Similar Datasets
Project description:In our studies we were searching for the new factors engaged in mitochondrial nucleic acids metabolism under stress conditions in humans. Quantitative proteomic approach revealed C6orf203 protein as a potential new factor engaged in response to perturbed mitochondrial gene expression. We showed that C6orf203 is a mitochondrial RNA binding protein which is able to rescue diminished mitochondrial transcription in stress conditions.
2019-06-13 | GSE123683 | GEO
Project description:Transcriptome analysis upon C6orf203 silencing
| PRJNA509589 | ENA
Project description:Transcriptome analysis upon REXO2 silencing
| PRJNA564828 | ENA
Project description:At each sexual cycle, during development of the somatic macronucleus (MAC) from the germline micronucleus (MIC), the genome of the ciliate Paramecium tetraurelia is massively rearranged through the reproducible elimination of germline-specific sequences. It has been reported previously that targeting of these sequences is mediated by non-protein-coding RNAs including different classes of small RNAs and longer non-coding transcripts. Using RNA interference, we showed that TFIIS4 gene encoding development-specific TFIIS elongation factor is essential for the formation of a functional somatic genome. We demonstrated that genome rearrangements taking place during MAC development were inhibited in TFIIS4-depleted cells, which led to high lethality in the sexual progeny. The role of TFIIS4 elongation factor in coding transcription at the genome-wide level was studied by performing a microarray hybridization experiment using RNA samples extracted during vegetative growth and at five time points during the progression of the sexual cycle (autogamy). Total RNA samples were extracted during vegetative growth and at five different time points of autogamy from mass cultures fed with bacteria producing dsRNA to induce TFIIS4 or ICL7a silencing. TFIIS4 gene encodes TFIIS elongation factor and is strongly induced during autogamy, a self-fertilization process. RNAi against TFIIS4 leads to strong lethality in post-autogamous progeny. ICL7a is a non-essential gene; the loss of function of this gene by with dsRNA feeding results in mutant phenotypes: absence of intraciliary lattice and defect in calcium-induced cell contractility.
2015-06-12 | E-GEOD-64682 | biostudies-arrayexpress
Project description:At each sexual cycle, during development of the somatic macronucleus (MAC) from the germline micronucleus (MIC), the genome of the ciliate Paramecium tetraurelia is massively rearranged through the reproducible elimination of germline-specific sequences. It has been reported previously that targeting of these sequences is mediated by non-protein-coding RNAs including different classes of small RNAs and longer non-coding transcripts. Using RNA interference, we showed that TFIIS4 gene encoding development-specific TFIIS elongation factor is essential for the formation of a functional somatic genome. We demonstrated that genome rearrangements taking place during MAC development were inhibited in TFIIS4-depleted cells, which led to high lethality in the sexual progeny. The role of TFIIS4 elongation factor in coding transcription at the genome-wide level was studied by performing a microarray hybridization experiment using RNA samples extracted during vegetative growth and at five time points during the progression of the sexual cycle (autogamy).
2015-06-12 | GSE64682 | GEO
Project description:Farnesol is a nonsterol isoprenoid produced by dephosphorylation of farnesyl pyrophosphate, a catabolite of the cholesterol biosynthetic pathway. These isoprenoids have been reported to inhibit proliferation and induce apoptosis in neoplastic cell lines as well as to be effective in chemotherapy in several in vivo cancer models. Recently, it was shown that farnesol triggers morphological features characteristic of apoptosis in the filamentous fungus Aspergillus nidulans. In order to investigate which pathways are involved under Farnesol treatment, we determined the transcriptional profile of A. nidulans wild type strain. Conidia were incubated at 37°C in complete medium for 16 hours and were esposed or not to 100 μM Farnesol for 2 hours. The mycelia were harvested by centrifugation and used for competitive microarray hybridizations. We detected differential regulation of genes involved in a variety of cellular processes whose specific modulation is likely to be implicated with A. nidulans adaptation to farnesol. We observed decreased mRNA abundance of several genes involved in RNA processing and modification, transcription, translation, ribosomal structure and biogenesis, amino acid transport and metabolism. Interestingly, several genes involved in the ergosterol biosynthesis (such as the homologues of erg4/24, 11A, -11B, -13, -25, and –28) have decreased mRNA accumulation and other genes encoding mitochondrial proteins [such as AN9103.3, AN4500.3, and AN5440.3, encoding the Apoptosis Inducing Factor (AIF)-like mitochondrial oxidoreductase, the mitochondrial ATPase inhibitor, and the cytochrome c peroxidase, respectively] have increased mRNA expression when A. nidulans was exposed to farnesol. We also observed as more expressed several genes encoding proteins involved in trehalose metabolism and chaperones. Keywords: farnesol effect
2008-03-06 | GSE10712 | GEO
Project description:The goal of the study was to understand whether mitochondrial-driven epigenetic changes regulate gene expression. Mitochondrial metabolism has been implicated in epigenetics but the extent to which this impacts gene expression is unclear. Here we show that loss of mitochondrial DNA (mtDNA) results in locus-specific alterations in histone acetylation, DNA methylation and expression of a subset of genes. Most of these changes are rescued by restoring mitochondrial electron transport in a way that maintains the oxidative tricarboxylic acid cycle, but not reactive oxygen species or ATP production, or by modulating the mitochondrial pool of acetyl-CoA. Changes in acetyl-CoA and histone acetylation precede overt mitochondrial dysfunction and significant changes in gene expression and DNA methylation. This suggests that acetyl-CoA levels signal mitochondrial status to the nucleus. Differentially expressed genes with altered histone marks or DNA methylation regulate amino acid degradation, which likely compensates for the changes in acetyl-CoA and one carbon metabolism. These have the potential to further affect methylation reactions, redox control and nucleotide levels. These results illustrate the extent to which mitochondria impact cell physiology through epigenetic remodeling.
