RNA-seq in NT, CAP-D3, and CAP-H2 expressing cells treated with DMSO or menadione
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE139540 | GEO | 2019/10/30
REPOSITORIES: GEO
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Project description:RNA-seq in NT, CAP-D3, and CAP-H2 expressing cells treated with DMSO or menadione
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Project description:Transcriptome analysis of two different mutants of the condensin II subunit CAP-D3. Four week-old plantlets from the T-DNA insertion lines SAIL_826_B06 (cap-d3 SAIL) and SALK_094776 (cap-d3 SALK) were compared to Col-0 wild-type plants.
2020-12-31 | E-MTAB-8969 | biostudies-arrayexpress
Project description:BACKGROUND & AIMS- More frequent interaction of bacteria with the colonic epithelium is associated with ulcerative colitis (UC). The identities of all proteins which promote bacterial clearance in colonic epithelial cells are unknown. Previously, we discovered that dCAP-D3 (Chromosome Associated Protein-D3), regulates responses to bacterial infection. We examined whether CAP-D3 promotes bacterial clearance in human colonic epithelium. METHODS- Clearance of Salmonella or adherent-invasive Escherichia coli LF82 was assessed by gentamycin protection assays in HT-29 and Caco-2 cells expressing CAP-D3 shRNA. CAP-D3 levels in colonic epithelial cells from healthy and UC patient tissues were analyzed by immunoblot. RNA-sequencing identified bacterially-induced CAP-D3 target genes. The role of CAP-D3 target genes in bacterial clearance was analyzed by gentamycin protection assays, immunofluorescent staining, and by using pharmacologic inhibitors. RESULTS- CAP-D3 expression was reduced in colonic epithelial cells from UC patients with active disease. Reduction of CAP-D3 expression inhibited autophagy and decreased intracellular bacterial clearance. The components of the heterodimeric SLC7A5/SLC3A2 amino acid transporter were identified as CAP-D3 target genes; their levels increased in infected, CAP-D3 deficient cell lines and in cells from UC patients. In HT-29 cells, this resulted in earlier SLC7A5 recruitment to Salmonella-containing vacuoles, increased mTOR activity, and enhanced bacterial survival. Inhibition of SLC7A5/SLC3A2 or mTOR activity rescued the bacterial clearance defect in CAP-D3 deficient cells. CONCLUSIONS- CAP-D3 attenuates amino acid transporter transcription to promote bacterial autophagy in colon epithelial cells. CAP-D3 protein levels are decreased in patients with active UC, suggesting that CAP-D3 is a potential therapeutic target to restore mucosal homeostasis in UC patients.
2015-09-15 | GSE62520 | GEO
Project description:BACKGROUND & AIMS- More frequent interaction of bacteria with the colonic epithelium is associated with ulcerative colitis (UC). The identities of all proteins which promote bacterial clearance in colonic epithelial cells are unknown. Previously, we discovered that dCAP-D3 (Chromosome Associated Protein-D3), regulates responses to bacterial infection. We examined whether CAP-D3 promotes bacterial clearance in human colonic epithelium. METHODS- Clearance of Salmonella or adherent-invasive Escherichia coli LF82 was assessed by gentamycin protection assays in HT-29 and Caco-2 cells expressing CAP-D3 shRNA. CAP-D3 levels in colonic epithelial cells from healthy and UC patient tissues were analyzed by immunoblot. RNA-sequencing identified bacterially-induced CAP-D3 target genes. The role of CAP-D3 target genes in bacterial clearance was analyzed by gentamycin protection assays, immunofluorescent staining, and by using pharmacologic inhibitors. RESULTS- CAP-D3 expression was reduced in colonic epithelial cells from UC patients with active disease. Reduction of CAP-D3 expression inhibited autophagy and decreased intracellular bacterial clearance. The components of the heterodimeric SLC7A5/SLC3A2 amino acid transporter were identified as CAP-D3 target genes; their levels increased in infected, CAP-D3 deficient cell lines and in cells from UC patients. In HT-29 cells, this resulted in earlier SLC7A5 recruitment to Salmonella-containing vacuoles, increased mTOR activity, and enhanced bacterial survival. Inhibition of SLC7A5/SLC3A2 or mTOR activity rescued the bacterial clearance defect in CAP-D3 deficient cells. CONCLUSIONS- CAP-D3 attenuates amino acid transporter transcription to promote bacterial autophagy in colon epithelial cells. CAP-D3 protein levels are decreased in patients with active UC, suggesting that CAP-D3 is a potential therapeutic target to restore mucosal homeostasis in UC patients. Three RNA samples from 3 independent experiments including timepoints taken at 0, 0.5 and 7 hours post-infection were analyzed on a bioanalyzer for quality; one of the 0.5 hour post-infection samples was excluded at this time due to poor RNA purity. Directional, cDNA libraries made from cellular mRNAs were generated from the other 8 samples and sequenced (paired-end sequencing of 100 bp reads) in the Genomics Core at the University of Chicago on an Illumina HiSeq2000.
2015-09-15 | E-GEOD-62520 | biostudies-arrayexpress
Project description:Influence of CAP-D3 in Arabidopsis thaliana transcription
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Project description:Genome instability is a characteristic of malignant cells, however, evidence for its contribution to tumorigenesis has been enigmatic. In this study we demonstrate that a complex containing the retinoblastoma protein, E2F1, and Condensin II localizes to major satellite repeats at pericentromeres. In the absence of this complex, this genomic region fails to properly replicate and H2AX phosphorylation at pericentromeric repeats is increased. Our data indicates that these lesions contribute to defective chromosome segregation in the ensuing mitosis. Surprisingly, loss of even one copy of the retinoblastoma gene was sufficient to reduce recruitment of Condensin II to pericentromeres and cause this phenotype. Furthermore, we determined that human RB1 mutation status in cancers of mesenchymal origin correlated with copy number variation, chromosomal gains and losses, as well as chromothriptic rearrangements. Importantly, the magnitude of these chromosomal abnormalities was indistinguishable between RB1+/- and RB1-/- genotypes. Lastly, using gene-targeted mice we determined that mutation of just one copy of the murine Rb1 gene causes sarcomas and lymphomas with increased chromosome copy number variation. Our study connects replication stress with a number of common chromosomal abnormalities in cancer through a dosage sensitive complex present at pericentromeric repeats. CAP-D3 localization was studied in two different genotypes: Rb+/+ and RbΔL/ΔL. As a control, input from the ChIP experiment was also sequenced. The CAP-D3 antibody used was raised against a GST fusion protein containing amino acids 1243-1506 (Coschi et al., 2010).
2014-06-19 | E-GEOD-55040 | biostudies-arrayexpress
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Project description:To elucidate the mode of actions of Plumbagin and Menadione, miRNA-profilling was performed after treating cells with vehicle (DMSO), Plumbagin (10uM), and Menadione (10uM) for 24 hours. Threel replicates for control and Menadione and two replicates for Plumbagin were subjected to miRNA-microarray.
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