Similar Datasets
Project description:Targeting of yeast with genetic or nutrient perturbation to assess mitochondrial membrane potential and its regulation.
2022-10-16 | GSE212790 | GEO
Project description:Reduction of mitochondrial membrane potential is a hallmark of mitochondrial dysfunction. It activates adaptive responses in organisms from yeast to human to rewire metabolism, remove depolarized mitochondria, and degrade unimported precursor proteins. It remains unclear how cells maintain mitochondrial membrane potential, which is critical for maintaining iron-sulfur cluster (ISC) synthesis, an indispensable function of mitochondria. Here we show that yeast oxidative phosphorylation mutants deficient in complex III, IV, V, and mtDNA respectively, have graded reduction of mitochondrial membrane potential and proliferation rates. Extensive omics analyses of these mutants show that accompanying mitochondrial membrane potential reduction, these mutants progressively activate adaptive responses, including transcriptional downregulation of ATP synthase inhibitor Inh1 and OXPHOS subunits, Puf3-mediated upregulation of import receptor Mia40 and global mitochondrial biogenesis, Snf1/AMPK-mediated upregulation of glycolysis and repression of ribosome biogenesis, and transcriptional upregulation of cytoplasmic chaperones. These adaptations disinhibit mitochondrial ATP hydrolysis, remodel mitochondrial proteome, and optimize ATP supply to mitochondria to convergently maintain mitochondrial membrane potential, ISC biosynthesis, and cell proliferation.
2020-11-27 | GSE162197 | GEO
Project description:We investigated the transcriptional response of yeast to the loss of a single copy of ARH1; an oxidoreductase of the mitochondrial inner membrane, which is among the few mitochondrial proteins that is essential for viability in yeast, ATM1; the mitochondrial inner membrane ATP-binding cassette (ABC) transporter, and of YFH1; the mitochondrial matrix iron chaperone, which oxidizes and stores iron, and interacts with Isu1p to promote Fe-S cluster assembly.
2019-08-13 | E-MTAB-7648 | biostudies-arrayexpress
Project description:Transcriptome comparisons between grx5, pet117 and mlp1 mutants. All of them are referenced to the same parental wild type sample using three independent samples and three independent nylon macroarrays. Each replicate pair (wt/mutant), hybridized on the same membrane, was normalized by lowess method. z-tests were performed to evaluate differential gene expression. Keywords = yeast Keywords = GRX5 Keywords = PET117 Keywords: other
2003-12-29 | GSE910 | GEO
Project description:Transcriptional profiles on different yeast strain mutants (DEgd2/1, DEgd2/Btt1)were identified by microarray analysis comparing total mutant RNA vs wild type RNA.
2013-04-05 | GSE45796 | GEO
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
2025-05-09 | GSE277766 | GEO
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
2025-05-09 | GSE277752 | GEO
Project description:Background: Mitochondria carry out essential functions in eukaryotic cells. The mitochondrial genome encodes factors critical to support oxidative phosphorylation and mitochondrial protein import necessary for these functions. However, organisms like budding yeast can readily lose their mitochondrial genome, yielding respiration-deficient petite mutants. The fission yeast Schizosaccharomyces pombe is petite-negative, but some nuclear mutations enable the loss of its mitochondrial genome.
Results: Here, we characterize the classical petite-positive mutation ptp1-1 as a loss of function allele of the proteasome 19S regulatory subunit component mts4/rpn1, involved in the ubiquitin-dependent degradation pathway. By comparison with another petite-enabling mutation in the g-subunit of the F1-ATPase, we show that ptp1-1 does not rescue mitochondrial membrane potential. Instead, the mutation results in increased levels of mitochondrial and cytoplasmic chaperones and an altered oxidative stress response.
Conclusions: ptp1-1 is a partial loss of function mutation of the proteasome that enables growth of cells devoid of mitochondrial DNA through a mechanism that is independent of mitochondrial membrane potential rescue and associated with proteasome dependent regulation of mitochondrial protein import precursors and the oxidative stress response.
2025-08-15 | MSV000098838 | MassIVE