title: Redistribution of mitochondria leads to bursts of ATP production during spontaneous mouse oocyte maturation.
abstract: During mammalian oocyte maturation there are marked changes in the distribution of mitochondria that supply the majority of the cellular ATP. Such redistribution of mitochondria is critical for oocyte quality, as oocytes with a poor developmental potential display aberrant mitochondrial distribution and lower ATP levels. Here we have investigated the dynamics of mitochondrial ATP production throughout spontaneous mouse oocyte maturation, using live measurements of cytosolic and mitochondrial ATP levels. We have observed three distinct increases in cytosolic ATP levels temporally associated with discrete events of oocyte maturation. These changes in cytosolic ATP levels are mirrored by changes in mitochondrial ATP levels, suggesting that mitochondrial ATP production is stimulated during oocyte maturation. Strikingly, these changes in ATP levels correlate with the distribution of mitochondria undergoing translocation to the peri-nuclear region and aggregation into clusters. Mitochondrial clustering during oocyte maturation was concomitant with the formation of long cortical microfilaments and could be disrupted by cytochalasin B treatment. Furthermore, the ATP production bursts observed during oocyte maturation were also inhibited by cytochalasin B suggesting that mitochondrial ATP production is stimulated during oocyte maturation by microfilament-driven, sub-cellular targeting of mitochondria.
authors.affiliation: Department of Obstetrics and Gynaecology, School of Medicine, Cardiff University, Heath Park, Cardiff, UK. yuy5@cardiff.ac.uk
authors.forename: Yuansong
authors.initials: Y
authors.lastname: Yu
authors.forename: Remi
authors.initials: R
authors.lastname: Dumollard
authors.forename: Andreas
authors.initials: A
authors.lastname: Rossbach
authors.forename: F Anthony
authors.initials: FA
authors.lastname: Lai
authors.forename: Karl
authors.initials: K
authors.lastname: Swann
mesh_terms: D008841:Actin Cytoskeleton / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D002478:Cells, Cultured; D003599:Cytoskeleton / Q000378:metabolism; D005260:Female; D008156:Luciferases / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D009154:Mutation; D015739:Nocodazole / Q000494:pharmacology; D009865:Oocytes / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D009866:Oogenesis / Q000502:physiology*; D050257:Tubulin Modulators / Q000494:pharmacology
chemical_list: D050257:Tubulin Modulators; D000255:Adenosine Triphosphate; D008156:Luciferases; D015739:Nocodazole