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The mitochondrial fusion protein OPA1 is dispensable in the live

ABSTRACT: Mitochondria are critical for metabolic homeostasis of the liver, and thus, mitochondrial dysfunction is a major cause of liver diseases. Optic atrophy 1 (OPA1) is a mitochondrial fusion protein that also plays a role in cristae shaping. Hence, the OPA1 gene disruption has been shown to cause mitochondrial dysfunction. However, the role of OPA1 in liver function is poorly understood. In this study, we deleted OPA1 in fully developed mouse liver and examined its effect.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Liver

SUBMITTER: Yisang Yoon

LAB HEAD: Yisang Yoon

PROVIDER: PXD040556 | Pride | 2023-10-30

REPOSITORIES: Pride

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The mitochondrial fusion protein OPA1 is dispensable in the liver and its absence induces mitohormesis to protect liver from drug-induced injury.

Lee Hakjoo H Lee Tae Jin TJ Galloway Chad A CA Zhi Wenbo W Xiao Wei W de Mesy Bentley Karen L KL Sharma Ashok A Teng Yong Y Sesaki Hiromi H Yoon Yisang Y

Nature communications 20231023 1

Mitochondria are critical for metabolic homeostasis of the liver, and their dysfunction is a major cause of liver diseases. Optic atrophy 1 (OPA1) is a mitochondrial fusion protein with a role in cristae shaping. Disruption of OPA1 causes mitochondrial dysfunction. However, the role of OPA1 in liver function is poorly understood. In this study, we delete OPA1 in the fully developed liver of male mice. Unexpectedly, OPA1 liver knockout (LKO) mice are healthy with unaffected mitochondrial respirat ...[more]

PMID: 37872238

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