Ontology highlight
ABSTRACT:
PROVIDER: PRJNA397951 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To determine how the mtDNA load at the beginning of tumorigenesis affects the DNA methylation patterns of TRFs during tumourigenesis. Different loads of mtDNA at the beginning of tumourigenesis have limited impact on the copy number variation contributing to tumorigenesis.
2018-12-31 | GSE98366 | GEO
Project description:How the mtDNA load at the beginning of tumorigenesis affects tumourigenesis
| PRJNA384905 | ENA
Project description:This study characterized variations in the methylation profile of mitochondrial DNA (mtDNA) during initial bovine embryo development and correlated the presence of methylation with mtDNA transcription. Bovine oocytes were obtained from abattoir ovaries and submitted to in vitro culture procedures. Oocytes and embryos were collected at various stages (immature oocyte, IM; mature oocyte, MII; zygote, ZY; 4-cells, 4C; 16-cells, 16C and blastocysts, BL). Total DNA (including mtDNA) was used for Whole Genome Enzymatic Methyl Sequencing and for quantification of mtDNA copy number. Extracted RNA was used for quantification of mitochondrial transcripts (ND6, CYTB, tRNA-Phe and tRNA-Gln) using Droplet Digital PCR. The number of mtDNA copies per oocyte/embryo was found to be similar, while methylation levels in mtDNA varied among stages. Higher total methylation levels were found mainly at 4C and 16C. In specific gene regions, higher methylation levels were also observed at 4C and 16C (ND6, CYTB and tRNA-Phe), as well as an inverse correlation with the quantity of transcripts for these regions. This is a first description of epigenetic changes occurring in mtDNA during early embryonic development. Our results indicate that methylation might regulate the mtDNA transcription at a local level, particularly around the time of embryonic genome activation.
2024-04-24 | GSE230476 | GEO
Project description:Mammalian mitochondrial DNA (mtDNA) is coated with mitochondrial transcription factor A (TFAM) and compacted into nucleoids. TFAM is not only the main component of mitochondrial nucleoids but its levels can also control mtDNA copy number. Here we show that the TFAM-to-mtDNA ratio is critical for maintaining normal mtDNA expression in different tissues of the mouse. BAC transgenic mice with a 1.5-fold increase in TFAM protein levels maintain a normal TFAM-to-mtDNA ratio in different tissues and as a consequence mitochondrial gene expression, nucleoid distribution and whole animal metabolism are all unaltered. In contrast, mice expressing TFAM from the CAG promoter in the ROSA26 locus have 4.5-fold increase of TFAM protein levels in heart and skeletal muscle and develop pathology leading to early postnatal lethality. The TFAM-to-mtDNA ratio varies widely between tissues in these mice and is very high in skeletal muscle where it causes strong repression of mtDNA expression and deficient oxidative phosphorylation (OXPHOS) despite normal mtDNA levels. In heart, mtDNA copy number is increased leading to a near normal TFAM-to-mtDNA ratio and maintained OXPHOS capacity. In the liver, mtDNA expression is maintained despite increased TFAM levels and normal mtDNA levels. Here, tissue-specific induction of the LONP1 protease and mitochondrial RNA polymerase (POLRMT) expression counteracts the silencing effect of high TFAM levels. We conclude that the TFAM-to-mtDNA ratio has an important role in maintaining mtDNA expression in vivo. TFAM acts as a general repressor of mtDNA expression and this effect can be counterbalance by tissue-specific expression of regulatory factors.
2021-08-18 | PXD023050 | Pride
Project description:How individual genes are regulated from a mitochondrial polycistronic transcript to have variable expression remains an enigma. Here, through bisulfite sequencing and strand-specific mapping, we show mitochondrial genomes in human and other animals were strongly biased to light (L)-strand non-CpG methylation with conserved peak loci preferentially located at gene-gene boundaries, which was also independently validated by MeDIP and FspEI digestion. Such mtDNA methylation patterns are conserved across different species and developmental stages, but display dynamic local or global changes during development and aging. Knockout of DNMT3A alone perturbed mtDNA regional methylation patterns, but not global levels, and altered mitochondrial gene expression, copy number, and oxygen respiration. Overexpression of DNMT3A strongly increased mtDNA methylation and strand bias. Overall, methylation at gene body and boundaries was negatively associated with mitochondrial transcript abundance and also polycistronic transcript processing. Furthermore, HPLC-MS confirmed the methylation signals on mitochondria DNA. Together, these data provide high-resolution mtDNA methylation maps that revealed a strand specific non-CpG methylation, its dynamic regulation and its impact on the polycistronic mitochondrial transcript processing.
2019-08-22 | GSE133964 | GEO
Project description:How individual genes are regulated from a mitochondrial polycistronic transcript to have variable expression remains an enigma. Here, through bisulfite sequencing and strand-specific mapping, we show mitochondrial genomes in human and other animals were strongly biased to light (L)-strand non-CpG methylation with conserved peak loci preferentially located at gene-gene boundaries, which was also independently validated by MeDIP and FspEI digestion. Such mtDNA methylation patterns are conserved across different species and developmental stages, but display dynamic local or global changes during development and aging. Knockout of DNMT3A alone perturbed mtDNA regional methylation patterns, but not global levels, and altered mitochondrial gene expression, copy number, and oxygen respiration. Overexpression of DNMT3A strongly increased mtDNA methylation and strand bias. Overall, methylation at gene body and boundaries was negatively associated with mitochondrial transcript abundance and also polycistronic transcript processing. Furthermore, HPLC-MS confirmed the methylation signals on mitochondria DNA. Together, these data provide high-resolution mtDNA methylation maps that revealed a strand specific non-CpG methylation, its dynamic regulation and its impact on the polycistronic mitochondrial transcript processing.
