title: Block of mitochondrial apoptotic pathways in lizard ovarian follicle cells as an adaptation to their nurse function.
abstract: Pyriforms are ovarian follicle nurse cells that undergo apoptosis at the end of previtellogenesis and are completely eliminated by the epithelium. This event is accompanied by the active transfer of organelles and macromolecules to the oocyte via an intercellular bridge. Since it would be a nonsense for damaged mitochondria to reach the oocyte, we have postulated that pyriform cells have adapted their apoptotic machinery to prevent mitochondrial degradation. To verify this hypothesis, we have studied mitochondrial morphology and functionality during follicle cell regression. Cytological and biochemical evidence indicates that mitochondria in pyriforms maintain their size, organization and membrane potential. This clearly indicates that they are not involved in apoptosis signalling/progression. This block would favour both the oocyte, by increasing the pool of organelles available from follicle cells, and also the regressing pyriforms, by maintaining the energy resources required for completion of their nurse function. The block is probably attributable to an over-expression of Bcl-2 and might be carried out by sequestering cytochrome c inside the organelles. As demonstrated by in vitro experiments, the mitochondrial apoptosis pathway can be activated by stress induction, such as serum deprivation, but not following physiological pro-apoptotic signalling, such as treatment with gonadotrophin-releasing hormone.
authors.affiliation: Dipartimento delle Scienze Biologiche, Section of Evolutionary and Comparative Biology, University of Naples Federico II, 80134 Naples, Italy.
authors.forename: Stefania
authors.initials: S
authors.lastname: Tammaro
authors.forename: Palma
authors.initials: P
authors.lastname: Simoniello
authors.forename: Silvana
authors.initials: S
authors.lastname: Filosa
authors.forename: Chiara Maria
authors.initials: CM
authors.lastname: Motta
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D016895:Culture Media, Serum-Free / Q000494:pharmacology; D045304:Cytochromes c / Q000378:metabolism; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology; D008116:Lizards / Q000502:physiology*; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects / Q000502:physiology; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D006080:Ovarian Follicle / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D015398:Signal Transduction; D014818:Vitellogenesis / Q000502:physiology
chemical_list: D016895:Culture Media, Serum-Free; D019253:Proto-Oncogene Proteins c-bcl-2; D007987:Gonadotropin-Releasing Hormone; D045304:Cytochromes c