Induction of germ cell formation by oskar

@article{Ephrussi1992InductionOG,
  title={Induction of germ cell formation by oskar},
  author={Anne Ephrussi and Ruth Lehmann},
  journal={Nature},
  year={1992},
  volume={358},
  pages={387-392}
}
The oskar gene directs germ plasm assembly and controls the number of germ cell precursors formed at the posterior pole of the Drosophila embryo. Mislocalization of oskar RNA to the anterior pole leads to induction of germ cells at the anterior. Of the eight genes necessary for germ cell formation at the posterior, only three, oskar, vasa and tudor, are essential at an ectopic site. 
View on Nature
ncbi.nlm.nih.gov
625 Citations
Highly Influential Citations
50
Background Citations
330
Methods Citations
25
Results Citations
5

625 Citations

Formation of germ cells in Drosophila.

Germ-plasm formation and germ-cell determination in Drosophila.

  • R. Lehmann
  • Biology
    Current opinion in genetics & development
  • 1992

Germ plasm and molecular determinants of germ cell fate.

Requirement for a Noncoding RNA in Drosophila Polar Granules for Germ Cell Establishment

Most pole cells in embryos produced by transgenic females expressing antisense Pgc RNA failed to complete migration and to populate the embryonic gonads, and females that developed from these embryos often had agametic ovaries.

Establishment of embryonic polarity during Drosophila oogenesis

Assembly of the Drosophila germ plasm.

Hedgehog Signaling in Germ Cell Migration

Repression of early zygotic transcription in the germline.

RNA localization and the development of asymmetry during Drosophila oogenesis.

Axis formation during Drosophila oogenesis.

...

References

SHOWING 1-10 OF 38 REFERENCES

oskar mRNA is localized to the posterior pole of the Drosophila oocyte

Abdominal segmentation, pole cell formation, and embryonic polarity require the localized activity of oskar, a maternal gene in drosophila

Organization of anterior pattern in the Drosophila embryo by the maternal gene bicoid

Cytoplasmic transplantation experiments reveal that bcd+-dependent activity is localized at the anterior pole of wild-type embryos and can induce anterior development in mutant embryos at any position along the antero-posterior axis.

tudor, a gene required for assembly of the germ plasm in Drosophila melanogaster

The role of localization of bicoid RNA in organizing the anterior pattern of the Drosophila embryo.

The organization of the anterior pattern in the Drosophila embryo is mediated by the maternal effect gene bicoid and the mRNA is localized at the anterior tip of oocyte and early embryo until the cellular blastoderm stage.

A molecular gradient in early Drosophila embryos and its role in specifying the body pattern

After fertilization, the protein products of the Drosophila homeobox gene caudal accumulate in a concentration gradient spanning the anteroposterior axis of the developing embryo, which causes abnormal zygotic expression of at least one segmentation gene (fushi tarazu) and alter the global body pattern.

The maternal gene nanos has a central role in posterior pattern formation of the Drosophila embryo.

It is suggested that the products of these genes provide the physical structure necessary for the localization of nanos-dependent activity and of germ line determinants.

Posterior localization of vasa protein correlates with, but is not sufficient for, pole cell development.

It is indicated that vasa protein, when properly localized, is not sufficient for induction of pole cell development, and that at least the tudor and valois wild-type functions are also required specifically for this process.

The product of the Drosophila gene vasa is very similar to eukaryotic initiation factor-4A

Isolation and characterization of vasa genomic and complementary DNA clones show that the transcript is abundant in the female germ line and early embryos only.

The ovo locus is required for sex-specific germ line maintenance in Drosophila.

The ovo locus is mapped to position 4E1-2 of the salivary gland X chromosome by using a set of cytologically visible deletions to map the sex-specific phenotype at late blastoderm and early gastrula stages of embryos homozygous for a loss-of-function allele.