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Fate of microinjected spermatid mitochondria in the mouse oocyte and embryo

Published online by Cambridge University Press:  01 August 1998

James M. Cummins
Affiliation:
School of Veterinary Studies, Murdoch University, Murdoch, Western Australia 6150
Teruhiko Wakayama
Affiliation:
Department of Anatomy and Reproductive Biology, University of Hawaii Medical School, Honolulu, Hawaii 96822, USA
Ryuzo Yanagimachi
Affiliation:
Department of Anatomy and Reproductive Biology, University of Hawaii Medical School, Honolulu, Hawaii 96822, USA

Abstract

Mouse round spermatids labelled with MitoTracker were microinjected into Sr2+-activated mouse oocytes. The labelled mitochondria were tracked up to the morula/blastocyst stage using fluorescence microscopy. The overall incidence of embryos with labelled mitochondria fell from 80% in the 1-cell zygote to 25% in 2-cell, 9% in 4-cell and ~1% in 8-cell or later stages. Thus it appears that almost all round spermatid mitochondria finally disappear from embryos during the 4-cell to 8-cell transition, as happens for mature spermatozoa (Cummins et al.Zygote 1997, 5: 301–8). The spermatid mitochondria remained tightly bound together during this process. In contrast, labelled primary spermatocyte and cumulus mitochondria dispersed rapidly throughout the oocyte cytoplasm within 3 h. We hypothesise that spermatid mitochondria may be bound together by cytoskeletal elements produced in the early haploid spermatid. These elements, together with terminal differentiation of the sperm mitochondria, may be central to the processes by which the embryo ‘recognises’ the sperm mitochondria and inhibits inheritance of paternal mitochondrial DNA. These results suggest that round spermatid injection for infertile men will not pose a significant risk to offspring by transmitting abnormal mitochondrial genomes.

Type
Research Article
Copyright
© 1998 Cambridge University Press

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