title: Chinese Herbal Formula (GCNY)-Medicated Serum Alleviates Peroxidation Induced by H2O2 in Human Microglial Cells

city: Guangzhou

first: Yanjuan

last: Chen

state: Guangdong

address: Guangzhou

department: Department of Geriatrics and Division of Rheumatology and Research

institute: The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital)

summary:
Transitional Chinese herbal medicine has a long history of applications for anti-aging and longevity purposes, and in our patent formula Gancao Nurish-Yin (GCNY) decoction, all of the ingredients show antioxidant properties. However, in real clinical practice, extractions of herbs are rarely applied alone but are prescribed as integrated formula.
In order to investigate whether GCNY possess anti-oxidation potential, we applied GCNY as a formula to treat rats in order to acquire medicated serum, which was then added on H2O2 (200 μM)-modeled human microglial cell line HMC-3 in comparison with its controls.

overall_design: To explore the impact of H2O2 modeling to HMC-3 cells and how GCNY-medicated serum affects transcriptome of H2O2 modeled cells, high-throughput RNA sequencing analysis was performed in NC, NC+H2O2 and GCNY groups of cells.

first: Yong

first: Baojiang

last: Wang

first: Wing-Fu

last: Lai

first: Rongbin

last: Pan

first: Zhongsheng

last: Tang

first: Dongzhou

last: Liu


title: The impact of the anticoagulant type in blood collection tubes on circulating plasma miRNA profiles revealed by small RNA sequencing

status: Public on Sep 07 2022

city: Moscow

first: Andrey

last: Zhelankin

address: Malaya Pirogovskaya 1a

country: Russia

institute: Federal Research and Clinical Center of Physical-Chemical Medicine of Federal Medical Biological Agency

type: Non-coding RNA profiling by high throughput sequencing

summary: Pre-analytic factors have a significant influence on circulating miRNA profiling. The aim of this study was the comprehensive NGS-based assessment of the impact of anticoagulant type in blood collection tubes on circulating plasma miRNA profiles.

overall_design: Comparative miRNA profiling analysis of miRNA-Seq data for plasma extracellular circulating miRNA obtained from blood collected with different anticoagulants (ACD-B, Sodium citrate, CTAD and K2-EDTA) from 10 healthy participants.

first: Liliia

last: Iulmetova

first: Eduard

last: Generozov

first: Elena

last: Sharova


title: Columbia University Irving Medical Center RNASeq of meningioma tumors

status: Public on Sep 06 2022

city: New York

first: Prabhjot

middle: Singh

last: Mundi

state: NY

address: 1130 St. Nicholas Avenue

department: Medicine; Systems Biology

country: USA

institute: COLUMBIA UNIVERSITY HEALTH SCIENCES

type: Expression profiling by high throughput sequencing

summary: We use a Master Regular-based precision cancer medicine framework to predict drug sensitivity to tumors.

overall_design: RNAseq profiles of 102 meningioma patient tumors sequenced at Columbia University Irving Medical Center used to derive a meningioma gene regulatory network (interactome).

middle: S

first: Mariano

middle: J

last: Alvarez

first: Andrea

last: Califano


title: A phenotypic rescue approach identifies lineage regionalization defects in a mouse model of DiGeorge syndrome.

city: Naples

first: Gabriella

last: Lania

address: Via Pietro Castellino

country: Italy

institute: IGB-CNR

summary:
Evaluate the effect of the vB12 treatment on transcriptional profile of Tbx1 haploinsufficiency embryos
we performed RNA-seq on whole E9.5 mouse embryos (21 somite stage) after treatment with vB12 (cyanocobalamin Sigma-Aldrich Prod. Number V2876) or vehicle (PBS) during pregnancy

overall_design: Comparative gene expression profiling analysis of RNA-seq data  from PBS-treated WT (n=3), PBS-treated Tbx1+/- (n=3), and vB12-treated Tbx1+/- (n=2) embryos

first: Antonio

last: Baldini

first: Monica

last: Franzese

first: Claudia

last: Angelini


title: COVID_19 lung autopsy samples

first: Shuibing

last: Chen

address: A 827B, 1300 York Ave

department: Surgery

institute: Weill Cornell Medical College

summary: The SARS-CoV-2 has already caused over 523 million COVID-19 cases and 6.27 million deaths worldwide. COVID-19 leads to a severe acute respiratory syndrome, a hyperinflammatory response, and widespread multi-organ damage. Common symptoms of COVID-19 include fever, cough, fatigue, shortness of breath, and loss of taste and smell. Here we offer an in-depth analysis of the transcriptional response to SARS-CoV-2. We performed RNA-seq analysis of lung tissues from three COVID-19 patients.

overall_design: RNA-sequencing of three COVID_19 lung autopsy samples

first: Robert

middle: E

last: Schwartz

first: Yuling

last: Han

first: Liuliu

last: Yang

first: Tuo

last: Zhang

first: Jenny

middle: Z

last: Xiang


title: Antigens expressed by breast cancer cells undergoing EMT stimulate cytotoxic CD8+ T cell immunity

city: Aurora

first: Tonya

last: Brunetti

state: CO

address: 12800 East 19th Avenue

department: Immunology and Microbiology

institute: University of Colorado Anschutz Medical Campus

summary: The transformation of carcinoma cells with epithelial characteristics to those with mesenchymal characteristics (termed EMT) facilitates the progression of localized breast cancer to metastatic disease. The EMT program also contributes to several immunosuppressive and immunoevasive properties, altering the susceptibility of the cells to immune cell recognition and killing. Therefore, the aim of our study was to identify antigens upregulated in the mesenchymal cell state and assess their ability to circumvent immune escape. We confirmed increased susceptibility to the killing of epithelial cells across all antigens tested.

overall_design: Neoantigen and intron retention neojunction analysis of the EO771 cell line compared across untreated, doxy empty vector, and doxy miR200c conditions

first: Faye

middle: A

last: Camp

middle: M

first: Michelle

last: Williams

first: Jessica

middle: L

last: Christenson

first: Zachary

last: Hay

first: Varsha

last: Sreekanth

first: James

last: Costello

first: Ross

last: Kedl

first: Jennifer

middle: K

last: Richer

first: Jill

last: Slansky


title: Potential Methylation-regulated Genes and Pathways in Hepatocellular Malignant Neoplasm, Not Otherwise Specified

city: Los Angeles

first: Shengmei

last: Zhou

state: CA

address: 4650 Sunset Blvd.

department: Pathology and Laboratory Medicine

institute: Children's Hospital Los Angeles

type: Methylation profiling by genome tiling array

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

overall_design: Refer to individual Series


title: PBAF loss leads to DNA damage induced inflammatory signalling through defective G2/M checkpoint maintenance

city: London

first: HUGANG

last: FENG

address: Chester Beatty Laboratories, 237 Fulham Road

department: Cancer Biology

country: United Kingdom

institute: The Institute of Cancer Research

summary: PBRM1 deficiency in immortalised fibroblast cell line 1BR3-hTERT after ionising radiation treatment leads to more mitotic progression and more formation of micronucleated cells. Here, we performed total RNA-seq in 1BR3-hTERT parental line and PBRM1 knockout clones (PBRM1 KO3&KO5) under untreated (UT) or 48 hr post 6Gy irradiation condition. We found that the annotated DREAM complex target genes are less transcriptionally repressed in the 1BR3-hTERT PBRM1 knockout clones compared to the parental line after ionising radiation treatment. The results confirm our findings that PBRM1 deficiency leads to delayed p21 induction and delayed p130 hypo-phosphorylation, which leads to defective DREAM target gene repression and misregulated G2/M progression after ionising radiation treatment.

overall_design: Total mRNA profiles of immortalised human fibroblast 1BR3-hTERT parenal and PBRM1 knockout cell lines with or without ionising radiation treatment

first: Hugang

last: Feng

last: Downs


title: OCT4-SOX2 dimers reshape the epigenome to promote neural crest multipotency [Group1-4]

city: Ithaca

first: Marcos

last: Simoes-Costa

state: New York

address: 526 Campus Rd

department: Molecular Biology and Genetics

institute: Cornell University

type: Genome binding/occupancy profiling by high throughput sequencing

summary: The transcription factors OCT4 and SOX2 play an essential role in the establishment and maintenance of pluripotent embryonic stem cells (ESCs). Yet, their function in specialized stem cell populations is still poorly understood. Here, we show that the OCT4 and SOX2 work as dimers to regulate the epigenomic landscape of neural crest cells. By isolating primary neural crest cells at a range of developmental stages, we characterized the transcriptomic and epigenomic changes that take place during specification, migration, and early differentiation. Analysis of these datasets revealed that the OCT4/SOX2 dimer promotes an epigenomic signature inherent to the multipotent neural crest. We found that the emergence of this epigenomic state requires the translocation of OCT4/SOX2 to tissue-specific cis-regulatory regions. By examining genome organization during the induction of hESCs into neural crest cells, we observed that the patterns of genomic occupancy of the dimer are modified during cell fate commitment. Dimer translocation is guided by neural crest-specific pioneer transcription factors, which physically interact with the OCT4/SOX to modify their genomic targets. Our results demonstrate how the ESC pluripotency program is repurposed in specialized stem cells to control chromatin organization and define the developmental potential of embryonic progenitors.

sample_organism:
Gallus gallus
Homo sapiens

platform_organism:
Gallus gallus
Homo sapiens

overall_design: There are four separate experiments in this submission. Groups 1-3 are for Human H1-derived cells transfected with either overexpression of TFAP2A or GFP and processed for RNA-Seq (Group 1), ATAC-Seq (Group 2), or Sox2 CUT&RUN (Group3). Group 4 - We electroporated chicken embryos with a TFAP2AE1-driven GFP reporter, which marks neural crest. We isolated GFP- Whole embryo cells via FACS from various stages across early chicken development, and subjected them to OMNI-ATAC-Seq

first: Austin

last: Hovland

first: Debadrita

last: Bhattacharya

first: Megan

last: Rothstein


title: OCT4-SOX2 dimers reshape the epigenome to promote neural crest multipotency [CUT&RUN]

overall_design: CUT&RUN


title: A novel lineage of RORγt+ antigen presenting cells instructs microbiota-dependent regulatory T cell differentiation and tolerance during early life [multiome scRNA-seq]

first: Chrysothemis

last: Brown

department: Immunology Program, Sloan Kettering Institute

institute: Memorial Sloan Kettering Cancer Center

summary: Tolerance to self- or innocuous foreign antigens is vital for preservation of organismal health. Within the thymus, medullary thymic epithelial cells (mTECs) expressing AutoImmune Regulator, Aire, play a critical role in self-tolerance through deletion of autoreactive T cells and promotion of thymic regulatory T (Treg) cell development. A second wave of Treg cell differentiation occurs in the periphery, upon exposure to dietary and commensal microbiota derived antigens within the first few weeks of life, yet the cell types responsible for the generation of peripheral Treg (pTreg) cells are not known. Here we identified a new lineage of tolerogenic RORγt+ antigen-presenting cells (APC) with a hybrid dendritic cell (DC)-mTEC phenotype, dubbed Thetis cells (TCs), comprising 4 major sub-groups (TC I-IV), We uncovered a developmental wave of TCs within intestinal lymph nodes during a critical early life window, coincident with the wave of pTreg cell differentiation. While Aire+ TC I and III bore remarkable homology with Aire+ mTECs, including expression of tissue restricted self-antigens, TC IV lacked Aire expression and were enriched for molecules required for pTreg generation, including the TGF-β activating integrin αvβ8. Loss of either MHCII or Itgb8 expression by TCs led to a profound impairment in intestinal pTreg differentiation, with onset of intestinal inflammation. In contrast, MHCII expression by RORγt+ group 3 innate lymphoid cells (ILC3) and classical DCs was neither sufficient nor required for pTreg generation, further implicating TCs as the critical tolerogenic RORγt+ APC. Our studies reveal parallel pathways for establishment of tolerance to self and foreign antigen within the thymus and periphery, marked by involvement of shared cellular and transcriptional programs.

