Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA394750 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5833400_1.fastq.gz | Fastqsanger.gz | |||
| SRR5833400_2.fastq.gz | Fastqsanger.gz | |||
| SRR5833401_1.fastq.gz | Fastqsanger.gz | |||
| SRR5833401_2.fastq.gz | Fastqsanger.gz | |||
| SRR5833402_1.fastq.gz | Fastqsanger.gz |
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Project description:We have performed RNA-seq on mouse islets lacking all p300 (p300 KO), all CBP (CBP-null), and one copy of CBP and all p300 (triallelic). The data revealed that p300 and CBP regulate some distinct but largely overlapping genes in islets. This was further confirmed by GO term and transcription factor target analyses, which suggested that these coactivators regulate genes that function similarly and converge to Hnf1a pathway.
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Project description:Organisms respond to mitochondrial stress by activating multiple defense pathways including the mitochondrial unfolded protein response (UPRmt). However, how different layers of UPRmt regulators are orchestrated to transcriptionally activate the stress responses remains largely unknown. Here we identified CBP-1, the worm ortholog of the mammalian acetyltransferases CBP/p300, as an essential regulator for UPRmt activation, as well as for mitochondrial stress-induced immune response, amyloid-β aggregation reduction and lifespan extension in Caenorhabditis elegans. Mechanistically, CBP-1 acts downstream of histone demethylases, JMJD-1.2/JMJD-3.1, and upstream of UPRmt transcription factors including ATFS-1, to systematically induce a broad spectrum of UPRmt genes and execute multiple beneficial functions. In mouse and human populations, transcript levels of CBP/p300 positively correlate with UPRmt transcripts and longevity. Furthermore, CBP/p300 inhibition disrupts, while forced expression of p300 is sufficient to activate, the UPRmt in mammalian cells. These results highlight an evolutionarily conserved mechanism that determines mitochondrial stress response, and promotes health and longevity through CBP/p300.
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Project description:Wild type or CBP/p300 fx/fx; Le-Cre-positive (CBP/p300-/-) surface ectoderm from E9.5 mouse embryos was laser micodissected from three embryos of each genotype. Total RNA was purified, pooled for each genotype and triplicate samples were reverse transcribed and amplified using a NuGEN kit. cDNA was biotinylated and hybridized to Illumina Mouse6 v2.0 bead arrays.
2013-09-24 | GSE49223 | GEO
Project description:Wild type or CBP/p300 fx/fx; Pax6-Cre-positive (CBP/p300-/-) surface ectoderm from E10.5 mouse embryos was laser micodissected from three embryos of each genotype. Total RNA was purified, pooled for each genotype and triplicate samples were reverse transcribed and amplified using a NuGEN kit. cDNA was biotinylated and hybridized to Illumina Mouse6v2.0 bead arrays.
2013-09-23 | GSE49218 | GEO
Project description:Reversible epsilon-amino acetylation of lysine residues regulates transcription as well as metabolic flux; however, roles for specific lysine acetyltransferases in skeletal muscle physiology and function remain enigmatic. In this study, we investigated the role of the homologous acetyltransferases p300 and CBP in skeletal muscle transcriptional homeostasis and physiology in adult mice. Mice with skeletal muscle-specific and inducible knockout of p300 and/or CBP were generated by crossing mice with a tamoxifen-inducible Cre recombinase expressed under the human alpha-skeletal actin (HSA) promoter with mice harboring LoxP sites flanking exon 9 of both the Ep300 and Crebbp genes. Knockout was induced at 13-15 weeks of age via oral gavage of tamoxifen. We demonstrate that loss of both p300 and CBP in adult mouse skeletal muscle severely impairs contractile function and results in lethality within one week – a phenotype that is reversed by the presence of a single allele of either p300 or CBP. The loss of muscle function in p300/CBP double knockout mice is paralleled by substantial transcriptional alterations in gene networks central to skeletal muscle contraction and structural integrity. Changes in protein expression patterns, determined by 10-plex TMT labeling, were linked to impaired muscle function also manifest within days (WT mice were compared to day 3 and day 5 knock out mice). Together, these data reveal the requirement of p300 and CBP for the control and maintenance of contractile function and transcriptional homeostasis in skeletal muscle, and ultimately, organism survival. By extension, modulating p300/CBP function holds promise for the treatment of disorders characterized by impaired contractile function in humans.
