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Human polar body transfer eliminates the transmission of inherited mitochondrial DNA variants

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE86650 | GEO | 2016/09/11

SECONDARY ACCESSION(S): PRJNA342524

REPOSITORIES: GEO

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Human polar body transfer eliminates the transmission of inherited mitochondrial DNA variants [methylation]

Project description:Although polar body transfer (PBT) has the potential to prevent the transmission of inherited mitochondrial DNA (mtDNA) diseases, the PBT technique is still at an early stage, as no human data are publicly available for PBT. Here, we investigated the comparative values of first and second PBT (PB1T, PB2T), spindle-chromosome and pronuclear transfer (ST, PNT), modified ST and PNT (mST and mPNT) to explore the efficiency and safety of these approaches. A comparative analysis confirmed that PB1T, mST, PB2T and mPNT could be used to donate mtDNA without resulting in significant heteroplasmy or alterations in the methylation profile and gene expression. Importantly, PB1T produced reconstructed embryos and embryonic stem cells (ESCs) in every generation with undetectable donor mtDNA. However, donor mtDNA seems to have a tendency to be amplified in generations of mPNT-ESCs with up to 3% heteroplasmy. These results suggest that PB1T holds great potential in eliminating mtDNA variants.

2016-09-11 | GSE86648 | GEO

Human polar body transfer eliminates the transmission of inherited mitochondrial DNA variants [mRNA]

2016-09-11 | GSE86570 | GEO

Human polar body transfer eliminates the transmission of inherited mitochondrial DNA variants

Project description:Human polar body transfer eliminates the transmission of inherited mitochondrial DNA variants

| PRJNA342524 | ENA

Nuclear genome transfer in human oocytes eliminates mitochondrial DNA variants.

Project description:Mitochondrial DNA mutations transmitted maternally within the oocyte cytoplasm often cause life-threatening disorders. Here we explore the use of nuclear genome transfer between unfertilized oocytes of two donors to prevent the transmission of mitochondrial mutations. Nuclear genome transfer did not reduce developmental efficiency to the blastocyst stage, and genome integrity was maintained provided that spontaneous oocyte activation was avoided through the transfer of incompletely assembled spindle-chromosome complexes. Mitochondrial DNA transferred with the nuclear genome was initially detected at levels below 1%, decreasing in blastocysts and stem-cell lines to undetectable levels, and remained undetectable after passaging for more than one year, clonal expansion, differentiation into neurons, cardiomyocytes or ?-cells, and after cellular reprogramming. Stem cells and differentiated cells had mitochondrial respiratory chain enzyme activities and oxygen consumption rates indistinguishable from controls. These results demonstrate the potential of nuclear genome transfer to prevent the transmission of mitochondrial disorders in humans.

| S-EPMC7924261 | biostudies-literature

Mitochondrial replacement in macaque monkey offspring by first polar body transfer.

Project description: Not available

| S-EPMC8027822 | biostudies-literature

DNA methylation data from ESCs derived by polar body transfer reconstructed embryos (PBTESCs)

Project description:Here we report the derivation of human ESCs from the polar body thansfer reconstructed embryos. We choose three cell lines from all the cell lines and compare the DNA methylation state. We use human methylation chip to compare genomic DNA methylation level among three PB1 transfer human ES cell lines and three PB2 transfer human ES cell lines.

2018-03-04 | GSE95761 | GEO

Herpes simplex virus eliminates host mitochondrial DNA.

Project description:Mitochondria have crucial roles in the life and death of mammalian cells, and help to orchestrate host antiviral defences. Here, we show that the ubiquitous human pathogen herpes simplex virus (HSV) induces rapid and complete degradation of host mitochondrial DNA during productive infection of cultured mammalian cells. The depletion of mitochondrial DNA requires the viral UL12 gene, which encodes a conserved nuclease with orthologues in all herpesviruses. We show that an amino-terminally truncated UL12 isoform-UL12.5-localizes to mitochondria and triggers mitochondrial DNA depletion in the absence of other HSV gene products. By contrast, full-length UL12, a nuclear protein, has little or no effect on mitochondrial DNA levels. Our data document that HSV inflicts massive genetic damage to a crucial host organelle and show a novel mechanism of virus-induced shutoff of host functions, which is likely to contribute to the cell death and tissue damage caused by this widespread human pathogen.

| S-EPMC1796774 | biostudies-literature

Elimination of mitochondrial DNA variants by nuclear genome transfer in human oocytes

Project description:Nuclear genome exchange between different oocytes results in efficient development and stem cell derivation 1 million cells was used for RNA extraction and labeling using the Illumina total prep RNA amplification kit. Parthenogenetic stem cell lines and embryonic stem cells

2012-12-01 | E-GEOD-42077 | biostudies-arrayexpress

Elimination of mitochondrial DNA variants by nuclear genome transfer in human oocytes.

Project description:Nuclear genome exchange between different oocytes results in efficient development and stem cell derivation. No differences in homozgyous CNVs were found between swaPS and pES lines. No differences in total copy number variations were found between the swaPS and pES lines. DNA was isolated from cultured cells. Affymetrix SNP arrays were used in accordance with the manufacturer's instructions. Copy number analysis was performed using NEXUS 6.0.

2013-01-01 | E-GEOD-42271 | biostudies-arrayexpress

Towards therapeutic application of pronuclear transfer to prevent transmission of mitochondrial DNA disease

Project description:Mitochondrial DNA (mtDNA) mutations are maternally inherited and are associated with a broad range of debilitating and fatal diseases. Assisted reproductive technologies designed to uncouple the inheritance of mtDNA from nuclear DNA may enable women who carry mtDNA mutations to have a genetically related child with a greatly reduced risk of disease. Here we report for the first time that pronuclear transplantation (PNT) between normally fertilised human zygotes provides an effective approach to preventing transmission of mtDNA disease. We found that the procedures previously used to perform PNT between abnormally fertilized human zygotes are highly inefficient when applied to those that undergo normal fertilization. We have therefore developed an alternative approach based on transplanting PN shortly after completion of the second meiotic division rather than shortly before onset of the first mitosis. This approach promotes highly efficient development to the blastocyst stage without affecting nuclear genome integrity. Furthermore, the expression profile of genes encoded by the nuclear and mitochondrial genomes was indistinguishable from unmanipulated control embryos. Importantly, levels of mtDNA transferred with the nuclear genome are below the threshold for mtDNA disease. Together these data indicate that transplantation of pronuclei early in the first cell cycle holds promise as a safe and effective approach to preventing transmission of mtDNA disease.

2016-06-03 | GSE76284 | GEO

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