Direct cell-to-cell transmission of retrotransposons
4 affiliations
- 1Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), Dr. Bohr-Gasse 3, 1030 Vienna, Austria
- 2Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), Dr. Bohr-Gasse 3, 1030 Vienna, Austria; Vienna BioCenter PhD Program, Doctoral School of the University of Vienna and Medical University of Vienna, Vienna, Austria
- 3Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), Dr. Bohr-Gasse 3, 1030 Vienna, Austria. Electronic address: [email protected]
- 4Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), Dr. Bohr-Gasse 3, 1030 Vienna, Austria. Electronic address: [email protected]
Abstract
Transposable elements are abundant in host genomes but are generally considered to be confined to the cell in which they are expressed, with the notable exception of endogenous retroviruses. Here, we identify a group of long terminal repeat (LTR) retrotransposons that infect the germline from somatic cells within the Drosophila ovary, despite lacking the fusogenic Envelope protein typically required for retroviral entry. Instead, these elements encode a short transmembrane protein, sORF2, which bears structural features reminiscent of viral cell-cell fusogens. Through genetics, imaging, and electron microscopy, we show that sORF2 localizes to invasive somatic protrusions that contain retroviral capsids and establish physical contact with the oocyte membrane. In the absence of sORF2, protrusion formation and soma-to-germline transmission of capsids are abolished. Remarkably, sORF2-like proteins are widespread among insect retrotransposons and also occur in piscine nackednaviruses and avian picornaviruses. These findings reveal a noncanonical, Envelope-independent transmission mechanism shared by retrotransposons and non-enveloped viruses.
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BibTeX
@article{voichek2026direct,
title = {{Direct cell-to-cell transmission of retrotransposons}},
author = {Maya Voichek and Andreas Bernhard and Lea Lauterjung and Maria Novatchkova and Dominik Handler and Paul Möseneder and Liudmila Protsenko and Baptiste Rafanel and Svetlana Iu. Iarovenko and Peter Duchek and Kirsten-André Senti and Julius Brennecke},
journal = {Cell},
year = {2026},
month = sep,
doi = {10.1016/j.cell.2026.08.047},
url = {https://doi.org/10.1016/j.cell.2026.08.047},
note = {CC BY},
}
RIS
TY - JOUR
TI - Direct cell-to-cell transmission of retrotransposons
AU - Maya Voichek
AU - Andreas Bernhard
AU - Lea Lauterjung
AU - Maria Novatchkova
AU - Dominik Handler
AU - Paul Möseneder
AU - Liudmila Protsenko
AU - Baptiste Rafanel
AU - Svetlana Iu. Iarovenko
AU - Peter Duchek
AU - Kirsten-André Senti
AU - Julius Brennecke
PY - 2026
DA - 2026/09/01
JO - Cell
DO - 10.1016/j.cell.2026.08.047
UR - https://doi.org/10.1016/j.cell.2026.08.047
AB - Transposable elements are abundant in host genomes but are generally considered to be confined to the cell in which they are expressed, with the notable exception of endogenous retroviruses. Here, we identify a group of long terminal repeat (LTR) retrotransposons that infect the germline from somatic cells within the Drosophila ovary, despite lacking the fusogenic Envelope protein typically required for retroviral entry. Instead, these elements encode a short transmembrane protein, sORF2, which bears structural features reminiscent of viral cell-cell fusogens. Through genetics, imaging, and electron microscopy, we show that sORF2 localizes to invasive somatic protrusions that contain retroviral capsids and establish physical contact with the oocyte membrane. In the absence of sORF2, protrusion formation and soma-to-germline transmission of capsids are abolished. Remarkably, sORF2-like proteins are widespread among insect retrotransposons and also occur in piscine nackednaviruses and avian picornaviruses. These findings reveal a noncanonical, Envelope-independent transmission mechanism shared by retrotransposons and non-enveloped viruses.
SN - 0092-8674
SN - 1097-4172
ER -