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First published online 25 April 2006
doi: 10.1242/jcs.02927

Journal of Cell Science 119, 2048-2055 (2006)
Published by The Company of Biologists 2006
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Research Article

Ca2+-linked upregulation and mitochondrial production of nitric oxide in the mouse preimplantation embryo

Rosemary C. Manser1 and Franchesca D. Houghton2,*

1 Department of Biology, University of York, PO Box 373, York, YO10 5YW, UK
2 Division of Human Genetics, University of Southampton, Duthie Building, Mailpoint 808, Southampton General Hospital, Tremona Road, Southampton, SO16 6YD, UK

* Author for correspondence (e-mail: fdh1{at}soton.ac.uk)

Accepted 1 February 2006

Previous studies have demonstrated a role for the signalling agent nitric oxide in regulating preimplantation embryo development. We have now investigated the biochemical mode of action of nitric oxide in mouse embryos in terms of mitochondrial function and Ca2+ signalling. DETA-NONOate, a nitric oxide donor, decreased day 4 blastocyst cell number and oxygen consumption, consistent with a role for nitric oxide in the inhibition mitochondrial cytochrome c oxidase. Using live cell imaging and the nitric-oxide-sensitive probe DAF-FM diacetate, nitric oxide was detected at all stages of preimplantation development and FRET analysis revealed a proportion of the nitric oxide to be colocalised with mitochondria. This suggests that mitochondria of preimplantation embryos produce nitric oxide to regulate their own oxygen consumption. Inhibiting or uncoupling the electron transport chain induced an increase in nitric oxide and [Ca2+]i as well as disruption of Ca2+ deposits at the plasma membrane, suggesting that mitochondrial disruption can quickly compromise cellular function through Ca2+-stimulated nitric oxide production. A link between antimycin-A-induced apoptosis and nitric oxide signalling is proposed.

Key words: Embryo, Nitric oxide, Mitochondria, Metabolism, Calcium






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