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The mitochondrial protein OPA1 regulates the quiescent state of adult muscle stem cells

ABSTRACT: The mitochondrial protein OPA1 regulates the quiescent state of adult muscle stem cells

PROVIDER: PRJNA859183 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20245708.fastq.gz	Fastqsanger.gz
	SRR20245708_1.fastq.gz	Fastqsanger.gz
	SRR20245708_2.fastq.gz	Fastqsanger.gz
	SRR20245709.fastq.gz	Fastqsanger.gz
	SRR20245709_1.fastq.gz	Fastqsanger.gz

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The mitochondrial protein OPA1 regulates the quiescent state of adult muscle stem cells

Project description:Regulation of quiescence is essential for adult stem cell maintenance, longevity and sustained regeneration potential. Our studies have uncovered that physiological and transient changes in mitochondrial shape regulate the quiescent state of adult muscle stem cells (MuSCs). We show that mitochondria in MuSCs rapidly fragment in response to an activation stimulus, via a systemic HGF/mTOR mechanism, to drive the exit from deep quiescence. Deletion of the mitochondrial fusion protein OPA1 and forced mitochondrial fragmentation is sufficient to transition MuSCs into G-alert quiescence causing premature activation and depletion upon a stimulus. Loss of OPA1 activates a glutathione (GSH) redox signaling pathway that promotes cell-cycle progression, myogenic gene expression and commitment. MuSCs with chronic OPA1 loss and mitochondrial fragmentation, leading to mitochondrial dysfunction, continue to reside in a primed state but acquire severe cell cycle defects. Additionally, we provide evidence that OPA1 decline and impaired mitochondrial dynamics may contribute to age-related MuSC dysfunction. These findings reveal a fundamental role for OPA1 and mitochondrial dynamics in establishing the quiescent state and activation potential of adult stem cells.

2022-08-24 | GSE208326 | GEO

The mitochondrial protein OPA1 regulates the quiescent state of adult muscle stem cells.

Project description:Quiescence regulation is essential for adult stem cell maintenance and sustained regeneration. Our studies uncovered that physiological changes in mitochondrial shape regulate the quiescent state of adult muscle stem cells (MuSCs). We show that MuSC mitochondria rapidly fragment upon an activation stimulus, via systemic HGF/mTOR, to drive the exit from deep quiescence. Deletion of the mitochondrial fusion protein OPA1 and mitochondrial fragmentation transitions MuSCs into G-alert quiescence, causing premature activation and depletion upon a stimulus. OPA1 loss activates a glutathione (GSH)-redox signaling pathway promoting cell-cycle progression, myogenic gene expression, and commitment. MuSCs with chronic OPA1 loss, leading to mitochondrial dysfunction, continue to reside in G-alert but acquire severe cell-cycle defects. Additionally, we provide evidence that OPA1 decline and impaired mitochondrial dynamics contribute to age-related MuSC dysfunction. These findings reveal a fundamental role for OPA1 and mitochondrial dynamics in establishing the quiescent state and activation potential of adult stem cells.

| S-EPMC10249109 | biostudies-literature

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

2024-06-17 | GSE233461 | GEO

Macrophage OPA1 maintains anti-inflammatory state and metabolic homeostasis by regulating metabolic reprogramming and mtDNA-cGAS-STING pathway

Project description:Adipose tissue macrophages (ATMs) play an important role in regulating adipose tissue inflammation and metabolic homeostasis. Mitochondria are pivotal hubs for macrophage-mediated inflammation. Here, we observed a negative correlation between macrophage optic atrophy type 1 (OPA1) and obesity in both humans and mice. Myeloid OPA1-deficient mice were susceptible to obesity and related systemic insulin resistance, glucose dysregulation, and hepatic steatosis upon high-fat diet (HFD). This is due to the impairment of M2-like macrophage features and the promotion of pro-inflammatory phenotypes. Mechanically, OPA1 loss resulted in metabolic reprogramming, as evidenced by reduced mitochondrial respiration, increased glycolysis, and elevated mtDNA release. This activated the cGAS-STING-IRF7 pathway in M2 macrophages, inducing anti-inflammatory conversion to a pro-inflammatory state. In contrast, myeloid OPA1 transgenic mice exhibited reduced inflammation and obesity. Collectively, we identified macrophage OPA1 as a novel regulator of immune metabolism. Targeting OPA1 may represent an effective therapeutic strategy against obesity and metabolic disorders.

2025-03-13 | GSE291869 | GEO

FoxO maintains a genuine quiescent muscle stem-cell state until geriatric age (ATAC-seq)

Project description:We identify two quiescent stem-cell states through relative CD34 expression: CD34High, with stemness properties (genuine state), and CD34Low, more committed to myogenic differentiation (primed state). The genuine-quiescent state is preserved into later life succumbing only in extreme old age due to acquisition of primed-state traits. We identified niche-derived IGF1-dependent Akt activation as detrimental to the genuine stem-cell state by imposing primed-state features via FoxO inhibition. Interventions to neutralize Akt and promote FoxO activity drive primed-to-genuine state conversion, while FoxO inactivation deteriorates the genuine state at young age, causing muscle regenerative failure, as in geriatric mice.

2020-10-29 | GSE155642 | GEO

FoxO maintains a genuine quiescent muscle stem-cell state until geriatric age (RNA-seq)

2020-10-29 | GSE157562 | GEO

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

Project description:To investigate the function of Opa1 in the regulation of adult neurogenesis, we created a conditional Opa1-knockout mouse line by cross-breeding Nestin-CreERT2;ROSA26YFP mice with Opa1-Flox mice. Using Tamoxifen, we induced Opa1 knockout on 8-weeks-old Nestin-CreERT2;ROSA26YFP;Opa1-Flox mice. We then sorted YFP-positive cells from the hippocampus using flow cytometry at 10 weeks. RNA was extracted from sorted cells and subjected to next generation sequencing.

2024-06-17 | GSE233464 | GEO

Heart proteome in Cox10 depending on Opa1 processing

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.

2024-08-10 | PXD048804 | Pride

The mitochondrial fusion protein OPA1 is dispensable in the live

Project description: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.

2023-10-30 | PXD040556 | Pride

Transcriptomic differences between juvenile and adult quiescent NSCs

Project description:Transcriptomic differences between juvenile and adult quiescent NSCs

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