-81297 alone or in combination with the BET bromodomain 2 selective inhibitor iBD2 for 60 minutes to determine the contribution of BD2 specifically to D1R-dependent gene expression. In Experiment 3 we treated primary striatal neurons with the D1R-selective agonist SKF-81297 alone or in combination with the non-selective BET inhibitor JQ1 for 24 hours to assess the effect of prolonged BET inhibition on basal gene expression and D1R-dependent gene expression.

overall_design: RNA sequencing of striatal cultures treated with varying combinations of D1R agonist and either JQ1 or iBD2, for either 60 minutes or 24 hours.

first: Jace

last: Jones-Tabah

last: Hebert

first: Paul

last: Clarke

first: Jason

last: Tanny


title: Whole transcriptome sequencing of gastric cancer and its adjacent paracancerous tissues

summary: We screened the differentially expressed lncRNA and circRNA in gastrointestinal cancer and its adjacent tissues by whole transcriptome sequencing

overall_design: lncRNA and circRNA expression profile of gastric cancer and  paracancerous normal tissues.A total of 12 samples were collected from 6 pairs of cancer and paracancerous normal tissues


title: Induction of a chromatin boundary in vivo upon insertion of a TAD border (MinION-nCATS)

city: Lausanne

first: Lucille

last: Lopez-Delisle

address: Station 19

country: Switzerland

institute: EPFL

summary: Mammalian genomes are partitioned into sub-megabase to megabase-sized units of preferential interactions called topologically associating domains or TADs, which are likely important for the proper implementation of gene regulatory processes. These domains provide structural scaffolds for distant cis regulatory elements to interact with their target genes within the three-dimensional nuclear space and architectural proteins such as CTCF as well as the cohesin complex participate in the formation of the boundaries between them. However, the importance of the genomic context in providing a given DNA sequence the capacity to act as a boundary element remains to be fully investigated. To address this question, we randomly relocated a topological boundary functionally associated with the mouse HoxD gene cluster and show that it can indeed act similarly outside its initial genomic context. In particular, the relocated DNA segment recruited the required architectural proteins and induced a significant depletion of contacts between genomic regions located across the integration site. The host chromatin landscape was re-organized, with the splitting of the TAD wherein the boundary had integrated. These results provide evidence that topological boundaries can function independently of their site of origin, under physiological conditions during mouse development.

overall_design: Characterization of the TgN(38-40) insertion by nanopore sequencing (MinION-nCATS)

first: Andréa

last: Willemin

first: Eddie

last: Rodríguez-Carballo

first: Denis

last: Duboule


title: Induction of a chromatin boundary in vivo upon insertion of a TAD border


title: Induction of a chromatin boundary in vivo upon insertion of a TAD border (Hi-C)

overall_design: Analysis of chromatin structure by Hi-C in developing mouse limbs upon ectopic integration of region CS38-40 (TgN(38-40))


title: Induction of a chromatin boundary in vivo upon insertion of a TAD border (4C-Seq)

overall_design: Analysis of chromatin structure by 4C-seq in developing mouse limbs upon ectopic integration of region CS38-40 (TgN(38-40))


title: Development of a Novel Live Attenuated Influenza A Virus Vaccine Encoding the IgA-Inducing Protein

city: Athens

first: Daniel

middle: Roberto

last: Perez

state: GA

address: 953 College Station Road

institute: University of Georgia

summary: Live attenuated influenza virus (LAIV) vaccines elicit a combination of systemic and mucosal  immunity by mimicking a natural infection. To further enhance protective mucosal responses,  we incorporated the gene encoding the IgA-inducing protein (IGIP) into the LAIV genomes of  the cold-adapted A/Leningrad/134/17/57 (H2N2) strain (caLen) and the experimental attenuated  backbone A/turkey/Ohio/313053/04 (H3N2) (OH/04att). Incorporation of IGIP into the caLen background  led to a virus that grew poorly in prototypical substrates. In contrast, IGIP in the OH/04att  background (IGIP-H1att) virus grew to titers comparable to the isogenic backbone H1att (H1N1)  without IGIP. IGIP-H1att- and H1caLen-vaccinated mice were protected against lethal challenge  with a homologous virus. The IGIP-H1att vaccine generated robust serum HAI responses in naive  mice against the homologous virus, equal or better than those obtained with the H1caLen vaccine.  Analyses of IgG and IgA responses using a protein microarray revealed qualitative differences in  humoral and mucosal responses between vaccine groups. Overall, serum and bronchoalveolar  lavage samples from the IGIP-H1att group showed trends towards increased stimulation of IgG  and IgA responses compared to H1caLen samples. In summary, the introduction of genes encoding  immunomodulatory functions into a candidate LAIV can serve as natural adjuvants to improve  overall vaccine safety and efficacy.

platform_organism:
Influenza A virus
Influenza B virus

overall_design: We incorporated the gene encoding the IgA-inducing protein (IGIP) into the LAIV genomes of  the cold-adapted A/Leningrad/134/17/57 (H2N2) strain (caLen) and the experimental attenuated  backbone A/turkey/Ohio/313053/04 (H3N2) (OH/04att). IGIP-H1att- and H1caLen-vaccinated mice were protected against lethal challenge  with a homologous virus. The IGIP-H1att vaccine generated robust serum HAI responses in na ve  mice against the homologous virus, equal or better than those obtained with the H1caLen vaccine.  Analyses of IgG and IgA responses using a protein microarray revealed qualitative differences in  humoral and mucosal responses between vaccine groups. Overall, serum and bronchoalveolar  lavage samples from the IGIP-H1att group showed trends towards increased stimulation of IgG  and IgA responses compared to H1caLen samples

first: Caceres

last: C. Joaquin.

first: Cardenas-Garcia

last: Stivalis

first: Jain

last: Aarti

first: Gay

last: L. Claire

first: Carnaccini

last: Silvia

first: Seibert

last: Brittany

first: Ferreri

last: Lucas M.

first: Geiger

last: Ginger

first: Jasinskas

last: Algimantas

first: Nakajima

last: Rie

first: Rajao

last: Daniela S.

first: Isakova-Sivak

last: Irina

first: Rudenko

last: Larisa

first: Vincent

last: Amy L.

first: Davies

last: D. Huw

first: Perez

last: Daniel R.


title: CircRtn4 Acts as the Sponge of miR-24-3p to Promote Neurite Growth by Regulating CHD5

city: Shenzhen

first: Yue

last: Qi

address: Lianhua

institute: Peking University

summary: To investigate the potential involved mRNAs, transcriptome RNA sequencing was employed to identify differential genes after circRtn4 knockdown in N2a cells.

overall_design: Examination differential genes in si-NC treated and si-circRtn4 treated N2a cells.

first: Nana

last: Ma

first: Xiaofan

last: Chen

first: Jun

last: Wan


title: Induction of a chromatin boundary in vivo upon insertion of a TAD border (TLA)

first: Lucille

last: Lopez-Delisle

overall_design: Characterization of the TgN(38-40) insertion using targeted locus amplification (TLA)

first: Andréa

last: Willemin

first: Eddie

last: Rodríguez-Carballo

first: Denis

last: Duboule


title: Single cell transcriptome analysis of primary murine EMP reveals complex erythroid, myeloid, and innate lymphoid lineage heterogeneity

city: Rochester

first: James

last: Palis

state: NY

address: 601 Elmwood Ave.

department: Pediatrics

institute: University of Rochester

overall_design: 2,952 single cells were captured using a chromium 10x platform and unbiased clustering was evaluated using Seurat. Further integration was performed with E12.5 fetal liver

first: Jacquelyn

last: Myers