title: Comparative analysis of gene expression of cell lines DU145 andLNCaP grown under standard and glutamine deprived condition

status: Public on Jul 01 2021

city: Dresden

first: Vasyl

last: Lukiyanchuk

address: Handelallee 26

institute: OncoRay

summary: By employing a global gene expression profiling, we performed analysis of the molecular pathways which are deregulated in prostate cancer cell lines DU145 and LNCaP grown under standard and glutamine deprived condition. Both oriignal cell lines and their radioresistant derivatives DU145-RR and LNCaP-RR were analyzed

overall_design: Standard and glutamine deprived culture were compared, both for original cell lines and for their radioresistant derivative sub lines DU145-RR and LNCaP-RR. Each of 8 samples has been prepared in 3 repeats, however repeat 2 was excluded at the stage of data analysis due to major inconsistency across all 8 samples. Presumably there was some technical problem with that repeat, therefore only repeats 1 and 3 were used for analysis as well as for this submission

first: Anna

last: Dubrovska

first: Oleg

last: Chen


title: Next Generation Sequencing Facilitates Quantitative Analysis of the Transcriptome of HIV-1-infected or uninfected MDMs

status: Public on Jul 21 2021

city: wuhan

first: meirong

last: wang

address: donghuroad

country: China

institute: wuhan university

type: Expression profiling by high throughput sequencing

summary:
Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The objective of this study was to compare transcriptome analysis (RNA-seq) with microarray and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) for HIV-1-infected and uninfected MDMs and to evaluate the optimal protocol for high-throughput data analysis
Methods: The mRNA profiles of HIV-1-infected and uninfected MDMs were generated by deep sequencing, in triplicate, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays.
Results: Using an optimized data analysis workflow, we mapped about 20 million sequence reads per sample to the human genome and identified 60505 transcripts in the HIV-1-infected or uninfected MDMs. RNA-seq data confirmed stable expression of 15 known housekeeping genes, and 10 of these were validated with qRT–PCR. RNA-seq data had a linear relationship with qRT–PCR for more than four orders of magnitude and a goodness of fit (R2) of 0.8953. Approximately 10% of the transcripts showed differential expression between the HIV-1-infected or uninfected MDMs, with a fold change ≥1.5 and p value <0.05. Altered expression of 48 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method.
Conclusions: Our study represents the detailed analysis of HIV-1-infected macrophages transcriptomes, with biologic replicates, generated by RNA-seq technology. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within a cell or tissue. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.

overall_design: MRNA profiles of MDMs with or without HIV-1 infection

first: Mei-Rong

last: Wang


title: Analysis of Transcriptional Responses to Altitude-Induced Hypoxia in Bronchial Epithelium, Bronchio-Alveolar Cells, and Blood Reveals Differences Between Smokers and Nonsmokers [blood]

status: Public on Sep 14 2021

city: Oklahoma City

first: Susan

middle: Kasko

last: Munster

state: OK

address: 6500 S. MacArthur Blvd.

department: Office of Aerospace Medicine

country: USA

institute: Federal Aviation Admininistration

summary: Blood, bronchial epithelium, and bronchio-alveolar cells were collected in a double blind study. Individuals were exposed to 'ground' and 'flight' conditions using a hypobaric chamber for approximately 5 hours. Blood samples were collected over 4 time points and both bronchial cells were collected at the last time point.

overall_design:
Samples were collected from 20 individuals, comprised of 10 smokers and 10 nonsmokers. Both subgroups of smokers and nonsmokers were comprised of 5 males and 5 females each.
Collection timepoint 1 = taken at time 0, before exposure to 'altitude'
Collection timepoint 2 = taken after 30 minutes exposure to 'altitude'
Collection timepoint 3 = taken after 4 hours exposure to 'altitude'
Collection timepoint 4 = taken 1.5 hours after exposure to 'altitude' ended

first: Scott

middle: J

last: Nicholson

middle: K

first: Hilary

middle: A

last: Uyhelji

first: David

middle: C

last: Hutchings

first: Vicky

middle: L

last: White

first: Dennis

middle: M

last: Burian

first: Jordan

last: Metcalf


title: Single-cell RNA sequencing reveals markers of disease progression in primary cutaneous T-cell lymphoma

status: Public on Sep 13 2021

city: Vienna

first: Katharina

last: Rindler

address: Waehringer Guertel 18-20

department: Dermatology

country: Austria

institute: Medical University of Vienna

summary:
Background: In early-stage mycosis fungoides (MF), the most common primary cutaneous T-cell lymphoma, limited skin involvement with patches and plaques is associated with a favorable prognosis. Nevertheless, approximately 20-30% of cases progress to tumors or erythroderma, resulting in poor outcome. At present, factors contributing to this switch from indolent to aggressive disease are only insufficiently understood.
Methods: In patients with advanced-stage MF, we compared patches with longstanding history to newly developed plaques and tumors by using single-cell RNA sequencing, and compared results with early-stage MF as well as nonlesional MF and healthy control skin.
Results: Despite considerable inter-individual variability, lesion progression was uniformly associated with downregulation of the tissue residency markers CXCR4 and CD69, the heat shock protein HSPA1A, the tumor suppressors and immunoregulatory mediators ZFP36 and TXNIP, and the interleukin 7 receptor (IL7R) within the malignant clone, but not in benign T cells. This phenomenon was not only found in conventional TCR-αβ MF, but also in a case of TCR-γδ MF, suggesting a common mechanism across MF subtypes. Conversely, malignant cells in clinically unaffected skin from MF patients showed upregulation of these markers.
Conclusions: Our data reveal a specific panel of biomarkers that might be used for monitoring MF disease progression. Altered expression of these genes may underlie the switch in clinical phenotype observed in advanced-stage MF.

overall_design:
Single-cell RNA-seq investigation of patch, plaque/tumor, and follow up lesions and nonlesional skin in CTCL patients.
------------------------------
Authors state "raw data are missing due to patient privacy concerns".

first: Constanze

last: Jonak

first: Natalia

last: Alkon

first: Felix

last: Thaler

first: Harald

last: Kurz

first: Lisa

middle: E

last: Shaw

first: Georg

last: Stingl

first: Wolfgang

last: Weninger

first: Florian

last: Halbritter

last: Bauer

first: Matthias

last: Farlik

first: Patrick

last: Brunner


title: The expression profiling of the early stage of multiple system atrophy model mice

status: Public on Jun 01 2021

city: Hirosaki

first: Shuji

last: Shimoyama

state: Aomori

address: 5 Zaifu-cho

department: Department of Neurophysiology

country: Japan

institute: Hirosaki University Graduate School of Medicine

summary:
Global transcriptional analysis of the brain of multiple system atrophy model mice after synuclein induction by tamoxifen.
Multiple system atrophy (MSA) is pathologically characterized by accumulation of phosphorylated α-synuclein in the oligodendrocytes. The pathophisiological mechinism under the early staige of disease pregression has been unknown. To clarify molecular alteration just after α-synuclein overexpression in the oligodendrocytes, we performed whole transcriptome analysis of the brain obtained from MSA model mice and control at 10 days after α-synuclein induction.

overall_design: Knock-in mice harboring human synuclein (Syn) gene with stop codon between loxp recognition sites were mated with mice expressing cre/estrogen receptor under the proteolipid protein (plp) promoter, which is an oligodendrocyte specific marker. Resulting mice (plp-Syn; Cre+/-) express human synuclein in the oligodedrocyte only after tamoxifen injection, and used as MSA model mice in this analysis. MSA model mice or control (plp-Syn; Cre-/-, n=3, respectively) were sacrified under deep anesthesia and brains were quickly removed. Right hemisphere of the brain from MSA model mice and control were subjected to transcriptome analysis or qRT-PCR.

first: Kunikazu

last: Tanji


title: Single cell analysis of the cellular heterogeneity and interactions in the injured mouse spinal cord

city: Miami

first: James

middle: S

last: Choi

state: FL

address: 1095 NW 14th Terrace

institute: University of Miami Miller School of Medicine

summary: The wound healing process that occurs after spinal cord injury is critical for maintaining tissue homeostasis and limiting tissue damage, but eventually results in a scar-like environment that is not conducive to regeneration and repair. A better understanding of this dichotomy is critical to developing effective therapeutics that target the appropriate pathobiology, but a major challenge has been the large cellular heterogeneity that results in immensely complex cellular interactions. In this study, we used single cell RNA sequencing to assess virtually all cell types that comprise the mouse spinal cord injury site. In addition to discovering novel subpopulations, we used expression values of receptor-ligand pairs to identify signaling pathways that are predicted to regulate specific cellular interactions during angiogenesis, gliosis, and fibrosis. Our dataset is a valuable resource that provides novel mechanistic insight into the pathobiology of not only spinal cord injury, but also other traumatic disorders of the CNS.

overall_design: Single cell RNA sequencing of uninjured and injured spinal cord at 1 dpi, 3 dpi, and 7 dpi of wild-type mice. In total, we sequenced three uninjured biological replicates (from five animals), three biological replicates at 1 dpi (from five animals), two biological replicates at 3 dpi (from three animals), and two biological replicates at 7dpi (from three animals). One biological replicate from each time point consisted of cells from a single animal's spinal cord. All other biological replicates consisted of cells pooled from two spinal cords. For these pooled samples, one of two spinal cords were processed to enrich for astrocytes using Miltenyi's Anti-ACSA-2 MicroBead kit. All samples were initially processed with Miltenyi Neural Tissue Dissociation Kit-P.

first: Lindsay

last: Milich

first: Christine

middle: B

last: Ryan

first: Susana

middle: R

last: Cerqueira

first: Sofia

last: Benavides

first: Stephanie

last: Yahn

first: Pantelis

last: Tsoulfas

first: Jae

last: Lee


title: Gene expression comparison of pre-osteoblastic and mature osteoblastic cell populations from 5 week old and 8 week old mice, a comparison of cell populations within and between age groups

status: Public on Aug 25 2021

city: Meblourne

first: Alistair

middle: Morgan

last: Chalk

state: VIC

address: 1G Royal Parade

department: Bioinformatics

country: Australia

institute: WEHI

summary: The aim of the study was to identify gene expression profiles that distinguished different stages of osteoblast commitment, and determine whether the same osteoblast cell populations from mice of different ages had distinguishable expression profiles that may indicate functional changes are apparent for the cell populations during different stages of skeletal development. Pre-osteoblastic and mature osteoblastic cells were isolated from collagenase digested bones from 5 week old and 8 week wild type C57BL6 mice by FACS based on Lin, Sca-1, CD51, and CD31 cell surface markers.

