Developmental competence of 8–16-cell stage bison embryos produced by interspecies somatic cell nuclear transfer
L. Antonio González-Grajales A , Laura A. Favetta A , W. Allan King A and Gabriela F. Mastromonaco A B CA Department of Biomedical Sciences, University of Guelph, 50 Stone Road E, Guelph, ON N1G 2W1, Canada.
B Reproductive Physiology, Toronto Zoo, Toronto, ON M1B 5K7, Canada.
C Corresponding author. Email: gmastromonaco@torontozoo.ca
Reproduction, Fertility and Development 28(9) 1360-1368 https://doi.org/10.1071/RD14376
Submitted: 4 October 2014 Accepted: 15 January 2015 Published: 13 March 2015
Abstract
Altered communication between nuclear and cytoplasmic components has been linked to impaired development in interspecies somatic cell nuclear transfer (iSCNT) embryos as a result of genetic divergence between the two species. This study investigated the developmental potential and mitochondrial function of cattle (Bos taurus), plains bison (Bison bison bison) and wood bison (Bison bison athabascae) embryos produced by iSCNT using domestic cattle oocytes as cytoplasts. Embryos in all groups were analysed for development, accumulation of ATP, apoptosis and gene expression of nuclear- and mitochondrial-encoded genes at the 8–16-cell stage. The results of this study showed no significant differences in the proportion of developed embryos at the 2-, 4- and 8–16-cell stages between groups. However, significantly higher ATP levels were observed in cattle SCNT embryos compared with bison iSCNT embryos. Significantly more condensed and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL)-positive nuclei were found in plains bison iSCNT embryos. No significant differences in the expression levels of nuclear respiratory factor 2 (NRF2) or mitochondrial subunit 2 of cytochrome c oxidase (mt-COX2) were found in any of the groups. However, mitochondrial transcription factor A (TFAM) expression significantly differed between groups. The results of this study provide insights into the potential causes that might lead to embryonic arrest in bison iSCNT embryos, including mitochondrial dysfunction, increased apoptosis and abnormal gene expression.
Additional keywords: ATP, apoptosis, heteroplasmy, mitochondrial incompatibility.
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