Actin Organization in the Early Drosophila Embryo

  1. Gregory Bock Organizer and
  2. Jamie Goode
  1. Eyal D. Schejter

Published Online: 7 OCT 2008

DOI: 10.1002/047001766X.ch11

Signalling Networks in Cell Shape and Motility: Novartis Foundation Symposium 269

Signalling Networks in Cell Shape and Motility: Novartis Foundation Symposium 269

How to Cite

Schejter, E. D. (2005) Actin Organization in the Early Drosophila Embryo, in Signalling Networks in Cell Shape and Motility: Novartis Foundation Symposium 269 (eds G. Bock and J. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/047001766X.ch11

Author Information

  1. Department of Molecular Genetics, Belfer Building, Weizmann Institute of Science, Rehovot 76100, Israel

Publication History

  1. Published Online: 7 OCT 2008
  2. Published Print: 9 SEP 2005

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780470011904

Online ISBN: 9780470017661

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Keywords:

  • microtubule-organizing centres (MTOCs);
  • yeast FRT-FLP recombination system;
  • nuclear migration;
  • Arp2/3 complex;
  • SCAR mutant embryos;
  • cortical actin structures;
  • CDM proteins;
  • guanine nucleotide exchange factor (GEF);
  • actin-based cytoskeleton

Summary

Organization of the cortical cytoplasm during the syncytial blastoderm stages of early Drosophila embryogenesis relies on cyclic transitions between transient microfilament structures. Microtubule-organizing centres (MTOCs) appear to provide the instructive cues governing this dynamic, cell-cycle-dependent process. Using a genetic approach, we have identified key roles for two molecular pathways in mediating these events. The conserved Arp2/3 microfilament nucleation machinery, likely acting in response to the activating element SCAR, plays an essential role in establishment of a cortical F-actin array, and contributes to specific aspects of cyclic microfilament restructuring. Defective cortical microfilament organization is the primary phenotypic feature of embryos derived from mothers bearing mutations in the sponge locus. Several lines of investigation suggest that the primary defect in sponge lies in a faulty cortical microfilament response, downstream of the centrosomal signal. We have determined that sponge encodes a Drosophila homologue of the evolutionarily-conserved CDM (DOCK180) protein family.