| Literature DB >> 33417886 |
Eyal Ben-David1, Pinelopi Pliota2, Sonya A Widen2, Alevtina Koreshova2, Tzitziki Lemus-Vergara3, Philipp Verpukhovskiy3, Sridhar Mandali4, Christian Braendle5, Alejandro Burga6, Leonid Kruglyak7.
Abstract
Toxin-antidote elements (TAs) are selfish genetic dyads that spread in populations by selectively killing non-carriers. TAs are common in prokaryotes, but very few examples are known in animals. Here, we report the discovery of maternal-effect TAs in both C. tropicalis and C. briggsae, two distant relatives of C. elegans. In C. tropicalis, multiple TAs combine to cause a striking degree of intraspecific incompatibility: five elements reduce the fitness of >70% of the F2 hybrid progeny of two Caribbean isolates. We identified the genes underlying one of the novel TAs, slow-1/grow-1, and found that its toxin, slow-1, is homologous to nuclear hormone receptors. Remarkably, although previously known TAs act during embryonic development, maternal loading of slow-1 in oocytes specifically slows down larval development, delaying the onset of reproduction by several days. Finally, we found that balancing selection acting on linked, conflicting TAs hampers their ability to spread in populations, leading to more stable genetic incompatibilities. Our findings indicate that TAs are widespread in Caenorhabditis species and target a wide range of developmental processes and that antagonism between them may cause lasting incompatibilities in natural populations. We expect that similar phenomena exist in other animal species.Entities:
Keywords: Caenorhabditis; gene drive; genetic incompatibility; natural genetic variation; selfish gene; speciation; toxin-antidote; toxin-antitoxin
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Year: 2021 PMID: 33417886 DOI: 10.1016/j.cub.2020.12.013
Source DB: PubMed Journal: Curr Biol ISSN: 0960-9822 Impact factor: 10.834