overall_design: Single cell multiome (ATAC + Gene Expression) sequencing of Lin–RORgt+MHCII+ cells from the mLN of 2-week-old Rorc_Venus-creERT2 pooled from 16 biological replicates.

first: Zakieh

last: Tayyebi


title: A novel lineage of RORγt+ antigen presenting cells instructs microbiota-dependent regulatory T cell differentiation and tolerance during early life


title: A novel lineage of RORγt+ antigen presenting cells instructs microbiota-dependent regulatory T cell differentiation and tolerance during early life [multiome scATAC-seq]

overall_design: Single cell multiome (ATAC + Gene Expression) sequencing of Lin–RORγt+MHCII+ cells from the mLN of 2-week-old Rorc_Venus-creERT2 mice pooled from 16 biological replicates.


title: OCT4-SOX2 dimers reshape the epigenome to promote neural crest multipotency [ATAC-Seq]

overall_design: There are three separate experiments in which we performed OMNI-ATAC-Seq. Group #1 - We electroporated chicken embryos with a TFAP2AE1-driven GFP reporter, which marks neural crest. We isolated GFP+ neural crest cells via FACS from various stages across early chicken development, and subjected them to OMNI-ATAC-Seq. Group #2 - We electroporated chicken embryos bilaterally. One side received a control vector (TFAP2AE1-GFP + empty PCI-H2B-RFP) and the other recieved an overexpression vector (TFAP2AE1-GFP +  PCI-OCT4-SOX2-H2B-RFP). We isolated GFP+/RFP+ cells from the control and treatment side of the embryos, and performed OMNI-ATAC-Seq on each sample. Group #3 - We generated induced neural crest (iNCCs) from hESC. Along their differentiation, we performed OMNI-ATAC-Seq at multiple timepoints.


title: A novel lineage of RORγt+ antigen presenting cells instructs microbiota-dependent regulatory T cell differentiation and tolerance during early life [Smart-seq2]

overall_design: SMART-seq2 single-cell RNA sequencing of Lin–RORγt+MHCII+ cells isolated from the mLN of 3-week-old Rorc_Venus-creERT2 mice in parallel with mLN Aire+ DCs and Aire+ mTECs from age-matched AireGFP mice.

first: Alexander

last: Rudensky

first: Christina

last: Leslie


title: Transcriptomic data from the liver of Ahr knockout mice

city: Seoul

first: Sang Geon

last: Kim

state: Seoul

address: San56-1, Sillim-dong, Kwanak-gu

department: College of Pharmacy

country: South Korea

institute: Seoul National University

summary: Alcoholic liver disease, which varies in severity from mild steatosis to cirrhosis and hepatitis, is one of the most prevalent chronic liver diseases worldwide. Excessive alcohol consumption remains the leading cause of ALD and alcohol-related complications and deaths. However, no medications have been developed to treat this disease and its pathogenesis remains elusive. Here, to understand alcohol-induced AhR activation in more detail, transcriptomic data was conducted using livers from mice subjected to either control or Lieber-DeCarli alcohol diets.

overall_design: Examination of RNA expression in the liver obtained from WT and Ahr HKO fed on Lieber-DeCarli alcohol liquid diet.

first: Y

first: S

middle: G


title: OCT4-SOX2 dimers reshape the epigenome to promote neural crest multipotency [RNA-Seq]

overall_design: RNA-seq.  We electroporated chicken embryos with a TFAP2AE1-driven GFP reporter, which marks neural crest. We isolated GFP+ neural crest cells and GFP- embryonic head cells from various stages across early chicken development, and subjected them to polyA RNA-selected stranded RNA-Seq library prep. These include all samples, some of which are excluded from the final analysis. An additional processed file, featureCountsFiltered.txt, has low-quality samples removed.


title: RNA-seq analysis about Pim-3 knocked out samples

status: Public on Sep 05 2022

city: Tianjin

first: Xuan

last: Zhao

state: Tianjin

address: No. 38 Tongyan Road, Haihe Education Park, Tianjin

department: State Key Laboratory of Medicinal Chemical Biology

country: China

institute: Nankai University

summary: Endogenous retroviruses (ERVs) are suppressed to maintain host genome stability and it’s regulatory mechanism remains unclear. To determine the restrain mechanism of MERVL, we knocked out Pim3 and analyzed the effect on the expression of transposable elements and coding genes. Our results show that Pim3 as a repressor of MERVL and 2-cell genes in ESCs. This study extends our understandings of the machanism by novel factors regulates MERVL.

overall_design: We knocked out Pim3 in E14 by CRISPR/Cas9 gene editing technology and performed RNA-seq analysis in order to exam the transcriptome after Pim3 knock out.

first: Xinyi

last: Lu

first: Xin

first: Jian

last: Shen


title: HBEGF-TNF induces a complex retinal pathology with macular degeneration hallmarks in human organoids

city: Leipzig

first: Jana

last: Schor

state: Saxony

address: Permoserstr. 15

department: Molecular Systems Biology

country: Germany

institute: Helmholtz Centre for Environmental Research

summary:
Methods: Profiles of individual human retinal organoids (HRO) at 150, 200 and 250 days of development days were treated for 10 days with HBEGF and TNF, and compared to solvent controls (CTRL). N=6 HROs per timepoint and variable. Single-end sequencing with 30 Mio reads per sample was performed at a length of 75 bases on HiSeq2500 (Illumina). The sequence reads that passed quality filters were analyzed at the transcripts level.
Results: Our data independently confirms that this protocol provides HROs with macular-like characteristics and shows low baseline variabilities for rods, cones and Müller glia. These features might be key for disease modeling, since most animal models lack a macula, and most other organoid protocols have low cone cell numbers. We found a significant reduction in the number of rod and cone photoreceptor cells after 10 days after HBEGF-TNF (HT) treatment. Specifically, some photoreceptors show pathologic changes, and some are apically displaced, with their nuclei protruding into or passing out of the retina. Histopathologic changes indicate photoreceptor extrusion of viable or dying cones and rods as a pathomechanism. Notably, photoreceptor displacement through the apical retinal border, and thus ectopy in the region of photoreceptor inner and outer segments, has been described in patients and animal models. In controls, photoreceptors were highly ordered, interspersed and interconnected with each other and with Müller glia processes, and these cell connections make up the outer limiting membrane. Upon HT, glial processes expanded in size, extended laterally along the retinal circumference, and replaced or covered photoreceptors over large areas – forming a seal-like glial scar. Taken together, HT induces photoreceptor degeneration via cell extrusion in conjunction with reactive gliosis, glial proliferation, retinal thickening/dyslamination, and glial seal-like scar formation, which reproduces a complex outer retinal atrophy. Interestingly, our transcriptome data revealed distinct gene expression patterns supporting our histological phenotype, specifically, cone and rod degeneration, reactive gliosis, glial proliferation, and photoreceptor cell extrusion.
Conclusions: We show that combined application of HBEGF and TNF, two neuropathology associated factors, is sufficient to induce a complex human retinal pathology. We discovered cone and rod cell extrusion as a pathomechanism for photoreceptor degeneration and a potential interrelationship with glial pathologies. Pharmacological inhibitor experiments support this, and PIEZO1 and MAPK signaling as untapped therapeutic targets, even for complex pathologies. Thus, our model provides mechanistic access to several pathologic processes as well as pathogenic functions of inflammation and biomechanics.

overall_design: Human retinal organoids transcript profiles of 150, 200 and 250 development days (Controls: CTRL), same time points were treated for 10 days with HBEGF and TNF, generated on HiSeq2500 (Illumina).

first: Ali

last: Yazbeck

first: Manuela

last: Völkner

first: Jörg

last: Hackermüller

first: Mike

middle: O

last: Karl


title: Integrative multi-omics landscape of fluoxetine action across 27 brain regions (single cell profiling for 2 regions)

status: Public on Sep 04 2022

city: Singapore

first: Nirmala

last: Arul Rayan

address: 60 Biopolis Street

country: Singapore

institute: Genome Institute of Singapore

summary: We constructed a comprehensive multi-omics map of the molecular effects of fluoxetine (an SSRI antidepressant) in 27 rat brain regions. We profiled gene expression (bulk RNA-seq, 210 datasets) and chromatin state (bulk chromatin immunoprecipitation sequencing (ChIP-seq) for the histone marker H3K27ac, 100 datasets) in a broad, unbiased panel of 27 brain regions across the entire rodent brain, in naive and fluoxetine-treated animals. We complemented this approach with single-cell RNA-seq (scRNA-seq) analysis of two brain regions (20 datasets). Remarkably, in the single-cell RNA-seq profiling we observed profound changes in the transcripts of hippocampal dorDG and venDG  (~500 DEGs in specific cell types). Using diverse integrative data analysis techniques we characterized the complex and multifaceted effects of fluoxetine on region-specific and cell-type-specific gene regulatory networks and pathways. We leveraged this atlas to identify fluoxetine-modulated genes and gene-regulatory loci, predict enriched motifs that suggest potential upstream regulators, and validate global mechanisms of fluoxetine action.

overall_design: To complement our multi-regional epigenome map, we used single cell RNA-seq to profile genome-wide fluoxetine-induced transcriptome changes in 2 hippocampal brain regions. Here we deposit these single cell RNA-seq profiles (2 regions, 2 treatment groups - Sham and Fluoxetine, 5 replicates; 30 MUX libraries, postQC- 3517 cells). To reduce the effects of inter-animal biological variation each RNA-seq sample was pooled from 3 animals (15 in Sham, 15 in FT; 30 animals in total).

first: Lim

last: Michelle

first: Shyam

last: Prabhakar


title: Mesenchymal stem cell administration changes transcriptomic profiles of non-inflamed lungs in mice.

city: Bialystok

first: Andrzej

last: Eljaszewicz

state: Podlaskie

address: Jana Kilinskiego 1

department: Centre for Regenerative Medicine

country: Poland

institute: Medical University of Bialystok

summary: Here, we report that intranasal administration of MSCs to non-inflamed lung microenvironment changed transcriptomic profiles compared to control group. We found 674 differentially regulated genes unique for the short-term model, while only 75 genes were unique for the prolonged observations, suggesting waning of the low-grade inflammation and active resolution in the longer time point. Moreover, we evaluated the enrichment of differentially expressed genes (DEGs) in the gene ontologies, signaling pathways, and mapped predicted interactions using clusterProfiler v.4.0.0. The normalized enrichment score (NES) analysis indicated activation of the innate and adaptive immune responses. More precisely, the analysis of activation canonical pathways in Ingenuity Pathway Analysis (IPA) software revealed the increase in IL-7 signaling, T and B cell signaling in the short- and long-term models compared to controls. In addition to this observation, we noted gradual downregulation in HIF1α signaling, IL-17 signaling, and B cell receptor signaling in the longer time-point. Furthermore, the analysis of expression of genes clustered to the terms and processes related to airway inflammation, namely Th1-, Th2-, Th17- driven immune responses development, tight junction molecules, and mucins, revealed a relatively low number of significantly changed genes. Next, we analyzed deeper the expression profiles of genes related to oxidative stress and immune responses, focusing on macrophages activation and phagocytosis. We noted the dysregulated expression of pattern recognition receptors (PRRs) macrophage activation, oxidative stress, phagocytosis, and inflammation of the respiratory system. Furthermore, we analyzed the most significant genes with altered z-scores at the investigated time-points according to the Ingenuity Pathway Analysis. We observed a trend in a longitudinal decrease in the expression of the shared genes. This study provides a new knowledge regarding a changes in lung transcriptomic profiles in mice administrated with adipose tissue- derived MSCs.

