Inherited defects of piRNA biogenesis cause transposon de-repression, impaired spermatogenesis, and human male infertility

Birgit Stallmeyer(University of Münster), Clara Bühlmann(University of Münster), Rytis Stakaitis(Oregon National Primate Research Center), Ann‐Kristin Dicke(University of Münster), Farah Ghieh(University of Münster), Luisa Meier(University of Münster), Ansgar Zoch(MRC Centre for Regenerative Medicine), David MacKenzie MacLeod(MRC Centre for Regenerative Medicine), Johanna Steingröver(University of Münster), Özlem Okutman(Université Libre de Bruxelles), Daniela Fietz(Justus-Liebig-Universität Gießen), Adrian Pilatz(Justus-Liebig-Universität Gießen), Antoni Riera‐Escamilla(Universitat Autònoma de Barcelona), Miguel J. Xavier(Newcastle University), Christian Rückert(University of Münster), Sara Di Persio(University Hospital Münster), Nina Neuhaus(University Hospital Münster), Ali Sami Gürbüz, Ahmet Şalvarcı, Nicolas Le May(Inserm), Kevin McEleny(Newcastle upon Tyne Hospitals NHS Foundation Trust), Corinna Friedrich(University of Münster), Godfried W. van der Heijden(Radboud University Nijmegen), Margot J. Wyrwoll(University of Münster), Sabine Kliesch(University Hospital Münster), Joris A. Veltman(Newcastle University), Csilla Krausz(Universitat Autònoma de Barcelona), Stéphane Viville(Inserm), Donald F. Conrad(Oregon National Primate Research Center), Dónal O’Carroll(MRC Centre for Regenerative Medicine), Frank Tüttelmann(University of Münster)
Nature Communications
August 9, 2024
Cited by 52Open Access
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Abstract

piRNAs are crucial for transposon silencing, germ cell maturation, and fertility in male mice. Here, we report on the genetic landscape of piRNA dysfunction in humans and present 39 infertile men carrying biallelic variants in 14 different piRNA pathway genes, including PIWIL1, GTSF1, GPAT2, MAEL, TDRD1, and DDX4. In some affected men, the testicular phenotypes differ from those of the respective knockout mice and range from complete germ cell loss to the production of a few morphologically abnormal sperm. A reduced number of pachytene piRNAs was detected in the testicular tissue of variant carriers, demonstrating impaired piRNA biogenesis. Furthermore, LINE1 expression in spermatogonia links impaired piRNA biogenesis to transposon de-silencing and serves to classify variants as functionally relevant. These results establish the disrupted piRNA pathway as a major cause of human spermatogenic failure and provide insights into transposon silencing in human male germ cells.


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