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Selvaraju, D.

Publications and source records attributed to Selvaraju, D..

3 recordsLinked to original sources

Rapid emergence of hyperparasitic elements may stop P-element invasions in the absence of a piRNA-based host defence

Transposable element (TE) invasions pose risks to both the TE and the host. All copies of a TE may be lost via genetic drift, or host populations may suffer fitness declines, potentially leading to extinction. By monitoring invasions of the P-element in experimental D. melanogaster populations for over 100 generations, we uncovered a novel risk for invading TEs. In two replicate populations, the P-element rapidly multiplied until a piRNA-based host defence emerged, leading to the plateauing of TE copy numbers. However, in one population (R2), P-element copy numbers stabilised at a significantly lower level, despite the absence of a piRNA-based host defence. We find that this stabilisation was likely driven by the propagation of non-autonomous insertions, characterised by internal-deletions, which out-competed the autonomous full-length insertions. Such a rapid proliferation of non-autonomous insertions could account for the high prevalence of P-element insertions with internal-deletions observed in natural D. melanogaster populations. Our work reveals that TEs may stochastically sabotage their own spread in populations due to the emergence of hyperparasites, rendering the establishment of a host defence unnecessary. The proliferation of hyperparasitic elements may also lead into an evolutionary dead end, where affected populations are resistant to re-invasion (e.g. following recurrent horizontal transfer), yet are unable to infect other species due to a lack of autonomous insertions.

genetics↗

P-element invasions in Drosophila erecta shed light on the establishment of host control over a transposable element

To prevent the spread of transposable elements (TEs) hosts have developed sophisticated defence mechanisms. In mammals and invertebrates this defence mechanism operates through piRNAs. It is unclear how piRNA-based defences are established against invading TEs. According to the trap model, a TE insertion into a piRNA cluster, i.e. a distinct genomic locus, activates the host defence. Alternatively, siRNAs, generated by cleavage of dsRNA, may be the trigger for host control. To investigate this we introduced the P-element, one of the most widely studied eukaryotic transposons, into naive lines of Drosophila erecta. We monitored the invasion in 3 replicates for more than 50 generations by sequencing the genomic DNA (using short and long-reads), the small RNAs and the transcriptome at regular intervals. A piRNA based host defence was rapidly established in 2 replicates but not in the third, where P-element copy numbers kept increasing for over 50 generations. We found that siRNAs emerged prior to piRNAs, supporting the view that siRNAs initiate host defence. However, neither insertions in piRNA clusters nor the formation of siRNAs were sufficient to stop the P-element. Instead the activation of the ping-pong cycle was shown to be crucial. We introduce a novel model, the crank-up model, which emphasizes activation of the ping-pong cycle as a critical event in establishing host control over a TE.

evolutionary biology↗

Reconstructing the invasion route of DNA transposons using extant population samples

Reconstructing invasion routes of transposable elements (TEs), so far, required capturing an ongoing invasion with population samples from different geographic regions and time points. Here, we propose a more accessible approach. Abundantly occurring internal deletions of DNA transposons allow to trace the direction as well as the path of an invasion, even hundreds of generations after the spread of a TE. We validated this hypothesis with computer simulations and by accurately reproducing the route of the P-element invasion in Drosophila melanogaster. Finally, we used our method to shed light on the controversial hobo invasion in D. melanogaster. Our approach solely requires sequenced samples from extant populations and sequences of TEs of interest. Hence, DNA transposons in a wide range of model and non-model organisms may be analyzed. Our approach will further our understanding of TE dynamics, migration patterns, and the ecology of species.

evolutionary biology↗