Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Whole Kidneys
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ABSTRACT:
PROVIDER: PRJNA427594 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6423150_1.fastq.gz | Fastqsanger.gz | |||
| SRR6423150_2.fastq.gz | Fastqsanger.gz | |||
| SRR6423160_1.fastq.gz | Fastqsanger.gz | |||
| SRR6423160_2.fastq.gz | Fastqsanger.gz | |||
| SRR6423170_1.fastq.gz | Fastqsanger.gz |
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Project description: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.
2019-07-01 | GSE108548 | GEO
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
Project description:Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Livers
| PRJNA427593 | ENA
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.
2020-09-01 | GSE157233 | GEO
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.
2020-09-05 | GSE157516 | GEO
Project description:Transcriptional profiling of mouse embryonic kidneys (E13.5) comparing UB HDAC1,2-/- kidneys with wild type kidneys. Studies in our lab showed that histone deacetylase 1 (HDAC1) and 2 (HDAC2) perform redundant, yet essential functions in the developing mouse ureteric bud (UB) tissue. Double deletion of HDAC1 and HDAC2 in the UB results in impaired UB branching morphogenesis, followed by severe kidney dysgenesis. The goal of the microarray analysis was to identify the genetic pathways controlled by HDAC1 and 2 in the UB. Two-condition experiment: E13.5 mutant kidneys (UB HDAC1,2-/-) vs. E13.5 wild type kidneys . Biological replicates: 4 control replicates, 4 UB HDAC1,2-/- replicates. Two-color Agilent 4x44k chips with dye-swaps on 2 of 4 arrays.
2012-01-31 | E-GEOD-35432 | biostudies-arrayexpress
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
Project description:Comparative gene expression profiling in livers of A1cf-transgenic, A1cf-knockout, and wild-type mice
| PRJNA660481 | ENA
Project description:Transcriptional profiling of mouse embryonic kidneys (E13.5) comparing UB HDAC1,2-/- kidneys with wild type kidneys. Studies in our lab showed that histone deacetylase 1 (HDAC1) and 2 (HDAC2) perform redundant, yet essential functions in the developing mouse ureteric bud (UB) tissue. Double deletion of HDAC1 and HDAC2 in the UB results in impaired UB branching morphogenesis, followed by severe kidney dysgenesis. The goal of the microarray analysis was to identify the genetic pathways controlled by HDAC1 and 2 in the UB.
2012-01-31 | GSE35432 | GEO
Project description:We used microarrays to detail the global gene expression in tissues from wild-type and Robo2 homozygous kidneys.
2019-09-12 | GSE137298 | GEO