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.
The small ovary (sov) locus was identified in a female sterile screen, yet its molecular identity and function remained a mystery for decades. In the present work, Benner et al. molecularly map...
variegation 23 24 2 Benner et al.; sov represses gene expression Abstract 25Repression is essential for coordinated cell type-specific gene regulation and for controlling the 26 expression of transposons. In the Drosophila ovary, stem cells regeneration and differentiation 27 require well-controlled expression, with de-repression leading to tissue degeneration and 28 ovarian tumors. Additionally, the ovary is acutely sensitive to deleterious consequences of 29 transposon de-repression. The small ovary (sov) locus was identified in a female sterile screen 30shows dramatic effects ovarian morphogenesis. We mapped the locus to the uncharacterized 31 gene CG14438 and reveal it encodes a zinc-finger protein that colocalizes with the essential 32Heterochromatin Protein 1 (HP1a). The distinct functions of Sov we report, including 33 repression of inappropriate signaling, transposon silencing, and effects on position-effect 34 variegation in the eye, suggest a central role in heterochromatin stabilization. 35 36 3 Benner et al.; sov represses gene expression produce a germline cyst interconnected by the fusome, a branched cytoskeletal structure. 49
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