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Deletion of the mitochondria-shaping protein Opa1 during early thymocyte maturation impacts mature memory T cell metabolism

ABSTRACT: Deletion of the mitochondria-shaping protein Opa1 during early thymocyte maturation impacts mature memory T cell metabolism

PROVIDER: PRJNA694994 | ENA |

REPOSITORIES: ENA

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Deletion of the mitochondria-shaping protein Opa1 during early thymocyte maturation impacts mature memory T cell metabolism

Project description:OPA1, a mitochondria-shaping protein controlling cristae biogenesis and respiration, is required for memory T cell function, but whether it affects intrathymic T cell development is unknown. Here we show that OPA1 is necessary for thymocyte maturation at the double negative (DN)3 stage when rearrangement of the T-cell receptor β (Tcrβ) locus occurs. By profiling mitochondrial function at different stages of thymocyte maturation, we find that DN3 cells rely on oxidative phosphorylation (OXPHOS). Consistently, Opa1 deletion during early T cell development impairs respiration of DN3 cells and reduces their number. Opa1-deficient DN3 cells indeed display stronger TCR signaling and are more prone to cell death. The surviving Opa1-/- thymocytes that reach the periphery as mature T cells display an Effector Memory phenotype even in the absence of antigenic stimulation but are unable to generate metabolically fit long-term memory T cells. Thus, mitochondrial defects early during T cell development affect mature T cell function.

2021-07-27 | GSE165579 | GEO

Deletion of the mitochondria-shaping protein Opa1 during early thymocyte maturation impacts mature memory T cell metabolism.

Project description: Not available

| S-EPMC8257785 | biostudies-literature

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

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.

2019-01-16 | GSE109228 | GEO

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

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

RNA sequencing of Opa1-silenced HUVECs.

Project description:The goal of this study is to compare the transcriptome of HUVECs silenced or not for Opa1

2021-10-31 | GSE122042 | GEO

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

RNA sequencing of Opa1-silenced HUVECs.

Project description:RNA sequencing of Opa1-silenced HUVECs.

| PRJNA503252 | ENA

Genotype data from induced Pluripotent Stem cells from OPA1 Haploinsufficiency patients

Project description:We have generated human induced Pluripotent Stem cells (hiPSc) from two individuals with OPA1 haploinsufficiency, and one control donor, using Sendai virus-mediated delivery of reprogramming factors. hiPSc lines have been screened using SNP array to assess chromosomal stability (alongside the fibroblast lines from which they derived), and validation of the pluripotency of the hiPSc lines is provided by Pluritest assessment of transcriptome datasets, prior to differentiation to dopaminergic neuronal clutures and downstream functional assays. Mitochondrial fragmentation in iPSC-derived dopaminergic neurons with OPA1 haploinsufficiency underpins increased apoptosis and syndromic Parkinsonism.

2017-02-03 | GSE94432 | GEO

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