<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cagnone GL</submitter><funding>NIA NIH HHS</funding><pagination>23229</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4796791</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>6</volume><pubmed_abstract>An increasing number of women fail to achieve pregnancy due to either failed fertilization or embryo arrest during preimplantation development. This often results from decreased oocyte quality. Indeed, reduced mitochondrial DNA copy number (mitochondrial DNA deficiency) may disrupt oocyte quality in some women. To overcome mitochondrial DNA deficiency, whilst maintaining genetic identity, we supplemented pig oocytes selected for mitochondrial DNA deficiency, reduced cytoplasmic maturation and lower developmental competence, with autologous populations of mitochondrial isolate at fertilization. Supplementation increased development to blastocyst, the final stage of preimplantation development, and promoted mitochondrial DNA replication prior to embryonic genome activation in mitochondrial D</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Restoration of normal embryogenesis by mitochondrial supplementation in pig oocytes exhibiting mitochondrial DNA deficiency.</pubmed_title><pmcid>PMC4796791</pmcid><funding_grant_id>R37 AG028730</funding_grant_id><pubmed_authors>Sinclair DA</pubmed_authors><pubmed_authors>Matthews P</pubmed_authors><pubmed_authors>Makanji Y</pubmed_authors><pubmed_authors>Wong AS</pubmed_authors><pubmed_authors>Wu LE</pubmed_authors><pubmed_authors>St John JC</pubmed_authors><pubmed_authors>Cagnone GL</pubmed_authors><pubmed_authors>Tsai TS</pubmed_authors><pubmed_authors>Gould J</pubmed_authors><pubmed_authors>Elgass KD</pubmed_authors><pubmed_authors>McKenzie M</pubmed_authors><pubmed_authors>Bonkowski MS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Restoration of normal embryogenesis by mitochondrial supplementation in pig oocytes exhibiting mitochondrial DNA deficiency.</name><description>An increasing number of women fail to achieve pregnancy due to either failed fertilization or embryo arrest during preimplantation development. This often results from decreased oocyte quality. Indeed, reduced mitochondrial DNA copy number (mitochondrial DNA deficiency) may disrupt oocyte quality in some women. To overcome mitochondrial DNA deficiency, whilst maintaining genetic identity, we supplemented pig oocytes selected for mitochondrial DNA deficiency, reduced cytoplasmic maturation and lower developmental competence, with autologous populations of mitochondrial isolate at fertilization. Supplementation increased development to blastocyst, the final stage of preimplantation development, and promoted mitochondrial DNA replication prior to embryonic genome activation in mitochondrial D</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Mar</publication><modification>2026-05-04T16:23:42.714Z</modification><creation>2019-03-27T02:11:23Z</creation></dates><accession>S-EPMC4796791</accession><cross_references><pubmed>26987907</pubmed><doi>10.1038/srep23229</doi></cross_references></HashMap>