Novel events associated with phenotypic reversion of a P element mutant in Drosophila melanogaster

Abstract

Transposable P elements have been used extensively for Drosophila mutagenesis. While their mutagenic activity has long been recognized, the mechanisms by which P elements cause mutations are varied and not completely understood. We describe here an experiment to replace a P element at vestigial (vg) that caused a strong mutant phenotype (P[21-3]) with a P element (P[21]) known to produce a very weak phenotype when inserted at vg. In addition to testing the feasibility of P element replacements at vg, our investigation led to the production of 7 new vg alleles and 1 apparent second site suppressor. All the vg21-3 revertants that we recovered had a P element inserted into the first exon of vg at the same location and in the same orientation as the original element in vg21-3, providing a unique opportunity to study the mechanism of transposon mutagenesis. A majority of the revertants arose from a previously described event: internal deletion of P sequences, including the P promoter. In addition, 3 novel reversions of the vg21-3 wing phenotype were recovered. The wings of homozygous vg21r36 flies were normal. However, vg21r36 in combination with a deletion of the vg locus exhibited a strong mutant wing phenotype. This was surprising, because the P element insertion in vg21r36 was very similar to that found in the vg21 allele, which showed only slight nicking of the wings in combination with a deletion. In vg21r4, reversion was caused by a tandem insertion of P[21] and the original P[21-3] element present in vg21-3. Finally, the vg21r7 revertant had a P[21-3] insert at vg and 3 additional P elements elsewhere in the genome. We hypothesize that reversion in the 3 novel cases might be caused by P repressor produced by an element at vg or, in the case of vg21r7, elsewhere in the genome. This raises an interesting aspect of P element evolution. While P transposons produce mutations that might prove deleterious to their host, their success in invading the genome of D. melanogaster may be explained by their ability to silence those same mutations by a range of repressor-producing elements.