Requirement of the ETS domain transcription factor D-ELG for egg chamber patterning and development during Drosophila oogenesis.

The D-elg gene encodes an ETS domain transcription factor that functions in Drosophila oogenesis. D-elg belongs to a small group of genes that are required for the formation of both the anteroposterior and dorsoventral axes of the egg chamber. During oogenesis in D-elg mutant females, the spatial localization of oskar and gurken mRNAs in the oocyte is disrupted and a follicle cell enhancer trap marker identifies dorsoventral polarity defects. Also, specialized follicle cells, called border cells, fail to migrate from their anterior location to a position adjacent to the developing oocyte. Consistent with these phenotypes, D-elg shows genetic interactions with two genes required for normal egg chamber differentiation.

bicaudal encodes the Drosophila beta NAC homolog, a component of the ribosomal translational machinery*.

bicaudal was the first Drosophila mutation identified as producing mirror-image pattern duplications along the anteroposterior axis of the embryo. However the mutation has been little studied due to its low penetrance and suppressibility. We undertook cloning of the bicaudal locus together with studies of the mutation's effects on key elements of the posterior embryonic patterning pathway. Our mapping studies place the bicaudal mutation within a approximately 2 kb region, 3' to the protein coding sequence of the Drosophila homolog of beta NAC, a subunit of Nascent polypeptide Associated Complex (NAC). Genomic DNA encoding beta NAC completely rescues the bicaudal phenotype. The lethal phenotype of Enhancer of Bicaudal, E(Bic), a mutation hypothesized to affect the bicaudal locus, is also completely rescued by the beta NAC locus. We further demonstrate that the E(Bic) mutation is caused by a P element insertion into the transcribed region of the beta NAC gene. NAC is among the first ribosome-associated entities to bind the nascent polypeptide after peptide bond formation. In contrast to other bicaudal-embryo-producing mutations, bicaudal leads to ectopic translation of mRNA for the posterior determinant nanos, without affecting the localization of mRNA for its upstream regulator, oskar, in the embryo. These findings suggest that repression of nanos mRNA translation occurs on the ribosome and involves a role for beta NAC.

Mutations in the predicted aspartyl tRNA synthetase of Drosophila are lethal and function as dosage-sensitive maternal modifiers of the sex determination gene Sex-lethal.

Stable activation of the Drosophila sex determination gene Sex-lethal in the female embryo is a multistep process. Early in embryogenesis Sex-lethal is regulated at the level of transcription, and then later in embryogenesis Sex-lethal regulation switches to an autoregulatory RNA splicing mechanism. Previous studies have shown that successful activation of Sxl requires both maternally and zygotically provided gene products, many of which are essential for viability and have other, non-sex specific functions. Using a screen for dosage-sensitive modifiers we identified a new maternally expressed gene, l(2)49Db, as a likely participant in Sxl activation. We show that the establishment of the Sxl autoregulatory splicing loop, but not the earlier steps in Sxl activation, is sensitive to the maternal dosage of l(2)49Db. We further demonstrate that l(2)49Db encodes an aspartyl tRNA synthetase. Finally we present evidence that this effect is indirect, by demonstrating that mutations in tryptophanyl tRNA synthetase are also dosage-sensitive maternal modifiers of Sex-lethal. These data suggest that stable activation of Sex-lethal in the embryo may be particularly sensitive to perturbation of the translational machinery.