title: Early development of mouse embryos null mutant for the cyclin A2 gene occurs in the absence of maternally derived cyclin A2 gene products.
abstract: Progression through the mammalian cell cycle is regulated by the sequential activation and inactivation of the cyclin-dependent kinases. In adult cells, cyclin A2-dependent kinases are required for entry into S and M phases, completion of S phase, and centrosome duplication. However, mouse embryos lacking the cyclin A2 gene nonetheless complete preimplantation development, but die soon after implantation. In this report, we investigated whether a contribution of maternal cyclin A2 mRNA and protein to early embryonic cell cycles might explain these conflicting observations. Our data show that a maternal stock of cyclin A2 mRNA is present in the oocyte and persists after fertilization until the second mitotic cell cycle, when it is degraded to undetectable levels coincident with transcriptional activation of the zygotic genome. A portion of maternally derived cyclin A2 protein is stable during the first mitosis and persists in the cytoplasm, but is completely degraded at the second mitosis. The ability of cyclin A2-null mutants to develop normally from the four-cell to the postimplantation stage in the absence of detectable cyclin A2 gene product indicates therefore that cyclin A2 is dispensable for cellular progression during the preimplantation nongrowth period of mouse embryo development.
authors.affiliation: Unité 370, Faculté Necker, Institut National de la Santé et de la Recherche Médicale, 156 Rue de Vaugirard, Paris, 75015, France.
authors.forename: N
authors.initials: N
authors.lastname: Winston
authors.forename: F
authors.initials: F
authors.lastname: Bourgain-Guglielmetti
authors.forename: M A
authors.initials: MA
authors.lastname: Ciemerych
authors.forename: J Z
authors.initials: JZ
authors.lastname: Kubiak
authors.forename: C
authors.initials: C
authors.lastname: Senamaud-Beaufort
authors.forename: M
authors.initials: M
authors.lastname: Carrington
authors.forename: C
authors.initials: C
authors.lastname: Bréchot
authors.forename: J
authors.initials: J
authors.lastname: Sobczak-Thépot
mesh_terms: D000546:Amanitins / Q000494:pharmacology; D000818:Animals; D001973:Bromodeoxyuridine / Q000378:metabolism; D019925:Cyclin A / Q000096:biosynthesis* / Q000235:genetics* / Q000502:physiology; D003513:Cycloheximide / Q000494:pharmacology; D004247:DNA / Q000096:biosynthesis; D004622:Embryo, Mammalian / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D005838:Genotype; D015151:Immunoblotting; D051379:Mice; D008817:Mice, Mutant Strains; D016296:Mutagenesis; D015739:Nocodazole / Q000494:pharmacology; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D009865:Oocytes / Q000378:metabolism; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D014158:Transcription, Genetic; D001616:beta-Galactosidase / Q000378:metabolism
chemical_list: D000546:Amanitins; D019925:Cyclin A; D019384:Nucleic Acid Synthesis Inhibitors; D011500:Protein Synthesis Inhibitors; D012333:RNA, Messenger; D004247:DNA; D003513:Cycloheximide; D001616:beta-Galactosidase; D001973:Bromodeoxyuridine; D015739:Nocodazole