2019-08-22 | GSE133963 | GEO
Project description:How individual genes are regulated from a mitochondrial polycistronic transcript to have variable expression remains an enigma. Here, through bisulfite sequencing and strand-specific mapping, we show mitochondrial genomes in human and other animals were strongly biased to light (L)-strand non-CpG methylation with conserved peak loci preferentially located at gene-gene boundaries, which was also independently validated by MeDIP and FspEI digestion. Such mtDNA methylation patterns are conserved across different species and developmental stages, but display dynamic local or global changes during development and aging. Knockout of DNMT3A alone perturbed mtDNA regional methylation patterns, but not global levels, and altered mitochondrial gene expression, copy number, and oxygen respiration. Overexpression of DNMT3A strongly increased mtDNA methylation and strand bias. Overall, methylation at gene body and boundaries was negatively associated with mitochondrial transcript abundance and also polycistronic transcript processing. Furthermore, HPLC-MS confirmed the methylation signals on mitochondria DNA. Together, these data provide high-resolution mtDNA methylation maps that revealed a strand specific non-CpG methylation, its dynamic regulation and its impact on the polycistronic mitochondrial transcript processing.
2019-08-22 | GSE133960 | GEO
Project description:How individual genes are regulated from a mitochondrial polycistronic transcript to have variable expression remains an enigma. Here, through bisulfite sequencing and strand-specific mapping, we show mitochondrial genomes in human and other animals were strongly biased to light (L)-strand non-CpG methylation with conserved peak loci preferentially located at gene-gene boundaries, which was also independently validated by MeDIP and FspEI digestion. Such mtDNA methylation patterns are conserved across different species and developmental stages, but display dynamic local or global changes during development and aging. Knockout of DNMT3A alone perturbed mtDNA regional methylation patterns, but not global levels, and altered mitochondrial gene expression, copy number, and oxygen respiration. Overexpression of DNMT3A strongly increased mtDNA methylation and strand bias. Overall, methylation at gene body and boundaries was negatively associated with mitochondrial transcript abundance and also polycistronic transcript processing. Furthermore, HPLC-MS confirmed the methylation signals on mitochondria DNA. Together, these data provide high-resolution mtDNA methylation maps that revealed a strand specific non-CpG methylation, its dynamic regulation and its impact on the polycistronic mitochondrial transcript processing.
2019-08-22 | GSE133959 | GEO
Project description:How individual genes are regulated from a mitochondrial polycistronic transcript to have variable expression remains an enigma. Here, through bisulfite sequencing and strand-specific mapping, we show mitochondrial genomes in human and other animals were strongly biased to light (L)-strand non-CpG methylation with conserved peak loci preferentially located at gene-gene boundaries, which was also independently validated by MeDIP and FspEI digestion. Such mtDNA methylation patterns are conserved across different species and developmental stages, but display dynamic local or global changes during development and aging. Knockout of DNMT3A alone perturbed mtDNA regional methylation patterns, but not global levels, and altered mitochondrial gene expression, copy number, and oxygen respiration. Overexpression of DNMT3A strongly increased mtDNA methylation and strand bias. Overall, methylation at gene body and boundaries was negatively associated with mitochondrial transcript abundance and also polycistronic transcript processing. Furthermore, HPLC-MS confirmed the methylation signals on mitochondria DNA. Together, these data provide high-resolution mtDNA methylation maps that revealed a strand specific non-CpG methylation, its dynamic regulation and its impact on the polycistronic mitochondrial transcript processing.
2019-08-22 | GSE133962 | GEO
Project description:How individual genes are regulated from a mitochondrial polycistronic transcript to have variable expression remains an enigma. Here, through bisulfite sequencing and strand-specific mapping, we show mitochondrial genomes in human and other animals were strongly biased to light (L)-strand non-CpG methylation with conserved peak loci preferentially located at gene-gene boundaries, which was also independently validated by MeDIP and FspEI digestion. Such mtDNA methylation patterns are conserved across different species and developmental stages, but display dynamic local or global changes during development and aging. Knockout of DNMT3A alone perturbed mtDNA regional methylation patterns, but not global levels, and altered mitochondrial gene expression, copy number, and oxygen respiration. Overexpression of DNMT3A strongly increased mtDNA methylation and strand bias. Overall, methylation at gene body and boundaries was negatively associated with mitochondrial transcript abundance and also polycistronic transcript processing. Furthermore, HPLC-MS confirmed the methylation signals on mitochondria DNA. Together, these data provide high-resolution mtDNA methylation maps that revealed a strand specific non-CpG methylation, its dynamic regulation and its impact on the polycistronic mitochondrial transcript processing.
2019-08-22 | GSE133961 | GEO