overall_design: Female 6-8-week-old C57BL/6 mice were divided into three groups. Mice were sacrificed after 2 (short-term) and 9 (long-term) days from adipose-tissue-derived MSCs administration intranasally. Biological material was collected and biobanked for further analysis.

first: Marlena

last: Tynecka

first: Adrian

last: Janucik

first: Magdalena

last: Niemira

first: Arkadiusz

last: Żbikowski

first: Nino

last: Stocker

first: Agnieszka

last: Tarasik

first: Aleksandra

last: Starosz

first: Kamil

last: Grubczak

first: Anna

last: Szalkowska

first: Urszula

last: Korotko

first: Joanna

last: Reszec

first: Miroslaw

last: Kwasniewski

first: Adam

last: Kretowski

first: Cezmi

last: Akdis

first: Milena

last: Sokolowska

first: Marcin

last: Moniuszko


title: Integrative multi-omics landscape of fluoxetine action across 27 brain regions

first: Nirmala

last: Arul Rayan

summary: We constructed a comprehensive multi-omics map of the molecular effects of fluoxetine (an SSRI antidepressant), in 27 rat brain regions. We profiled gene expression (bulk RNA-seq, 210 datasets) and chromatin state (bulk chromatin immunoprecipitation sequencing (ChIP-seq) for the histone marker H3K27ac, 100 datasets) in a broad, unbiased panel of 27 brain regions across the entire rodent brain, in naive and fluoxetine-treated animals. We complemented this approach with single-cell RNA-seq (scRNA-seq) analysis of two brain regions. Using diverse integrative data analysis techniques we characterized the complex and multifaceted effects of fluoxetine on region-specific and cell-type-specific gene regulatory networks and pathways. Remarkably, we observed profound molecular changes across the brain (>4,000 differentially expressed genes and differentially acetylated ChIP-seq peaks each) that were highly region-dependent. We leveraged this atlas to identify fluoxetine-moduated genes and gene-regulatory loci, predict enriched motifs that suggest potential upstream regulators, and validate global mechanisms of fluoxetine action.

overall_design: To complement our multi-regional transcriptome map, we used H3K27ac ChIP-seq to profile genome-wide fluoxetine-induced histone acetylation changes in 27 brain regions. Here we deposit these ChIP-seq profiles (27 regions, 2 treatment groups - Sham and Fluoxetine, 2 replicates; 27*4 = 108 chromatin profiles before QC, 106 post-QC). To reduce the effects of inter-animal biological variation each ChIP sample was pooled from 10 animals (20 in Sham, 20 in FT; 40 animals in total).  H3K27ac profiling was chosen as this histone mark is the most well-studied acetylation signature of active regulatory elements such as enhancers and promoters.

first: Vibhor

last: Kumar

first: Shyam

last: Prabhakar


title: Angel2 phosphatase activity is required for non-canonical mitochondrial RNA processing in metazoa

city: Perth

first: Stefan

last: Siira

state: Western Australia

address: 15 Hospital Ave, Nedlands

department: Precision Health

country: Australia

institute: The Kids Research Institute Australia

summary: Canonical RNA processing in mammalian mitochondria necessitates that tRNAs are recognised by nucleases to release flanking transcripts. However, not all mitochondrial transcripts are punctuated by tRNAs, and the mechanism and factors involved in their processing has remained unsolved. Here, we demonstrate that phosphatase activity of the carbon catabolite repressor 4 domain containing family member ANGEL2 is required for the hydrolysis of 3′ phosphates, resulting from non-canonical processing. Interaction studies in Drosophila further identify that members of the FAST kinase domain containing protein family are involved in the formation of these 3′ phosphates. Our results therefore resolve the mechanism of RNA processing in metazoan mitochondria, by defining the outstanding non-canonical processing mechanism.

overall_design: Ribosome profiling of two AngelKO and two wild-type samples from Drosophila melanogaster, in technical quadruplicate

first: Paula

last: Clemente

first: Javier

last: Calvo-Garrido

first: Sarah

middle: F

last: Pearce

first: Florian

last: Schober

first: Megumi

last: Hamasaki

first: Isabelle

last: Laine

first: Henrik

last: Spåhr

first: Yohei

last: Kirino

first: Rolf

last: Wibom

first: Oliver

last: Rackham

last: FIlipovska

last: Rorbach

first: Christoph

last: Freyer

last: Wredenberg


title: ChIP-seq analysis about Hdac4/5 samples

first: Xuan

last: Zhao

summary: To identify whether Hdac4/5 were enriched in MuERVL directly, we performed Hdac4/5 ChIP-seq with anti-Hdac4/5 antibody in wildtype ESCs. we conclude that Hdac4/5 binding were enriched on MuERVL-int region and weakly enriched on MT2, suggesting a direct regulatory role of Hdac4/5 on MuERVL expression.

overall_design: We carried out Hdac4/5 ChIP-seq with anti-Hdac4/5 antibody in wildtype ESCs in order to  identify whether Hdac4/5 were enriched in MuERVL. We performed two biological replicates of ChIP-seq for HDAC4/5 respectively.

first: Xinyi

last: Lu

first: Xin

first: Jian

last: Shen


title: Transcriptome analysis of brain microglia

city: Chongqing

first: jiangyong

last: he

address: Tiansheng Li Street of Beibei District

institute: southwest university

summary: the scRNA-seq data for exploring the heterogenity of zebrafish brain microglia are listed in below

overall_design: the 200 zebrafish brains are collected as a sample to dissect and sort coro1a-DsRed+ cells to perform 10X genomic ananlysis

first: F

middle: Y

first: J

last: He

first: L

last: Li


title: Influenza A virus activates Tropomyosin receptor kinase A (TrkA) signaling to promote viral replication and lung inflammation

city: Saint Paul

first: Yuying

last: Liang

state: MN

address: 1988 Fitch Avenue, Room 295 AS/VM

institute: University of Minnesota

summary: Influenza A virus (IAV) infection causes acute respiratory disease with potential severe and deadly complications. Viral pathogenesis is not only due to the direct cytopathic effect of viral infections but also to the exacerbated host inflammatory responses. Influenza viral infection can activate various host signaling pathways that function to activate or inhibit viral replication. Our previous studies have shown that a receptor tyrosine kinase TrkA plays an important role in the replication of influenza viruses in vitro, but its biological roles and functional mechanisms in influenza viral infection have not been characterized. Here we show that IAV infection strongly activates TrkA in vitro and in vivo. Using a chemical-genetic approach to specifically control TrkA kinase activity through a small molecule compound 1NMPP1 in a TrkA knock-in (TrkA KI) mouse model, we show that 1NMPP1-mediated TrkA inhibition completely protected mice from a lethal IAV infection by significantly reducing viral loads and lung inflammation. Using primary lung cells isolated from the TrkA KI mice, we show that specific TrkA inhibition reduced viral RNA synthesis in airway epithelial cells (AECs) but not in alveolar macrophages (AMs). Transcriptomic analysis confirmed the cell-type-specific role of TrkA in viral RNA synthesis, and identified distinct gene expression patterns under the TrkA regulation in IAV-infected AECs and AMs. Among the TrkA-activated targets are various proinflammatory cytokines and chemokines such as IL6, IL-1, IFNs, CCL-5, and CXCL9, supporting the role of TrkA in mediating lung inflammation. Indeed, TrkA inhibitor 1NMPP1 administered after the peak of IAV replication, though had no effect on viral load, was able to decrease lung inflammation and provide partial protection in mice. Taken together, our results have demonstrated for the first time an important biological role of TrkA signaling in IAV infection, identified its cell-type-specific contribution to viral replication, and revealed its functional mechanism in virus-induced lung inflammation. This study suggests TrkA as a novel host target for therapeutics against influenza viral disease.

overall_design: To characterize the cell-type-specific role of the TrkA signaling in influenza A Virus (IAV) infection, we conducted transcriptomic analysis of virus-infected Alveolar epithelial cells (AECs) and alveolar macrophages (AMs) with or without the TrkA inhibition. Primary AECs and AMs seeded on 6-well plates were subjected to three treatments: mock infection, A/WSN infection (MOI=10), and A/WSN infection (MOI=10) in the presence of 1NMPP1 (10 µm), each in triplicates. Total RNAs at 10 hpi were stored in RNAlater and submitted to University of Minnesota Genomic Center (UMGC) for RNA extraction, mRNA enrichment, library construction, and RNA-sequencing.

first: Vikram

last: Verma

first: Mythili

last: Dileepan

first: Thu

last: Phan

first: Wei-Shou

last: Hu

first: Hinh

last: Ly


title: RNA-seq for cell populations from blastocyst seeding in pig

first: Chang-Kyu

last: Lee

address: 1 Gwanak-ro, Gwanak-gu

department: Department of Agricultural Biotechnology

summary: RNA sequencing data from blastocyst seeding in pig. Four types of cell population were produced from single protocol.

overall_design: Expression profiling of four cell types originated from blastocyst seeding experiment. Triplicates for each type

first: Jong-Nam

last: Oh

first: Jinsol

last: Jung

first: Mingyun

first: Gyung

middle: C

last: Choe

first: Seung-Hun

last: Kim

first: Kwang-Hwan

last: Choi

first: Dong-Kyung


title: Examining RNA Transcript Changes in Stem Cells Undergoing Differentiation, Using Short and Long Reads Sequencing Technologies [Illumina short reads]

city: Rehovot

first: Bareket

last: Dassa

address: 234 Herzl st.

department: Life Sciences Core Facilities

country: Israel

institute: Weizmann Institute of Science

summary: We explored changes at gene-level or transcript-level in embryonic stem cells, before and after in vitro differentiation with retinoic acid. RNA was sequenced both via Illumina short reads, and with Oxford Nanopore Technology with cDNA and direct RNA sequencing.

overall_design: Mouse embryonic stem cells were grown for 4 days in mES growth medium (DMEM, 15% FBS, L-Glutamine, Non-Essential Amino Acids) were harvested and named sample "undiff". Cells after additional treatmeant for 4 days with 2microM Retinoic Acid were harvested and named "day4". RNA was extracted and prepared for both Illumina TruSeq Strand Specific sequencing, and to nanopore cDNA and direct RNA sequencing.

first: Dena

last: Leshkowitz

first: Merav

last: Kedmi

first: David

last: Pilzer

first: Yael

last: Fried

first: Hadas

last: Keren-Shaul

first: Elena

last: Ainbinder


title: Examining RNA Transcript Changes in Stem Cells Undergoing Differentiation, Using Short and Long Reads Sequencing Technologies [Nanopore long reads]

overall_design: Mouse embryonic stem cells were grown for 4 days in mES growth medium (DMEM, 15% FBS, L-Glutamine, Non-Essential Amino Acids) were harvested and named sample "undiff". Cells after additional treatmeant for 4 days with 2microM Retinoic Acid were harvested and named "day4". RNA was extracted and prepared for Illumina TruSeq Strand Specific sequencing, and to nanopore cDNA and direct RNA sequencing.


title: Gene expression profile at single cell level of Bronchoalveolar Lavage fluid (BALF) cells from mice

status: Public on Sep 03 2022

city: OMAHA

first: Meng

last: Niu

state: NE

address: 42nd and Emile

department: Department of Neurological sciences

institute: University of Nebraska Medical Center

summary: Bronchoalveolar Lavage cells include resident and infiltrating immune cells in repsone to infections. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of BALF cells.

overall_design: BALF cells in mice were isolated and analyzed using scRNAseq.

