forked, Gypsys, and suppressors in Drosophila

Interactions among the gypsy transposable element and the yellow and the suppressor of hairy-wing loci in Drosophila melanogaster.

“…The gypsy transposable element gives rise to a major 6.5-kb RNA; this transcript probably starts at the promoter element located in one of the LTRs and extends all the way to the termination signals placed in the second LTR. The transcription of the 6.5-kb RNA in wild-type flies is not constant during development but rather is modulated in a temporalspecific fashion during different stages of the Drosophila life cycle, reaching maximal expression in the midstages of pupal life (24). The pattern of transcription of the gypsy element in the mutant y2 is the same as that in wild-type flies, as deduced from Northern analysis of poly(A)-containing RNA from different developmental stages of these mutant flies (Fig.…”

“…While other transposable elements, such as copia, seem to interfere with proper transcription termination (14), little is known about the molecular basis of gypsy-induced mutations or the mechanisms by which mutations at the siu(Hw) locus reverse the phenotype of these mutations. To approach these problems, we cloned and characterized the forked (24) and yellow loci of D. inelanogaster to use as a model system in which to ask questions related to the phenomenon of suppression. This paper describes the studies carried out on the yellow (y, 1-0.0) locus, which is involved in controlling the pattern of pigmentation of the body of the fly; the visible phenotypic effect of y mutations is an altered pigmentation of the adult body cuticle and its derivative structures.…”

An allelic series reveals essential roles for FY in plant development in addition to flowering-time control

“…However, hypomorphic mutations that are viable can also be recovered (Ohnacker et al, 2000;Zhao et al, 1999). Viable mutations in the Drosophila polyadenylation factor, suppressor of forked (su(f)) were identified as modifiers of retrotransposon insertions in the Forked gene (Parkhurst and Corces, 1985;Parkhurst and Corces, 1986). The su(f) mutation modified usage of premature polyadenylation sites within the retrotransposon long terminal repeats, restoring forked gene expression (Parkhurst and Corces, 1985;Parkhurst and Corces, 1986).…”

“…Viable mutations in the Drosophila polyadenylation factor, suppressor of forked (su(f)) were identified as modifiers of retrotransposon insertions in the Forked gene (Parkhurst and Corces, 1985;Parkhurst and Corces, 1986). The su(f) mutation modified usage of premature polyadenylation sites within the retrotransposon long terminal repeats, restoring forked gene expression (Parkhurst and Corces, 1985;Parkhurst and Corces, 1986). However, strong or null su(f) alleles are cell-autonomous, lethal mutations that prevent mitotic proliferation (Audibert et al, 1998;Audibert and Simonelig, 1999).…”

Bidirectional transcription from a solo long terminal repeat of the retrotransposon TED: symmetrical RNA start sites.

“…These alterations occur at the level of transcription and are presumably due to insertion of new promoters, termination signals, or both, located within the retrotransposon. The mutagenic effects of inserted copia, gypsy, and Ty elements are suppressed by additional mutations at unlinked loci which restore transcription of the affected genes to wild-type levels (25,32,51). Mutation of the S. cerevisiae SPT3 (suppressor of Ty) gene, for instance, abolishes normal Ty transcription, which suggests that the mutational effect of certain Ty insertions is due to transcription originating from the element (51).…”