2018-03-21 | GSE100249 | GEO
Project description:The goal of the study was to understand whether mitochondrial-driven epigenetic changes regulate gene expression. Mitochondrial metabolism has been implicated in epigenetics but the extent to which this impacts gene expression is unclear. Here we show that loss of mitochondrial DNA (mtDNA) results in locus-specific alterations in histone acetylation, DNA methylation and expression of a subset of genes. Most of these changes are rescued by restoring mitochondrial electron transport in a way that maintains the oxidative tricarboxylic acid cycle, but not reactive oxygen species or ATP production, or by modulating the mitochondrial pool of acetyl-CoA. Changes in acetyl-CoA and histone acetylation precede overt mitochondrial dysfunction and significant changes in gene expression and DNA methylation. This suggests that acetyl-CoA levels signal mitochondrial status to the nucleus. Differentially expressed genes with altered histone marks or DNA methylation regulate amino acid degradation, which likely compensates for the changes in acetyl-CoA and one carbon metabolism. These have the potential to further affect methylation reactions, redox control and nucleotide levels. These results illustrate the extent to which mitochondria impact cell physiology through epigenetic remodeling.
2018-03-21 | GSE99834 | GEO
Project description:The goal of the study was to understand whether mitochondrial-driven epigenetic changes regulate gene expression. Mitochondrial metabolism has been implicated in epigenetics but the extent to which this impacts gene expression is unclear. Here we show that loss of mitochondrial DNA (mtDNA) results in locus-specific alterations in histone acetylation, DNA methylation and expression of a subset of genes. Most of these changes are rescued by restoring mitochondrial electron transport in a way that maintains the oxidative tricarboxylic acid cycle, but not reactive oxygen species or ATP production, or by modulating the mitochondrial pool of acetyl-CoA. Changes in acetyl-CoA and histone acetylation precede overt mitochondrial dysfunction and significant changes in gene expression and DNA methylation. This suggests that acetyl-CoA levels signal mitochondrial status to the nucleus. Differentially expressed genes with altered histone marks or DNA methylation regulate amino acid degradation, which likely compensates for the changes in acetyl-CoA and one carbon metabolism. These have the potential to further affect methylation reactions, redox control and nucleotide levels. These results illustrate the extent to which mitochondria impact cell physiology through epigenetic remodeling.
2018-03-21 | GSE100133 | GEO
Project description:The goal of the study was to understand whether mitochondrial-driven epigenetic changes regulate gene expression. Mitochondrial metabolism has been implicated in epigenetics but the extent to which this impacts gene expression is unclear. Here we show that loss of mitochondrial DNA (mtDNA) results in locus-specific alterations in histone acetylation, DNA methylation and expression of a subset of genes. Most of these changes are rescued by restoring mitochondrial electron transport in a way that maintains the oxidative tricarboxylic acid cycle, but not reactive oxygen species or ATP production, or by modulating the mitochondrial pool of acetyl-CoA. Changes in acetyl-CoA and histone acetylation precede overt mitochondrial dysfunction and significant changes in gene expression and DNA methylation. This suggests that acetyl-CoA levels signal mitochondrial status to the nucleus. Differentially expressed genes with altered histone marks or DNA methylation regulate amino acid degradation, which likely compensates for the changes in acetyl-CoA and one carbon metabolism. These have the potential to further affect methylation reactions, redox control and nucleotide levels. These results illustrate the extent to which mitochondria impact cell physiology through epigenetic remodeling.
2018-03-21 | GSE100132 | GEO