first: E

last: Baker

first: A

last: Green

first: J

last: Quach

first: T

last: Jovic

first: S

first: C

last: Walkley

first: L

last: Purton


title: The study of the effects of dauricine(dau) on human pancreatic carcinoma cells

status: Public on Jun 05 2021

city: Harbin

first: Yun

last: Bai

state: Hei Long Jiang

address: No.24 heping Street, XiangFang district

institute: Hei Long Jiang University of Chinese medicine

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

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

platform_organism:
Homo sapiens
Mus musculus
Rattus norvegicus

overall_design: Refer to individual Series

first: Ling

last: Jiang


title: A mitochondrial long-chain fatty acid oxidation defect leads to uncharged tRNA accumulation and activation of the integrated stress response in the mouse heart

status: Public on Jun 11 2021

city: New York

first: Sander

last: Houten

state: NY

address: 1425 Madison Avenue, Box 1498

department: Genetics and Genomic Sciences

institute: Icahn School of Medicine at Mount Sinai

summary: The heart relies mainly on mitochondrial fatty acid beta-oxidation (FAO) for its high energy requirements. Cardiomyopathy and arrhythmias can be severe complications in patients with inherited defects in mitochondrial long-chain FAO, reinforcing the importance of FAO for cardiac health. However, the pathophysiological mechanisms that underlie the cardiac abnormalities in long-chain FAO disorders remain largely unknown. Here, we investigated the cardiac transcriptional adaptations to the FAO defect in the long-chain acyl-CoA dehydrogenase (LCAD) knockout (KO) mouse. We found a prominent activation of the integrated stress response (ISR) mediated by the eIF2a/ATF4 axis in both fed and fasted states, accompanied by a reduction in cardiac protein synthesis during a short period of food withdrawal. Notably, we found an accumulation of uncharged tRNAs in LCAD KO hearts, consistent with a reduced availability of cardiac amino acids, in particular, glutamine. We replicated the activation of the cardiac ISR in hearts of mice with a muscle-specific deletion of carnitine palmitoyltransferase 2 deletion (Cpt2M-/-). Our results show that perturbations in amino acid metabolism caused by long-chain FAO deficiency impact cardiac metabolic signaling, in particular the ISR, and may play a role in the associated cardiac pathology.

overall_design: We analyzed mRNA expression in 24 mouse heart samples with genetic defects of mitochondrial fatty acid oxidation (Acadl and Acadvl knockout) using RNA sequencing

first: Carmen

last: Argmann

first: Aaron

last: Bender

first: Pablo

last: Ranea-Robles


title: Histone ChIP-seq from middle frontal area 46 (ENCSR943TBH)

status: Public on May 23 2021

city: Stanford

first: ENCODE

last: DCC

state: CA

address: 300 Pasteur Dr

institute: ENCODE DCC

type: Genome binding/occupancy profiling by high throughput sequencing

summary:
H3K4me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (90 or above years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR935EPK)

summary:
H3K4me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (87 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR901ZXU)

summary:
H3K27me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (88 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR497URO)


title: Histone ChIP-seq from middle frontal area 46 (ENCSR888NRO)

summary:
H3K4me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (74 years) originated from dorsolateral prefrontal cortex

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


title: Gene expression analysis of 5 osteoblastic subtypes obtained from 8 week old mice

summary: The aim of the study was to identify gene expression profiles in different OB cell types. Isolated by novel facs markers.

overall_design: Osteoblastic cells were isolated from collagenase digested bones from 8 week old wild type C57BL6 mice by FACS based on Lin, Sca-1, CD51, CD31, PDGFRa, PDGFRb cell surface markers.

first: R


title: Histone ChIP-seq from middle frontal area 46 (ENCSR852VZG)

summary:
H3K27me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (90 or above years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR256OOR)

summary:
H3K27me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (87 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR957YLX)


title: Histone ChIP-seq from middle frontal area 46 (ENCSR206CIN)

summary:
H3K27me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (74 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR768YDB)

summary:
H3K4me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (88 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR914RMX)


title: Histone ChIP-seq from middle frontal area 46 (ENCSR675VCH)

summary:
H3K27me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (89 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR092IWZ)

summary:
H3K27me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (83 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR064QOA)


title: Histone ChIP-seq from middle frontal area 46 (ENCSR055JGU)

summary:
H3K27me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (81 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR147VUC)


title: Histone ChIP-seq from middle frontal area 46 (ENCSR589CXZ)

summary:
H3K4me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (84 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR622QCU)

summary:
H3K4me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (89 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR083FDD)


title: Histone ChIP-seq from middle frontal area 46 (ENCSR053KIS)


title: Histone ChIP-seq from middle frontal area 46 (ENCSR549BWF)


title: Transcriptomic analysis of the impact of EHHADH deficiency on male mouse kidney

status: Public on Mar 26 2021

summary: Background: Proximal tubular (PT) cells are enriched in mitochondria and peroxisomes. Whereas mitochondrial fatty acid oxidation (FAO) plays an important role in kidney function by supporting the high-energy requirements of PT cells, the role of peroxisomal metabolism remains largely unknown. EHHADH, also known as L-bifunctional protein, catalyzes the second and third step of peroxisomal FAO.  Methods: RNA was isolated using QIAzol lysis reagent followed by purification using the RNeasy kit (Qiagen). RNA samples were submitted to the Genomics Core Facility at the Icahn Institute and Department of Genetics and Genomic Sciences for further processing. mRNA-focused cDNA libraries were generated using Illumina reagents (polyA capture), and samples were run on an Illumina HiSeq 2500 sequencer to yield a read depth of approximately 56 million 100 nucleotide single-end reads per samples. Reads from fastq files were aligned to the mouse genome mm10 (GRCm38.75) with STAR (release 2.4.0 g1) and summarized to gene- and exon- level counts using featureCounts. Only genes with at least one count per million in at least 2 samples were considered. Differential gene expression analysis was conducted with the R package limma. Differentially expressed genes (DEGs) were defined using an adjusted p value of < 0.05 with no logFC cut-off.   Results: Transcriptome analysis unveiled a gene expression signature similar to PT injury in acute kidney injury mouse models.  Conclusions: Our data highlight the importance of EHHADH and peroxisomal metabolism in male kidney physiology and reveal peroxisomal FAO as a sexual dimorphic metabolic pathway in mouse kidneys.

overall_design: WT vs Ehhadh KO adult kidneys were used (n=4 per genotype, male animals). Dataset includes two more WT samples, one from a DBA_2J mouse, the other from a 129_SvPasCrl mouse.


title: Multiple interactions of the oncoprotein transcription factor MYC with the SWI/SNF chromatin remodeler

status: Public on May 01 2021

city: Nashville

first: Jing

last: Wang

state: TN

address: 2220 Pierce Avenue

institute: Vanderbilt University Medical Center

summary: We report that even though SNF5 is the most well-documented SWI/SNF subunit to bind MYC, MYC can use multiple interaction surfaces to interact with SWI/SNF subunits independently of SNF5. In line with this, MYC interacts with the pan-SWI/SNF subunit, BAF155, in multiple SNF5-null malignant rhabdoid tumor (MRT) cell lines and almost all of MYC co-localizes with SWI/SNF subunits on chromatin in MRT. In the MRT cell line, G401, MYC binds to essential genes, although for a purpose that appears distinct from chromatin remodeling, and loss of MYC leads to widespread gene expression changes. Analysis of specific MYC-SWI/SNF target genes in G401 cells reveals that this group of genes are associated with core biological functions linked to protein synthesis and their transcription is directly activated by MYC. These data provide a solid framework in which to interrogate the influence of SWI/SNF on MYC function in cancers in which SWI/SNF or MYC are altered.

overall_design: The G401 MRT cell line was engineered to express a lentiviral version of c-MYC containing a N-terminal HA-FKBP12F36V dTAG module and then endogenous MYC was removed by CRISPR-Cas9, resulting in G401 cells expressing MYC that could be removed by addition of dTAG47 molecule. For ChIP-seq and Pro-Seq, engineered G401 cells were treated for 4 hours with dTAG47, or DMSO control. For ATAC-seq and RNA-seq, engineered G401 cells were treated for 24 hours with dTAG47 or DMSO control. For RNA-seq of parental G401 cell lines treated with dTAG47, the experiment was also performed at the 24 hour timepoint.

first: William

middle: P

last: Tansey

first: April

last: Weissmiller

first: Qi

last: Liu


title: Histone ChIP-seq from middle frontal area 46 (ENCSR538GXY)


title: Histone ChIP-seq from middle frontal area 46 (ENCSR532STE)

summary:
H3K4me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (83 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR166WJU)

summary:
H3K27me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (78 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR022FAQ)

summary:
H3K4me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (78 years) originated from dorsolateral prefrontal cortex

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


title: Histone ChIP-seq from middle frontal area 46 (ENCSR548QRE)

summary:
H3K4me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (81 years) originated from dorsolateral prefrontal cortex

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


title: DNA methylation profile of cancerous and non-cancerous renal tissues

status: Public on Feb 15 2021

city: Vilnius

first: Raimonda

last: Kubiliūtė

state: Saulėtekis

address: Sauletekio al., 7

department: Life Sciences Center

country: Lithuania

institute: Vilnius University

type: Methylation profiling by genome tiling array

summary: Renal cell carcinoma (RCC), particularly clear cell RCC (ccRCC), is the most common type of kidney tumors characterized by the highest mortality rate of the genitourinary cancers. Lack of symptoms leads to late detection of the disease using conventional imagining procedures. There is an urgent need for new diagnostic biomarkers with the potential for early detection and prediction of high risk of progression. In the present study, based on microarray profiling of DNA methylation in 11 pairs of ccRCC and noncancerous renal tissues (NRT), the methylation at regulatory regions of six putative ccRCC biomarkers was further analyzed in 123 ccRCC and 45 NRT samples by means of methylation specific PCR (MSP). Thereafter, the quantitative MSP was applied for the methylation analysis in the urine samples of 123 ccRCC patients and 93 asymptomatic controls (ASC). The comparison of ccRCC and NRT samples revealed significant methylation differences in 1319 genes, of which 191 were hypermethylated and 1128 were hypomethylated. DNA methylation of selected genes were validated by means of MSP and significantly higher methylation frequencies for all genes was found in ccRCC tissues compared to NRT (33-60% vs. 0-11%). Methylated status of at least one gene was significantly related with various adverse clinical-pathological parameters of the patients, including larger tumor size, higher tumor pathological stage, grade, intravascular and fat invasion as welll as tumor necrosis. The multivariate Cox regression model revealed  the methylation in a panel of  selected  three genes as independent prognostic biomarker of ccRCC. Moreover, five genes were characterised by higher methylation intensity in the urine samples of ccRCC patients, as compared to ASC, and various combination of these biomarkers revealed moderate-to-high sensitivity and specificity values for the diagnosis of ccRCC.

overall_design: DNA methylation profile was analyzed in 11 ccRCC cases and paired NRT samples (as a control). No biological replicates were performed.

