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Ae. aegypti has a large piRNA complement that maps to transposons but primarily gene sequences, including many viral-derived sequences.
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The libraries were mapped to transposons allowing two mismatches.
Remarkably for an organism with such a high transposon load we show that a much lower percentage of Ae. aegypti piRNAs map to transposons than in D. melanogaster.
As such the piRNA profile of this mosquito is more similar to that of mice than D. melanogaster in which the majority of piRNA sequences map to transposons.
Estimated piRNA sequence diversity was comparable between Ae. aegypti and D. melanogaster, but surprisingly only 19% of mosquito piRNAs mapped to transposons compared to 51% for D. melanogaster.
In addition, there remain a large set of ~ 27,000 TCs that overlap TCs on complementary strands, which is characteristic of TCs mapping to transposons.
However, while piRNA clusters in D. melanogaster and mouse generate sequences that predominantly map to transposons [ 4, 6] fewer than a quarter of potential piRNAs generated from Ae. aegypti clusters matched known transposons.
There were 3134 tag clusters among which 45.4 % (1424) of the tag clusters mapped to first coding exons or their proximal predicted 5′UTR regions and 1.0%% (31) tag clusters mapping to transposons, within a threshold of 100 tags per cluster.
By contrast, tap 125 mutation did not lead to any statistically significant decrease in the piRNAs mapping to transposons targeted by piRNAs in both germline and somatic cells and those predominantly in in somatic cells.
The single or double mutants did not have any reduction in piRNAs mapping to transposons predominantly expressed in gonadal somatic cells or those derived from unidirectional clusters such as flamenco.
The piRNAs mapping to transposons predominantly targeted in germline were more severely reduced in the tej 48 5 -tap 125 mutants (88%, Z-score: −3.98, P = 0.00006,) than the tej mutants (80%, Z-score: −3.8, P = 0.0001; Figure 7A, left panel).
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