Jana Krauss

Publications (2)15 Total impact

• Article: Myosin-V regulates oskar mRNA localization in the Drosophila oocyte.

  Jana Krauss, Sonia López de Quinto, Christiane Nüsslein-Volhard, Anne Ephrussi
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  ABSTRACT: Intracellular mRNA localization is an effective mechanism for protein targeting leading to functional polarization of the cell. The mechanisms controlling mRNA localization and specifically how the actin and microtubule (MT) cytoskeletons cooperate in this process are not well understood. In Drosophila, Oskar protein accumulation at the posterior pole of the oocyte is required for embryonic development and is achieved by the transport of oskar mRNA and its exclusive translation at the posterior pole. oskar mRNA localization requires the activity of the MT-based motor Kinesin, as well as the formation of a transport-competent ribonucleoprotein (RNP) complex. Here, we show that didum, encoding the Drosophila actin-based motor Myosin-V, is a new posterior group gene that promotes posterior accumulation of Oskar. Myosin-V associates with the oskar mRNA transport complex preferentially at the oocyte cortex, revealing a short-range actomyosin-based mechanism that mediates the local entrapment of oskar at the posterior pole. Our results also show that Myosin-V interacts with Kinesin heavy chain and counterbalances Kinesin function, preventing ectopic accumulation of oskar in the cytoplasm. Our findings reveal that a balance of microtubule- and actin-based motor activities regulates oskar mRNA localization in the Drosophila oocyte.
  Current biology: CB 07/2009; 19(12):1058-63. · 10.99 Impact Factor
• Source

  Available from: Stefan Luschnig

  Article: An F1 genetic screen for maternal-effect mutations affecting embryonic pattern formation in Drosophila melanogaster.

  Stefan Luschnig, Bernard Moussian, Jana Krauss, Isabelle Desjeux, Josip Perkovic, Christiane Nüsslein-Volhard
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  ABSTRACT: Large-scale screens for female-sterile mutations have revealed genes required maternally for establishment of the body axes in the Drosophila embryo. Although it is likely that the majority of components involved in axis formation have been identified by this approach, certain genes have escaped detection. This may be due to (1) incomplete saturation of the screens for female-sterile mutations and (2) genes with essential functions in zygotic development that mutate to lethality, precluding their identification as female-sterile mutations. To overcome these limitations, we performed a genetic mosaic screen aimed at identifying new maternal genes required for early embryonic patterning, including zygotically required ones. Using the Flp-FRT technique and a visible germline clone marker, we developed a system that allows efficient screening for maternal-effect phenotypes after only one generation of breeding, rather than after the three generations required for classic female-sterile screens. We identified 232 mutants showing various defects in embryonic pattern or morphogenesis. The mutants were ordered into 10 different phenotypic classes. A total of 174 mutants were assigned to 86 complementation groups with two alleles on average. Mutations in 45 complementation groups represent most previously known maternal genes, while 41 complementation groups represent new loci, including several involved in dorsoventral, anterior-posterior, and terminal patterning.
  Genetics 06/2004; 167(1):325-42. · 4.01 Impact Factor