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The impact of conditional Opa1 Knockout on gene expression profile at single cell level during adult neurogenesis in the hippocampus

ABSTRACT: The impact of conditional Opa1 Knockout on gene expression profile at single cell level during adult neurogenesis in the hippocampus

PROVIDER: PRJNA976307 | ENA |

REPOSITORIES: ENA

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The impact of conditional Opa1 Knockout on gene expression profile at single cell level during adult neurogenesis in the hippocampus

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The impact of conditional Opa1 Knockout in neural stem cells on transcriptome changes

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Project description:The impact of conditional Opa1 Knockout

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The impact of conditional Opa1 Knockout

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-06-17 | GSE233465 | GEO

Neuronal TIMP2 regulates hippocampus-dependent plasticity and extracellular matrix complexity

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Project description:Mitochondrial fusion and fission accompany adaptive responses to stress and altered metabolic demands. Inner membrane fusion and cristae morphogenesis depends on Optic Atrophy 1 (Opa1), which is expressed in different isoforms and is cleaved from a membrane-bound, long to a soluble, short form. Here, we have analyzed the physiological role of Opa1 isoforms and Opa1 processing by generating mouse lines expressing only one cleavable Opa1 isoform or a non-cleavable variant thereof. Our results show that expression of a single cleavable or non-cleavable Opa1 isoform preserves embryonic development and the health of adult mice. Opa1 processing is dispensable under metabolic and thermal stress, but prolongs lifespan and protects against mitochondrial cardiomyopathy in OXPHOS-deficient Cox10-/- mice. Mechanistically, loss of Opa1 processing disturbs the balance between mitochondrial biogenesis and mitophagy, suppressing cardiac hypertrophic growth in Cox10-/- hearts. Our results highlight the critical regulatory role of Opa1 processing, mitochondrial dynamics and metabolism for cardiac hypertrophy.

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