RESUMEN
Transcriptional quiescence, an evolutionarily conserved trait, distinguishes the embryonic primordial germ cells (PGCs) from their somatic neighbors. In Drosophila melanogaster, PGCs from embryos maternally compromised for germ cell-less (gcl) misexpress somatic genes, possibly resulting in PGC loss. Recent studies documented a requirement for Gcl during proteolytic degradation of the terminal patterning determinant, Torso receptor. Here we demonstrate that the somatic determinant of female fate, Sex-lethal (Sxl), is a biologically relevant transcriptional target of Gcl. Underscoring the significance of transcriptional silencing mediated by Gcl, ectopic expression of a degradation-resistant form of Torso (torsoDeg) can activate Sxl transcription in PGCs, whereas simultaneous loss of torso-like (tsl) reinstates the quiescent status of gcl PGCs. Intriguingly, like gcl mutants, embryos derived from mothers expressing torsoDeg in the germline display aberrant spreading of pole plasm RNAs, suggesting that mutual antagonism between Gcl and Torso ensures the controlled release of germ-plasm underlying the germline/soma distinction.
Asunto(s)
Proteínas de Drosophila/genética , Drosophila melanogaster/embriología , Péptidos y Proteínas de Señalización Intercelular/genética , Proteínas de Unión al ARN/genética , Proteínas Tirosina Quinasas Receptoras/genética , Procesos de Determinación del Sexo , Animales , Proteínas de Drosophila/metabolismo , Drosophila melanogaster/genética , Drosophila melanogaster/metabolismo , Embrión no Mamífero/embriología , Femenino , Péptidos y Proteínas de Señalización Intercelular/metabolismo , Masculino , Proteínas de Unión al ARN/metabolismo , Proteínas Tirosina Quinasas Receptoras/metabolismo , Transcripción GenéticaRESUMEN
Heterochromatin-mediated repression is essential for controlling the expression of transposons and for coordinated cell type-specific gene regulation. The small ovary (sov) locus was identified in a screen for female-sterile mutations in Drosophila melanogaster, and mutants show dramatic ovarian morphogenesis defects. We show that the null sov phenotype is lethal and map the locus to the uncharacterized gene CG14438, which encodes a nuclear zinc-finger protein that colocalizes with the essential Heterochromatin Protein 1 (HP1a). We demonstrate Sov functions to repress inappropriate gene expression in the ovary, silence transposons, and suppress position-effect variegation in the eye, suggesting a central role in heterochromatin stabilization.
