Mitochondrial dynamics regulates iron homeostasis and nuclear genome stability [RNA-seq]
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ABSTRACT:
PROVIDER: PRJNA1164125 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30767400_1.fastq.gz | Fastqsanger.gz | |||
| SRR30767400_2.fastq.gz | Fastqsanger.gz | |||
| SRR30767401_1.fastq.gz | Fastqsanger.gz | |||
| SRR30767401_2.fastq.gz | Fastqsanger.gz | |||
| SRR30767402_1.fastq.gz | Fastqsanger.gz |
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Project description:Mitochondrial membrane dynamics control the shape, number, and distribution of mitochondria and regulate energy production and cell health. Defective mitochondrial dynamics in humans are related to optic atrophy, neuropathies, cardiomyopathies, or dementia. In a screen for yeast mutants with increased levels of templated insertions (TINS) in the nuclear genome, we identified mitochondrial fusion deficient mutants (mgm1, ugo1, fzo1). We found that fusion mutants activate the iron regulon, have decreased iron-sulfur clusters (ISC) and increased DNA damage, suggesting a role of iron homeostasis in preventing TINS. Consistently, a secondary screen found many iron homeostasis mutants to exhibit high TINS. We propose that iron dysregulation leading to oxidative DNA damage coupled with compromised DNA repair drives TINS. Poor growth, iron dyshomeostasis, and genome instability can be suppressed in fusion mutants by increasing mitochondrial membrane potential, suggesting a new therapeutic approach. These studies link mitochondrial dynamics to iron homeostasis deficiency and genome stability
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Project description:Mitochondrial dynamics regulates iron homeostasis and nuclear genome stability
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Project description:Mitochondrial membrane dynamics control the shape, number, and distribution of mitochondria and regulate energy production and cell health. Defective mitochondrial dynamics in humans are related to optic atrophy, neuropathies, cardiomyopathies, or dementia. In a screen for yeast mutants with increased levels of templated insertions (TINS) in the nuclear genome, we identified mitochondrial fusion deficient mutants (mgm1, ugo1, fzo1). We found that fusion mutants activate the iron regulon, have decreased iron-sulfur clusters (ISC) and increased DNA damage, suggesting a role of iron homeostasis in preventing TINS. Consistently, a secondary screen found many iron homeostasis mutants to exhibit high TINS. We propose that iron dysregulation leading to oxidative DNA damage coupled with compromised DNA repair drives TINS. Poor growth, iron dyshomeostasis, and genome instability can be suppressed in fusion mutants by increasing mitochondrial membrane potential, suggesting a new therapeutic approach. These studies link mitochondrial dynamics to iron homeostasis deficiency and genome stability
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Project description:Mitochondria are the energy-generating hubs of the cell. In spite of considerable advances, our understanding of the factors that regulate the molecular circuits that govern mitochondrial function remains incomplete. Using a genome-wide functional screen, we have identified the poorly characterized protein Zinc finger CCCH-type containing 10 (Zc3h10) as regulator of mitochondrial physiology. We show that Zc3h10 is a nuclear RNA binding protein that controls the fate of Slc25a37 and Prelid3a mRNA transcripts, two nuclear-encoded mitochondrial proteins central for iron and cardiolipin homeostasis. Depletion of Zc3h10 results in mitochondrial dysfunction and reduced TCA cycle flux. Notably, we have identified a loss-of-function mutation of Zc3h10 in humans (Tyr105 to Cys105) that is associated with decreased mitochondrial function, increased body mass index, fat mass, fasting glucose and triglycerides. Cells from Cys105 homozygotes display alterations in Slc25a37 and Prelid3a levels and defects in mitochondrial iron and cardiolipin homeostasis that derive in mitochondrial dysfunction.
