Fish metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB10626 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR249530_1.fastq.gz | Fastqsanger.gz | |||
| DRR249530_2.fastq.gz | Fastqsanger.gz | |||
| DRR249531_1.fastq.gz | Fastqsanger.gz | |||
| DRR249531_2.fastq.gz | Fastqsanger.gz | |||
| DRR249532_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 1070 |
Similar Datasets
Project description:This dataset investigates the transcriptional effect of mitochondrial 12S rRNA hypermethylation, both by overexpressing the mitochondrial methyltransferase mtTFB1 in HeLa cells and by using A1555G cybrids, where the 12S rRNA is hypermethylated. HeLa cells overexpressing a methyltransferase-deficient mtTFB1 (mtTFB1[G65A]) and wild-type A1555A cybrids were used as controls. four samples with 12S rRNA hypermethylation (two cell lines, with two biological replicates each) versus four samples with basal 12S rRNA methylation (two cell lines, with two biological replicates each)
2012-09-18 | E-GEOD-33780 | biostudies-arrayexpress
Project description:This dataset investigates the transcriptional effect of mitochondrial 12S rRNA hypermethylation, both by overexpressing the mitochondrial methyltransferase mtTFB1 in HeLa cells and by using A1555G cybrids, where the 12S rRNA is hypermethylated. HeLa cells overexpressing a methyltransferase-deficient mtTFB1 (mtTFB1[G65A]) and wild-type A1555A cybrids were used as controls.
2012-09-18 | GSE33780 | GEO
Project description:Metabolic syndrome is a growing concern in developed societies and due to its polygenic nature, the genetic component is only slowly being elucidated. Common mitochondrial DNA sequence variants have been associated with symptoms of metabolic syndrome and may therefore be relevant players in the genetics of metabolic syndrome. We investigate the effect of mitochondrial sequence variation on the metabolic phenotype in conplastic rat strains with identical nuclear but unique mitochondrial genomes, challenged by high-fat diet. We find that the variation in mitochondrial rRNA sequence represents risk factor in the insulin resistance development, which is caused by diacylglycerols accumulation induced by tissue-specific reduction of the oxidative capacity. These metabolic perturbations stem from the 12S rRNA sequence variation affecting mitochondrial ribosome assembly and translation. Our work demonstrates that physiological variation in mitochondrial rRNA might represent a relevant underlying factor in the progression of metabolic syndrome.
2024-08-13 | PXD052976 | Pride
Project description:Objectives: Metabolic syndrome and its associated comorbidities are a growing concern in developed societies. Due to its polygenic nature, the genetic component of metabolic syndrome is only slowly being elucidated. Common mitochondrial DNA sequence variants have been associated with late-onset human diseases, including cardiovascular disease or type 2 diabetes mellitus, and may therefore be relevant players in the genetics of metabolic syndrome. Methods: In the present study, we investigate the effect of mitochondrial sequence variation on the metabolic phenotype in conplastic rat strains with identical nuclear but unique mitochondrial genomes that differ in the sequence of oxidative phosphorylation structural proteins, tRNAs and rRNAs. Results: Exposure to the high-fat diet led to the development of insulin resistance in the conplastic animals, which was associated with the reduced oxidative capacity of the heart (but not the liver) mitochondria. Reduced fatty acid oxidation led to the accumulation of bioactive diacylglycerols and subsequent inhibition of insulin signaling. Conclusions: We propose that these metabolic perturbations stem from the 12S rRNA sequence variation, which affects mitoribosome assembly and thus mitochondrial translation. Our work has demonstrated that physiological sequence variation in mitochondrial rRNA may be a relevant underlying factor in the progression of metabolic syndrome.
2024-08-13 | PXD045910 | Pride
Project description:mitochondrial 12S rRNA sequences Cynomolgus macaque
| PRJEB49348 | ENA
Project description:The mechanisms of RNA-binding proteins (RBPs)-mediated post-transcriptional regulation of pre-existing mRNAs, which is essential for spermatogenesis, remains poorly understood. Here, we identify a germline-specific mitochondrial RBP AMG-1, a homolog of mammalian LRPPRC, required for spermatogenesis in C. elegans. amg-1 mutation hinders germline development without affecting somatic development and leads to the aberrant mitochondrial morphology and structure associated with mitochondrial dysfunctions specifically in germline. We demonstrate that AMG-1 is most frequently bound to mtDNA-encoded 12S and 16S ribosomal RNA, the essential components of mitochondrial ribosome, and that 12S rRNA expression mediated by AMG-1 is crucial for germline mitochondrial protein homeostasis. Besides, mitochondrial dysfunction by AMG-1 mutation triggers sperm apoptosis in C. elegans. Furthermore, SLRP-1, the homolog of mammalian SLIRP in C. elegans, interacts with AMG-1 genetically to regulate germline development and reproductive success in C. elegans. Taken together, these findings reveal the novel function of mtRBP in specifically regulating germline development.
2023-01-16 | GSE222138 | GEO
Project description:The mechanisms of RNA-binding proteins (RBPs)-mediated post-transcriptional regulation of pre-existing mRNAs, which is essential for spermatogenesis, remains poorly understood. Here, we identify a germline-specific mitochondrial RBP AMG-1, a homolog of mammalian LRPPRC, required for spermatogenesis in C. elegans. amg-1 mutation hinders germline development without affecting somatic development and leads to the aberrant mitochondrial morphology and structure associated with mitochondrial dysfunctions specifically in germline. We demonstrate that AMG-1 is most frequently bound to mtDNA-encoded 12S and 16S ribosomal RNA, the essential components of mitochondrial ribosome, and that 12S rRNA expression mediated by AMG-1 is crucial for germline mitochondrial protein homeostasis. Besides, mitochondrial dysfunction by AMG-1 mutation triggers sperm apoptosis in C. elegans. Furthermore, SLRP-1, the homolog of mammalian SLIRP in C. elegans, interacts with AMG-1 genetically to regulate germline development and reproductive success in C. elegans. Taken together, these findings reveal the novel function of mtRBP in specifically regulating germline development.
2023-01-16 | GSE222137 | GEO
Project description:We analyzed samples from fourteen deaf individuals (Affected 1 through 14), fifteen hearing maternally related family members (Unaffected 1-15), six marry-in controls (Controls 1-6) from extended pedigree from Arab-Israeli village, and nine individuals from another Arab-Israeli village (Controls 7-15). All affected and unaffected maternally-related individuals carry homoplasmic mutation in the 12S rRNA gene of the mitochondrial DNA, associated with both non-syndromic and aminoglycosides-induced deafness. Keywords: Comparison of genome-wide expression in cell lines of maternally-related individuals with mitochondrial mutation and controls carrying wild-type mitochondrial chromosome.
2009-06-01 | GSE9822 | GEO