Syncytin-A and syncytin-B, two fusogenic placenta-specific murine envelope genes of retroviral origin conserved in Muridae.
Anne Dupressoir,Geoffroy Marceau,Cécile Vernochet,Laurence Bénit,Colette Kanellopoulos,Vincent Sapin,Thierry Heidmann +6 more
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Together, these data strongly argue for a critical role of syncytin-A and -B in murine syncytiotrophoblast formation, thus unraveling a rather unique situation where two pairs of endogenous retroviruses, independently acquired by the primate and rodent lineages, would have been positively selected for a convergent physiological role.Abstract:
Recently, we and others have identified two human endogenous retroviruses that entered the primate lineage 25–40 million years ago and that encode highly fusogenic retroviral envelope proteins (syncytin-1 and -2), possibly involved in the formation of the placenta syncytiotrophoblast layer generated by trophoblast cell fusion at the materno–fetal interface. A systematic in silico search throughout mouse genome databases presently identifies two fully coding envelope genes, present as unique copies and unrelated to any known murine endogenous retrovirus, that we named syncytin-A and -B. Quantitative RT-PCR demonstrates placenta-specific expression for both genes, with increasing transcript levels in this organ from 9.5 to 14.5 days postcoitum. In situ hybridization of placenta cryosections further localizes these transcripts in the syncytiotrophoblast-containing labyrinthine zona. Consistently, we show that both genes can trigger cell–cell fusion in ex vivo transfection assays, with distinct cell type specificities suggesting different receptor usage. Genes orthologous to syncytin-A and -B and disclosing a striking conservation of their coding status are found in all Muridae tested (mouse, rat, gerbil, vole, and hamster), dating their entry into the rodent lineage ≈20 million years ago. Together, these data strongly argue for a critical role of syncytin-A and -B in murine syncytiotrophoblast formation, thus unraveling a rather unique situation where two pairs of endogenous retroviruses, independently acquired by the primate and rodent lineages, would have been positively selected for a convergent physiological role.read more
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TL;DR: The results of an international collaboration to produce and make freely available a draft sequence of the human genome are reported and an initial analysis is presented, describing some of the insights that can be gleaned from the sequence.
Journal ArticleDOI
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TL;DR: The results of an international collaboration to produce a high-quality draft sequence of the mouse genome are reported and an initial comparative analysis of the Mouse and human genomes is presented, describing some of the insights that can be gleaned from the two sequences.
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Chung-I Wu,Wen-Hsiung Li +1 more
TL;DR: It is found that rodents evolve significantly faster than man when the coding regions of 11 genes from rodents (mouse or rat) and man are compared with those from another mammalian species (usually bovine).
Evidence for higher rates of nucleotide substitution in rodents than in man (molecular clock/generation-time effect/synonymous substitution/nonsynonymous substitution/neutral theory)
Chung-I Wu,Wen-Hsiung Lit +1 more
TL;DR: Rodents evolve significantly faster than humans as discussed by the authors, and the ratio of the number of nucleotide substitutions in the rodent lineage to that in the human lineage since their divergence is 2.0 for synonymous substitutions and 1.3 for nonsynonymous substitutions.
Journal ArticleDOI
An Envelope Glycoprotein of the Human Endogenous Retrovirus HERV-W Is Expressed in the Human Placenta and Fuses Cells Expressing the Type D Mammalian Retrovirus Receptor
Jean-Luc Blond,Dimitri Lavillette,Valérie Cheynet,Olivier Bouton,Guy Oriol,Sylvie Chapel-Fernandes,Bernard Mandrand,François Mallet,François-Loïc Cosset +8 more
TL;DR: It is demonstrated here that the product of the HERV-W env gene is a highly fusogenic membrane glycoprotein, suggesting that they may play a physiological role during pregnancy and placenta formation.