Conversion of one P-derived transposon into another has already been shown
to occur with a measurable frequency. However, the mechanism responsible fo
r such replacements has remained controversial. We: previously proposed a m
echanism involving three partners. We assumed that after excision of the P-
element inserted at the target site, the double-strand break was repaired u
sing, first, the homologous P sequences on the sister chromatid, and second
, a remote template, the donor P-derived transposon. However, two other mec
hanisms have been proposed. The first involves two partners only, the broke
n end and the remote template, while the second involves transposition of t
he donor into the target P-element, followed by a double recombination even
t. Here we describe the conversion of a defective P-element using as a remo
te template an enhancer-trap element that is itself unable to transpose bec
ause it lacks 21 bp at its 5' end. This result makes it possible to exclude
the possibility that this conversion event occurred after transposition. T
he new allele was molecularly and genetically characterized. The occurrence
of a polymorphism at position 33 of the P-element sequence and of an imper
fect copy of the template on the 3' side of the converted transposon confir
med that the sister chromatid was absolutely necessary as a partner for rep
air. Our results show that targeting of a marked P-element is possible, eve
n when this element is unable to transpose. This provides a means of improv
ing recovery of conversion events by eliminating unwanted transpositions ca
talyzed by the P transposase.