first: Keer

last: Sun


title: Deciphering transcriptome alterations in bone marrow hematopoiesis at single-cell resolution in immune thrombocytopenia

city: Jinan

first: Yan

last: Liu

state: Shandong

address: 107 West Wenhua Rd, Lixia

department: Department of Hematology

institute: Qilu Hospital, Cheeloo College of Medicine, Shandong University

summary:
Purpose and Methods: Immune thrombocytopenia (ITP), an autoimmune disorder, is mainly caused by megakaryocyte dysfunction, although the underlying mechanisms remain unclear. Here, we performed single-cell transcriptome profiling of bone marrow (BM) CD34+ hematopoietic stem and progenitor cells (HSPCs) to determine defects in megakaryopoiesis in ITP.
Results: Gene expression, cell-cell interactions, and transcriptional regulatory networks varied in HSPCs of ITP, particularly in natural killer/T cell progenitors and a pre-B cell subset, highlighting the selective immune aberratixon associated with defective megakaryopoiesis in ITP. CD9 can be used to enrich megakaryocyte-biased HSPCs, and CD9+Lin−CD34+CD45RA− HSPCs have the potential to be novel diagnostic and therapeutic targets in ITP. Further analysis revealed that megakaryocytic progenitors (MkP) can be divided into seven subclusters with different gene expression patterns and functions. The ITP-associated DEGs were MkP subtype-specific, with most DEGs concentrated in the subcluster possessing dual functions of immunomodulation and platelet generation.
Conclusions: This study comprehensively dissects defective hematopoiesis and provides novel therapeutic targets for ITP.

overall_design: We performed scRNA-seq of BM CD34+ HSPCs from four newly diagnosed treatment-naïve ITP patients and four healthy donors on the 10X Chromium platform to determine the megakaryopoiesis defects in ITP.

first: Xinyi

last: Zuo

first: Peng

last: Chen

first: Shihui

last: Ma

first: Shuwen

last: Wang

first: Jun

last: Peng


title: P300-mediated adaptive conversion of glioma stem cells to vascular-like cells in response to therapeutic stress promotes tumor recurrence [ATAC_SeqIRC646]

status: Public on Sep 09 2022

first: Riki

last: Kawaguchi

address: 760 Westwood Plaza, Room 37-420

department: Department of Psychiatry and Neurology Department of Psychiatry

institute: University of California, Los Angeles

summary: Purpose: The goal of the experiment is to determine chromatin accessibility changes induced by radiation and treatment with P300 HAT inhibitor C646 in gliomaspheres by ATAC-sequencing

overall_design: ATAC-sequencing of control and 2-day radiated gliomaspheres treated with or without C646

first: Sree

middle: D

last: Muthukrishnan

first: Harley

last: Kornblum


title: Integrative multi-omics landscape of fluoxetine action across 27 brain regions [bulk RNA-seq]

first: Nirmala

last: Arul Rayan

overall_design:
To complement our multi-regional epigenome map, we used bulk RNA-seq to profile genome-wide fluoxetine-induced transcriptome changes in 27 brain regions. Here we deposit these RNA-seq profiles (27 regions,2 treatment groups - Sham and Fluoxetine, 4 replicates; 27*8= 216 profiles, postQC- 210 RNAseq datasets). To reduce the effects of inter-animal biological variation each RNA-seq sample was pooled from 10 animals (40 in Sham, 40 in FT; 80 animals in total).
Some samples lack raw data due to file corruption.

first: Vibhor

last: Kumar

first: Shyam

last: Prabhakar

first: Michael

last: Meaney


title: Transcriptomic analysis of the rpn12a-236 stay-green mutant

status: Public on Sep 02 2022

city: Umea

first: Clement

last: Boussardon

address: Umeå Plant Science Centre Department of Plant Physiology Umeå University

department: Plant Physiology

country: Sweden

institute: Umeå Plant Science Centre

summary: The 19S proteasome mutant rpn12a-236 exhibits a stay-green phenotype upon individually darkened leaf treatment (IDL). To gain insight into the molecular mechanisms conferring this extended longevity to rpn12a-236 in response to darkness, we performed RNA-seq analysis on WT and mutant leaves sampled after 0 hour (light control), 6 hours, 1 day, 3 days and 6 days of IDL treatment.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for Col-0 WT plants and rpn12a-236 EMS mutant during IDL

first: Olivier

last: Keech

first: Nicolas

last: Delhomme


title: Transcriptome changes induced by perturbed expression of circRNA hsa_circ_0062682 in HCC cell lines

city: LJubljana

first: Tadeja

last: Rezen

address: Vrazov trg 2

department: Faculty of Medicine

country: Slovenia

institute: University of Ljubljana

summary:
Circular RNAs (circRNAs) have been shown to play an important role in the pathogenesis of hepatocellular carcinoma (HCC). By implementing available transcriptomic analyses of HCC patients, we identified an upregulated circRNA hsa_circ_0062682. The aim of the study was to evaluate the oncogenic potential of this circRNA in HCC model cell lines.
Using  microarrays we evaluated the transcriptome changes induced by perturbation of circRNA expression.

overall_design: We have performed a transient overexpression of hsa_circ_0062682 in Huh-7 and generated a stable knockdown of hsa_circ_0062682 in SNU-449 cell lines.

first: Rok

last: Razpotnik

last: Režen


title: Role of ZNF281 in intestinal fibroblast activation: new insights in IBD-related fibrosis

city: Roma

first: valerio

last: fulci

address: Vle regina Elena, 324

department: Dipartimento di Medicina Molecolare

institute: Università i Roma "La Sapienza"

summary:
Serious complications of Crohn’s disease (CD), a form of Inflammatory Bowel Disease (IBD), involve the formation of intestinal fibrotic stenosis followed by obstruction. Chronic inflammatory state activates resident fibroblasts and myofibroblasts, that are the key effector cells in fibrosis, being responsible for the synthesis of ECM proteins.
Exposure of human colon fibroblasts (CCD18-Co) to the pro-fibrotic cytokine TGF-β1 is sufficient to induce the expression of genes associated with myofibroblast features such as cell migration, ECM remodeling and contraction. Furthermore, during TGFβ1-mediated myofibroblast differentiation, the transcription factor ZNF281 is increased and is required to reshape the expression of genes encoding for myofibroblast markers, suggesting an active role for ZNF281 as a master regulator of intestinal myofibroblast functions.

overall_design: 12 samples

first: Valerio

last: Fulci

first: Ilaria

last: Laudadio

first: Laura

last: Stronati


title: Potential Methylation-regulated Genes and Pathways in Hepatocellular Malignant Neoplasm, Not Otherwise Specified (EPIC850)

city: Los Angeles

first: Shengmei

last: Zhou

address: 4650 Sunset Blvd.

department: Pathology and Laboratory Medicine

institute: Children's Hospital Los Angeles

summary: genome-wide profiling of DNA methylation (EPIC850) was performed on 4 pairs of pre-treatment HCN-NOS tumors and adjacent non-tumor controls.

overall_design: Bisulphite converted DNA from the 8 samples were hybridised to the Illumina Infinium MethylationEPIC BeadChip array

first: Meng

last: Li

first: Dejerianne

last: Ostrow

first: David

last: Ruble

first: Leo

last: Mascarenhas

first: Bruce

last: Pawel

first: Jonathan David

last: Buckley

first: Timothy J

last: Triche


title: Examining RNA Transcript Changes in Stem Cells Undergoing Differentiation, Using Short and Long Reads Sequencing Technologies

first: Bareket

last: Dassa

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

overall_design: Refer to individual Series


title: Potential Methylation-regulated Genes and Pathways in Hepatocellular Malignant Neoplasm, Not Otherwise Specified (RNA-seq)

summary: genome-wide profiling of gene expression (RNAseq) was performed on 4 pairs of pre-treatment HCN-NOS tumors and adjacent non-tumor controls.

overall_design: Examination of differentially expressed genes between tumors and controls.


title: Integrated genomic, transcriptomic and metabolomic analysis reveals MDH2 mutation-induced metabolic disorder in recurrent focal segmental glomerulosclerosis

city: Hangzhou

first: QIXIA

last: SHEN

state: Zhejiang

address: Qinchun Rd.79, Hangzhou

institute: The first affiliated hospital, Hangzhou, China

summary: Focal segmental glomerulosclerosis (FSGS) has an over 30% risk of recurrence after kidney transplantation (Ktx) and is associated with an extremely high risk of graft loss. However, mechanisms remain largely unclear. Thus, this study identifies novel genes related to the recurrence of FSGS (rFSGS). Whole genome-wide sequencing and next-generation RNA sequencing were used to identify the candidate mutant genes associated with rFSGS in peripheral blood mononuclear cells (PBMCs) from patients with biopsy-confirmed rFSGS after KTx. To confirm the functional role of the identified gene with the MDH2 c.26C >T mutation, a homozygous MDH2 c.26C >T mutation in HMy2.CIR cell line was induced by CRISPR/Cas9 and co-cultured with podocytes, mesangial cells, or HK2 cells, respectively, to detect the potential pathogenicity of the c.26C >T variant in MDH2. A total of 32 nonsynonymous single nucleotide polymorphisms (SNPs) and 610 differentially expressed genes (DEGs) related to rFSGS were identified. DEGs are mainly enriched in the immune and metabolomic-related pathways. A variant in MDH2, c.26C >T, was found in all patients with rFSGS, which was also accompanied by lower levels of mRNA expression in PBMCs from relapsed patients compared with patients with remission after KTx. Functionally, co-cultures of HMy2.CIR cells overexpressing the mutant MDH2 significantly inhibited the expression of synaptopodin, podocin, and F-actin by podocytes compared with those co- cultured with WT HMy2.CIR cells or podocytes alone. We identified that MDH2 is a novel rFSGS susceptibility gene in patients with recurrence of FSGS after KTx. Mutation of the MDH2 c.26C >T variant may contribute to progressive podocyte injury in rFSGS patients.

overall_design: Three healthy kidney donors (HC group) and six adult patients with biopsies confirming primary FSGS were enrolled in this study. Of them, three recurred after KTx within one month (RC group) and three had remission for as long as 2 to 5 years (RM group). Whole blood was collected from them, peripheral blood mononulear cells were isolated and use d for RNA-sequencing.

first: Qixia

last: Shen

first: Luying

last: Guo

first: Hongfeng

last: Huang

first: Jianghua

last: Chen

first: Hong

last: Jiang


title: Transcriptomic profiling of cardiac tissues from SARS-CoV-2 patients identifies DNA damage

city: brisbane

first: Arutha

last: Kulasinghe

address: 37 kent st

institute: University of Queensland

summary: In this study, we investigated the landscape of cardiac tissues collected at rapid autopsy from 7 SARS-CoV-2, 2 pH1N1, and 6 control patients using targeted spatial transcriptomics approaches. The main outcomes for the study were to profile rapid autopsy samples collected from the COVID-19, pH1N1 and normal, non-viral deaths to determine transcriptional changes between the different cohorts. Although SARS-CoV-2 was not detected in cardiac tissue, host transcriptomics showed upregulation of genes associated with DNA damage and repair, heat shock, and M1-like macrophage infiltration in the cardiac tissues of COVID-19 patients. The DNA damage present in the SARS-CoV-2 patient samples, were further confirmed by g-H2Ax immunohistochemistry. In comparison, pH1N1 showed upregulation of Interferon-stimulated genes (ISGs), in particular interferon and complement pathways, when compared with COVID-19 patients.

sample_organism:
Homo sapiens
blank sample

platform_organism:
Homo sapiens
blank sample

overall_design: In this dataset, we capture GeoMx DSP RNA profiles of myocardial tissue from SARS-CoV2 infected patients aswell as pH1N1 and control specimens

first: A

first: C

middle: W

last: Tan


title: Single-cell RNA transcriptome analysis of murine male and female forebrain tissue after recovery from West Nile virus encephalitis

status: Public on Sep 01 2022

city: St Louis

first: Sarah

last: Rosen

state: MO

address: 320 S. Euclid Ave.

