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Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Whole Kidneys

ABSTRACT: Purpose: A1CF is an RNA binding protein that has not been extensively studied on a transcriptome-wide scale. Here we profile the whole kidneys of wild-type and A1cf knockout mice to detect differences in gene expression. Methods: mRNA profiles of 6-8 week old wild-type and A1cf knockout mice were generated by deep sequencing using Illumina HiSeq 2500. Reads that passed quality filters were aligned to mm10 genome and analyzed for differential expression using CuffDiff2 and DESeq2. Results: We mapped reads to the mm10 genome and found a subset of fewer than 500 differentially expressed genes in A1CF deficiency. Conclusions: Our study represents the first transcriptomic profiling of A1CF deficiency in the kidney.

ORGANISM(S): Mus musculus

PROVIDER: GSE108548 | GEO | 2019/07/01

REPOSITORIES: GEO

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Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Livers

Project description:Purpose: A1CF is an RNA binding protein that has not been extensively studied on a transcriptome-wide scale. Here we profile the livers of wild-type and A1cf knockout mice to detect differences in gene expression. Methods: mRNA profiles of 6-8 week old wild-type and A1cf knockout mice were generated by deep sequencing using Illumina HiSeq 2500. Reads that passed quality filters were aligned to mm10 genome and analyzed for differential expression using CuffDiff2 and DESeq2. Results: We mapped reads to the mm10 genome and found a subset of fewer than 500 differentially expressed genes in A1CF deficiency. Conclusions: Our study represents the first transcriptomic profiling of A1CF deficiency in the liver.

2019-10-31 | GSE108547 | GEO

Comparative gene expression profiling in livers of A1cf-transgenic, A1cf-knockout, and wild-type mice

Project description:Rationale: RNA binding protein Apobec1 Complementation Factor (A1CF) regulates posttranscriptional ApoB mRNA editing but the range of RNA targets and long-term impact of altered A1CF expression on liver function are unknown. Objective: We studied hepatocyte-specific A1cf transgenic (A1cf +/Tg), A1cf+/Tg Apobec1– /– and A1cf –/– mice fed chow or high fat/high fructose diets using RNA-Seq, RNA-CLIP Seq and tissue microarrays from human hepatocellular cancer (HCC). Findings: A1cf +/Tg mice exhibited increased hepatic proliferation and steatosis, with increased lipogenic gene expression (Mogat1, Mogat2, Cidea, Cd36) associated with shifts in polysomal RNA distribution. Aged A1cf +/Tg mice developed spontaneous fibrosis, dysplasia and HCC, which was accelerated on a high fat/fructose diet and independent of Apobec1. RNA-Seq revealed increased expression of mRNAs involved in oxidative stress (Gstm3, Gpx3, Cbr3), inflammatory response (Il19, Cxcl14, Tnfα, Ly6c), extracellular matrix organization (Mmp2, Col1a1, Col4a1), proliferation (Kif20a, Mcm2, Mcm4, Mcm6) with a subset of mRNAs (including Sox4, Sox9, Cdh1) identified in RNA CLIP-Seq. Increased A1CF expression in human HCC correlated with advanced fibrosis and with reduced survival in a subset with nonalcoholic fatty liver disease. Conclusions: Hepatic A1CF overexpression selectively alters polysomal distribution and mRNA expression, promoting lipogenic, proliferative and inflammatory pathways leading to HCC.

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Comparative gene expression profiling in livers of A1cf-transgenic, A1cf-knockout, and wild-type mice

Project description:Comparative gene expression profiling in livers of A1cf-transgenic, A1cf-knockout, and wild-type mice

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Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Whole Kidneys

Project description:Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Whole Kidneys

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Comparative gene expression profiling in livers of A1cf-transgenic and wild-type mice

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RNA-seq of 8hr LPS-stimulated bone marrow-derived macrophages from wild type, Ch25h-deficient, and LXRab knockout mice

Project description:25-hydroxycholesterol has been demonstrated to regulate SREBP processing, yet Ch25h-deficient mice have no cholesterol abnormalities. Using RNA-seq, we find that LPS-stimulated, Ch25h-deficient BMDMs have dysregulated SREBP target genes, demonstrating that 25-hydroxycholesterol is an induced repressor of SREBP during inflammatory settings. mRNA profiles from day 7 M-CSF bone marrow-derived macrophages (wild type, Ch25h-knockout, LXR-double knockout, were generated by deep sequencing on an Illumina HiSeq 2500. Sequence reads passing a quality filter were aligned to the mouse genome (mm10) using STAR.

