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Highlights

Multiplying mitochondria for competence.

Remarkably little is known regarding what underlies acquisition by oocytes of developmental competence to develop to term. On p. 327 of this issue, Spikings et al. provide evidence that the timing of mitochondrial DNA (mtDNA) replication during maturation contributes to competence. Replication of mtDNA requires the action of nuclear-encoded replication factors that regulate mtDNA copy number, which correlates with oxidative phosphorylation capacity. Spikings et al. show that competent oocytes, with low levels of glucose-6-phosphate dehydrogenase activity, replicate their mtDNA during maturation (and express nuclear-encoded replication factors), while oocytes of reduced competence exhibit a marked delay in mtDNA replication. Inhibition of mtDNA replication in competent oocytes decreased their developmental competence. These findings have potential clinical ramifications for oocyte reconstruction protocols in treating human infertility and for selecting oocytes to improve nuclear transfer outcomes, such as in generation of embryonic stem cells.

Emma C. Spikings, Jon Alderson, and Justin C. St. John. Regulated Mitochondrial DNA Replication During Oocyte Maturation Is Essential for Successful Porcine Embryonic Development. Biol Reprod 2007; 76:327–335. Published online ahead of print 11 October 2006; DOI 10.1095/biolreprod.106.054536

Modifiers to the rescue.

Maternal factors in the ooplasm must recognize and interact with paternal factors in order for normal development to ensue. An excellent example of the consequences when this goes wrong is the "DDK syndrome" of embryonic lethality resulting from an incompatibility of a maternal factor, the product of the Om gene, and a paternal factor located within the Slfn (Schlafen) gene cluster. In an article on p. 286 of this issue, Ideraabdullah et al. report a genetic approach to discover and map modifier genes that rescue DDK syndrome lethality; two such loci, Rmod1 and Rmod2, were identified. The interaction of these factors with DDK factors gives us a view of the complexity of zygotic gene interactions, and while the identity of the encoded products of these genes remains to be determined, it will surely inform us about maternal factors required for early embryogenesis.

Folami Y. Ideraabdullah, Kuikwon Kim, Daniel Pomp, Jennifer L. Moran, David Beier, and Fernando Pardo-Manuel de Villena. Rescue of the Mouse DDK Syndrome by Parent-of-Origin Dependent Modifiers. Biol Reprod 2007; 76:286–293. Published online ahead of print 18 October 2006; DOI 10.1095/biolreprod.106.056739

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