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No recombination suppression in asexually produced males of Daphnia pulex

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Molinier,  C       
Reproductive Isolation and Speciation in Brown Algae Group, Department Algal Development and Evolution, Max Planck Institute for Biology Tübingen, Max Planck Society;
Department Algal Development and Evolution, Max Planck Institute for Biology Tübingen, Max Planck Society;

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Citation

Molinier, C., Lenormand, T., & Haag, C. (2023). No recombination suppression in asexually produced males of Daphnia pulex. Evolution: international journal of organic evolution, 77(9): qpad114, pp. 1987-1999. doi:10.1093/evolut/qpad114.


Cite as: https://hdl.handle.net/21.11116/0000-000D-52A9-8
Abstract
Obligate parthenogenesis (OP) is often thought to evolve by disruption of reductional meiosis and suppression of crossover recombination. In the crustacean Daphnia pulex, OP lineages, which have evolved from cyclical parthenogenetic (CP) ancestors, occasionally produce males that are capable of reductional meiosis. Here, by constructing high-density linkage maps, we find that these males show only slightly and non-significantly reduced recombination rates compared to CP males and females. Both meiosis disruption and recombination suppression are therefore sex-limited (or partly so), which speaks against the evolution of OP by disruption of a gene that is essential for meiosis or recombination in both sexes. The findings may be explained by female-limited action of genes that suppress recombination, but previously identified candidate genes are known to be expressed in both sexes. Alternatively, and equally consistent with the data, OP might have evolved through a re-use of the parthenogenesis pathways already present in CP and through their extension to all events of oogenesis. The causal mutations for the CP to OP transition may therefore include mutations in genes involved in oogenesis regulation and may not necessarily be restricted to genes of the "meiosis toolkit". More generally, our study emphasizes that there are many ways to achieve asexuality, and elucidating the possible mechanisms is key to ultimately identify the genes and traits involved.