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Effect of cardiac specific depletion of one allele of Mrps5 on gene expression in heart at postnatal day 4

ABSTRACT: Effect of cardiac specific depletion of one allele of Mrps5 on gene expression in heart at postnatal day 4

PROVIDER: PRJNA827591 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18779955_1.fastq.gz	Fastqsanger.gz
	SRR18779955_2.fastq.gz	Fastqsanger.gz
	SRR18779956_1.fastq.gz	Fastqsanger.gz
	SRR18779956_2.fastq.gz	Fastqsanger.gz
	SRR18779957_1.fastq.gz	Fastqsanger.gz

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Effect of cardiac specific depletion of one allele of Mrps5 on gene expression in heart at postnatal day 4

Project description:To investigate the function of reduction in Mrps5 expression in the regulation of cardiomyocyte proliferation and postnatal heart development, we established the mouse with cardiac specific depletion of one allele of Mrps5 through Cre-Loxp system by crossing Mrps5 fl/fl mouse with Myh6-Cre mouse. We cross Mrps5 fl/fl mouse with Myh6-Cre mouse to obtain the Mrps5 fl/+;Myh6-Cre mouse and its control littermates Mrps5 fl/+ mouse. So that one allele of Mrps5 gene was depleted upon Myh6 gene promoter drivened Cre expression at the later stage of embyronic stage. We then performed gene expression profiling analysis using data obtained from RNA-seq of Mrps5 fl/+; Myh6-Cre and Mrps5 fl/+ mouse hearts at postnatal day 4.

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Project description:To gain insight into the function of Mrps5 in cardiac development We conducted RNA sequencing to profile the transcriptomes of Mrps5 fl/fl and Mrps5 fl/fl; cTNT-Cre mouse hearts at embryonic 12 days, prior to the onset of embryos lethality.

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Effect of Mrps5 on gene expression in Mrps5 null heart at embryonic 12 days after Mrps5 knockout

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Phenotype of Mrps5-associated polymorphisms is intimately linked to mitoribosomal misreading

Project description:Recently, we have identified a point mutation V338Y in mammalian nuclear-encoded mitochondrial protein MrpS5 that confers error-prone mitochondrial protein synthesis. In-vivo, mutation V338Y was associated with a distinct phenotype including impaired mitochondrial function, enhanced susceptibility to noise-induced hearing damage, anxiety-related behavioral alterations, and age-associated metabolic changes in muscle. To challenge the link between V338Y-mediated misreading and in-vivo phenotype, we introduced mutation G315R into the MRPS5 gene; MRPS5 G315R is homologous to the established bacterial ram mutation uS5 G104R. In contrast to the phylogenetically closely related bacterial translation, the corresponding MRPS5 G315R mutation did not affect the accuracy of mitochondrial protein synthesis. In addition, in the absence of mitochondrial misreading, homozygous mutant MRPS5G315R/G315R mice did not show phenotype distinct from wild-type animals.

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Effect of cardiac specific depletion of Mrps5 on gene expression in heart at 12 weeks after gene knockout

Project description:To understand the molecular mechanism underlying Mrps5 function in the heart, we performed RNA sequencing of Mrps5cKO and Mrps5fl/fl hearts 12 weeks after tamoxifen induction. We chose this stage because the mutant hearts have just started to exhibit detectable defects and the changes in the transcriptome state would more accurately correlate with the onset of the phenotype.

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