last: Kubiliute

first: Sonata

last: Jarmalaite


title: An organoid model to assay the role of CFTR in the human epididymis epithelium

status: Public on Jan 16 2021

city: Cleveland

first: Ann

last: Harris

state: OH

address: 10900 Euclid Ave

institute: Case Western Reserve Uni

summary: Organoid cultures derived from primary human tissues facilitate the study of disease processes and the development of new therapeutics. We used human epididymis epithelial cell (HEE) organoids and polarized HEE cell cultures to assay the CF transmembrane conductance regulator (CFTR) in the human epididymis.

overall_design: Use single-cell RNA sequencing to map cell-type-specific gene expression in the HEE organoids.

first: Shih-Hsing

last: Leir

first: Shiyi

last: Yin

first: Jenny

last: Kerschner


title: Epigenetic and chromatin profiling of wild-type and Dnmt3a-deficient B1 and B2 B cells.

status: Public on Feb 22 2021

city: Cambridge

first: Vinay

last: Mahajan

state: MA

address: 65 Landsdowne Street

institute: Brigham and Women's Hospital

type: Methylation profiling by high throughput sequencing

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


title: Transcriptome profiles of different light-signaling mutants

status: Public on Jan 01 2021

city: Cerdanyola del Vallès

first: Guiomar

last: Martín

state: Barcelona

address: Vall Moronta

country: Spain

institute: Centre for Research in Agricultural Genomics

summary: RNA-seq experiment of WT, hy5, phyab and pifq mutant seedlings grown for 3 days in darkness or continuous white light.

overall_design: Transcriptome profiles of the wild-type (WT), hy5, phytochromeaphytochromeb (phyab) and pif1pif3pif4pif5 (pifq)  mutant seedlings grown for 3 days in the dark or continuous white light irradiation (13 µmol·m-2·s-1). Triplicate biological samples were analyzed.

first: Paula

last: Duque


title: Transcriptome changes in human endothelial cells with reduced cMYC signaling.

status: Public on Jan 05 2021

city: Almada

first: Ana

middle: Rita

last: Grosso

address: Campus de Caparica

department: Departamento Ciências da Vida

country: Portugal

institute: Unidade de Ciências Biomoleculares Aplicadas (UCIBIO)/Faculdade de Ciências e Tecnologia - Universidade Nova de Lisboa

summary: Transcriptome profiling of human umbilical vein endothelial cells (HUVECs) transduced with lentiviruses encoding FLAG-CAS9 nuclease and control- (gCTL) or cMYC-targeting (gMYC) gRNAS to identify cMYC regulated genes.

overall_design: HUVECs were engineered by CRISPR/CAS9 to ablate cMYC expression.  A pool of stable cells for control and MYC-depleted HUVECs was selected after puromycin treatment.

first: Jorge

last: Andrade

first: Barbara

last: Zimmermann

first: Stefan

last: Gunther

first: Michael

last: Potente


title: Genome-wide maps of FOXO1 binding sites in human endothelial cells

summary: ChIP-Seq profiling of human umbilical vein endothelial cells (HUVECs) overexpressing constitutively active FOXO1 to identify FOXO1 DNA binding sites and to assess changes in the histone modifications H3K4me3 and H3K27ac.

overall_design: HUVECs with or without constitutively active FOXO1 were analyzed 24 h post adenoviral transduction. FOXO1 binding and the histone modifications H3K4me3 and H3K27ac were analyzed by ChIP-seq with antibodies targeting FOXO1, H3K4me3 and H3K27ac.


title: A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression [Hi-C]

status: Public on Feb 23 2021

city: Chapel Hill

first: Zachary

last: Carico

state: NC

address: 250 Bell Tower Dr, CB7100

department: Integrative Biological and Genome Sciences program

institute: University of North Carolina

summary:
Purpose: Chromatin loop formation and maintenance is regulated by the cohesin complex. Here, we investigate whether a cancer mutation to a cohesin complex subunit, SMC1A-R586W, alters genome architecture.
Method: Genome wide chromatin looping patterns were assessed via Hi-C in both wildtype and CRISPR-Cas9 genome edited SMC1A-R586W mouse embryonic stem cells (mESCs).

overall_design: Hi-C was performed in wild type and SMC1A-R586W mESCs. Two replicates from wildtype cells were collected, and one replicate each of two SMC1A-R586W mES clones were collected.

first: Jill

last: Dowen

first: Holden

last: Stefan

first: Megan

middle: N

last: Justice


title: Transcriptional regulation by FOXO1 and 2HG in human endothelial cells


title: Cortical neuropathology RNA expression time-course after diffuse traumatic brain injury

status: Public on Nov 15 2020

city: Columbus

first: Kristina

middle: Grace

last: Witcher

address: 460 Medical Center Dr

department: Neuroscience

institute: Ohio State University

summary:
Traumatic brain injury (TBI) can lead to significant neuropsychiatric problems and neurodegenerative pathologies, which develop and persist years after injury. Neuroinflammatory processes evolve over this same period. Therefore, we aimed to determine the contribution of microglia to neuropathology at acute (1-day post-injury; dpi), subacute (7 dpi), and chronic (30 dpi) time-points. Microglia were depleted with PLX5622, a CSF1R antagonist, prior to midline fluid percussion injury in male mice and cortical neuropathology/inflammation was assessed using a neuropathology mRNA panel.
NanoString Neuropathology gene expression panel was used to quantify expression from RNA microdissected from the mouse cortex.

overall_design: Tissue was collected from mice fed either vehicle or PLX5622 (CSF1R inhibitor) diet; from both control (naïve) and injured (TBI) mice

first: Witcher

last: Kristina

first: Godbout

last: Jonathan


title: Transcriptomic analysis of cultured primed synovial fibroblasts from monosodium urate crystal-induced arthritis in the mouse (validation set of samples)

status: Public on Dec 24 2020

city: Erlangen

first: Steffen

last: Uebe

address: Kussmaulallee 4

department: Humangenetisches Institut

country: Germany

institute: Uniklinikum Erlangen

summary: Repeated challenge of synovial fibroblasts with MSU crystals in vivo induced inflammatory priming

overall_design: Differential gene expression analysis of cultured synovial fibroblasts derived from mouse joints 9 days after the first (-/MSU) or the second (MSU/MSU) injection of MSU crystals

first: Markus

last: Hoffmann

first: Arif

last: Ekici

first: Philipp

last: Kirchner


title: Epigenetic and chromatin profiling of wild-type and Dnmt3a-deficient B1 and B2 B cells. (RNA)

first: Vinay

last: Mahajan

summary: We have comprehensively interrogated wild type B1 and B2 B lineage cells and their progenitors. In mice bearing a conditional deletion of Dnmt3a in the B lineage, we integrated a variety of whole-genome profiling approaches including WGBS, TAB-Seq, RNA-seq, ATAC-Seq and CUT&RUN. The results reveal a stable “foundational methylome” in all B cells that establishes lymphocyte lineage identity. Superimposed on this foundational methylome is a “dynamic methylome” which is differentially modulated  in B1 and B2 B cells by the coincident activity/recruitment of DNMT3A and TET enzymes.

overall_design: We compared the transcriptomes of wild-type and Dnmt3a-deficient B1 and B2 B cells.


title: Epigenetic and chromatin profiling of wild-type and Dnmt3a-deficient B1 and B2 B cells. (CUT&RUN)

overall_design: We profiled and compared the histone modifications of wild-type and Dnmt3a-deficient B1 and B2 B lineage cells using CUT&RUN.


title: HIF1α/HIF2α-miR210-3p network promotes glioblastoma proliferation and tumorigenesis through EGFR-PI3K/AKT signaling pathway with a positive feedback

status: Public on Nov 24 2020

city: Chongqing

first: liao

last: bin

address: 118 Xingguang Avenue

institute: Chongqing General Hospital, Chongqing University

type: Non-coding RNA profiling by high throughput sequencing

summary: HIF1α promotes glioblastoma cell proliferation and tumorigenesis under hypoxia conditions, leading to poor prognosis; however, none of the targeted therapies of HIF1α for glioblastoma is success nowadays. Therefore, we focused to look for the reason and wondered whether HIF2α contributed GBM growth. We did gene-chip and found that HIF2α contributed to the malignant progression of glioblastoma while blocking of HIF1α. Furthermore, our results revealed knock-out of HIF1α and HIF2α simultaneously improved the chemo-sensitization significantly. Moreover, miR-210-3p induced HIF1α expression but inhibited HIF2α, which meant the existence of regulation of cycle between HIF1α/HIF2α and miR-210-3p. Traditional studies have proved EGF as an upstream gene regulator of HIF1α in hypoxia conditions through EGFR-PI3K/AKT-mTOR signaling pathway. However, in this study, besides the signaling pathways mentioned above, we found the upstream regulators HIF1α and HIF2α also promoted EGF with the binding regions AGGCGTGG and GGGCGTGG. Briefly, in hypoxia microenvironment HIF1α/HIF2α-miR210-3p network promotes malignant progression of glioblastoma through EGFR-PI3K/AKT-mTOR signaling pathway with a positive feedback.

overall_design: The control cells without HIF1α and HIF2α interference, HIF1α-ko, HIF2α-ko and HIF1α/HIF2α knock-out simultaneously cells were cultured under hypoxia conditions for 24h and then the cells were collected. The cells were then sent to undergo miRNA-Seq.

first: Pan

last: Wang

first: Sheng

last: Gong

first: Lu

last: Zhao

last: WU

first: Bin

last: Liao


title: Development and application of a high-throughput gene expression profiling of per- and polyfluoroalkyl substances (PFAS) in primary liver human spheroids to inform read-across

status: Public on Dec 22 2020

city: Ottawa

first: Matthew

last: Meier

state: Ontario

address: 251 Sir Frederick Banting Driveway

department: Health Canada

country: Canada

institute: Government of Canada

summary: Study of PFAS chemicals

overall_design: PFAS TempO-Seq Experiment: Sequencing data from 10 concentrations, 4 time points from PFOS, PFOA, PFBS, PFDS

first: Andrea

last: Rowan-Carroll

first: Karen

last: Leingartner

first: Byron

last: Kuo

first: Remi

last: Gagne

first: Andrew

last: Williams

first: Julie

last: Bourdon-Lacomb

first: Anthony

last: Reardon

first: Ivy

last: Moffat

first: Stephen

last: Ferguson

first: Luigi

last: Lorusso

first: Christine

last: Levicki

first: Ella

last: Atlas

first: Carole

last: Yauk


title: Cryptococcus neoformans reactivation in different media and temperatures

status: Public on Aug 26 2020

city: Edinburgh

first: Edward

middle: William Joseph

last: Wallace

address: Waddington Building, Max Born Crescent

department: Institute for Cell Biology, School of Biological Sciences

country: United Kingdom

institute: University of Edinburgh

summary:
We wanted to find out the transcriptomic response of growth-arrested Cryptococcus yeast cells when initially placed in environments in which they could reactivate or "wake up", focusing on the difference between a rich microbial media (YPD) and a common cell culture media, RPMI + 10% heat-inactivated fetal calf serum.