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Interactomics Analyses of Wild-type and Mutant A1CF Reveal Diverged Functions in Regulating Cellular Lipid Metabolism

Project description:Population genetic studies highlight a missense variant (G398S) of A1CF that is strongly associated with higher levels of blood triglycerides (TGs) and total cholesterol (TC). Functional analyses suggest that the mutation accelerates the secretion of very low-density lipoprotein (VLDL) from the livers by an unknown mechanism. Here, we used multi-omics approaches to interrogate the functional difference between the WT and mutant A1CF. Using metabolomics analyses, we captured the cellular lipid metabolite changes induced by the transient expression of the proteins, confirming that the mutant A1CF is able to relieve the TG accumulation induced by WT A1CF. Using a proteomics approach, we obtained the interactomic data of WT and mutant A1CF. Networking analyses show that WT A1CF interacts with three functional protein groups, RNA/mRNA processing, cytosolic translation and, surprisingly, mitochondrial translation. The mutation diminishes these interactions, especially with the group of mitochondrial translation. Differential analyses show that the WT A1CF-interacting proteins most significantly different from the mutant are those for mitochondrial translation, whereas the most significant interacting proteins with the mutant are those for cytoskeleton and vesicle-mediated transport. RNA-seq analyses validate that the mutant, but not the WT, A1CF increases the expression of the genes responsible for cellular transport processes. On the contrary, WT A1CF affected the expression of mitochondrial matrix proteins and increased cell oxygen consumption. Thus, our studies confirm the previous hypothesis that A1CF plays broader roles in regulating gene expression. The interactions of the mutant A1CF with the vesicle-mediated transport machinery provide mechanistic insight in understanding the increased VLDL secretion in the A1CF mutation carriers.

2022-06-30 | GSE152807 | GEO

RNA-binding protein A1CF modulates plasma triglyceride levels through posttranscriptional regulation of stress-induced VLDL secretion

Project description:A recent human exome-chip study on plasma lipids identified a missense mutation in the 3 A1CF (APOBEC1 complementation factor) gene that associates with elevated TG levels, but how A1CF, 4 an RNA binding protein, influences plasma TG is unknown.

2024-07-31 | GSE117633 | GEO

Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Livers

Project description:Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Livers

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and poh1-/- splenic foxp3＋Treg cells

Project description:Purpose: The goals of this study are to compare the transcriptome profiling of Wild Type and poh1-/- splenic foxp3＋Treg cells Methods:Splenic CD4+Foxp3+ (YFP+) cells mRNA profiles of 2-week-old poh1+/+ Foxp3Cre+ wild type and poh1fl/fl Foxp3Cre+ mice were generated by deep sequencing, using Illumina HiSeq 2500. The sequence reads that passed quality filters were analyzed with edgeR. qRT–PCR validation was performed using SYBR Green assays Results:Using an optimized data analysis workflow, we mapped about 50 million sequence reads per sample to the mouse genome (build mm10). Among all genes expressed, 1067 genes were upregulated and1391 genes were downregulated in poh1−/− Foxp3+ Treg cells relative to their expression in POH1 +/+ Treg cells. The gene-expression altered in POH1-ablated cells adversely correlated with those expressed in Treg cells in TCR-dependent manner. The gene sets were downreglated in POH1-deficiency Treg cells encoding various cell-surface receptors and intracellular molecules involved in migration, suppressive function and signature of Treg cells. Conclusions:Gene expression in POH1-deficiency Treg cells was markedly diverse compared with that in POH1-sufficient Treg cells.

2020-12-12 | GSE110084 | GEO

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