department: Infectious Diseases

institute: Washington University School of Medicine

summary: Single-cell RNA-seq analysis of cortex and hippocampus tissue from murine males and females after recovery from West Niles virus encephalitis

overall_design: Murine cortical and hippocampal tissue was obtained and cells isolated and sequenced at 25 days after intracranial infection with 10^4 PFU of WNV-NS5-E218A

first: Robyn

last: Klein


title: OCT4-SOX2 dimers reshape the epigenome to promote neural crest multipotency

city: Ithaca

first: Marcos

last: Simoes-Costa

address: 526 Campus Rd

department: Molecular Biology and Genetics

institute: Cornell University


title: Chemotherapy-induced complement signaling modulates immunosuppression and metastatic relapse in breast cancer [RNA-seq]

city: Tel Aviv

first: Nour

last: Ershaid

state: Israel

address: Postal code 2373,

institute: Tel Aviv University

summary: Mortality from breast cancer is almost exclusively a result of tumor metastasis and resistance to therapy and therefore understanding the underlying mechanisms is an urgent challenge. Chemotherapy, routinely used to treat breast cancer, induces extensive tissue damage, eliciting an inflammatory response that may hinder efficacy and promote metastatic relapse. Here we show that systemic treatment with chemotherapy following resection of a triple-negative breast tumor induced the expression of complement factors in lung fibroblasts and modulated an immunosuppressive metastatic niche that supported lung metastasis. CAF-derived complement signaling mediated the recruitment of myeloid-derived suppressor cells (MDSCs) to the metastatic niche, thus promoting T cell dysfunction. Functionally, we show that pharmacological targeting of complement signaling in combination with chemotherapy alleviated immune dysregulation and attenuated lung metastasis. Our findings suggest that combining cytotoxic treatment with blockade of complement signaling in triple-negative breast cancer patients may attenuate the adverse effects of chemotherapy, thus offering a promising approach for clinical use.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for fibroblasts isolated from early stage metastatic lungs of mice treated with doxorubicin (Dox n=5) or saline as control (Pbs, n=4).

first: Lea

last: Monteran

first: Hila

last: Doron

first: Yael

last: Zait

first: Yeela

last: Scharff

first: Shahar

last: Ben-Yosef

first: Camila

last: Avivi

first: Iris

last: Barshack


title: Single-nucleus RNA sequencing of the mouse hypothalamus in the fed and fasted state

city: Cambridge

first: Brian

middle: Yee Hong

last: Lam

address: Box 289 Addenbookes Hospital, Hills Road

department: Metabolic Research Laboratories

institute: University of Cambridge

summary:
To provide a summary of cells within the mouse hypothalamus in the fed and fasted state, we performed single nucleus RNA sequencing on 12 mice fed ad libitum, and 6 mice that were fasted overnight.
Hypothalami were dissected and stored at -80ºC overnight. The next day single nucleus supensions were made, pooling together hypothalamic from the same feeding condition (2 x ad libitum prepared on separate days; 1 x overnight fast). Susepensions were FACS sorted for DRAQ5 positive events. Single nucleus RNA sequencing libraries were generated using the 10X Chromium single cell 3' reagents.

overall_design: The hypothalamus was dissected from 12 adlib fed (2 cohorts) and 6 overnight (16 hr) fasted mice, and a single nucleus suspension was created using a dounce homogenizer and purified using FACS, sorting for DRAQ5 positive events. These samples (2 adlib fed and 1 overnight fasted) were submitted for single nucleus RNA sequencing

first: Georgina

last: Dowsett

first: Sara

middle: N

last: Khonke

first: Giles

last: Yeo


title: RNA-seq and ChIP-seq in subcutaneous white adipoce tissue cells

city: Tokyo

first: Juro

last: Sakai

address: 4-6-1, Komaba, Meguro-ku

department: Division of Metabolic Medicine

country: Japan

institute: Research Center for Advanced Science and Technology, The University of Tokyo


title: Genome-wide analysis of JMJD1A binding in immortalized subcutaneous white adipose tissue cells.

summary: Protein kinase A promotes beige adipogenesis downstream from β-adrenergic receptor signaling by phosphorylating proteins, including histone H3 lysine 9 (H3K9) demethylase JMJD1A. To ensure homeostasis, this process needs to be reversible however, this step is not well understood. We show that myosin phosphatase target subunit 1- protein phosphatase 1β (MYPT1-PP1β) phosphatase activity is inhibited via PKA-dependent phosphorylation, which increases phosphorylated JMJD1A and beige adipogenesis. Mechanistically, MYPT1-PP1β depletion resulted in JMJD1A-mediated H3K9 demethylation and activation of the Ucp1 enhancer/promoter regions. Interestingly, MYPT1-PP1β also dephosphorylates myosin light chain which regulates actomyosin tension-mediated activation of YAP/TAZ which directly stimulates Ucp1 gene expression. Preadipocyte specific Mypt1 deficiency increases cold tolerance with higher Ucp1 levels in subcutaneous white adipose tissues compared to control mice, confirming this regulatory mechanism in vivo. Thus, we have uncovered new regulatory cross-talk involved in beige adipogenesis that coordinates epigenetic regulation with direct activation of the mechano-sensitive YAP/TAZ transcriptional co-activators.

overall_design: Preadipocytes derived from inguinal subcutaneous white adipose tissue were immortalized. Preadipocytes were differentiated for ChIP-seq analysis of JMJD1A using Illumina HiSeq 2500.

first: Yoshihiro

last: Matsumura


title: Transcriptome Analysis of Oxytocin-Treated Human Induced Pluripotent Stem Cell-Derived Epicardial Cells

city: East Lansing

first: Aitor

last: Aguirre

state: MI

address: 775 Woodlot Dr

department: Biomedical Engineering

institute: Michigan State University

summary: Cardiovascular disease (CVD) is one of the leading causes of mortality worldwide, and frequently leads to massive heart injury and the loss of billions of cardiac muscle cells and associated vasculature.  Critical work in the last two decades demonstrated that these lost cells can be partially regenerated by the epicardium, the outermost mesothelial layer of the heart, in a process that highly recapitulates its role in heart development.  Upon cardiac injury, mature epicardial cells activate and undergo an epithelial-mesenchymal transition (EMT) to form epicardial-derived progenitor cells (EpiPCs), multipotent progenitors that can differentiate into several important cardiac lineages, including cardiomyocytes and vascular cells.  In mammals, this process alone is insufficient for significant regeneration, but it may be possible to prime it by administering specific reprogramming factors, leading to enhanced EpiPC function. Here, we compared changes in gene expression induced by oxytocin in epicardial cells to determine potential pro-regenerative effects.

overall_design: RNA sequencing of hiPSC-derived epicardial cells treated with and without oxytocin

first: Aaron

middle: H

last: Wasserman


title: Aging is associated with increased chromatin accessibility and reduced polymerase pausing in liver [NET-seq]

city: Cologne

first: Peter

last: Tessarz

state: Nordrhein-Westfalen

address: Joseph-Stelzman-Str 9b

institute: Max Planck Institute

summary: Regulation of gene expression is linked to the organization of the genome. With age, chromatin alterations occur on all levels of genome organization, accompanied by changes in the gene expression profile. However, little is known about the changes on the level of transcriptional regulation. Here, we used a multi-omics approach and integrated ATAC-, RNA- and NET-seq to identify age-related changes in the chromatin landscape of murine liver and to investigate how these are linked to transcriptional regulation. We provide the first systematic inventory of the connection between aging, chromatin accessibility and transcriptional regulation in a whole tissue. Aging in murine liver is characterized by an increase in chromatin accessibility at promoter regions, but not in an increase of transcriptional output. Instead, aging is accompanied by a decrease of promoter-proximal pausing of RNA polymerase II (Pol II), while initiation of transcription is not decreased as assessed by RNA polymerase mapping using CUT&RUN. Based on the data reported we propose that these age-related changes in transcriptional regulation are due to a reduced stability of the pausing complex.

overall_design: tNET-seq of murine liver tissue using 3 biological replicates per age group and 3 age groups (3, 12, 18 months)

first: Mihaela

last: Bozukova

first: Chrysa

last: Nikopoulou

first: Niklas

last: Kleinenkuhnen

first: Dora

last: Grbavac

first: Katrin

last: Goetsch


title: Aging is associated with increased chromatin accessibility and reduced polymerase pausing in liver [ATAC-seq]

overall_design: ATAC-seq of murine liver tissue using 3 biological replicates from 3-month-old mice and 3(+1) biological replicates from 18-month old mice; for the latter, two different liver lobules were used as two separate biological replicates, i.e. 3 old animals in total were used


title: Aging is associated with increased chromatin accessibility and reduced polymerase pausing in liver [CUT&RUN]

overall_design: CUT&RUN of murine liver tissue using 3 different antibodies (CTD, S2, S5) and 4 biological replicates per age group (3 and 18 months)


title: In vitro and In vivo analysis of gene expression changes in mouse neural progenitor cells derived from embryonic stem cells after exposure to specific molecules or grafting into traumatic spinal cord injury

city: Boston

first: Timothy

last: O'Shea

state: MA

address: 44 Cummington Mall, ERB Room 521

institute: Boston University

summary: Comparison of genomic data from neural progenitor cells derived from mouse embryonic stem cells under different experimetnal conditions in vitro and invivo. We conducted genome-wide RNA sequencing of immunoprecipitated specific ribosome-associated mRNA using RiboTag methods from: (i) mouse embryonic stem cell (ESC), (ii) derived neural progenitor cells, (iii) differentiated neural progenitor cells (in vitro), (iv) grafted neural progenitor cells (recovered from different in vivo tissue enivornments - healthy spinal cord, spinal cord injury lesions) and (v) host astrocytes using GFAp-Cre RiboTag mice.

overall_design: Mouse ESC were derived from the inner cell mass of E3.5 blastocyst stage embryos generated from crosses of male homozygous B6N.129-Rpl22tm1.1 Psam/J “Ribotag” mice to females hemizygous for a dominant, maternal effect cre allele, B6.Cg-Tg(SOX2-cre)1Amc/J and heterozygous for the “RiboTag” allele. NPC were derived by neural induction and expansion protocols. Neural progenitors were differenetaitatd in vitro for 4 days by removal of progenitor maintaing mitogens (EGF/FGF) and treatment with either CNTF, IGF-1 or FBS in different concentrations. NPC mRNA was recoveved using the RiboTag protocol. NPC were grafted into young adult mice that underwent severe crush SCI at thoracic level T10. NPC grafting was performed at 2 days after injury. NPC mRNA was recoveved using the RiboTag protocol at 5 and 14 days after injury.

first: Michael

middle: V

last: Sofroniew


title: Aging is associated with increased chromatin accessibility and reduced polymerase pausing in liver [RNA-seq]

overall_design: RNA-seq of murine liver tissue using 3 biological replicates per age group and 3 age groups (3,12  and 18 months)


title: Gene expression in stickleback (Apeltes quadracus) spine and fins

city: Stanford

first: David

last: Kingsley

address: 279 Campus Drive

department: Developmental Biology

institute: Stanford University

summary: Apeltes quadracus gene expression differences between developing spines and fins as assessed by RNA-seq

overall_design:
The spines and fins were individually dissected from Apeltes quadracus with 4 dorsal spines from Louisbourg population.  RNA was extracted to investigate gene expression differences between the different spines
The processed file also includes samples/data whose raw files have already been submitted under GSE184886 (which were analyzed in an allele specific manner), and contains non-allele specific processed data.