Please contact Edward.Wallace@ed.ac.uk if you use this data and ask for citation information; we are currently (August 2020) working on a publication.

overall_design: 36-sample RNA-seq timecourse of reactivation of growth-arrested Cryptococcus neoformans H99 in two media at two temperatures. Two biological samples of cells were pre-grown for 5 days in 10mL YPD. A sample of this was taken as the "0 minute" control timepoint. We then inoculated to OD 0.1 in 4 different cultures of 100mL pre-warmed media: (YPD, RPMI+) x (25C, 37C), and grew for 10, 30, 60, or 120 min. We also obtained a timepoint in more standard growth conditions of YPD, 30C, 180mins.

first: Elizabeth

last: Ballou


title: Single-cell RNAseq of Normoxic and OIR mouse retina by Drop-seq

status: Public on Aug 20 2020

city: Montréal

first: Gael

middle: Louis Max

last: Cagnone

state: QC

address: 3175 Chemin de la Côte-Sainte-Catherine

department: The Montreal single-cell Academy

institute: CHU Sainte Justine

summary: Proliferative retinopathy is associated with abnormal vascular development (neovascularisation) of the retina. In mouse, the oxygen-induced retinopathy (OIR) model mimics the proliferative retinopathy found in extreme premature babies (Retinopathy of Prematurity) and in patients suffering from diabetic retinopathy. Using Drop-seq, we performed single-cell RNAseq analysis of mouse retina under physiological, normoxic (NORM) condition and retina under OIR condition, at postnatal day 14 and day 17, periods associated with a peak of neovascularisation. We used both whole retina cells or rod (CD73) depleted retina cells. Sorting conditions (whole vs. rod-depleted) derived count matrices were aligned with Seurat CCA and processed for dimensionality reduction and clustering.

overall_design:
We analysed the effect of OIR/NORM by single-cell RNAseq (Drop-seq) of C57B6 retina (whole retina n =7, and rod-depleted n=5) from P14 and P17 animals.

Contributor: Vision Health Research Network

first: G

first: F

last: Wünnemann

first: S

last: Leclerc

first: P

last: Sapieha

last: Andelfinger

first: J

last: Joyal


title: Single-cell atlas of human leptomeningeal metastasis

status: Public on Jul 16 2020

city: Leuven

first: Jan

last: Remsik

address: Campus Gasthuisberg, Herestraat 49

department: Center for Cancer Biology

country: Belgium

institute: VIB

summary: The tumor microenvironment plays a critical regulatory role in cancer progression, especially in metastases to the central nervous system. Cancer cells inhabiting the cerebrospinal spinal fluid (CSF)-filled leptomeningeal space face substantial microenvironmental challenges including inflammation and sparse extracellular iron. Unlike CSF leukocytes, we find that cancer cells within the CSF express the iron-binding protein LCN2 and its receptor SCL22A17. Employing mouse models of LM, we find that the LCN2/SLC22A17 system is necessary to support leptomeningeal cancer cell growth. We find that infiltrating CSF macrophages generate inflammatory cytokines that induce cancer cell LCN2 expression. This LCN2/SLC22A17 system provides cancer cells superior access to limiting extracellular iron, allowing LCN2-expressing cancer cells to outcompete CSF macrophages for this resource. Finally, pharmacologic interruption of these interactions prevents cancer cell growth within the leptomeninges.

overall_design: 10x single-cell RNA-sequencing of human leptomeningeal metastasis

first: Yudan

last: Chi

first: Vaidotas

last: Kiseliovas

first: Dana

last: Pe'er

first: Linas

last: Mazutis

first: Adrienne

last: Boire


title: Histone ChIP-seq from middle frontal area 46 (ENCSR798YAU)

first: ENCODE

last: DCC

summary:
H3K27me3 ChIP-seq on dorsolateral prefrontal cortex tissue female adult (84 years) originated from dorsolateral prefrontal cortex

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


title: Dissecting esophageal squamous-cell carcinoma ecosystem by single-cell transcriptomic analysis

status: Public on Oct 29 2020

city: Beijing

first: Xiannian

last: Zhang

address: 10 YouAnMen Xitoutiao, Fengtai District

department: Department of neurology

institute: Captital Medical University

summary: Esophageal squamous-cell carcinoma (ESCC), one of the most prevalent and lethal malignant disease, has a complex but unknown tumor ecosystem. Here, we decipher for the first time the full compositions of ESCC tumor based on analyzing 208,659 single-cell transcriptomes in ESCC derived from 60 individuals. We identify 8 essential expression programs from malignant epithelial cells and discovered 43 cell types including 26 immune cell and 17 nonimmune stromal cell subtypes in the tumor microenvironment (TME), and also explicate the interactions between cancer cells and other cells and the interactions among different cell types in the TME. Moreover, we have linked the cancer cell transcriptomes to the somatic mutations and identified several markers significantly associated with survival time in patients, which may be relevant to precision cares of ESCC patients. These results renew our understanding of ESCC and provide a valuable example and resource for investigating other types of solid tumor.

overall_design:
We performed scRNA-seq on 60 ESCC tumor and 4 adjacent normal tissue samples obtained from 60 individuals using 10X Genomics platform.
Raw data is available at https://bigd.big.ac.cn/gsa-human/ under the accession ID of HRA000195.

For the details or customized demand of Raw and Processed data, please feel free to contact Prof Zhang (xiannian@ccmu.edu.cn). We are glad to help.

first: Linna

last: Peng

first: Yingying

last: Guo

first: Wenjia

first: Jiacheng

last: Yao

first: Mingming

last: Shao

first: Wenyi

last: Fan

first: Yamei

last: Chen

first: Qionghua

last: Cui

first: Yiyi

last: Xi

first: Yanxia

last: Sun

first: Xiangjie

last: Niu

first: Xuan

last: Zhao

first: Liping

first: Yuqian

last: Wang

first: Yachen

last: liu

first: Jianbin

first: Chen

last: Wu

first: Dongxin

last: Lin


title: Targeting CD38 with Daratumumab in refractory Systemic Lupus Erythematosus

status: Public on Sep 11 2020

city: Berlin

first: Pawel

last: Durek

address: Charitéplatz 1

institute: Deutsches Rheuma-Forschungszentrum

summary: Single cell transcriptome and TCR sequencing of FACS-sorted memory T cells in one patient under treatment with the anti CD38-antibody Daratumumab. The patient received Daratumumab at days 0, 7, 14 and 21. Analyses were performed on day 0, 41 and 74.

overall_design: Sequencing of RNA and TCR was performed from FACS sorted memory (not CD45+CCR7+) T cells from the peripheral blood of 1 patient with the anti-CD38 antibody Daratumumab on day 0, 41 and 74, using the 10X Genomics platform with the Single Cell 5’ Library & Gel Bead Kit

first: Lennard

last: Ostendorf

first: Gitta

last: Heinz

first: Panagiotis

last: Garantziotis

first: Frederik

last: Heinrich

first: Falk

last: Hiepe

first: Andreas

last: Radbruch

first: Mir-Farzin

last: Mashreghi

first: Tobias

last: Alexander


title: Macrophage Gene Expression in PyMT Tumor Progression

status: Public on Sep 02 2020

city: San Francicso

first: Allison

last: Drain

address: 513 Parnassus Ave HSE 560

institute: UCSF

summary: Exome sequencing on macrophages sorted by flow cytometry from the mammary gland of 8- and 11-week-old female PyMT mice

overall_design: We report the identification of distinct gene expression profiles from macrophages sorted from early vs. late PyMT mammary gland tumors. The mammary glands of female FVB/n MMTV-PyMT mice were collected, digested, and stained with fluorescently tagged antibodies for immune cell markers to enable flow sorting of macrophages.

first: Valerie

last: Weaver

first: Ori

last: Maller

first: Kirk

last: Hansen


title: Transcriptome of human endothelial cells treated with R-2HG or S-2HG

first: Ana

last: Grosso

summary: Transcriptome profiling of human umbilical vein endothelial cells (HUVECs) treated with R-2HG or S-2HG to identify isomer-specific gene regulation.

overall_design: Analysis of HUVECs treated for 24h with cell-permeable R-2HG or S-2HG compared to control vehicle (DMSO).

first: Jorge

last: Andrade

first: Barbara

last: Zimmermann

first: Stefan

last: Gunther

first: Michael

last: Potente


title: Transcriptome changes in human endothelial cells with constitutively active FOXO1

summary: Transcriptome profiling of human umbilical vein endothelial cells (HUVECs) overexpressing constitutively nuclear FOXO1 to identify FOXO1 target genes.

overall_design: Analysis of HUVECs transduced with an adenovirus encoding for an AKT-insensitive (nuclear) FOXO1 mutant compared to HUVECs transduced with a control adenovirus (Ad-Null). Expression analysis was performed 16h, 24h and 32h post transduction.


title: Cancer cells deploy lipocalin-2 to collect limiting iron in leptomeningeal metastasis

first: Jan

last: Remsik

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

overall_design: Refer to individual Series


title: The transcription factor EGR2 is the molecular linchpin connecting STAT6 activation to the stable epigenomic program of alternative macrophage polarization

status: Public on Sep 15 2020

city: New York

first: Laszlo

last: Halasz

address: 1470 Madison Avenue

department: Department of Oncological Sciences

institute: Mount Sinai Icahn School of Medicine

summary: Macrophages polarize into functionally distinct subtypes while responding to microenvironmental cues. The identity of proximal transcription factors (TFs) downstream of the polarization signals are known, but their activity is typically transient, failing to explain the long-term, stable epigenomic programs developed. Here, we mapped the early and late epigenomic changes of interleukin-4 (IL-4)-induced alternative macrophage polarization. We identified the TF, Early Growth Response 2 (EGR2), bridging the early-transient and late-stable gene expression program of polarization. EGR2 is a direct target of IL-4-activated STAT6, having broad action indispensable for 77% of the induced gene signature of alternative polarization, including its autoregulation and a robust, downstream TF cascade involving PPARG. Mechanistically, EGR2 binding results in chromatin opening and the recruitment of chromatin remodelers and RNA-polymerase II. Egr2 induction is evolutionarily conserved during alternative polarization of mouse and human macrophages. In the context of tissue resident macrophages, Egr2 expression is most prominent in the lung of a variety of species. Thus, EGR2 is an example of an essential and evolutionarily conserved broad acting factor, linking transient polarization signals to stable epigenomic and transcriptional changes in macrophages.

overall_design: Transcriptomic and epigenetic profiling of IL-4 treated bone-marrow derived macrophages (BMDMs), using high throughput sequencing (RNA-seq, ChIP-seq and ATAC-seq).

