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Mitochondrial gene expression is required for platelet function and blood clotting

ABSTRACT: Mitochondrial gene expression is required for platelet function and blood clotting

PROVIDER: PRJNA851354 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19795758_1.fastq.gz	Fastqsanger.gz
	SRR19795758_2.fastq.gz	Fastqsanger.gz
	SRR19795759_1.fastq.gz	Fastqsanger.gz
	SRR19795759_2.fastq.gz	Fastqsanger.gz
	SRR19795760_1.fastq.gz	Fastqsanger.gz

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Mitochondrial gene expression is required for platelet function and blood clotting

Project description:Platelets are anucleate blood cells that contain mitochondria, that regulate blood clotting in response to injury. Mitochondria contain their own gene expression machinery which relies on nuclear encoded factors for the biogenesis of the oxidative phosphorylation (OXPHOS) system to produce energy, ions and metabolites required for thrombosis. The autonomy of the mitochondrial gene expression machinery from the nucleus is not known and platelets provide a valuable model to understand the importance of mitochondrial gene expression in anucleate cells. We generated three different platelet-specific conditional knockout mouse models, each lacking a gene that is essential for mitochondrial gene expression at the level of RNA processing, stability and translation (Elac2Pf4∆/Pf4∆, Ptcd1Pf4∆/Pf4 and Mtif3Pf4∆/Pf4∆). Loss of ELAC2, PTCD1 or MTIF3, leads to increased megakaryocyte ploidy, elevated circulating levels of reticulated platelets, thrombocytopenia and consequent extended bleeding time. Loss of ELAC2, PTCD1 and MTIF3 reduced agonist induced platelet activation. Transcriptomic and proteomic analyses showed that mitochondrial gene expression and protein synthesis facilitate fibrinolysis, haemostasis and blood coagulation in response to injury.

2023-10-03 | GSE206543 | GEO

Mitochondrial gene expression is required for platelet function and blood clotting

Project description:Platelets are anucleate blood cells that contain mitochondria and regulate blood clotting in response to injury. Mitochondria contain their own gene expression machinery which relies on nuclear encoded factors for the biogenesis of the oxidative phosphorylation (OXPHOS) system to produce energy, ions and metabolites required for thrombosis. The autonomy of the mitochondrial gene expression machinery from the nucleus is not known and platelets provide a valuable model to understand the importance of mitochondrial gene expression in anucleate cells. We generated three different platelet-specific conditional knockout mouse models, each lacking a gene that is essential for mitochondrial gene expression at the level of RNA processing, stability and translation (Elac2Pf4?/Pf4?, Ptcd1Pf4?/Pf4 and Mtif3Pf4?/Pf4?). Loss of ELAC2, PTCD1 or MTIF3, leads to increased megakaryocyte ploidy, elevated circulating levels of reticulated platelets, thrombocytopenia and consequent extended bleeding time. Furthermore, impaired RNA metabolism also reduced agonist induced platelet activation. Transcriptomic and proteomic analyses showed that mitochondrial gene expression and protein synthesis facilitate fibrinolysis, haemostasis and blood coagulation in response to injury.

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Proteasome Function is Required for Platelet Production

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Mitochondrial carrier SLC25A19 is required for respiratory chain function

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Cardiac mitochondrial function depends on BUD23 mediated ribosome programming

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