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Project description:Mitochondria are the energy-generating hubs of the cell. In spite of considerable advances, our understanding of the factors that regulate the molecular circuits that govern mitochondrial function remains incomplete. Using a genome-wide functional screen, we have identified the poorly characterized protein Zinc finger CCCH-type containing 10 (Zc3h10) as regulator of mitochondrial physiology. We show that Zc3h10 is a nuclear RNA binding protein that controls the fate of Slc25a37 and Prelid3a mRNA transcripts, two nuclear-encoded mitochondrial proteins central for iron and cardiolipin homeostasis. Depletion of Zc3h10 results in mitochondrial dysfunction and reduced TCA cycle flux. Notably, we have identified a loss-of-function mutation of Zc3h10 in humans (Tyr105 to Cys105) that is associated with decreased mitochondrial function, increased body mass index, fat mass, fasting glucose and triglycerides. Cells from Cys105 homozygotes display alterations in Slc25a37 and Prelid3a levels and defects in mitochondrial iron and cardiolipin homeostasis that derive in mitochondrial dysfunction.
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Project description:Mitochondria are the energy-generating hubs of the cell. In spite of considerable advances, our understanding of the factors that regulate the molecular circuits that govern mitochondrial function remains incomplete. Using a genome-wide functional screen, we have identified the poorly characterized protein Zinc finger CCCH-type containing 10 (Zc3h10) as regulator of mitochondrial physiology. We show that Zc3h10 is a nuclear RNA binding protein that controls the fate of Slc25a37 and Prelid3a mRNA transcripts, two nuclear-encoded mitochondrial proteins central for iron and cardiolipin homeostasis. Depletion of Zc3h10 results in mitochondrial dysfunction and reduced TCA cycle flux. Notably, we have identified a loss-of-function mutation of Zc3h10 in humans (Tyr105 to Cys105) that is associated with decreased mitochondrial function, increased body mass index, fat mass, fasting glucose and triglycerides. Cells from Cys105 homozygotes display alterations in Slc25a37 and Prelid3a levels and defects in mitochondrial iron and cardiolipin homeostasis that derive in mitochondrial dysfunction.
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Project description:Zc3h10 controls mitochondrial function coupling iron and cardiolipin homeostasis.
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Project description:Disruption of local iron homeostasis is a common feature of neurodegenerative diseases. We focused on dopaminergic neurons, asking how iron transport proteins modulate iron homeostasis in vivo. Inactivation of the transmembrane iron exporter ferroportin had no apparent consequences. However, loss of the transferrin receptor 1, involved in iron uptake, caused profound, age-progressive neurodegeneration with features similar to Parkinson’s disease. There was gradual loss of dopaminergic projections in the striatum with subsequent death of dopaminergic neurons in the substantia nigra. After depletion of 30% of the neurons the mice developed neurobehavioral parkinsonism, with evidence of mitochondrial dysfunction and impaired mitochondrial autophagy. Molecular analysis revealed strong signatures indicative of attempted axonal regeneration, a metabolic switch to glycolysis and the unfolded protein response. We speculate that cellular iron deficiency may contribute to neurodegeneration in human patients Using Ribotag technology, from mouse ventral midbrain lysates, we isolated actively translated mRNA species from control and Transferrin receptor 1-null dopaminergic neurons. Two mouse ages were used 3 wks (early neurodegeration) 10 wks (late neurodegeneration)
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Project description:Histones and their modifications such as methylation and acetylation play an important role in the regulation of gene transcription and cellular metabolism. Cells in response to iron deficiency induce iron metabolism, especially the expression of iron uptake-related genes, but the role of histone modifications in their induction is unclear. We report here that compared to other histone modification enzymes, loss of histone acetylates Gcn5p and Sas2p has a stronger effect on the induction of iron homeostasis genes. Among the studied histone modification enzymes, Gcn5p and Rtt109p have a specific role in regulating the cellular response under the deficiency of the mitochondrial iron-sulfur cluster biosynthesis. Therefore, the histone acetylation, specifically regulated by Gcn5p, Rtt109p and Sas2p, plays an important role in the response to iron-deficiency conditions.
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