first: Julia

middle: I

last: Wucherpfennig


title: Aging is associated with increased chromatin accessibility and reduced polymerase pausing in liver


title: Aging is associated with increased chromatin accessibility and reduced polymerase pausing in liver [ChIP-Seq]

overall_design: ChIP-seq of SPT4 in murine liver tissue using 2 biological replicates per age group (3 and 18 months)


title: Velcrin-induced selective cleavage of tRNALeu(TAA) by SLFN12 causes cancer cell death [RNA-Seq]

first: Stephanie

last: Hoyt

address: 415 Main St

department: Cancer Program

institute: Broad Institute of MIT and Harvard

summary: Velcrin compounds kill cancer cells expressing high levels of phosphodiesterase 3A (PDE3A) and Schlafen family member 12 (SLFN12) by inducing complex formation between these two proteins, but the mechanism of cancer cell killing by the PDE3A–SLFN12 complex is not fully understood. Here, we report that the physiological substrate of SLFN12 RNase is tRNALeu(TAA). SLFN12 selectively digests tRNALeu(TAA), and velcrin treatment promotes the cleavage of tRNALeu(TAA) by inducing PDE3A–SLFN12 complex formation in vitro. We found that distinct sequences in the variable loop and acceptor stem of tRNALeu(TAA) are required for substrate digestion. Velcrin treatment of sensitive cells results in downregulation of tRNALeu(TAA), ribosome pausing at Leu-TTA codons and global inhibition of protein synthesis. Velcrin-induced cleavage of tRNALeu(TAA) by SLFN12 and the concomitant global inhibition of protein synthesis thus define a new mechanism of apoptosis initiation.

overall_design: Ribosome profiling of Hela cells treated with DMSO control or DNMDP in duplicate

first: Sooncheol

last: Lee

first: Xiaoyun

last: Wu

first: Colin

last: Garvie

first: Joseph

last: McGaunn

first: Andrew

last: Cherniack

first: Matthew

last: Meyerson

first: Heidi

last: Greulich


title: The quantitative analysis of transcriptomes derived from malignant rhabdoid tumor cells treated with EZH1/2 dual inhibitor or EZH2 selective inhibitor

first: Haruka

last: Shinohara

address: 5-1-1 Tsukiji, Chuo-ku

institute: National Cancer Center Research Institute

summary: We found that both EZH1 and EZH2 contributes to cell growth and H3K27 methylation, and EZH1/2 dual inhibitors induce growth inhibition in malignant rhabdoid tumor (MRT). To investigate the molecular mechanism underlying the growth inhibition of EZH inhibitors in MRT cells, we performed RNA-sequencing analysis and compared differentially expressed genes between A204.1 cells treated with EZH1/2 dual inhibitor DS-3201b or EZH2 selective inhibitor EPZ-6438.

overall_design: The comparisons of transcriptomes among EZH inhibitors (DS-3201b or EPZ-6438)-treated and non-treated (Control) A204.1 or TTC549 cells. A204.1 or TTC549 cells were treated with DS-3201b (100 nM) or EPZ-6438 (100 nM) for 14 days, followed by RNA-sequencing (RNA-seq) analysis.

first: Issay

last: Kitabayashi


title: Velcrin-induced selective cleavage of tRNALeu(TAA) by SLFN12 causes cancer cell death

overall_design: Refer to individual Series


title: Allele-specific gene expression in stickleback (Apeltes quadracus) spine and fins

summary: Apeltes quadracus gene expression differences in developing spines and fins as assessed by allele-specific RNA-seq.

overall_design: Apeltes quadracus with different HOXDB alleles were crossed to each other to generate F1 hybrids. The spines and fins were individually dissected. RNA was extracted to investigate gene expression differences between the alleles.


title: Allele-specific gene expression in stickleback spine, fins, and embryos

sample_organism:
Gasterosteus aculeatus
Apeltes quadracus


title: RNA-seq of spleen monocytes from IL-4Rα+/+ and IL-4Rα-/- mice on a C57BL/6J background

city: Vienna

first: Patrick

last: Haider

address: Waehringer Guertel 18-20

country: Austria

institute: Medical University of Vienna

summary: Monocytes are immune cells which differentiate into subsets through sequential transition. The life-time differs between the individual subsets ranging from 1 day to 1 week. We studied the involvement of IL-4 receptor signaling on monocyte survival in mice lacking IL-4 receptors in a total knockout and a myeloid knockout. Circulating leukocytes were reduced by 25% in both knockouts, which was mainly caused by a 50% reduction of monocytes. Using RNA sequencing we were able to demonstrate that spleen monocytes in IL-4Rα deficient mice express lower amounts of anti-apoptotic genes and increased amounts of cell adhesion molecules hinting to an increase in apoptotic potential of these cells. This data were also verified in spleen samples were we found an increase of apoptotic monocytes identified by TUNEL and cleaved caspase 3 staining. Mechanistically we were able to show that IL-4 signaling directly affects the lifespan of monocytes in vivo. Therefore, we identified a previously unknown function of basal IL-4 levels in homeostasis of monocytes by regulating the lifespan and preventing apoptosis of the cells.

overall_design: RNA-seq of spleen monocytes from 3 IL-4Rα+/+ and 3 IL-4Rα-/- mice, isolated from splenocytes by negative selection using a commercial antibody cocktail and magnetic beads

first: Philipp

last: Hohensinner

first: Sophia

last: Derdak


title: Regulation and bioinformatic analysis of circ_0015891/miR-129-1-3p axis in methamphetamine-induced dopaminergic apoptosis

status: Public on Aug 31 2022

city: Changsha

first: Yong

last: Wang

state: Hunan

address: No. 172 Tongzipo Road

institute: Central South University

summary:
To investigated the role of noncoding RNAs in methamphetamine-induced dopaminergic neurotoxicity
We then performed gene expression profiling analysis using data obtained from RNA-seq of SH-SY5Y cells with or without methamphetamine treatment (2 mM).

overall_design:
Comparative gene expression profiling analysis of RNA-seq data for SH-SY5Y cells with or without methamphetamine treatment (2 mM).

>>Submitter states that raw data are not available due to hardware failure<<<

first: Bingpeng

last: Deng


title: Allele-specific gene expression in stickleback (Gasterosteus aculeatus) embryos

first: David

last: Kingsley

state: CA

summary: Population-specific Gasterosteus aculeatus gene expression differences at an embryonic time point as assessed by RNA-seq.

overall_design: Two different populations of stickleback were crossed to each other to generate F1 hybrids. RNA was extracted from the F1 progeny at an embryonic time point to investigate gene expression differences between the two populations.


title: Allele-specific gene expression in stickleback (Gasterosteus aculeatus) spine and fins

summary: Population-specific Gasterosteus aculeatus gene expression differences in developing spines and fins as assessed by RNA-seq.

overall_design: Two different populations of stickleback were crossed to each other to generate F1 hybrids. The spines and fins were individually dissected. RNA was extracted to investigate gene expression differences between the two populations.

first: Julia

last: Wucherpfennig


title: Velcrin-induced selective cleavage of tRNALeu(TAA) by SLFN12 causes cancer cell death [Ribo-Seq]

first: Stephanie

last: Hoyt


title: Identification and analysis of microRNA editing events in recurrent bladder cancer based on RNA sequencing: microRNA editing level is a potential novel biomarker

city: Xuzhou

first: Jiaxin

last: Qin

address: Jiefang South Road, No. 199, Xuzhou, Jiangsu, China

institute: Department of Urology, Xuzhou Clinical College of Xuzhou Medical University, Xuzhou, Jiangsu, China

summary: To identify and compare miRNA editing events in primary and recurrent bladder cancer, as well as to investigate the potential molecular mechanism and its impact on patient prognosis. We examined the mRNA and miRNA transcriptomes of 12 recurrent bladder cancer cases and 13 primary bladder cancer cases.

overall_design: In this study, we performed RNA sequencing on tissue specimens from 25 bladder cancer(BC) patients (12 recurrent BC and 13 primary BC) and performed a comprehensive analysis of mRNAseq and miRNAseq to determine miRNA editing in bladder cancer.

first: Zhenduo

last: Shi

first: Conghui

last: Han


title: The role of extracellular vesicle miRNAs and tRNAs in synovial fibroblast senescence

city: Wien

first: Andreas

middle: B

last: Diendorfer

address: Leberstraße 20

institute: TAmiRNA GmbH

summary: We studied extracellular vesicles (EVs) from synovial fibroblast (SF). EVs were isolated from the secretome of non-senescent and irradiation-induced senescent SFs using size exclusion chromatography. EV RNA was extracted and subject to small RNA sequencing on an Illumina NovaSeq SP using 100bp, single end reads. After mapping against GRCh38.p12 and miRBase v22.1 differential expression analysis was undertaken with edgeRv3.28 using a quasi-likelihood negative binomial generalized log-linear model. We identified a panel of differentially expressed small non-coding RNAs.

overall_design: Examination of small non-coding RNAs of extracellular vesiscles derived form the secretome of synovial fibroblasts from osteoathritic joint tissue using pairwise comparisons.

first: Mandy

last: Peffers

first: James

last: Anderson

first: Matthias

last: Hackl

first: Simon

last: Jones

first: Susanne

last: Wijesinghe

first: Victoria

last: James


title: RNA-seq of MAIT cells in aGVHD patients and healthy controls

city: Tianjin

first: Zhao

address: No. 24, Fukang Road, Nankai District

institute: Tianjin First Central Hospital

summary: We report the application of next generation sequencing technology for high-throughput transcriptom profiling of  mucosal associated invariant T  (MAIT) cells from patients with or without acute graft versus host disease (aGVHD) post allogenetic hematopoietic stem cell transplantation, and the healthy subjects as the contorls. Totally, MAIT cells from 4 patients with aGVHD, 3 patients without aGVHD and 3 healthy controls were detected in this study. Gene Set Enrichment Analysis (GSEA) on the sequencing data show the enrichments of interferon alpha response pathway in recipients with aGVHD and recipients without aGVHD, in comparison with healthy controls. Enrichment of primary immunodeficiency gene set is found in recipients without aGVHD when compared with aGVHD patients  and healthy controls. This study provides some preliminary investigation to the mechanical mechanism of MAIT cells in the aGVHD development.

overall_design: mRNA profiles of MAIT cells from patients with or without aGVHD, as well as healthy controls

first: Sizhou

last: Feng


title: RNA-Seq Facilitates Quantitative Analysis of Wild Type and Bnc1tr/tr ovary Transcriptomes

first: Dan

last: Zhang

address: Yuhang Road 866

institute: Zhejiang University

summary: Primary ovarian insufficiency (POI) is a clinical syndrome of ovarian dysfunction characterized by premature exhaustion of primordial follicles. POI causes infertility, serious daily life disturbances and long-term health risks. However, the underlying mechanism remains largely unknown. We have previously identified Basonuclin1 (BNC1) mutation from a large Chinese POI pedigree and find the targeted Bnc1 mutation mouse exhibites POI. In this study, we find that BNC1 plays a key role in the dynamic balance of ovarian reserve, and maintaining lipid metabolism and redox homeostasis in oocytes during follicular development. Deficiency of BNC1 results in premature follicular activation and accelerated follicular atresia, but doesn’t affect the ovarian primordial follicle reserve. Mechanistically, BNC1 targets the NF2-YAP pathway to trigger oocyte ferroptosis. Inhibition of ferroptosis significantly rescues POI. These findings uncover a novel pathologic mechanism of POI based on BNC1 deficiency and is the first report showing ferroptosis involved in oocyte death.

overall_design: ovary mRNA profiles of 8-weeks old wild type (WT) and Bnc1tr/tr mice

first: Feixia

first: Yifeng

last: Liu

first: Feida

last: Ni


title: SnFFPE-Seq: towards scalable single nucleus RNA-seq of formalin-fixed paraffin-embedded (FFPE) tissues

first: Hattie

last: Chung

institute: Broad Institute

summary: Profiling cellular heterogeneity in formalin-fixed paraffin-embedded (FFPE) tissues is key to characterizing clinical specimens for biomarkers, therapeutic targets, and drug responses. Here, we optimize methods for isolating intact nuclei and single nucleus RNA-seq from FFPE tissues in the mouse brain, and demonstrate a pilot application to a human clinical specimen of lung adenocarcinoma. Our method opens the way to broad applications of snRNA-Seq to archival tissues, including clinical samples.

