title: Degradation of maternal mRNA in mouse embryos: selective degradation of specific mRNAs after fertilization.
abstract: During oogenesis, mRNA is actively transcribed and accumulated in growing oocytes, but this transcription stops before the oocytes grow to their full size. The accumulated maternal mRNA is used for protein synthesis in the oocytes during meiotic maturation and even in the embryos to sustain development after fertilization. Therefore, the degradation of accumulated maternal mRNA starts during meiotic maturation, but its rate is slow. Nevertheless, some mRNA species should rapidly degrade after fertilization if they encode proteins that play a role in specific events during meiosis and are detrimental for development after fertilization. In this study, to identify the selective degradation of maternal transcripts after fertilization, we sought mRNAs that are degraded in the early hours after fertilization by constructing an oocyte cDNA library after subtracting the cDNA of embryos at the mid one-cell stage. H1oo, c-mos, tPA (tissue type plasminogen activator gene), and Gdf9 were identified as genes whose transcripts undergo rapid degradation after fertilization. RT-PCR analysis showed that none of these transcripts was expressed during pre-implantation development once they were eliminated, suggesting that the mRNA species that are required for oogenesis, but not for early pre-implantation development, are degraded rapidly after fertilization. Microinjection of chimeric mRNAs in which the coding and 3'-untranslated regions (3'UTR) were exchanged between c-mos and hypoxanthine phosphoribosyltransferase mRNAs revealed that the 3'UTR plays a role in the rapid degradation that occurs after fertilization. Cytoplasmic polyadenylation elements (CPEs) was found near a poly(A) signal in the 3'UTR of all the mRNA species identified as rapidly degrading mRNA. The mechanism for the selective degradation is discussed, in relation to its biological significance.
authors.affiliation: Department of Integrated Biosciences, Graduate School of Frontier Sciences, University of Tokyo, Chiba, Japan.
authors.forename: Zohreh
authors.initials: Z
authors.lastname: Alizadeh
authors.forename: Shun-Ichiro
authors.initials: S
authors.lastname: Kageyama
authors.forename: Fugaku
authors.initials: F
authors.lastname: Aoki
mesh_terms: D020413:3' Untranslated Regions / Q000235:genetics; D000818:Animals; D015152:Blotting, Northern; D055430:Bone Morphogenetic Protein 15; D017931:DNA Primers; D004622:Embryo, Mammalian / Q000378:metabolism / Q000502:physiology*; D005260:Female; D005306:Fertilization / Q000235:genetics / Q000502:physiology*; D018507:Gene Expression Regulation, Developmental; D015723:Gene Library; D016258:Genes, mos / Q000235:genetics; D055429:Growth Differentiation Factor 9; D006657:Histones; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics; D051379:Mice; D009865:Oocytes / Q000737:chemistry; D011247:Pregnancy; D011506:Proteins / Q000235:genetics; D020871:RNA Stability / Q000235:genetics / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000235:genetics; D039221:mRNA Cleavage and Polyadenylation Factors / Q000378:metabolism
chemical_list: D020413:3' Untranslated Regions; C525902:Bmp15 protein, mouse; D055430:Bone Morphogenetic Protein 15; D017931:DNA Primers; C525898:Gdf9 protein, mouse; D055429:Growth Differentiation Factor 9; C423383:H1f8 protein, mouse; D006657:Histones; D036341:Intercellular Signaling Peptides and Proteins; D011506:Proteins; D039221:mRNA Cleavage and Polyadenylation Factors; D010959:Tissue Plasminogen Activator