last: Nagy


title: Different expression profiles of lncRNAs, mRNAs and circRNAs in degenerative and healthy cervical cartilage endplate (ceRNA)

status: Public on Jul 04 2020

city: Nanchang

first: Jinghong

last: Yuan

state: Jiangxi

address: No.1 Minde Road

institute: The Secondly Affiliated Hospital of Nanchang University

summary: The degeneration of cartilage endplate in cervical disc is considered as a basis of cervical spondylosis. Owing to the important role of post-transcriptional gene regulation in phenotypes and functions of cells, non-coding ribonucleic acid (ncRNA) molecules contributed to the regulation.Degenerated cervical vertebral endplate cartilage specimens were collected from patients with cervical intervertebral disc degeneration (CIDD) that suffered from cervical spondylosis myelopathy, who had received anterior cervical discectomy and fusion (ACDF). CE specimens of healthy subjects were obtained from patients with a cervical fracture who received ACDF at The Second Affiliated Hospital of Nanchang University (Nanchang, China) and adopted SBC human ceRNA array V1.0（4×180K）. The results revealed that expressions of369 lncRNAs, 246 mRNAs, 578 circRNAs were different between degenerated cartilage endplate and healthy cartilage endplate. The functions of differentially expressed lncRNAs and co-expressed potential targeting genes were predicted by analyzing Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) biological pathway analysis. Furthermore, we analyzed and find the co-expression and interaction patterns of different RNAs and possible ceRNA mechanism. The present study provided a systematic perspective on the potential function of non-coding RNAs (ncRNAs) in the degeneration of cartilage endplate in CIDD.

overall_design: 6 cartilage endplate of cervical disc samples from 3  patients with cervical spondylosis myelopathy and 3 healthy subjects were obtained from patients with a cervical fracture who received ACDF. there were no replicates, control and/or reference Samples or dye-swaps.

first: Jingyu

last: Jia

first: Tianlong

last: Wu

first: Xigao

last: Cheng


title: Epigenetic Inheritance of DNA Methylation Changes in Fish Living in Hydrogen Sulfide-rich Springs

status: Public on Dec 09 2020

city: Pullman

last: Skinner

state: WA

address: Abelson 507

department: SBS

institute: WSU

summary: Although hydrogen sulfide is toxic to most organisms, a fish, Poecilia mexicana, has adapted to survive in environments with high levels of hydrogen sulfide. The epigenetic changes in response to this environmental stress were examined by assessing DNA methylation alterations in the nucleated red blood cells (RBC) in the fish. In addition to collecting wild males and females from sulfidic and non-sulfidic environments, wild males and females in these environments were collected and moved to a non-sulfidic environment in the laboratory and propagated for two generations in a non-sulfidic environment. We compared epimutations between sexes and field and laboratory populations. The F0 generation sulfidic wild fish were compared to the non-sulfidic wild fish and found to have significant differential DNA methylation regions (DMRs) in the RBC DNA. The F2 generation laboratory fish were also compared between the sulfidic and non-sulfidic populations, and a significant number of DMRs were also identified. The DMRs have stable generational inheritance in the absence of the sulfidic environment. The DMRs in the F0 generation wild fish had an over 80% overlap with the F2 generation laboratory non-sulfidic environment propagated fish. This is one of the first examples of epigenetic generational stability after the removal of an environmental stressor. The DMR associated genes were found to be relevant to sulfur toxicity and metabolism processes.

overall_design: Wild P. mexicana males and females from sulfidic and non-sulfidic environments were collected. Additionally, wild males and females in these environments were collected and moved to a non-sulfidic environment in the laboratory and propagated for two generations in a non-sulfidic environment. We compared epimutations between sexes and field and laboratory populations.

first: Joanna

last: Kelley

last: Tobler

first: Daniel

last: Beck

first: Ingrid

last: Sadler-Riggleman

first: Corey

last: Quackenbush

first: Lenin

last: Rodriguez


title: A Thalamic Orphan Receptor Drives Variability in Short Term Memory

status: Public on Oct 01 2020

city: Ithica

first: Praveen

last: Sethupathy

address: Cornell University College of Veterinary Medicine, Box 17

institute: Cornell University

summary: Working memory is a form of short-term memory that involves maintaining and updating task relevant information toward goal-directed pursuits. Classical models posit persistent activity in prefrontal cortex (PFC) as a primary neural correlate, but emerging views suggest additional mechanisms may exist. We screened ~200 genetically diverse mice on a working memory task and identified a genetic locus on Chromosome 5 that contributes to a substantial proportion (17%) of the phenotypic variance. Within the locus, we identified a gene encoding an orphan G-protein coupled receptor, Gpr12, which is sufficient to drive substantial and bi-directional changes in working memory. Molecular, cellular, and imaging studies revealed that Gpr12 enables high thalamus-PFC synchrony to support memory maintenance and choice accuracy. These findings identify a novel orphan receptor as a potent modifier of short-term memory, and supplement classical PFC-based models with an emerging thalamus-centric framework for the mechanistic understanding of working memory.

overall_design: Examination of short term memory using Diversity Outbred mice and interrigation through QTL and RNAseq analysis.

first: Priiya

last: Rajasethupathy

first: Matt

last: Kanke


title: Circulating MicroRNAs and Treatment Response in Childhood Asthma

status: Public on Jul 08 2020

city: Boston

first: Jiang

last: Li

state: Massachusetts

address: 181 Longwood Avenue

department: Medicine

institute: Brigham and Women's Hospital

summary: Total RNA was isolated from serum samples by the Qiagen miRNeasy Serum/Plasma extraction kit and QIAcube automation. All samples were quantified using the Nanodrop spectrophotometer prior to plating. Small RNA-seq libraries were prepared using the Norgen Biotek Small RNA Library Prep Kit and then sequenced on the Illumina NextSeq 500 platform at 51bp single end reads. ExceRpt was employed to assess the read quality and annotate miRNAs. The read count was log transformed and normalized by quantile normalization.

overall_design: Stratified analysis in treatment group and interaction analysis between treatment group and placebo group.

first: Ronald

last: Panganiban

first: Alvin

middle: T

last: Kho

middle: J

last: McGeachie

first: Leanna

last: Farnam

first: Robert

last: Chase

first: Scott

last: Weiss

first: Quan

last: Lu

first: Kelan

middle: G

last: Tantisira


title: Expression data of kidneys from Wild-type (WT) or Mincle-deficient (KO) mouse subjected to renal ischemia-reperfusion injury.

status: Public on Jul 15 2020

city: nagoya

first: Marie

last: Saka-Tanaka

state: aichi

address: furoutyou tikusaku

department: Department of  Molecular Medicine and Metabolism

institute: nagoya university

summary:
Mincle (Macrophage inducible C-type lectin) is a pattern recognition receptor expressed in innate immune cells and can sense cell death, suggesting a role in sterile inflammation. We induced renal ischemia–reperfusion injury to KO and WT mice and collected the kidneys to compare the gene expression.
Microarray analysis revealed that the overlap between the genes upregulated in injured kidney vs. sham kidney in WT mice and the genes downregulated in injured kidney in KO mice vs. WT mice included inflammation-related pathways on day 3.

overall_design: We induced renal ischemia–reperfusion injury and collected kidneys at day 1 and day 3 for RNA extraction and hybridization on Affymetrix microarrays.

first: Miyako

last: Tanaka

first: Takayosi

last: Suganami


title: Single cell sequencing of murine ApoB-reactive CD4+ T cells

status: Public on May 21 2020

city: La Jolla

first: Klaus

last: Ley

address: 9420 Athena Cir

institute: La Jolla Institute for Immunology

summary: We report the single cell transcriptome of atherosclerosis-specific murine CD4+ T cells that recognize a peptide from ApoB-100, the core protein of low-density lipoprotein (LDL). Our data reveal a unique single cell transcriptome of ApoB-specific T cells that is similar to T-regulatory T but shows an overlap with the transcriptome of pathogenic T-helper type -1 and -17 cells on a single cell level.

overall_design: We used a novel tetramer of MHC-II to track CD4+ T cells reactive to the mouse self-peptide ApoB978-993 (ApoB+). ApoB+ T cells were isolated by flow cytometry and MHC-II tetramer staining from peripheral lymph nodes of atherosclerotic ApoE-deficient mice. Their transcriptome (scRNAseq) was compared to non-specific T cells (ApoB-neg.).

first: Dennis

last: Wolf

first: Teresa

last: Gerhard

first: Holger

last: Winkels

first: Nathaly

last: Anto Michel

first: Akula

last: Pramod

first: Yanal

last: Ghosheh

first: Simon

last: Brunel

first: Konrad

last: Buscher

first: Jacqueline

last: Miller

first: Sara

last: McArdle

first: Livia

last: Baas

first: Kouji

last: Kobiyama

first: Melanie

last: Vassallo

first: Erik

last: Ehinger

first: Thamotharampillai

last: Dileepan

first: Amal

last: Ali

first: Maximilian

last: Schell

first: Zbigniew

last: Mikulski

first: Daniel

last: Sidler

first: Takayuki

last: Kimura

first: Xia

last: Sheng

first: Hauke

last: Horstmann

first: Sophie

last: Hansen

first: Lucia

last: Sol Mitre

first: Peter

last: Stachon

first: Ingo

last: Hilgendorf

first: Dalia

last: Gaddis

first: Catherine

last: Hedrick

first: Chris

middle: A

last: Benedict

first: Bjoern

last: Peters

first: Andreas

last: Zirlik

first: Alessandro

last: Sette


title: Transcriptional changes in kidney allografts with histology of antibody-mediated rejection

status: Public on Nov 10 2020

first: Jasper

last: Callemeyn

address: Herestraat 49

department: Microbiology, Immunology and Transplantation

institute: KU Leuven University

summary:
Circulating anti-HLA donor-specific antibodies (HLA-DSA) are often absent in serum of kidney allograft recipients with biopsies demonstrating histology of antibody-mediated rejection (ABMRh).
In this multicenter study, we aimed to elucidate whether the transcriptional profile of biopsies with HLA-DSA negative ABMRh can indicate an undetected humoral etiology, or whether HLA-DSA negative ABMRh should be considered as a distinct histomolecular entity.

overall_design: We performed microarray analysis of 224 kidney allograft biopsies, collected from unique recipients in 4 European centers. The transcriptional profile of biopsies without ABMRh (n=168), DSA negative ABMRh (n=26) and DSA positive ABMRh (n=30) was compared.

first: Maarten

last: Naesens


title: Pathogenic autoimmunity in atherosclerosis evolves from initially protective ApoB-reactive CD4+ T-regulatory cells

first: Klaus

last: Ley


title: H3K36 methyltransferase SETD2 regulates lymphoid and neural development [MIXCR]

status: Public on Mar 23 2020

first: Scott

last: Armstrong

address: 450 Brookline Ave

department: pediatric oncology

institute: Dana Farber Cancer Institute

summary: Complete Amplicon Sequencing of a 500bp  V(D)J recombination products from proB cells sorted from control and Setd2KO mice to Vh558, Vh7183 and Vhq52 variable gene familes to JH4 joining gene fragment to determine CDR3

overall_design: Genomic DNA from proB cells (B220+Cd43+IgM-CD25-) sorted from control and Setd2 knockout mice were isolated and subjected to V(D)J recombination PCR using a primer for either Vh558, Vh7183, or Vhq52 gene families and JH4 gene.  This 500bp PCR fragment was extracted and subjected to NGS (single 150bp read of amplicon pair)

first: Haihua

last: Chu

first: Charlie

last: Hatton


title: RNA-sequencing of ApoB-reactive CD4+ T cells in mice

summary: We report the transcriptome of atherosclerosis-specific murine CD4+ T cells in atherosclerosis that recognize a peptide from ApoB-100, the core protein of low-density lipoprotein (LDL). Our data reveal a unique transcriptome of ApoB-specific T cells that is similar to T-regulatory T cells and changes during disease progression in a pathogenic T-helper type -1 and -17 like transcriptome.

