Tex19 paralogs are new members of the piRNA pathway controlling retrotransposon suppression - Archive ouverte HAL Accéder directement au contenu
Article Dans Une Revue (Data Paper) Journal of Cell Science Année : 2023

Tex19 paralogs are new members of the piRNA pathway controlling retrotransposon suppression

Yara Tarabay
Mayada Achour
Marius Teletin
  • Fonction : Auteur
Tao Ye
Aurélie Teissandier
  • Fonction : Auteur
Manuel Mark
  • Fonction : Auteur
Déborah Bourc'His
  • Fonction : Auteur
  • PersonId : 1215490
Stéphane Viville

Résumé

Tex19 genes are mammalian specific and duplicated in Tex19.1 and Tex19.2 in some species, such as the mouse and rat. It has been demonstrated that mutant Tex19.1 males display a variable degree of infertility whereas they all upregulate MMERVK10C transposons in their germ line. In order to study the function of both paralogs in the mouse, we generated and studied double knockout (Tex19DKO) mutant mice. Adult Tex19DKO males exhibited a fully penetrant phenotype, similar to the most severe phenotype observed in single Tex19.1KO mice, with small testes and impaired spermatogenesis, defects in meiotic chromosome synapsis, persistence of DNA double-strand breaks during meiosis, lack of post-meiotic germ cells and upregulation of MMERVK10C expression. The phenotypic similarities with Piwi KO mice prompted us to check and then demonstrate, by immunoprecipitation and GST pulldown followed by mass spectrometry analyses, that TEX19 paralogs interact with PIWI proteins and their VPTEL domain directly binds piRNAs in adult testes. We therefore identified two new members of the postnatal piRNA pathway.

Dates et versions

hal-03940633 , version 1 (16-01-2023)

Identifiants

Citer

Yara Tarabay, Mayada Achour, Marius Teletin, Tao Ye, Aurélie Teissandier, et al.. Tex19 paralogs are new members of the piRNA pathway controlling retrotransposon suppression. Journal of Cell Science, 2023, ⟨10.1242/jcs.188763⟩. ⟨hal-03940633⟩
5 Consultations
0 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More