Abstract
Without transposon-silencing Piwi-interacting RNAs (piRNAs), transposition causes an ovarian atrophy syndrome in
called gonadal dysgenesis (GD).
(
) strains with
-elements cause severe GD in F1 daughters when
fathers mate with mothers lacking
-element-piRNAs (i.e.
strain). To address the mystery of why
induces severe GD, we bred hybrid
with
genomic fragments into the
background to create
lines that still cause
ysgenesis or are
on-dysgenic, respectively. In these lines, we discovered a highly truncated
-element variant we named '
' as the most frequent de novo insertion. Although
lines still contain full-length
-elements,
lines lost functional
-transposase but retained
's that when crossed back to
-transposase restores GD induction. Finally, we uncovered
-element-piRNA-directed repression on
transmitted paternally to suppress somatic transposition. The
short
and full-length
-elements relationship parallels the MITEs/DNA-transposase in plants and SINEs/LINEs in mammals.