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Mitochondria Metabolism Sets the Species-Specific Tempo of Neuronal Development

ABSTRACT: Mitochondria Metabolism Sets the Species-Specific Tempo of Neuronal Development

PROVIDER: PRJNA907814 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22506349_1.fastq.gz	Fastqsanger.gz
	SRR22506349_2.fastq.gz	Fastqsanger.gz
	SRR22506350_1.fastq.gz	Fastqsanger.gz
	SRR22506350_2.fastq.gz	Fastqsanger.gz
	SRR22506351_1.fastq.gz	Fastqsanger.gz

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Mitochondria Metabolism Sets the Species-Specific Tempo of Neuronal Development

Project description:Neuronal development in the human cerebral cortex is considerably prolonged compared to that of other mammals. We explored whether mitochondria influence the species-specific timing of cortical neuron maturation. By comparing human and mouse cortical neuronal maturation at high temporal and cell resolution, we found a slower mitochondria development in human cortical neurons compared with that in the mouse, together with lower mitochondria metabolic activity, particularly that of oxidative phosphorylation. Stimulation of mitochondria metabolism in human neurons resulted in accelerated development in vitro and in vivo, leading to maturation of cells weeks ahead of time, whereas its inhibition in mouse neurons led to decreased rates of maturation. Mitochondria are thus important regulators of the pace of neuronal development underlying human-specific brain neoteny.

2023-02-01 | GSE219253 | GEO

Mitochondria Metabolism Sets the Species-Specific Tempo of Neuronal Development

Project description:Mitochondria dynamics and metabolism drive the species-specific developmental timing of cortical neurons.

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An epigenetic barrier sets the timing of human neuronal maturation

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Neuronal mitochondria transport Pink1 mRNA via Synaptojanin 2 to support local mitophagy

Project description:PTEN-induced kinase 1 (PINK1) is a very short-lived protein that is required for the removal of damaged mitochondria through Parkin translocation and mitophagy. Because the short half-life of PINK1 limits its ability to be trafficked into neurites, local translation is required for this mitophagy pathway to be active far from the soma. The Pink1 transcript is associated with and cotransported with neuronal mitochondria. In concert with translation, the mitochondrial outer membrane protein Synaptojanin 2 Binding Protein (SYNJ2BP) and Synaptojanin 2 (SYNJ2) are required for tethering Pink1 mRNA to mitochondria via an RNA-binding domain in SYNJ2. This neuron-specific adaptation for local translation of PINK1 provides distal mitochondria with a continuous supply of PINK1 for activation of mitophagy.

2022-01-14 | GSE193443 | GEO

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Project description:Inflammation in the central nervous system (CNS) can impair the function of neuronal mitochondria and contributes to axon degeneration in the common neuroinflammatory disease multiple sclerosis (MS). Here we combine cell type-specific mitochondrial proteomics with in vivo biosensor imaging to dissect how inflammation alters the molecular composition and functional capacity of neuronal mitochondria. Neuroinflammatory lesions in the mouse spinal cord cause widespread and persisting axonal ATP depletion, which precedes mitochondrial oxidation and calcium overload. This early axonal energy crisis is associated with impaired electron transport chain function, but also an upstream dysbalance of tricarboxylic acid (TCA) cycle enzymes. Isocitrate dehydrogenase 3 (Idh3), the rate limiting enzyme of the TCA cycle, is depleted in neuronal mitochondria in experimental models and in human MS lesions. Notably, viral overexpression of Idh3 can rectify the axonal energy deficits, suggesting that TCA cycle dysfunction in neuroinflammation may be amendable to therapy.

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Mitochondria drive neuronal differentiation by metabolising nuclear-encoded RNA [RNA-seq]

Project description:Mitochondria drive neuronal differentiation by metabolising nuclear-encoded RNA [RNA-seq]

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Mitochondria drive neuronal differentiation by metabolising nuclear-encoded RNA [ATAC-seq]

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Project description:Mitochondria are the ‘power-houses’ of all cells, generating ATP to fuel numerous pathways which are vital for cellular form and function (1). Neuronal processes and synapses present a constant demand for ATP to maintain ionic gradients and neurotransmission events (2), promoting sub-populations of mitochondria to be enriched pre- and post-synaptically (3, 4). These mitochondria display unique enzymatic (5), calcium buffering (6, 7) and antioxidant properties (8) and have thus been associated in the pathogenesis of a variety of neurodegenerative diseases where the synapse is the primary target. In this study, we employed label-free proteomics to characterize the proteomes of synaptic and non-synaptic mitochondria following biochemical isolation (5). Discrete proteomic profiles exist between the two subpopulations of mitochondria and a molecular fingerprint of these differences is seemingly conserved between mammalian species. The majority of the constituents of this grouping have been previously associated with diseases of the nervous system. In addition, bioinformatic analysis of this conserved expression pattern indicated that differences in the properties of protein complex I may represent an important specialisation of synaptic mitochondria. Following this, in vivo assays of mitochondrial candidates using Drosophila larval fillet preparations were performed. Our data demonstrates that selective knock-down of intrinsic mitochondrial proteins alter synaptic morphology which may contribute to pathological processes during ageing and disease.

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