overall_design: Intact nuclei were isolated from scrolls of FFPE specimens of the mouse cortex, after deparaffinization, rehydration, and tissue lysis

first: Aviv

last: Regev


title: RNA-Seq Facilitates Quantitative Analysis of Wild Type and Bnc1tr/tr oocyte Transcriptomes

overall_design: Oocyte mRNA profiles of 12-weeks old wild type (WT) and Bnc1tr/tr mice

last: Wang


title: Molecular Chaperone RUVBL2 Activates Oncogenes by Modulation of Transcriptional Condensates [Mnase-seq]

status: Public on Aug 30 2022

city: Beijing

first: Xiong

last: Ji

address: Yiheyuan Road

department: School of life science

institute: Peking University

summary: Transcription regulators and apparatuses compartmentalize into transcriptional condensates in part through molecular interactions among intrinsically disordered regions. To better understand how these fundamental condensates are regulated, we performed time-series analyses of transcriptome, genome and imaging to show that the previously characterized molecular chaperone RUVBL2 assembles Pol II condensates by its ATPase activity and prevalently interacting with diverse oncogenic transcription factors at promoters, thereby maintaining active transcription in mammalian cells. Besides, RUVBL2 is overexpressed in various cancers, has higher expression levels and preferential chromatin binding compared with RUVBL1. Remarkably, acute protein degradation and chemical perturbations of RUVBL2 with the nucleoside compound cordycepin result in the repression of oncogenes in embryonic stem cells and breast cancer cells, respectively. Our results suggest that molecular chaperone RUVBL2 safeguards the hemostasis of transcriptional condensates at promoters. Thus, pharmacological perturbations of RUVBL2 is a promising strategy to restore these condensates in breast cancers.

overall_design: We performed ChIP-Seq, PRO-Seq, MNase and RNA-Seq to explore the mechanism of RUVBL2 regulating transcription

first: Hui

first: Boyuan

last: Li


title: Molecular Chaperone RUVBL2 Activates Oncogenes by Modulation of Transcriptional Condensates

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

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus


title: DNA Replication Stress Generates Distinctive landscapes of DNA copy number alterations and chromosome scale losses

city: London

first: Eleni

last: Maniati

address: John Vane Science Centre, Charterhouse Square

department: Barts Cancer Institute

institute: Queen Mary University of London

summary: Diploid human cell lines were treated with aphidicolin as a model to see how DNA replication stress affects the genome, by identifying which copy number alterations appear in the first cell cycle. RNAseq was used to see whether there is any link between loci with recurrent CNAs and gene transcription in the genes located there.

overall_design: RNAseq analysis was performed on the BJ and RPE-1 cell lines treated with Aphidicolin or DMSO control. Three replicates were analysed per condition.

first: Nadeem

last: Shaikh

first: Alice

last: Mazzagatti

first: Sarah

last: McClelland


title: Molecular Chaperone RUVBL2 Activates Oncogenes by Modulation of Transcriptional Condensates [ChIP-Seq]

overall_design: We performed ChIP-Seq, PRO-Seq and RNA-Seq to explore the mechanism of RUVBL2 regulating transcription


title: Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Jhd2 S321A S340A mutant Transcriptomes

status: Public on Aug 29 2022

city: wuhan

first: Yu

last: Qi

state: Hubei

address: xujiapeng

department: College of life sciences

institute: Hubei university

summary: Cells need to coordinate gene expression with their metabolic states to maintain cell homeostasis and growth. However, how cells transduce nutrient availability to appropriate gene expression response via histone modifications remains poorly understood. Here, we report that glycolysis promotes H3K4me3 by activating Tpk2, the catalytic subunit of protein kinase A (PKA) via the Ras-cyclic AMP (cAMP) pathway. Further study showed that Tpk2 antagonizes Jhd2-catalyzed H3K4 demethylation by phosphorylating Jhd2 at S321 and S340 in response to glucose availability.Mechanistically, Tpk2-catalyzed Jhd2 phosphorylation inhibits its overall binding to chromatin and promotes its polyubiquitination by the E3 ubiquitin ligase Not4 and degradation by the proteasome. In addition, Tpk2-catalyzed Jhd2 phosphorylation also maintains H3K14ac by preventing the binding of Rpd3 to chromatin. By inhibiting the activity of Jhd2 and Rpd3, Tpk2-catalyzed Jhd2 phosphorylation regulates gene expression and promotes autophagy. Thus, regulation of Jhd2 by the Ras-cAMP-PKA pathway shed lights on how cells rewire their biological responses to glucose availability.

overall_design: Total RNA was isolated from exponential growing yeast cells by standard phenol-chloroform extraction procedures and the quality of RNA was examined using Agilent Bioanalyzer according to the manufacturer’s instructions. Library construction, sequencing and bioinformatics analysis were performed by MegaGenomics Inc. (Beijing, China). There are three biological replicates for WT  and Jhd2 S2A mutants. Differential expression levels of aligned sequences were calculated using significant thresholds set at fold change over 1.5 and adjusted P-value < 0.05


title: Single nuclei RNAseq from non-tumour and HCC human liver tissues

status: Public on Aug 26 2022

city: NEW YORK

first: Robert

last: Schwabe

state: NY

address: 1130 ST NICHOLAS AVE - ROOM 916B

department: Medicine

institute: Columbia University

summary: Hepatocellular carcinoma (HCC), the fourth leading cause of cancer mortality, develops almost exclusively in patients with chronic liver disease (CLD) and advanced fibrosis. Here we interrogated functions of hepatic stellate cells (HSC), the main source of liver fibroblasts, during hepatocarcinogenPesis. Genetic depletion, activation or inhibition established HSC as tumour-promoting in mouse models of HCC. HSC were enriched in the preneoplastic environment, where they closely interacted with hepatocytes and modulated hepatocarcinogenesis by regulating hepatocyte proliferation and death. Analysis of mouse and human HSC subpopulations and their associated mediators by single cell RNA-sequencing in conjunction with genetic ablation revealed dual functions of HSC in hepatocarcinogenesis. Hepatocyte growth factor, enriched in quiescent and cytokine-producing HSC (cyHSC), protected from hepatocyte death and HCC development. In contrast, type I collagen, enriched in activated myofibroblastic HSC (myHSC), promoted proliferation and tumour development via increased stiffness and TAZ activation in pretumoural hepatocytes and via activation of discoidin domain receptor 1 in established tumours. An increasing HSC dysbalance between cyHSC and myHSC during liver disease progression was associated with elevated HCC risk in patients. In summary, the dynamic shift of HSC subpopulations and their mediators during CLD is associated with a switch from HCC protection to HCC promotion.

overall_design: Single nucleus RNA sequencing of non-tumor (background liver cirrhosis with steatohepatitis) and matched tumor liver tissues from patient with Hepatocellular Carcinoma (n=2 cases). ****Authors state "IRB protocol do not allow uploading the human raw data."

first: Aveline

last: Filliol

first: Ajay

last: Nair


title: Genome-wide maps of chromatin modifiers and histone modification in saccharomyces cerevisiae

overall_design: ChIP-Seq examination of Histone H3 and H3K4me3 as well as Jhd2 and Rpd3 in WT, Jhd2 S2A mutant .


title: Hepatic Stellate Cells inhibition induced by YAP deletion

summary: Gene expression by bulk RNAseq in isolated mouse Hepatic Stellate Cells (HSC) YAP ko compared to HSC YAP floxed (wt).

overall_design:
Bullk RNA sequencing was used to characterize gene expression of primary mouse hepatic stellate cells (HSC) under the following condition:
1) HSC from YAP floxed mice (wt, without LratCre) treated with 6xCCl4 and
2) HSC YAP ko (from YAP floxed mice carrying LratCre) treated with 6xCCl4.


title: ATAC-seq data from Lmna knock-out mouse embryonic fibroblasts (Lmna-/- MEFs) and wild type (Lmna+/+ MEFs)

city: Copenhagen N

first: Mads

last: Lerdrup

address: Blegdamsvej 3C

department: Department of Cellular and Molecular Medicine

country: Denmark

institute: University of Copenhagen

summary: Using ATAC seq analysis, we showed that the MEFs with a knockout of Lmna gene (i.e., missing the lamin A/C nuclear scaffolding protein) (Lmna-/- MEFs) display a striking change in chromatin accessibility landscape (peak signals that are both up and down), both within and outside lamina-associated domains (LADs); moreover, there was a clear overrepresentation of peaks with a gain in chromatin accessibility (within and outside LADs) in the Lmna-/- MEFs, and within LADs compared to outside LADs.

overall_design: ATAC-seq of four biological replicates of mouse embryonic fibroblasts (MEFs) with the genotypes Lmna-/- and Lmna+/+.

first: Scott

last: Maynard

first: Muhammad

last: Shoaib

first: Jens

last: Johansen

first: Claus

middle: S

last: Sørensen

first: Jiri

last: Bartek


title: Deciphering Multi-way Interactions in the Human Genome

city: Ann Arbor

first: Gabrielle

last: Dotson

state: Michigan

address: 1600 Huron Parkway

institute: University of Michigan

summary: Chromatin architecture, a key regulator of gene expression, can be inferred using chromatin contact data from chromosome conformation capture, or Hi-C. However, classical Hi-C does not preserve multi-way contacts. Here we use long sequencing reads to map genome-wide multi-way contacts and investigate higher order chromatin organization in the human genome. We use hypergraph theory for data representation and analysis, and quantify higher order structures in neonatal fibroblasts, biopsied adult fibroblasts, and B lymphocytes. By integrating multi-way contacts with chromatin accessibility, gene expression, and transcription factor binding, we introduce a data-driven method to identify cell type-specific transcription clusters. We provide transcription factor-mediated functional building blocks for cell identity that serve as a global signature for cell types.

overall_design: Genome-wide multi-way chromatin interaction capture (Pore-C sequencing) for primary adult fibroblasts and neonatal fibroblasts (BJ cell line), in addition to RNA-sequencing for primary adult fibroblasts.

middle: A

first: Can

last: Chen

first: Stephen

last: Lindsly

first: Anthony

last: Cicalo

first: Sam

last: Dilworth

first: Charles

last: Ryan

first: Sivakumar

last: Jeyarajan

first: Walter

last: Meixner

first: Cooper

last: Stansbury

first: Nicholas

last: Beckloff

first: Amit

last: Surana

first: Max

last: Wicha

first: Lindsey

last: Muir

first: Indika

last: Rajapakse


title: RNA-seqence analysis of MYPT1 target genes in subcutaneous white adipoce tissue cells.

first: Juro

last: Sakai

address: 4-6-1, Komaba, Meguro-ku

institute: Research Center for Advanced Science and Technology, The University of Tokyo

summary: Protein kinase A promotes beige adipogenesis downstream from β-adrenergic receptor signaling by phosphorylating proteins, including histone H3 lysine 9 (H3K9) demethylase JMJD1A. To ensure homeostasis, this process needs to be reversible however, this step is not well understood. We show that myosin phosphatase target subunit 1- protein phosphatase 1β (MYPT1-PP1β) phosphatase activity is inhibited via PKA-dependent phosphorylation, which increases phosphorylated JMJD1A and beige adipogenesis. Mechanistically, MYPT1-PP1β depletion resulted in JMJD1A-mediated H3K9 demethylation and activation of the Ucp1 enhancer/promoter regions. Interestingly, MYPT1-PP1β also dephosphorylates myosin light chain which regulates actomyosin tension-mediated activation of YAP/TAZ which directly stimulates Ucp1 gene expression. Preadipocyte specific Mypt1 deficiency increases cold tolerance with higher Ucp1 levels in subcutaneous white adipose tissues compared to control mice, confirming this regulatory mechanism in vivo. Thus, we have uncovered new regulatory cross-talk involved in beige adipogenesis that coordinates epigenetic regulation with direct activation of the mechano-sensitive YAP/TAZ transcriptional co-activators.

