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OPA1 mice gut micobiome

ABSTRACT: OPA1 mice gut micobiome

PROVIDER: PRJEB83275 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR14050120_1.fastq.gz	Fastqsanger.gz
	ERR14050120_2.fastq.gz	Fastqsanger.gz
	ERR14050121_1.fastq.gz	Fastqsanger.gz
	ERR14050121_2.fastq.gz	Fastqsanger.gz
	ERR14050122_1.fastq.gz	Fastqsanger.gz

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Gene expression analysis of the cochlea of Opa1 KO mice

Project description:RNA was extracted from dissected cochlea at post-natal day 15, from either Opa1+/- mice of their wild-type littermates.

2024-02-26 | GSE232051 | 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 loss of OPA1 accelerates intervertebral disc degeneration and osteoarthritis in aged mice

Project description:NP cells of the intervertebral disc and articular chondrocytes reside in avascular and hypoxic tissue niches. As a consequence of these environmental constraints the cells are primarily glycolytic in nature and were long thought to have a minimal reliance on mitochondrial function. Recent studies have challenged this long-held view and highlighted the increasingly important role of mitochondria in the physiology of these tissues. However, the foundational understanding of mechanisms governing mitochondrial dynamics and function in these tissues is lacking. We investigated the role of mitochondrial fusion protein OPA1 in maintaining the spine and knee joint health in mice. OPA1 knockdown in NP cells altered mitochondrial size and cristae shape and increased the oxygen consumption rate without affecting ATP synthesis. OPA1 governed the morphology of multiple organelles, including peroxisomes, early endosomes and cis-Golgi and its loss resulted in the dysregulation of NP cell autophagy. Metabolic profiling and 13C-flux analyses revealed TCA cycle anaplerosis and altered metabolism in OPA1-deficient NP cells. Noteworthy, Opa1AcanCreERT2 mice with Opa1 deletion in disc and cartilage showed age-dependent disc degeneration, osteoarthritis, and vertebral osteopenia. Our findings underscore that OPA1 regulation of mitochondrial dynamics and multi-organelle interactions is critical in preserving metabolic homeostasis of disc and cartilage.

2025-04-26 | GSE270889 | 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.

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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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Transcriptome analysis in brown adipose tissue of mice lacking the mitochondrial protein optic atrophy 1 (OPA1) in thermogenic adipocytes

Project description:mRNA expression profiles from interscapular brown adipose (iBAT) tissue of 7-week-old OPA1 BAT KO mice and their WT counterparts.

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Necroptosis inhibition protects from dopaminergic neuronal cell death in OPA1 mutant Parkinson’s disease patient neurons and MPTP treated mice

Project description:Dysfunctions in mitochondria dynamics and metabolism are common pathological processes associated with Parkinson’s disease (PD). Recently, it was shown that an inherited form of PD and dementia is caused by new mutations in the OPA1 gene, which encodes for a key player of mitochondrial fusion and structure. iPSC-derived neural cells from these patients exhibited severe mitochondrial fragmentation, respiration impairment, ATP deficits and heightened oxidative stress. Reconstitution of normal levels of OPA1 in PD-derived neural cells normalized mitochondria morphology and function. OPA1 mutated neuronal cultures showed reduced survival in vitro. Intriguingly, selective inhibition of necroptosis effectively rescued this survival deficit. Additionally, dampening necroptosis in MPTP treated mice protected from DA neuronal cell loss. This human iPSC-based model captures both the early pathological events in OPA1 mutant neural cells and the beneficial effects of blocking necroptosis, highlighting this cell death process as a promising therapeutic target for PD.

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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

Genome-wide analysis of Ctr and OPA1 knock-down transcriptomes

Project description:Through the genome-wide analysis of Ctr and OPA1 knock-down group, we reveal the transcriptome changes with OPA1 down-regulation

2019-07-31 | GSE135089 | GEO

Gene expression analysis of the cochlea of Opa1 KO mice

Project description:Gene expression analysis of the cochlea of Opa1 KO mice

| PRJNA970712 | ENA