Levels of P-element-induced hybrid dysgenesis in Drosophila simulans are uncorrelated with levels of P-element piRNAs

Author:

Paulouskaya Olga12ORCID,Romero-Soriano Valèria1ORCID,Ramirez-Lanzas Claudia3ORCID,Price Tom A R1ORCID,Betancourt Andrea J1ORCID

Affiliation:

1. Department of Evolution, Ecology and Behaviour, University of Liverpool , L69 7ZB Liverpool , UK

2. Institute of Biology Leiden, Leiden University , PO Box 9505, 2300 RA, Leiden , The Netherlands

3. Institut für Populationsgenetik, Vetmeduni Vienna , A-1210 Vienna , Austria

Abstract

Abstract Transposable elements (TEs) are genomic parasites that proliferate within host genomes, and which can also invade new species. The P-element, a DNA-based TE, recently invaded two Drosophila species: Drosophila melanogaster in the 20th century, and D. simulans in the 21st. In both species, lines collected before the invasion are susceptible to “hybrid dysgenesis”, a syndrome of abnormal phenotypes apparently due to P-element-inflicted DNA damage. In D. melanogaster, lines collected after the invasion have evolved a maternally acting mechanism that suppresses hybrid dysgenesis, with extensive work showing that PIWI-interacting small RNAs (piRNAs) are a key factor in this suppression. Most of these studies use lines collected many generations after the initial P-element invasion. Here, we study D. simulans collected early, as well as late in the P-element invasion of this species. Like D. melanogaster, D. simulans from late in the invasion show strong resistance to hybrid dysgenesis and abundant P-element-derived piRNAs. Lines collected early in the invasion, however, show substantial variation in how much they suffer from hybrid dysgenesis, with some lines highly resistant. Surprisingly, although, these resistant lines do not show high levels of cognate maternal P-element piRNAs; in these lines, it may be that other mechanisms suppress hybrid dysgenesis.

Funder

Austrian Science Fund

ERC

Publisher

Oxford University Press (OUP)

Subject

Genetics (clinical),Genetics,Molecular Biology

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