Reactivation of a somatic errantivirus and germline invasion in Drosophila ovaries
Marianne Yoth,
Stéphanie Maupetit-Méhouas,
Abdou Akkouche,
Nathalie Gueguen,
Benjamin Bertin,
Silke Jensen () and
Emilie Brasset ()
Additional contact information
Marianne Yoth: iGReD, Université Clermont Auvergne, CNRS, INSERM, Faculté de Médecine
Stéphanie Maupetit-Méhouas: iGReD, Université Clermont Auvergne, CNRS, INSERM, Faculté de Médecine
Abdou Akkouche: iGReD, Université Clermont Auvergne, CNRS, INSERM, Faculté de Médecine
Nathalie Gueguen: iGReD, Université Clermont Auvergne, CNRS, INSERM, Faculté de Médecine
Benjamin Bertin: LIMAGRAIN EUROPE, Centre de recherche
Silke Jensen: iGReD, Université Clermont Auvergne, CNRS, INSERM, Faculté de Médecine
Emilie Brasset: iGReD, Université Clermont Auvergne, CNRS, INSERM, Faculté de Médecine
Nature Communications, 2023, vol. 14, issue 1, 1-15
Abstract:
Abstract Most Drosophila transposable elements are LTR retrotransposons, some of which belong to the genus Errantivirus and share structural and functional characteristics with vertebrate endogenous retroviruses. Like endogenous retroviruses, it is unclear whether errantiviruses retain some infectivity and transposition capacity. We created conditions where control of the Drosophila ZAM errantivirus through the piRNA pathway was abolished leading to its de novo reactivation in somatic gonadal cells. After reactivation, ZAM invaded the oocytes and severe fertility defects were observed. While ZAM expression persists in the somatic gonadal cells, the germline then set up its own adaptive genomic immune response by producing piRNAs against the constantly invading errantivirus, restricting invasion. Our results suggest that although errantiviruses are continuously repressed by the piRNA pathway, they may retain their ability to infect the germline and transpose, thus allowing them to efficiently invade the germline if they are expressed.
Date: 2023
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-41733-5
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DOI: 10.1038/s41467-023-41733-5
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