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Effect of overexpression of A3B and RNA editing calling in mouse tissues [RNA-seq]

ABSTRACT: To test if A3B has RNA editng activity we performed SNV calling from RNA-seq of 6 mouse lungs (Samples 7-12), 8 mouse livers (Samples 14-20) and 8 pancreas (Samples 21-28) We then performed gene expression profiling analysis using data obtained from RNA-seq of 6 mouse livers (Samples 1-6), 6 mouse lungs (Samples 7-12), 8 mouse livers (Samples 14-20) and 8 pancreas (Samples 21-28)

ORGANISM(S): Mus musculus

PROVIDER: GSE209721 | GEO | 2023/07/25

REPOSITORIES: GEO

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Effect of overexpression of A3B and RNA editing calling in mouse tissues [WES]

Project description:To test if A3B has RNA editing activity we performed SNV calling from WES of 8 mouse livers (Samples 1-8) and 8 pancreas (Samples 7-16)

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Effect of depletion of A3B on gene expression of 92.1 cells and overexpression of A3B on gene expression of MEL290 cells

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Decoding the Genes that A3B regulated

Project description:Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for A3B in OMM2.3 and 92.1 cells.

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Decoding the Genomic regions that R-loop distributed associated with A3B expression

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2019-12-02 | GSE141259 | GEO

Reversible and irreversible PAH in a rat model for MCT+Shunt-induced PAH and hemodynamic unloading.

Project description:PAH was induced by 60mg/kg MCT and an aorto-caval shunt. At different timepoints of PAH progression (day 14, 21 and 28 after MCT-injection), the left lung with PAH was hemodynamically unloading by unilateral orthotopic transplatation into a syngeneic, healthy recipient. All day 14 and 7/10 day 21 transplanted lungs showed reversal of PAH after LTx. All day 28 and 3/10 day 21 transplanted lungs showed PAH progression after LTx. Lung tissue of Reversible and Irreversible PAH and normal controls, acquired at LTx, was compared using RNA-seq.

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SNP microarray of T-REx-293-based clones overexpressing the DNA cytosine deaminase APOBEC3B

Project description:A conditional and isogenic system for APOBEC3B (A3B) induction in T-REx-293 cells. Cells were engineered to express doxycycline-inducible A3B-eGFP or eGFP constructs and subjected to 10 rounds of A3B-eGFP exposure causing 80-90% cell death. Control pools (eGFP) were subjected to parallel rounds of non-toxic eGFP exposure, and dilutions were done each round to mimic A3B-eGFP induced population fluctuations. DNA was extracted and subjected to SNP analyses using the Human OmniExpress-24v1-0 BeadChip (Illumina, San Diego, CA). Genotyping was performed using the humanomniexpress_24v1-0_a cluster file. SNP data is avaiable for a total of 16 samples, all derived from single cells mother lines A and C. For each series, each consisting of 8 samples, A3B-eGFP and eGFP daugther clones were processed on the SNP microarray, as well as 3 A3B-eGFP and 3 eGFP grand-daugther clones.

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Multifunctional Activity-Based Protein Profiling of the Developing Lung

Project description:Data includes proteomics analysis of P450-ABP (2EN, ATW8, ATW12), FP-2, and ATP-ABP labeled mouse lung lysate S9. Lungs from the following developmental stages were used in the study: gestational day 17, post natal days 0, 21, and 42. Also included are global analyses of the same mice lungs.

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Epigenetic effects of acrylamide exposure in mice

Project description:Acrylamide, a high-production-volume chemical and food contaminant in baked and fried carbohydrate-rich foods has been classiﬁed as a “Group 2A carcinogen” (probable human carcinogen) by the IARC. The carcinogenicity of acrylamide is attributed to its well-recognized genotoxicity; however, evidence suggests that acrylamide may also induce non-genotoxic alterations. In the present study female B6C3F1 mice were exposed to 0.70mM acrylamide in drinking water for 28 days and genotoxic and transcriptomic effects were investigated in the lung, a target organ for acrylamide carcinogenicity in mice, and the liver, a non-target organ. Acrylamide exposure resulted in a dose-dependent formation of N7-(2-carbamoyl-2-hydroxyethyl)guanine and N3-(2-carbamoyl-2-hydroxyethyl)adenine in lung and liver DNA at the similar levels. In contrast, whole genome gene expression profiles in the lungs and livers revealed the tissue-specific gene expression alterations. By using a SurePrint G3 Mouse Gene Expression v2 8x60K Microarray Kit (Agilent Technologies), we identified 123 and 363 genes that were found to be differentially expressed in the lungs and livers of acrylamide-treated mice; however, only 5 genes were in common between the organs. A detailed analysis of differentially expressed genes revealed that the major difference in the effect of acrylamide on the transcriptome in the lungs and livers was related to a different trend of gene expression changes. In the lungs, acrylamide exposure caused an inhibition of gene expression (54 up-regulated and 69 down-regulated genes), whereas the opposite effect, characterized by twice the number of up-regulated as compare to down-regulated genes (245 up-regulated and 118 down-regulated), was found in the livers of exposed mice.

2019-01-30 | GSE125851 | GEO

The RB/E2F pathway controls expression of the cancer genomic DNA deaminase APOBEC3B

Project description:Mutations in cancer are due in part to DNA cytosine deamination by APOBEC3B (A3B). While low in healthy tissues, A3B expression and activity are elevated in tumors and further increase in metastases. However, molecular mechanisms responsible for A3B transcriptional regulation are poorly understood. Here, we address whether the RB/E2F pathway, which is often dysregulated in breast cancer, is a molecular trigger of A3B overexpression. First, an A3B promoter-driven luciferase reporter was used to demonstrate reporter activation by disruption of only one out of five predicted E2F binding sites. Second, A3B-luciferase reporter activation was also triggered by expressing the BK polyomavirus T-antigen, which inactivates RB and thereby alleviates repression of E2F regulated genes. Importantly, A3B-luciferase reporter induction by BK polyomavirus T-antigen could not be further increased by mutating the functional E2F binding site. Third, both CRISPR disruption and targeted base substitutions in the endogenous E2F binding site caused strong A3B upregulation and confirmed importance of this regulatory element. Fourth, proteomics experiments showed that members of the DREAM and PRC1.6-complexes including multiple E2F family members are able to bind to wild-type but not E2F mutant promoter sequences. Finally, a combination of genetic and biochemical studies implicated E2F4 and E2F6 in endogenous A3B gene repression. Altogether, our studies demonstrate that A3B expression is suppressed in normal cells by the RB/E2F axis and that viral or mutational disruption of this pathway causes overexpression of this DNA deaminase in cancer and contributes mutational fuel to tumor evolution.

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