overall_design: We used a novel tetramer of MHC-II to track CD4+ T cells reactive to the mouse self-peptide ApoB978-993 (ApoB+). ApoB+ T cells were sorted by flow cytometry from peripheral lymph nodes at different time points in atherosclerotic or healthy ApoE-deficient mice and their transcriptome by scRNAseq was compared to non-specific T cells (ApoB-neg.).

first: Dennis

last: Wolf

first: Teresa

last: Gerhard

first: Holger

last: Winkels

first: Nathaly

last: Anto Michel

first: Akula

last: Pramod

first: Yanal

last: Ghosheh

first: Simon

last: Brunel

first: Konrad

last: Buscher

first: Jacqueline

last: Miller

first: Sara

last: McArdle

first: Livia

last: Baas

first: Kouji

last: Kobiyama

first: Melanie

last: Vassallo

first: Erik

last: Ehinger

first: Thamotharampillai

last: Dileepan

first: Amal

last: Ali

first: Maximilian

last: Schell

first: Zbigniew

last: Mikulski

first: Daniel

last: Sidler

first: Takayuki

last: Kimura

first: Xia

last: Sheng

first: Hauke

last: Horstmann


title: H3K36 methyltransferase SETD2 regulates lymphoid and neural development [RNA-seq]

first: Scott

last: Armstrong

summary: Transcript analysis of RNA from murine proB cells to determine B cell repertoire and variable gene usage

overall_design: RNA proB cells (B220+Cd43+IgM-CD25-) sorted from control and Setd2 knockout mice was analyzed for expression and use in the TRUST B/T cell repertoire algorithm

first: Haihua

last: Chu

first: Charlie

last: Hatton


title: The genome-wide transcriptional consequences of the deletions of sulfur metabolism genes in Drosophila melanogaster

status: Public on Apr 07 2020

city: Moscow

first: Alexander

middle: Pertovich

last: Rezvykh

state: Moscow

address: Vavilova, 32

department: Russian Academy of Sciences

country: Russia

institute: Engelhardt Molecular Biology Institute

summary: The gasotransmitter hydrogen sulfide (H2S), produced by transsulfuration pathway, in recent years has been recognized as a biological mediator playing important role under normal conditions and in various pathologies both in eukaryotes and prokaryotes. The transsulfuration pathway (TSP) includes the conversion of homocysteine to cysteine following the breakdown of methionine.   In Drosophila melanogaster and other eukaryotes H2S is produced by cystathionine B-synthase (CBS), cystathionine y-lyase (CSE), and 3-mercaptopyruvate sulftransferase (MST). In the experiments reported here we were able exploring CRISPR technique to obtain single and double deletions of these three major genes responsible for H2S production. In most cases the deletion of one studied gene does not result in the compensatory induction of two other genes responsible for H2S production. Transcriptomic studies demonstrated that the deletions of the above genes alter the genome expression to different degree with more pronounced effect exerted by deletions of CBS gene. Furthermore, the double deletion of both CBS and CSE resulted in cumulative effect on the transcription in the resulted strains. Overall, we found that the obtained deletions affected numerous genes involved in various biological pathways. Characteristically, genes involved in oxidative reduction process, stress-response genes, house-keeping genes, genes participating in olfactory and reproduction were among the most affected. Furthermore, characteristic differences in the response to the deletions of the studied genes were apparently organ specific and have clear-cut gender character. Importantly, the deletions altered global methylation and chromatin state of the experimental strains by increasing the level of inactive chromatin of the genome. Single and double deletions of the three genes responsible for the production of H2S helped to understand new aspects of biological significance of this vital physiological mediator.

overall_design: 5-day old whole fly derived mRNA transcriptome profiling in background of deletions of CBS,CSE,MST genes, implicated in sulfur metabolism

first: A


title: S6K2 IS A NOVEL TARGET IN MAPKi-RESISTANT NRAS-MUTANT MELANOMA

status: Public on Mar 06 2020

city: Philadelphia

first: Priyankara

last: Wickramasinghe

state: PA

address: 3601 Spruce Street

department: Bioinformatics

institute: The Wistar Institute

summary: Melanoma is often driven by NRAS mutations. Although oncogenic NRAS activates MAPK signaling, inhibition of this pathway has limited efficacy in NRAS-mutant tumors. As there are limited options to treat these tumors, there is a pressing need to identify NRAS-mutant-specific vulnerabilities that can be therapeutically exploited.  Metabolic reprogramming is one of the hallmarks of RAS-mutant tumors, creating a dependency on key metabolic pathways. This dependency could be leveraged to combat these tumors.  We discovered that abrogation of S6K2, a mTORC1 effector, triggers accumulation of unsaturated fatty acids, lipid peroxidation and cell death selectively in NRAS-mutant melanoma cells that are resistant to MAPK inhibition.  S6K2 depletion induced upregulation of S6K1 and PPAR, triggering apoptotic and ferroptosis-like cell death.   Conversely, depletion of S6K1 diminished lipid synthesis and cell proliferation, without eliciting cell death.  Collectively, our data indicate that a fine balance between S6K1 and S6K2 activity and metabolic homeostasis is required to prompt cell death of NRAS-mutant melanoma.  S6K2 is hence a novel therapeutic target for MAPKi-resistant NRAS-mutant melanoma.

overall_design: RNA-seq for WT, and knockdown of S6K1 and S6K2

first: Jessie

last: Villanueva

first: Hsin-Yi

last: Chen


title: Single-cell RNA-seq data of Arabidopsis root

status: Public on Jul 02 2020

city: Durham

first: Philip

middle: N.

last: Benfey

state: North Carolina

address: 130 Science Drive

department: Biology

institute: Duke University

summary: We report both raw and processed scRNA-seq data that are used to build transcriptomic atlas of Arabidopsis root.

overall_design:
scRNA-seq of 18 wild-type, 2 scr-4 and 2 shr-2 mutant Arabidopsis root samples. Three wild-type samples are from published data (two from Denyer et al. 2019 [PMID: 30913408] and one from Ryu et al. 2019 [PMID: 30718350]).
Denyer et al. (GSE123818): GSM3511858, WT Arabidopsis root cells - dc1; GSM3511859, WT Arabidopsis root cells - dc2
Ryu et al. (GSE123013): GSM3490689, WT Arabidopsis root cells - pp1

first: Rachel

last: Shahan

first: Che-Wei

last: Hsu

first: Trevor

last: Nolan

first: Benjamin

last: Cole

first: Isaiah

middle: W

last: Taylor

first: Laura

last: Greenstreet

first: Stephen

last: Zhang

first: Anton

last: Afanassiev

first: Anna

last: Vlot

first: Geoffrey

last: Schiebinger

first: Uwe

last: Ohler


title: A stem cell-driven lymphoangiogenic switch coordinates tissue regeneration

status: Public on Feb 19 2020

first: Hanseul

last: Yang

state: NY

address: 1230 York Avenue

institute: Rockefeller University

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

overall_design: Mouse hair follicle stem cells were purified from Krt14-H2BGFP mice along the hair cycle. The sorted cells were analyzed by RNAseeq.

first: Shiri

last: Gur-Cohen

first: Elaine

last: Fuchs


title: RNA sequencing from the microglia of mice with acute GvHD against syngeneic bone marrow transplanted and untreated controls

status: Public on Jan 13 2020

city: Freiburg

first: Geoffroy

last: Andrieux

address: Breisacherstr 153

institute: University clinics Freiburg

summary: Understanding the role of myeloid cells in GvHD of CNS. Microglia are the major immune cells of the CNS. We intend to understand if microglia play a role in GvHD of the CNS.

overall_design: In order to study this, mice were lethally irradiated and transplanted with either syngeneic or allogeneic bone marrow and T cells. We isolated  RNA from sorted microglia cells of the brain on day14 after transplantation to understand the molecular changes occurring within microglia. Four mice were analyzed per group

first: Janaki

middle: M

last: Vinnakota

first: Robert

last: Zeiser

first: Melanie

last: Boerries


title: H3K36 methyltransferase SETD2 regulates NHEJ during lymphoid and neural development

first: Richard

last: Koche

state: New York

institute: Memorial Sloan Kettering Cancer Center

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

overall_design: Refer to individual Series


title: Cellular milieu of the neural retina informs complement immune regulation

status: Public on Jan 24 2020

first: Dwight

middle: Edward

last: Stambolian

address: 422 Curie Blvd.

department: Opthalmalogy

institute: University of Pennsylvania

sample_organism:
Homo sapiens
Mus musculus

platform_organism:
Homo sapiens
Mus musculus


title: Differential gene expression profiles between two novel murine prostate cancer cell lines derived from androgen‑dependent (PLum‑AD cells) and androgen‑independent (PLum‑AI cells) prostate cancer

status: Public on May 27 2020

city: Beirut

first: Wassim

last: Abou-Kheir

address: Bliss St. DTS Bldg.

department: Department of Anatomy, Cell Biology, and Physiological Sciences

country: Lebanon

institute: American University of Beirut

summary:
Orthotopic tumors were previously generated from parental Prostate Luminal (PLum) cells under androgen‑dependent (PLum-AD) and androgen‑independent (PLum-AI) conditions in order to establish cellular models of prostate cancer progression (Abou-Kheir et al., 2011; doi: 10.1371/journal.pone.0026112).
We used microarrays to evaluate the differential gene expression profiles underlying progression of prostate cancer from primary androgen-dependent stage to advanced androgen-independent stage using newly isolated murine prostate cancer cell lines. Those cell lines represent novel in vitro models of androgen‑dependent and –independent prostate cancer, recapitulating the progression of the disease to a more invasive phenotype upon androgen deprivation.

overall_design: A total of 3 microarray analyses representing 3 biological replicates were conducted for each of the two cell lines: PLum-AD and PLum-AI.

first: Hisham

middle: F

last: Bahmad


title: MLL-Menin inhibition reverses pre-leukemic progenitor self-renewal induced by NPM1c mutations [ChIP-Seq]

status: Public on Feb 11 2020

first: Scott

last: Armstrong

summary: Menin binding to MLL1 is required to maintain self-renewal properties of NPM1c progenitors at different stages of leukemia development

overall_design: Mouse NPM1c knock-in cells and human AML cell lines  carrying NPM1c mutations were analyzed for the gene expression changes induced by NPM1c and in response to Menin inhibitor VTP-50469.