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Project description:Conditional knockout of p300 and Cbp in mouse rod photoreceptors
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Project description:Wild type or CBP/p300 fx/fx; Pax6-Cre-positive (CBP/p300-/-) surface ectoderm from E10.5 mouse embryos was laser micodissected from three embryos of each genotype. Total RNA was purified, pooled for each genotype and triplicate samples were reverse transcribed and amplified using a NuGEN kit. cDNA was biotinylated and hybridized to Illumina Mouse6v2.0 bead arrays. Three wild type and three knockout embryos were used. The RNA from embryos of the same genotype was purified and pooled and triplicate samples were amplified and used for microarray analysis.
2013-09-23 | E-GEOD-49218 | biostudies-arrayexpress
Project description:Wild type or CBP/p300 fx/fx; Le-Cre-positive (CBP/p300-/-) surface ectoderm from E9.5 mouse embryos was laser micodissected from three embryos of each genotype. Total RNA was purified, pooled for each genotype and triplicate samples were reverse transcribed and amplified using a NuGEN kit. cDNA was biotinylated and hybridized to Illumina Mouse6 v2.0 bead arrays. Three wild type and three knockout embryos were used. The RNA from embryos of the same genotype was purified and pooled and triplicate samples were amplified and used for microarray analysis.
2013-09-24 | E-GEOD-49223 | biostudies-arrayexpress
Project description:The CH1 protein interaction domain of the transcriptional coactivators p300 and CBP is thought to interact with HIF-1alpha and this interaction is thought to be critical to the expression of HIF-1alpha target genes in response to hypoxia. To test the requirement of the CH1 domain for gene expression in response to hypoxia, rimary mouse embryonic fibroblasts (MEFs) were generated from C57Bl/6x129/Sv F2 e14.5 embryos that contain a deletion in the CH1 domain of three of four alleles of CBP and p300. The remaining allele of p300 or CBP was a conditional knock out allele. Control MEFs with only a single conditional knockout allele of p300 or CBP were also generated. At passage 3 MEFs were infected with Cre Adenovirus and grown until they had expanded at least 100 fold. Subconfluent MEFs were treated with 21% oxygen (normoxia) or 0.1% oxygen (hypoxia) with 5% carbon dioxide at 37 C in a humid chamber for 6hrs. At the start of treatment, medium was removed and replaced with medium (DMEM+10% FBS+pen-strep+ l-glu) that had been preequilibrated overnight in normoxia or hypoxia as appropriate. Immediately after treatment, cells were lysed in Trizol for RNA extraction. 12 samples; 4 genotypes [CBP+/flox (flox1), p300 +/flox (flox2), CBP CH1/flox;p300 CH1/CH1 (triCH1flox1),CBP CH1/CH1;p300 CH1/flox (triCH1flox2)] , 2 treatments (normoxia and hypoxia).
2007-12-15 | E-GEOD-3196 | biostudies-arrayexpress
Project description:Histone acetyltransferases (HATs) GCN5/PCAF and CBP/p300 are transcription coactivators. However, how these HATs regulate ligand-induced nuclear receptor target gene expression remains unclear. Here we show in mouse embryonic fibroblasts (MEFs), deletion of GCN5/PCAF specifically eliminates acetylation on H3K9 (H3K9Ac) while deletion of CBP/p300 selectively reduces acetylation on H3K18 and H3K27 (H3K18/27Ac). Treating MEFs with a specific ligand for nuclear receptor PPARdelta induces sequential increases of H3K18/27Ac and H3K9Ac on the promoter of PPARdelta target gene Angptl4, which correlates with a robust ligand-induced Angptl4 expression. Inhibiting transcription elongation blocks ligand-induced H3K9Ac but not H3K18/27Ac on Angptl4 promoter. Finally, we show CBP/p300 and their HAT activities are required, while GCN5/PCAF and H3K9Ac are dispensable, for ligand-induced PPARdelta target gene expression in MEFs. These results highlight the substrate and site specificities of HATs in cells, and suggest that GCN5/PCAF- and CBP/p300-mediated histone acetylations play distinct roles in regulating ligand-induced nuclear receptor target gene expression. PCAF and GCN5 have some redundant function. To identify PCAF/GCN5-regulated genes, immortalized MEFs with PCAF knockout and GCN5 conditional knockout were infected with retroviruses expressing either Cre recombinase or vector alone. We prepared duplicated RNAs from either vector or Cre infected cells (PCAF-/-;GCN5+/- or PCAF-/-;GCN5+/-) and RNAs from either Vector or Cre infected the other independently immortalized cells for 6 affymetrix microarray.
2013-12-31 | E-GEOD-20008 | biostudies-arrayexpress