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.

中文翻译：

---

无生殖细胞和躯干之间的拮抗调节生殖细胞/体细胞区别的转录静止

转录静止是一种进化上保守的特征，它将胚胎原始生殖细胞 (PGC) 与其体细胞邻居区分开来。在黑腹果蝇中，来自母体胚胎的 PGC 因无生殖细胞 (gcl) 体细胞基因而受损，可能导致 PGC 丢失。最近的研究记录了在末端图案决定因子躯干受体的蛋白水解降解过程中对 Gcl 的需求。在这里，我们证明了女性命运的体细胞决定因素，性致死 (Sxl)，是 Gcl 的生物学相关转录靶标。强调由 Gcl 介导的转录沉默的重要性，抗降解形式的躯干 (torsoDeg) 的异位表达可以激活 PGC 中的 Sxl 转录，而同时失去躯干样 (tsl) 会恢复 gcl PGC 的静止状态。