Conflicts and coalitions among selfish toxin-antidote elements shape the evolution of hyperdivergent haplotypes
5 affiliations
- 1Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), Dr. Bohr-Gasse 3, 1030 Vienna, Austria.
- 2Vienna BioCenter PhD Program, Doctoral School of the University of Vienna and Medical University of Vienna, A-1030, Vienna, Austria.
- 3These authors contributed equally.
- 4Max Perutz Labs, Vienna BioCenter (VBC), Medical University of Vienna, Austria.
- 5Université Côte d’Azur, CNRS, Inserm, IBV, Nice, France.
Abstract
Genetic conflict drives evolutionary innovation, yet most research has focused on arms races between selfish elements and their hosts. A second layer-competition among selfish elements-remains largely unexplored. Here, we uncover such a conflict between two antagonistic toxin-antidote elements (TAs), loki-1/sgyn-1 and thor-1/sif-1, in Caenorhabditis tropicalis. Each toxin, LOKI-1 or THOR-1, selectively kills progeny homozygous for the opposing haplotype, favoring heterozygotes. Their antidotes, SGYN-1 and SIF-1, evolved from F-box proteins, although SIF-1 subsequently lost its F-box domain. We solved the crystal structure of the THOR-1-SIF-1 complex and used in vivo mutagenesis to validate the binding interface, supporting direct toxin neutralization independently of F-box-mediated degradation. A survey of 676 wild isolates revealed two contrasting evolutionary outcomes of antagonizing TAs: independently evolved loki-1/sgyn-1 and thor-1/sif-1 remain confined to alternative hyperdivergent haplotypes, whereas other homologous TAs can recombine to form composite haplotypes. Altogether, our findings establish competition among selfish elements as a distinct form of genetic conflict, and support models in which antagonistic TAs act as barriers that restrict gene flow between neighboring populations.
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BibTeX
@misc{koreshova2026conflicts,
title = {{Conflicts and coalitions among selfish toxin-antidote elements shape the evolution of hyperdivergent haplotypes}},
author = {Alevtina Koreshova and Andreas Hagmüller and Arda Kara and Pinelopi Pliota and Tianhua Liao and George Kobakhidze and Joseph Gokcezade and Peter Duchek and Christian Braendle and Gang Dong and Alejandro Burga},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.22.760680},
url = {https://www.biorxiv.org/content/10.64898/2026.10.22.760680v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Conflicts and coalitions among selfish toxin-antidote elements shape the evolution of hyperdivergent haplotypes
AU - Alevtina Koreshova
AU - Andreas Hagmüller
AU - Arda Kara
AU - Pinelopi Pliota
AU - Tianhua Liao
AU - George Kobakhidze
AU - Joseph Gokcezade
AU - Peter Duchek
AU - Christian Braendle
AU - Gang Dong
AU - Alejandro Burga
PY - 2026
DA - 2026/10/22
PB - bioRxiv
DO - 10.64898/2026.10.22.760680
UR - https://www.biorxiv.org/content/10.64898/2026.10.22.760680v1
AB - Genetic conflict drives evolutionary innovation, yet most research has focused on arms races between selfish elements and their hosts. A second layer-competition among selfish elements-remains largely unexplored. Here, we uncover such a conflict between two antagonistic toxin-antidote elements (TAs), loki-1/sgyn-1 and thor-1/sif-1, in Caenorhabditis tropicalis. Each toxin, LOKI-1 or THOR-1, selectively kills progeny homozygous for the opposing haplotype, favoring heterozygotes. Their antidotes, SGYN-1 and SIF-1, evolved from F-box proteins, although SIF-1 subsequently lost its F-box domain. We solved the crystal structure of the THOR-1-SIF-1 complex and used in vivo mutagenesis to validate the binding interface, supporting direct toxin neutralization independently of F-box-mediated degradation. A survey of 676 wild isolates revealed two contrasting evolutionary outcomes of antagonizing TAs: independently evolved loki-1/sgyn-1 and thor-1/sif-1 remain confined to alternative hyperdivergent haplotypes, whereas other homologous TAs can recombine to form composite haplotypes. Altogether, our findings establish competition among selfish elements as a distinct form of genetic conflict, and support models in which antagonistic TAs act as barriers that restrict gene flow between neighboring populations.
SN - 2692-8205
ER -