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Restoration of normal embryogenesis by mitochondrial supplementation in pig oocytes exhibiting mitochondrial DNA deficiency

Cagnone, Gael L. M., Tsai, Te-Sha, Makanji, Yogeshwar, Matthews, Pamela, Gould, Jodee, Bonkowski, Michael S., Elgass, Kirstin D., Wong, Ashley S. A., Wu, Lindsay E., McKenzie, Matthew, Sinclair, David A. and St. John, Justin C. 2016, Restoration of normal embryogenesis by mitochondrial supplementation in pig oocytes exhibiting mitochondrial DNA deficiency, Scientific reports, vol. 6, pp. 1-15, doi: 10.1038/srep23229.

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Title Restoration of normal embryogenesis by mitochondrial supplementation in pig oocytes exhibiting mitochondrial DNA deficiency
Author(s) Cagnone, Gael L. M.
Tsai, Te-Sha
Makanji, Yogeshwar
Matthews, Pamela
Gould, Jodee
Bonkowski, Michael S.
Elgass, Kirstin D.
Wong, Ashley S. A.
Wu, Lindsay E.
McKenzie, MatthewORCID iD for McKenzie, Matthew orcid.org/0000-0001-7508-1800
Sinclair, David A.
St. John, Justin C.
Journal name Scientific reports
Volume number 6
Article ID 23229
Start page 1
End page 15
Total pages 15
Publisher Nature Publishing Group
Place of publication London, Eng.
Publication date 2016-03-18
ISSN 2045-2322
Keyword(s) Animals
Blastocyst
Culture Media
DNA Copy Number Variations
DNA, Mitochondrial
Embryo Culture Techniques
Embryonic Development
Female
Fertilization in Vitro
Gene Expression Profiling
Mitochondria
Oocytes
Pregnancy
Sus scrofa
Swine
Science & Technology
Multidisciplinary Sciences
Science & Technology - Other Topics
EMBRYONIC STEM-CELLS
CRESYL BLUE TEST
COPY NUMBER
POLYMERASE-GAMMA
REPLICATION
FERTILIZATION
DIFFERENTIATION
HETEROPLASMY
EXPRESSION
MATURATION
Summary 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 DNA deficient oocytes but not in oocytes with normal levels of mitochondrial DNA. Blastocysts exhibited transcriptome profiles more closely resembling those of blastocysts from developmentally competent oocytes. Furthermore, mitochondrial supplementation reduced gene expression patterns associated with metabolic disorders that were identified in blastocysts from mitochondrial DNA deficient oocytes. These results demonstrate the importance of the oocyte's mitochondrial DNA investment in fertilization outcome and subsequent embryo development to mitochondrial DNA deficient oocytes.
Language eng
DOI 10.1038/srep23229
HERDC Research category C1.1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2016, The Authors
Free to Read? Yes
Use Rights Creative Commons Attribution licence
Persistent URL http://hdl.handle.net/10536/DRO/DU:30111626

Document type: Journal Article
Collections: School of Life and Environmental Sciences
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.