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MPST sulfurtransferase maintains mitochondrial protein import and cellular bioenergetics to attenuate obesity

ABSTRACT: MPST sulfurtransferase maintains mitochondrial protein import and cellular bioenergetics to attenuate obesity

PROVIDER: PRJNA831095 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18900902.fastq.gz	Fastqsanger.gz
	SRR18900903.fastq.gz	Fastqsanger.gz
	SRR18900904.fastq.gz	Fastqsanger.gz
	SRR18900905.fastq.gz	Fastqsanger.gz
	SRR18900906.fastq.gz	Fastqsanger.gz

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MPST sulfurtransferase maintains mitochondrial protein import and cellular bioenergetics to attenuate obesity

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Mitochondrial protein import stress augments alpha-synuclein aggregation and neurodegeneration independent of bioenergetics

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Mitochondrial protein import clogging as a mechanism of disease

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Project description:Mitochondrial functions are essential for cell viability and rely on protein import into the organelle. Physiological perturbations and disease conditions can lead to mitochondrial import defect. We find that in budding yeast, mitochondrial import defects result in activation of a surveillance mechanism, which we termed mitoCPR. The mitoCPR is aimed at ameliorating mitochondrial import and protecting mitochondria during import stress. This is mediated by the mitoCPR effector, Cis1, which associates with mitochondria to reduce the accumulation of mitochondrial preproteins at the organelle's surface. Clearance of preproteins depends on the AAA-ATPase Msp1 and the proteasome, suggesting that Cis1 facilitates the degradation of unimported proteins that accumulate at the mitochondrial surface. We further show that mitoCPR is critical for maintaining mitochondrial functions during mitochondrial import stress and provide evidence that it is an ancient, conserved mitochondrial protection mechanism.

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mitoCPR - a surveillance pathway that protects mitochondria in response to mitochondrial import stress [human]

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