first: Hannah

last: Uckelmann

first: Charlie

last: Hatton


title: Genome-wide replication dynamics quantification reveals stress-induced delayed/under-replication as a hallmark of CFSs

status: Public on Dec 29 2019

city: Paris

first: Chunlong

last: Chen

address: 26 rue d’Ulm

country: France

institute: Institut Curie

summary: We report Repli-Seq analysis of the replication program in human lymphoblasts grown in the absence or in the presence of aphidicolin, an inhibitor of replicative DNA polymerases used in vitro to destabilize CFSs. We identified regions displaying specific replication delay upon aphidicolin treatment, resulting in under-replication. We then further study the mechanisms leading to such specific delayed/under-replication within CFSs and show that transcription-dependent segregation of initiation events out of the gene body generates long-traveling forks in large transcribed domains, which elicits the replication timing delay responsible for CFS instability upon replication stress.

overall_design: Repli-Seq experiments of human lymphoblastoid cells grown in the absence (3 biological replicates) or in the presence of 600 nM aphidicolin of 16h (2 biological replicates).

first: Sami

last: EL-Hilali

first: Olivier

last: Brison

first: Dana

last: Azar

first: Stéphane

last: Koundrioukoff

first: Mélanie

last: Schmidt

first: Viola

last: Naehse-Kumpf

first: Yan

last: Jaszczyszyn

first: Anne-Marie

last: Lachages

first: Bernard

last: Dutrillaux

first: Claude

last: Thermes

first: Michelle

last: Debatisse

first: Chun-Long


title: Identifying genomic predictors of sensitivity to immune checkpoint therapy in mouse models of TNBC

status: Public on Nov 13 2019

city: Chapel Hill

first: Charles

middle: M.

last: Perou

address: 12-044 Lineberger Comprehensive Cancer Center CB# 7295

department: Professor of Genetics, and Pathology & Laboratory Medicine; Lineberger Comprehensive Cancer Center

institute: University of North Carolina at Chapel Hill

summary: We created new mouse mammary tumor models to identify biomarkers of sensitivity to immune checkpoint inhibitors. Using these models in a syngeneic transplant system and treating with anti-PD1/anti-CTLA4 combination therapy, we profiled treated and non-treated tumors by RNA-SEQ. Herein, the profiled tumors represent models that are resistant or senstitive to immune checkpoint inhibitors at distinct timepoints of therapy and tumor progression.

overall_design: 283 samples

first: Dan

last: Hollern


title: MLL-Menin inhibition reverses pre-leukemic progenitor self-renewal induced by NPM1c mutations [RNA-Seq]

first: Scott

last: Armstrong

first: Hannah


title: Single cell sequencing of murine CD4+ T cells from atherosclerotic aortas

first: Klaus

last: Ley

state: CA

summary: We report the single cell transcriptome of CD4+ T cells from atherosclerotic aortas from ApoE-deficient mice that have been fed a western diet (WD) with aggravated atherosclerosis or with a standard chow diet (CD) with moderate atherosclerosis. We show that aortic T cells have a unique transcriptome with a mixed phenotype overlapping with T-regulatory and pathogenic T-helper type -1 and -17 cells.

overall_design: Leukocytes from atherosclerotic aortas were extracted by enzymatic digestion and flow sorting of viable CD45+ leukocytes. Leukocytes underwent single cell sequencing by the 10x Genomics drop-sequencing workflow. CD4+ T cells were identified by marker gene expression in computational down-stream analysis and T cell heterogeneity and gene expression was revealed by dimensionality reduction and unsupervised cluster detection.

first: Dennis

last: Wolf

first: Teresa

last: Gerhard

first: Holger

last: Winkels

first: Nathaly

last: Anto Michel

first: Akula

middle: B

last: Pramod

first: Yanal

last: Ghosheh

first: Simon

last: Brunel

first: Konrad

last: Buscher

first: Jacqueline

last: Miller

first: Sara

last: McArdle

first: Livia

last: Baas

first: Kouji

last: Kobiyama

first: Melanie

last: Vassallo

first: Erik

last: Ehinger

first: Thamotharampillai

last: Dileepan

first: Amal

last: Ali

first: Maximilian

last: Schell

first: Zbigniew

last: Mikulski

first: Daniel

last: Sidler

first: Takayuki

last: Kimura

first: Xia

last: Sheng

first: Hauke

last: Horstmann

first: Sophie

last: Hansen

first: Lucia

last: Sol Mitre

first: Peter

last: Stachon

first: Ingo

last: Hilgendorf

first: Dalia

last: Gaddis

first: Catherine

last: Hedrick

first: Chris

last: Benedict

first: Bjoern

last: Peters

first: Andreas

last: Zirlik

first: Alessandro

last: Sette


title: A novel Menin-MLL inhibitor induces specific chromatin changes and eradicates disease in models of MLL-rearranged leukemia [RNA-Seq II]

status: Public on Nov 06 2019

first: Scott

last: Armstrong

summary: Using 3-end RNA-seq followed by digital gene expression analyses we assessed genes that change expression upon genetic loss of MEN1 for 6 days in triplicates of samples.

overall_design: Using 3-end RNA-seq followed by digital gene expression analyses we assessed genes that change expression after knock-out MEN1 at 6 days

first: Charlie

last: Hatton

first: Andrei

last: Krivtsov


title: A novel Menin-MLL inhibitor induces specific chromatin changes and eradicates disease in models of MLL-rearranged leukemia [ChIP-seq]

summary: Treatment of cells carrying MLL-rearrangements with VTP-50469 (specific Menin-MLL1 inhibitor) displaces Menin from high molecular weight complexes and chromatin genome-wide. Since VTP-50469 block Menin interaction with MLL1 we tested using chip-seq if treatment with VTP-50469 also displaces MLL1 or MLL-fusions from chromatin. We found that the VTP-50469 treatment displaced MLL-fusions from only a subset of MLL-fusion binding sites. Since DOT1L is associated with MLL-AF9 we then tested if displacement of MLL1 also leads to loss of DOT1L association with chromatin on MLL-AF9 binding sites. We found that DOT1L binds to thousands of genes, treatment with VTP-50469 leads to genome wide loss of DOT1L binding including the same subset of MLL-fusion binding sites.

overall_design: Using ChIP-seq we examined Menin, MLL1, and DOT1L genome binding sites as well as methylation of lysine 79 on Histone H3 (H3K79me2) in cell lines carrying MLL-rearrangements MOLM13 (MLL-AF9), RS4;11 (MLL-AF4) and ML-2 (MLL-AF6) treated with VTP-50469 (100-330nM) or DMSO for 2-4 days.


title: A novel Menin-MLL inhibitor induces specific chromatin changes and eradicates disease in models of MLL-rearranged leukemia


title: A novel Menin-MLL inhibitor induces specific chromatin changes and eradicates disease in models of MLL-rearranged leukemia [Cut&Run]

summary: CRISPR mediated gene inactivation of MEN1 does not lead to loss of MLL1n chromatin occupancy.

overall_design: Using MLL1n Cut&Run-seq we examined if CRISPR mediated MEN1 gene inactivation lead to loss of MLL1n chromatin occupancy in MOLM13 cells.


title: Transcriptome analysis of freshly isolated young and aged rat oligodendrocyte progenitor cells (OPCs)

status: Public on Nov 01 2019

city: St Louis

first: Sabine

last: Dietmann

state: MO

address: 4565 McKinley Avenue

institute: Washington University School of Medicine

summary: The age-related failure to regenerate lost oligodendrocytes from oligodendrocyte progenitor cells (OPCs) is associated with irreversible neurodegeneration in multiple sclerosis. Consequently, regenerative therapies for chronic demyelinating diseases remain a long sought after but elusive goal. Here we show that adult OPCs lose their inherent differentiation potential with increasing age. Moreover, aged OPCs do not remain responsive to pro-differentiation signals, posing significant constraints on the effectiveness of remyelination therapies based on the enhancement of OPC differentiation. We show that this reduced regenerative capacity is associated with hallmarks of cellular ageing, including reduced metabolic function and increased DNA damage. We find that fasting or treatment with metformin can reverse these changes and restore the regenerative capacity of aged OPCs, improving remyelination in aged animals following white matter injury.  Importantly, aged OPCs treated with metformin regain their responsiveness to pro-differentiation factors, suggesting a potential for synergistic effects of rejuvenation and pro-differentiation therapies. Our findings have direct implications for understanding oligodendrocyte regeneration failure with ageing and how it might be reversed therapeutically.

overall_design: We compared the RNA expression of oligodendrocyte progenitor cells (OPCs) isolated from young and aged female rats.

first: Roey

last: Baror

first: Robin

last: Franklin


title: Transcriptome and open chromatin analysis of 5-month mouse liver and blood by the TaRGET II consortium

status: Public on May 20 2020

city: SAINT LOUIS

first: Daofeng

last: Li

address: 4515 McKinley Avenue

department: Genetics

institute: Washington University in St. Louis

summary: The TaRGET (Toxicant Exposures and Responses by Genomic and Epigenomic Regulators of Transcription) program is a research consortium funded by the National Institute of Environmental Health Sciences (NIEHS). The goal of the collaboration is to address the role of environmental exposures in disease pathogenesis as a function of epigenome perturbation, including understanding the environmental control of epigenetic mechanisms and assessing the utility of surrogate tissue analysis in mouse models of disease-relevant environmental exposures (https://targetepigenomics.org).

overall_design:
RNA-seq and ATAC-seq of liver and blood samples from 5-month mice that were subjected to disease-relevant environmental exposures.
The TaRGET II consortium (https://targetepigenomics.org/about/)


title: A novel Menin-MLL inhibitor induces specific chromatin changes and eradicates disease in models of MLL-rearranged leukemia [RNA-seq]

summary: Cells carrying MLL-rearrangements are sensitive to treatment with VTP-50469 with IC50 in 20-60 nM. We treated MOLM13 or RS4;11 cells with DMSO (0.33%) or VTP-50469 (100-330nM), followed by digital gene expression analyses of 3'end RNA-seq data. We found that very few genes significantly change expression >2-fold after 2 days of treatment, while after 7-day treatment more genes significantly changed expression >2-fold. The genes that lost expression after VTP-50469 treatment were enriched in MLL-fusion target genes and DOT1L-sensitive genes. Moreover, treatment with both EPZ-5676 and VTP-50469 suppress similar subsets of genes, however VTP-50469 suppress genes faster as compared to EPZ-5676. Treatment of PDX with VTP-50469 suppressed similar gene sets, namely MLL-fusion targets and DOT1L-sensitive genes.

overall_design: Using 3-end RNA-seq followed by digital gene expression analyses we assessed genes that change expression upon treatment with VTP-50469 in cell lines (2 and 7 days) and PDX (28 day dosing) in triplicates of samples.


