Abstract
We have determined that two P elements, P[21-3] and P[21r36], residing in the 5'-UTR of the vestigial wing gene, encode functional repressors in eye tissue. However, neither element fits a previous categorization of repressor-making elements as Type I or II. Both elements encode polypeptides that are shorter than the canonical elements they most closely resemble. DNA sequencing reveals that P[21r36] encodes an intact THAP domain that is missing in the P[21] element, which does not encode a functional repressor. Recovery of P[21-3] at sites other than vestigial (where it causes the wing mutant, vg(21-3)) reveals that the element can make repressor in wing tissue of sufficient activity to repress the mutant phenotype of vg(21-3). Why the P[21-3] element fails to produce repressor when located at vestigial may be explained by our observation that three different mutants in the RNA interference pathway cause a partial reversion of vg(21-3). We speculate that the vg and P-initiated transcripts that arise at the vg locus in the vg(21-3) mutant trigger an RNA interference response that results in the mutual degradation of both transcripts.
