Antagonism between <i>germ cell-less</i> and Torso receptor regulates transcriptional quiescence underlying germline/soma distinction.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 33459591.
- Also identified by DOI 10.7554/eLife.54346 and PMC identifier 7843132.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Transcriptional quiescence, an evolutionarily conserved trait, distinguishes the embryonic primordial germ cells (PGCs) from their somatic neighbors. In <i>Drosophila melanogaster</i>, PGCs from embryos maternally compromised for <i>germ cell-less</i> (<i>gcl</i>) 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, <i>Sex-lethal</i> (<i>Sxl</i>), 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 (<i>torso<sup>Deg</sup></i>) can activate <i>Sxl</i> transcription in PGCs, whereas simultaneous loss of <i>torso-like</i> (<i>tsl</i>) reinstates the quiescent status of <i>gcl</i> PGCs. Intriguingly, like <i>gcl</i> mutants, embryos derived from mothers expressing <i>torso<sup>Deg</sup></i> 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.
Medical subject headings
- Drosophila Proteins
- Drosophila melanogaster
- Intercellular Signaling Peptides and Proteins
- RNA-Binding Proteins
- Receptor Protein-Tyrosine Kinases
- Sex Determination Processes