title: The mammalian-specific Tex19.1 gene plays an essential role in spermatogenesis and placenta-supported development.
abstract: OBJECTIVE
  What is the consequence of Tex19.1 gene deletion in mice?
  
  
  CONCLUSIONS
  The Tex19.1 gene is important in spermatogenesis and placenta-supported development.
  
  
  BACKGROUND
  Tex19.1 is expressed in embryonic stem (ES) cells, primordial germ cells (PGCs), placenta and adult gonads. Its invalidation in mice leads to a variable impairment in spermatogenesis and reduction of perinatal survival.
  
  
  METHODS
  We generated knock-out mice and ES cells and compared them with wild-type counterparts. The phenotype of the Tex19.1 knock-out mouse line was investigated during embryogenesis, fetal development and placentation as well as during adulthood.
  
  
  METHODS
  We used a mouse model system to generate a mutant mouse line in which the Tex19.1 gene was deleted in the germline. We performed an extensive analysis of Tex19.1-deficient ES cells and assessed their in vivo differentiation potential by generating chimeric mice after injection of the ES cells into wild-type blastocysts. For mutant animals, a morphological characterization was performed for testes and ovaries and placenta. Finally, we characterized semen parameters of mutant animals and performed real-time RT-PCR for expression levels of retrotransposons in mutant testes and ES cells.
  
  
  RESULTS
  While Tex19.1 is not essential in ES cells, our study points out that it is important for spermatogenesis and for placenta-supported development. Furthermore, we observed an overexpression of the class II LTR-retrotransposon MMERVK10C in Tex19.1-deficient ES cells and testes.
  
  
  CONCLUSIONS
  The Tex19.1 knock-out phenotype is variable with testis morphology ranging from severely altered (in sterile males) to almost indistinguishable compared with the control counterparts (in fertile males). This variability in the testis phenotype subsequently hampered the molecular analysis of mutant testes. Furthermore, these results were obtained in the mouse, which has a second isoform (i.e. Tex19.2), while other mammals possess only one Tex19 (e.g. in humans).
  
  
  CONCLUSIONS
  The fact that one gene has a role in both placentation and spermatogenesis might open new ways of studying human pathologies that might link male fertility impairment and placenta-related pregnancy disorders.
  
  
  BACKGROUND
  This work was supported by the Centre National de la Recherche Scientifique (CNRS), the Institut National de la Santé et de la Recherche Médicale (INSERM) (Grant Avenir), the Ministère de l'Education Nationale, de l'Enseignement Supérieur et de la Recherche, the Université de Strasbourg, the Association Française contre les Myopathies (AFM) and the Fondation pour la Recherche Médicale (FRM) and Hôpitaux Universitaires de Strasbourg.The authors have nothing to disclose.
authors.affiliation: Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Institut National de Santé et de Recherche Médicale (INSERM) U964/Centre National de Recherche Scientifique (CNRS) UMR 1704/Université de Strasbourg, 67404 Illkirch, France.
authors.forename: Yara
authors.initials: Y
authors.lastname: Tarabay
authors.forename: Emmanuelle
authors.initials: E
authors.lastname: Kieffer
authors.forename: Marius
authors.initials: M
authors.lastname: Teletin
authors.forename: Catherine
authors.initials: C
authors.lastname: Celebi
authors.forename: Aafke
authors.initials: A
authors.lastname: Van Montfoort
authors.forename: Natasha
authors.initials: N
authors.lastname: Zamudio
authors.forename: Mayada
authors.initials: M
authors.lastname: Achour
authors.forename: Rosy
authors.initials: R
authors.lastname: El Ramy
authors.forename: Emese
authors.initials: E
authors.lastname: Gazdag
authors.forename: Philippe
authors.initials: P
authors.lastname: Tropel
authors.forename: Manuel
authors.initials: M
authors.lastname: Mark
authors.forename: Déborah
authors.initials: D
authors.lastname: Bourc'his
authors.forename: Stéphane
authors.initials: S
authors.lastname: Viville
mesh_terms: D000818:Animals; D001755:Blastocyst / Q000166:cytology; D053595:Embryonic Stem Cells; D005260:Female; D047109:Fetal Development / Q000235:genetics*; D005855:Germ Layers / Q000166:cytology; D020287:In Situ Nick-End Labeling; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009154:Mutation; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D010929:Placentation / Q000235:genetics*; D011247:Pregnancy; D016601:RNA-Binding Proteins; D013091:Spermatogenesis / Q000235:genetics*; D013737:Testis / Q000473:pathology
chemical_list: D009687:Nuclear Proteins; D016601:RNA-Binding Proteins; C528631:Tex19 protein, mouse
keywords: Tex19; meiosis; spermatogenesis; stem cells; transposons