Abstract
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.
Highlights
Following fertilization, a Drosophila embryo undergoes 14 consecutive nuclear divisions to give rise to the cellular blastoderm
Lending further credence to the idea that transcription misregulation plays an important role in disrupting primordial germ cells (PGCs) development in gcl embryos, we found that expression of a mutant form of Torso that is resistant to Gcl-dependent degradation ectopically activates transcription of two Gcl targets, sis-b and Sxl, in pole buds (PBs) and PGC nuclei
Leatherman et al reported that a second X-chromosome counting elements (XCEs), sis-a, is not properly turned off in gcl PBs and PGCs
Summary
A Drosophila embryo undergoes 14 consecutive nuclear divisions to give rise to the cellular blastoderm. Studies by Leatherman et al, 2002 suggested that the defects in PGC formation in gcl mutant embryos are linked to failing to inhibit somatic transcription They found that when PBs first form during NC 9 in wild-type (WT) embryos, levels of CTD phosphorylation PB are only marginally less than in nuclei elsewhere in the embryo. The studies of Leatherman et al, 2002 indicated that two of the key X chromosomal counting elements, sis-a and sis-b, were inappropriately expressed in gcl PBs and PGCs. Since transcription factors encoded by these two genes function to activate the Sxl establishment promoter, Sxl-Pe, in somatic nuclei of female embryos, their findings raised the possibility that Sxl might be ectopically expressed in PBs/PGCs of gcl embryos. Stabilization of Torso in early PGCs mimics another gcl phenotype, the failure to properly sequester key PGC determinants in PBs and newly formed PGCs
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