Abundant A-to-I RNA editing in spermatocytes may suppress transposons to compensate for piRNA downregulation in male germlines

The germline genome serves as a crucial battleground for transposon expansion, as transposons can increase their copy numbers in offspring when activated within germ cells. Unexpectedly, during <i>Drosophila</i> spermatogenesis, the piRNA pathway, typically responsible for transposon silencing in female germ cells, is significantly downregulated, coinciding with a burst of transposon expression in spermatocytes. This suggests that germ cells might rely on alternative mechanisms for transposon suppression. By leveraging single-cell Smart-seq transcriptomic data, we found that transposon expression, <i>Adar</i> expression, and A-to-I RNA editing efficiency are markedly elevated in <i>Drosophila</i> spermatocytes. <i>Adar</i> mutant flies exhibit higher testicular TE expression, likely resulting from the loss of editing-mediated suppression. In the absence of a fully functional piRNA pathway in male germline, Adar-mediated RNA editing may act as an alternative mechanism for transposon silencing, highlighting a potential role for Adar in maintaining genome integrity.