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Mus musculus

ABSTRACT: Expression profiling analysis of mouse P4 cerebellum in CitK mutant mice proficient or knockout for P53

PROVIDER: PRJNA326069 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3679460.fastq.gz	Fastqsanger.gz
	SRR3679461.fastq.gz	Fastqsanger.gz
	SRR3679462.fastq.gz	Fastqsanger.gz
	SRR3679463.fastq.gz	Fastqsanger.gz
	SRR3679464.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:Expression profiling analysis of mouse P4 cerebellum in CitK mutant mice proficient or knockout for P53

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Expression profiling analysis of mouse P4 cerebellum in CitK mutant mice proficient or knockout for P53

Project description:Purpose: Citron kinase (CitK) knockout mice show a severe form of primary microcephaly, associated with ataxia and lethal epilepsy. This phenotype is caused by massive apoptosis occuring during embryonic and post-natal brain development, associated with cytokinesis failure. Cerebellum is the tissue showing highest sensitivity to CitK loss. The clinical phenotype of CitK knockout mice is significantly resued by P53 inactivation. In addition, CitK/P53 double knockout brains have almost normal levels of apoptosis, but display high percentage of binucleated and multinucleated cells. The aim of this study was to analyze the gene expression changes produced in developing neural tissue by CitK loss and to determine which alterations are P53-dependent. expression changes Methods: We analyzed by RNA sequencing total RNA extracted from P4 cerebellum of mice characterized by the following genotypes: 1. CitK +/-, P53 +/- (CTRL); 2. CitK -/-, P53 +/- (CitK-KO); 3. CitK +/-, P53 -/- (P53-KO); 4. CitK -/-, P53 -/- (D-KO). Biological triplicates were analyzed per every genotype. Conclusions: The loss of CitK leads to a strong reduction of the expression of pro-neural genes and induces a P53-related pro-apoptotic gene sets. The analysis of D-KO mice reveals that most of these changes are P53-dependent, but many genes implicated in growth arrest are induced through P53-independent mechanisms.

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p53 K316P mutation results in increased liver triglyceride levels and increased rates of de novo lipogenesis.

Project description:Our lab generated the p53 K316P mouse, which mimicks a common amino acid change found in bats. The K316P mutation, found in the nuclear localization signal of p53, results in increased cytoplasmic localization of p53. We found that K316P mutant mice develop several metabolic phenotypes, including increased body fat percentage, and increased liver lipid levels. In order to determine the mechanism through which K316P mutation increases liver lipid levels, we performed metabolomic analysis of mouse livers from WT and K316P mutant mice. Mouse livers were isolated from four wild type (WT) and four p53 K316P (M) mice for lipidomic analysis. Samples were isolated and flash frozen in liquid nitrogen. Lipids were then extracted from each liver sample and analyzed using mass spectrometry.

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Project description:Progesterone (P4) acting through its cognate receptor, the progesterone receptor (PR), plays an important role in uterine physiology. The PR knockout (PRKO) mouse has demonstrated the importance of the P4-PR axis in the regulation of uterine function. To define the molecular pathways regulated by P4-PR in the mouse uterus, Affymetrix MG U74Av2 oligonucleotide arrays were used to identify alterations in gene expression after acute and chronic P4 treatments. In the analysis, retinoic acid metabolic genes, cytochrome P 450 26a1 (Cyp26a1), alcohol dehydrogenase 5, and aldehyde dehydrogenase 1a1 (Aldh1a1); kallikrein genes, Klk5 and Klk6; and specific transcription factors, GATA-2 and Cited2 [cAMP-corticosterone-binding protein/p300-interacting transactivator with glutamic acid (E) and aspartic acid (D)-rich tail], were validated as regulated by the P4-PR axis. Identification and analysis of these responsive genes will help define the role of PR in regulating uterine biology. Ovariectomized wild-type and progesterone receptor knockout mice were injected with either vehicle or 1 mg/mouse progesterone. The injections were repeated every 12 h, and groups of mice were killed 4 h after the first injection (acute P4 treatment) or 4 h after the fourth injection (chronic P4 treatment).

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