overall_design: Primary or immortalized preadipocytes derived from inguinal subcutaneous white adipose tissue (scWAT or im-scWAT) were cultured. Mouse Mypt1 was knocked-down by siRNA. Preadipocytes were differentiated for RNA extraction and RNA-sequence analysis using Illumina HiSeq 2500.

first: Yoshihiro

last: Matsumura


title: Endothelial Cell Cycle State Determines Propensity for Arterial-Venous Fates (ATAC-Seq)

status: Public on Aug 28 2022

city: Charlottesville

last: Chavkin

address: 415 Lane Road

institute: University of Virginia

summary: Formation and maturation of a functional blood vascular system is required for the development and maintenance of all tissues in the body. During the process of blood vessel development, primordial endothelial cells are formed and become specified toward arterial or venous fates to generate a circulatory network that provides nutrients and oxygen to, and removes metabolic waste from, all tissues. Specification of arterial and venous endothelial cells occurs in conjunction with suppression of endothelial cell cycle progression, and endothelial cell hyperproliferation is associated with potentially lethal arterial-venous malformations. However, the mechanistic role that cell cycle state plays in arterial-venous specification is unknown. Herein, studying vascular development in Cdh5-CreERT2;R26FUCCI2aR reporter mice, we find that venous and arterial endothelial cells exhibit a propensity for different cell cycle states during development and in adulthood. That is, venous endothelial cells are predominantly FUCCI-Negative, while arterial endothelial cells are enriched for the FUCCI-Red reporter. Single cell RNA sequencing analysis of developing retinal endothelial cells reveals that venous endothelial cells are enriched for the FUCCI-Negative state and BMP signaling, while arterial endothelial cells are enriched for the FUCCI-Red state and TGF-b signaling. Further transcriptional analyses and live imaging of cultured endothelial cells expressing the FUCCI reporter show that reporter-negative corresponds to an early G1 state and reporter-red corresponds to late G1 state. We find the early G1 state is essential for BMP4-induced venous gene expression, whereas late G1 state is essential for TGF-b1-induced arterial gene expression. In a mouse model of endothelial cell hyperproliferation and disrupted arterial-venous specification, pharmacological inhibition of endothelial cell cycle prevents the vascular defects. Collectively, our results show that endothelial cell cycle control plays a key role in arterial-venous network formation, and distinct cell cycle states provide distinct windows of opportunity for the molecular induction of arterial vs. venous specification.

overall_design: Subconfluent, HUVEC-FUCCI were lifted and sorted into early G1 and late G1 cell cycle states, then immediately collected for ATAC-sequencing analysis (n = 4 biological replicates).

first: Karen

last: Hirschi


title: Single cell RNAseq of isolated hepatic cells and Col1a1+ cells from mouse fibrotic livers

first: Robert

last: Schwabe

summary: Gene expression was measured by scRNAseq in isolated liver cells from mice treated with CCl4 and in non parenchymal Col1a1+ cells from a 3 month old Mdr2KO mouse.

overall_design:
The Single cell RNA sequencing in this series were obtained from mouse livers as followed:
1) isolated hepatic cells from injured liver induced by 8xCCl4 (RS045 and RS046, n=2)
2)  isolated Col1a1+ liver cells from the fibrotic liver induced by Mdr2KO (RS024, n=1)

first: Aveline

last: Filliol

first: Ajay

last: Nair


title: IL-2 and IL-15 drive intrathymic development of distinct periphery-seeding CD4+Foxp3+ regulatory T lymphocytes

city: Toulouse

first: Joost

last: Van Meerwijk

state: HG

address: CHU Purpan BP 3028

department: CPTP U1043

country: France

institute: INSERM

summary:
Development of Foxp3-expressing regulatory T-lymphocytes (Treg) in the thymus is controlled by signals delivered in T-cell
precursors via the TCR, co-stimulatory receptors, and cytokine receptors. In absence of IL-2, IL-15 or their receptors, fewer Treg
apparently develop in the thymus. However, it was recently shown that a substantial part of thymic Treg are cells that had
recirculated from the periphery back to the thymus, troubling interpretation of these results. We therefore reassessed the
involvement of IL-2 and IL-15 in the development of Treg, taking into account Treg-recirculation. In three-week-old mice, when
substantial amounts of recirculating Treg are present in the thymus, we found similarly reduced proportions of newly developed
Treg in absence of IL-2 or IL-15, and in absence of both cytokines even less Treg developed. In neonates, when practically no
recirculating Treg were found in the thymus, the absence of IL-2 led to substantially more reduced Treg-development than
deficiency in IL-15. IL-2 and IL-15 differentially modulated the CD25, GITR, OX40, and CD73-phenotypes of thymus-egress-competent
and periphery-seeding Treg. Interestingly, IL-2 and IL-15 also modulated the TCR-repertoire expressed by developing Treg. Upon
transfer into Treg-less Foxp3sf mice, thymus-exit-competent Treg from IL-2- (and to a lesser extent IL-15-) deficient mice
suppressed immunopathology less efficiently than wt Treg. Taken together, our results firmly establish important non-redundant
quantitative and qualitative roles for IL-2 and, to a lesser extent, IL-15 in intrathymic Treg-development.

overall_design: CD4+CD8−Thy1.1+GFP+ thymic Treg (10^5) were FACS sorted from individual three week-old wt (n=4), Il2o (n=4), or Il15o (n=4) Rag2-Gfp Foxp3-Thy1a Tcra +/o Kaa TCRbeta-transgenic B6 mice.

first: Cécile

last: Apert

first: Ariel

last: Galindo-Albarran

first: Sarah

last: Castan

first: Claire

last: Detraves

first: Héloise

last: Michaud

first: Nicola

last: McJannett

first: Bart

last: Haegeman

first: Simon

last: Fillatreau

first: Bernard

last: Malissen

first: Georg

last: Holländer

first: Saulius

last: Žuklys

first: Jérémy

last: Santamaria

first: Olivier

last: Joffre

first: Paola

last: Romagnoli

middle: P

last: van Meerwijk


title: Velcrin-induced selective cleavage of tRNALeu(TAA) by SLFN12 causes cancer cell death [tRNA seq]

city: Cambridge

first: Stephanie

last: Hoyt

address: 415 Main St

institute: Broad Institute of MIT and Harvard

summary: Velcrin compounds kill cancer cells expressing high levels of phosphodiesterase 3A (PDE3A) and Schlafen family member 12 (SLFN12) by inducing complex formation between these two proteins, but the mechanism of cancer cell killing by the PDE3A–SLFN12 complex is not fully understood. Here, we report that the physiological substrate of SLFN12 RNase is tRNALeu(TAA). SLFN12 selectively digests tRNALeu(TAA), and velcrin treatment promotes the cleavage of tRNALeu(TAA) by inducing PDE3A–SLFN12 complex formation in vitro. We found that distinct sequences in the variable loop and acceptor stem of tRNALeu(TAA) are required for substrate digestion. Velcrin treatment of sensitive cells results in downregulation of tRNALeu(TAA), ribosome pausing at Leu-TTA codons and global inhibition of protein synthesis. Velcrin-induced cleavage of tRNALeu(TAA) by SLFN12 and the concomitant global inhibition of protein synthesis thus define a new mechanism of apoptosis initiation.

overall_design: Ribosome profiling of Hela cells treated with DMSO control or DNMDP in duplicate

first: Sooncheol

last: Lee

first: Xiaoyun

last: Wu

first: Colin

last: Garvie

first: Joseph

last: McGaunn

first: Andrew

last: Cherniack

first: Matthew

last: Meyerson

first: Heidi

last: Greulich


title: Genome-wide maps of chromatin state in Wild Type mouse ovary

city: Hangzhou

first: Dan

last: Zhang

overall_design: oavry DNA profiles of 8-weeks old wild type (WT) mice

first: Feixia

last: Wang

first: Yifeng

last: Liu

first: Feida

last: Ni


title: RNA-sequencing of WT and P2Y4 KO pericardial adipose tissue (PAT) 24 hours after left anterior descending artery (LAD) ligation

status: Public on Aug 25 2022

city: Brussels

first: Didier

last: Communi

address: Route de Lennik 808

department: IRIBHM

country: Belgium

institute: Université Libre de Bruxelles

summary: We identified differentially regulated genes in the pericardial adipose tissue of wild type (WT) and P2Y4 KO mice, 24 hours after left anterior descending artery (LAD) ligation as a model of myocardial infarction (MI). Differentially regulated genes were involved in metabolism, brown fat cell differentiation, immune response and inflammation. P2Y4 KO mice displayed adipocyte beiging with increased PD-L1 expression and a higher number of regulatory leukocytes in their PAT 24 hours after LAD ligation. Up-regulated genes linked to adipocyte beiging included Ucp1, Cited1 and Prdm16.

overall_design: 2 samples were analyzed, a pool of the RNA of 3 WT PAT and a pool of the RNA of 3 P2Y4 KO PAT. PAT was freshly harvested 24 hours after LAD ligation.

first: Esteban

last: Diaz Villamil

first: Michael

last: Horckmans

first: Frédérick

last: Libert


title: Molecular Chaperone RUVBL2 Activates Oncogenes by Modulation of Transcriptional Condensates [PRO-Seq]

first: Xiong

last: Ji

first: Hui

first: Boyuan

last: Li


title: Integrative single cell and spatial transcriptomic analysis reveal reciprocal microglia-plasma cell crosstalk in the mouse brain during chronic Trypanosoma brucei infection

city: Manchester

first: Juan

middle: Fernando

last: Quintana

address: 2.18c CTF, Grafton Street

department: Lydia Becker Institute of Immunology and Inflammation

institute: University of Manchester

summary: Human African trypanosomiasis, or sleeping sickness, is caused by the protozoan parasite Trypanosoma brucei and induces profound reactivity of glial cells and neuroinflammation when the parasites colonise the central nervous system. However, the transcriptional and functional responses of the brain to chronic T. brucei infection remain poorly understood. By integrating single cell and spatial transcriptomics of the mouse brain, we identified that glial responses triggered by infection are readily detected in the proximity to the circumventricular organs, including the lateral and 3rd ventricle. This coincides with the spatial localisation of both slender and stumpy forms of T. brucei. Furthermore, in silico predictions and functional validations led us to identify a previously unknown crosstalk between homeostatic Cx3cr1+ microglia and Cd138+ plasma cells mediated by IL-10 and B cell activating factor (BAFF) signalling. This study provides important insights and resources to improve understanding of the molecular and cellular responses in the brain during infection with African trypanosomes.

overall_design: Single cell and spatial transcriptomics of murine brain at two time points of chronic infection with Trypanosoma brucei

first: Praveena

last: Chandrasegaran

last: Sinton

first: Emma

last: Briggs

first: Thomas

last: Otto

first: Rhiannon

last: Heslop

first: Calum

last: Bentley-Abbot

last: Loney

first: Luis

last: de Lecea

first: Neil

last: Mabbott

first: Annette

last: MacLeod


title: Molecular Chaperone RUVBL2 Activates Oncogenes by Modulation of Transcriptional Condensates [RNA-Seq]

last: Wang


title: Effect of overexpression of NCAL1 on gene expression profile of NK92MI cells

city: Changchun

first: Chao

last: Niu

state: Jilin

address: Xinmin Street #1

department: Cancer Center

institute: The First Hospital of Jilin University

summary: To investigate NCAL1 effect on NK92MI cells , we performed a whole-transcriptome RNA sequencing experiment for NK92MI cells overexpressing NCAL1 and established differntial expression profile comparing to control NK92MI cells.

overall_design: Comparative gene expression profiling analysis of RNA-seq data for NCAL1 overexpressing NK92MI cells and control NK92MI cells.

first: Jiuwei

last: Cui