title: FoxG1 function in hippocampus

status: Public on Oct 22 2019

first: Tanja

last: Vogel

address: Albertstr. 17

department: Institute for Anatomy and Cell Biology

institute: University of Freiburg

summary: The forkhead box transcription factor FoxG1 is known to influence forebrain development by determining regional brain specification as well as by regulating expansion of neuronal progenitors and timing of their differentiation. In the adult brain, FoxG1 is expressed in cortex and hippocampus. In the latter it is involved in postnatal neurogenesis in the dentate gyrus by influencing maintenance of the progenitor pool as well as survival and maturation of postmitotic neurons. In humans, haploinsufficiency of FoxG1 causes the congenital version of the Rett syndrome, a progressive neurologic developmental disorder. We use FoxG1 mutant mice to screen for global changes in mRNA expression after partial loss of FoxG1 protein in hippocampi of six week-old mice. Data analysis points to a specific function for FoxG1 in adult hippocampus besides its known involvement in dentate gyrus neurogenesis. We analyse transcriptional changes in the different CA-fields and show that especially the CA-1 field is influenced by lack of FOXG1 protein. Furthermore, data analysis shows altered expression of genes that have also been implicated in the classical form of the Rett syndrome and other autism spectrum disorders.

overall_design: mRNA from four different WT and four different FoxG1cre/+hippocampi was analysed

first: Stefan

last: Weise

first: Christine

last: Hacker

first: Ganeshkumar

last: Arumugam

first: Pavankumar

last: Videm

first: Rolf

last: Backofen


title: Induction of extracellular adenosine salvage and metabolic quiescence regulate the transitional to follicular B cell checkpoint in humans.

status: Public on Oct 11 2019

city: Cambridge

first: Vinay

middle: S

last: Mahajan

address: 65 Landsdowne Street

institute: Brigham and Women's Hospital

summary: Transcriptional profiling of transitional and follicular B cells showed that metabolic quiescence was acquired at the follicular B cell stage in both humans and mice, characterized by an orchestrated reduction of mTORC1 signaling, aerobic respiration and expression of genes involved in ribosome biogenesis.

overall_design: RNAseq analysis of transitional and follicular B cells from healthy human donors and C57BL/6 (wild-type) mice

first: Jocelyn

last: Farmer


title: Glioblastoma epigenome profiling identifies SOX10 as a master regulator of molecular tumour subtype - mouse RNAseq experiments

status: Public on Feb 20 2020

city: Heidelberg

first: Bernhard

last: Radlwimmer

address: Im Neuenheimer Feld 280

department: Department of Molecular Genetics

institute: Deutsches Krebsforschungszentrum / German National Cancer Research Centre

summary: Glioblastomas in adult patients are classified into four subtypes, IDH, MES, RTK I, and RTK II, based on DNA-methylation and RNA-expression data. Tumour subtype transitions are common during treatment, and transitions to the mesenchymal (MES) subtype are associated with therapy resistance and adverse prognosis. Here, we present DNA methylome and histone modification data of glioblastoma primary tumours and find that glioblastoma subtypes differ in their enhancer landscapes. Using Core Regulatory Circuitry analysis of chromatin and orthogonal analysis of RNA-derived gene regulatory networks, we identified 38 subtype Master Regulators whose cell population-specific activities we further mapped in single-cell RNA sequencing data. These analyses identified the oligodendrocyte precursor marker and chromatin modifier SRY-Box 10 (SOX10) as a master regulator in RTK I tumours. In vitro functional studies demonstrated that SOX10 loss causes a subtype switch analogous to the proneural-mesenchymal Transition observed in patients at the transcriptomic, epigenetic and phenotypic levels. This subtype transition is dependent on the activity of the SOX10 and enhancer co-factor Bromodomain Containing 4 (BRD4). Sox10 repression in an in vivo syngeneic graft glioblastoma mouse model results in increased tumour invasion, immune cell infiltration and significantly reduced survival, reminiscent of progressive human glioblastoma. These results identify SOX10 as a bona fide master regulator of the RTK I subtype, with both tumour cell-intrinsic and microenvironmental effects, highlighting that both glioblastoma cell plasticity and their tumour-microenvironment interactions are important contributors to tumour phenotypes.

overall_design: A Proneural/RTK I-like mouse glioblastoma cell line (mGBM2) was used to characterise the effects of Sox10 loss in vivo. mGBM2 cells were transduced with lentiviral construct targeting Sox10 or a non-targetting control, and implanted into syngenic C57/Bl6 mice (n=3 control, n=5 shSox10). Tumours were characterised using RNA-seq and histopathological analysis.

first: Carl

last: Herrmann

first: Zuguang

last: Gu

first: Qi

last: Wang

first: Yonghe

last: Wu

first: Michael

middle: N

last: Fletcher


title: The majority of A-to-I RNA editing is not required for mammalian homeostasis

status: Public on Oct 27 2019

city: Meblourne

first: Alistair

middle: Morgan

last: Chalk

state: VIC

address: 1G Royal Parade

institute: WEHI

summary: RNAseq of Adult Brain in ADAR1 E861A, ADAR2 knock out,  ADAR1 E861A x ADAR2 knock out het, and ADAR1 E861A x ADAR2 knock out mice generated by deep sequencing.

overall_design: Whole brain from 3 replicates of each genotype were subjected to RNA sequencing.

first: Jacki

middle: E

last: Heraud-Farlow

first: Scott

last: Taylor

first: Ankita

last: Gupte

middle: R

last: Walkley


title: MLL-Menin inhibition reverses pre-leukemic progenitor self-renewal induced by NPM1c mutations

last: Armstrong

state: MA

institute: Dana Farber Cancer Institute


title: Single cell RNAseq analysis of Cxcl12-GFP+ bone marrow stromal cells

status: Public on Sep 06 2019

city: Houston

first: Noriaki

last: Ono

state: Texas

department: School of Dentistry

institute: University of Texas Health Science Center at Houston

summary: A single cell transcriptional profile of CXCL12-abundant reticular stromal cells of 4 weeks-old murine bone marrow

overall_design: Cxcl12-GFP+ were FACS-isolated from postnatal day 28 (P28) femurs of Cxcl12-GFP; Cxcl12-creER; R26R-tdTomato mice, with tamoxifen injection at P21. 18,000 cells were loaded onto 10X Genomic Chromium Single Cell Expression Solution version 3. platform. cDNA was sequenced by Illumina NovaSeq 6000.


title: Niche stiffness underlies the aging of CNS progenitor cells.

status: Public on Jul 06 2019

first: Kevin

last: Chalut

address: Tennis Court Road

department: Stem Cell Institute

institute: University of Cambridge

summary: Next generation sequencing of OPCs grown on stiff and soft hydrogels

overall_design: Illumina HiSeq4000 PE150 Sequencing

last: Segel

first: Bjorn

last: Neumann

first: Robin

last: Franklin


title: Single-cell RNA transcriptome of induced noradrenergic (iNA) neurons from astrocytes and mouse embryonic fibroblasts

status: Public on Sep 01 2019

city: Shanghai

first: Sanlan

last: Li

address: 320 Yueyang Road, Xuhui District

institute: Institute of Neuroscience, Chinese Academy of Sciences

summary: We reported the generation of iNA neurons from astrocytes and MEFs by direct cell reprogramming. To compare the transcriptome of iNA neurons induced from this two kinds of starter cells, we prepared the single-cell cDNA library of iNA neurons induced from both starter cells in vitro for 28 days by 10x Genomics. Our results show that the single-cell RNA transcriptome of iNA neurons induced from astrocytes and MEFs is similar.

overall_design: Control astrocytes, MEFs, mCherry+ induced neurons at 28 days in vitro generated from astrocytes and MEFs of Dbh-2a-mCherry mice were enriched by FACS and put to library construction by 10x Genomics. The single-cell cDNA library were sequenced using Hiseq 6000 platform.

first: Zhenning

last: Zhou

first: Libing

last: Shen

first: Leping

last: Cheng


title: The MMTV-Wnt1 murine model produces two phenotypically distinct subtypes of mammary tumors with unique therapeutic responses to an EGFR inhibitor (RNA-seq)

status: Public on Jun 26 2019

first: Charles

last: Perou

state: NC

summary: The Wnt gene family is an evolutionarily conserved group of proteins that regulate cell growth, differentiation, and stem cell self-renewal. Aberrant Wnt signaling in human breast tumors has been proposed to be an attractive drug target, especially in the basal-like subtype where canonical Wnt signaling is both enriched and predictive of poor clinical outcomes. The development of effective Wnt based therapeutics, however, has been slowed in part by a limited understanding of the context dependent nature with which these aberrations influence breast tumorigenesis. We recently reported that MMTV-Wnt1 mice, which are an established model for studying Wnt signaling in breast tumors, develop two subtypes of tumors by gene expression classification: Wnt1-EarlyEx and Wnt1-LateEx. Here, we extend this initial observation and show that Wnt1-EarlyEx tumors had high expression of canonical Wnt, non-canonical Wnt, and EGFR signaling pathway signatures. Therapeutically, Wnt1-EarlyEx tumors had a dynamic reduction in tumor volume when treated with an EGFR inhibitor. Wnt1-EarlyEx tumors also had primarily Cd49fpos/Epcamneg FACS profiles, but were unable to be serially transplanted into wild-type FVB female mice. Wnt1-LateEx tumors, conversely, had a bloody gross pathology, which was highlighted by the presence of ‘blood lakes’ by H&E staining. These tumors had primarily Cd49fpos/Epcampos FACS profiles, but also contained a secondary Cd49fpos/Epcamneg subpopulation. Wnt1-LateEx tumors were enriched for activating Hras1 mutations and were capable of reproducing tumors when serially transplanted into wild-type FVB female mice. This study definitely shows that the MMTV-Wnt1 mouse model produces two phenotypically distinct subtypes of mammary tumors. Importantly, these subtypes differ in their therapeutic response to an EGFR inhibitor, suggesting that a subset of human tumors with aberrant Wnt signaling may also respond to erlotinib.

overall_design: Agilent gene expression microarrays were performed comparing RNA from FVB/n MMTV-Wnt1 mammary tumors to a common mouse reference sample. Agilent CGH microarrays were performed comparing DNA from FVB/n MMTV-Wnt1 mammary tumors to DNA from FVB wild-type mice. RNAseq libraries were prepared from FVB/n MMTV-Wnt1 mammary tumors using a TruSeq RNA kit before being submitted to the Lineberger Comprehensive Cancer Center Genomics Core to be run on the Illumina HiSeq 2000.

first: Adam

middle: D

last: Pfefferle

last: Mott


title: The MMTV-Wnt1 murine model produces two phenotypically distinct subtypes of mammary tumors with unique therapeutic responses to an EGFR inhibitor (Agilent gene expression)


title: The MMTV-Wnt1 murine model produces two phenotypically distinct subtypes of mammary tumors with unique therapeutic responses to an EGFR inhibitor (Agilent CGH)

type: Genome variation profiling by genome tiling array