TitleSCAR is a primary regulator of Arp2/3-dependent morphological events in Drosophila.
Publication TypeJournal Article
Year of Publication2002
AuthorsZallen, JA, Cohen, Y, Hudson, AM, Cooley, L, Wieschaus, E, Schejter, ED
JournalJ Cell Biol
Date Published2002 Feb 18
KeywordsActin-Related Protein 2, Actin-Related Protein 3, Actins, Amino Acid Sequence, Animals, Axons, Base Sequence, Blastoderm, Brain, Cytoplasm, Cytoskeletal Proteins, DNA, Complementary, Drosophila, Drosophila Proteins, Genes, Insect, Humans, Insect Proteins, Microfilament Proteins, Molecular Sequence Data, Morphogenesis, Mutagenesis, Oogenesis, Ovum, Proteins, Sequence Homology, Amino Acid, Wiskott-Aldrich Syndrome Protein

The Arp2/3 complex and its activators, Scar/WAVE and Wiskott-Aldrich Syndrome protein (WASp), promote actin polymerization in vitro and have been proposed to influence cell shape and motility in vivo. We demonstrate that the Drosophila Scar homologue, SCAR, localizes to actin-rich structures and is required for normal cell morphology in multiple cell types throughout development. In particular, SCAR function is essential for cytoplasmic organization in the blastoderm, axon development in the central nervous system, egg chamber structure during oogenesis, and adult eye morphology. Highly similar developmental requirements are found for subunits of the Arp2/3 complex. In the blastoderm, SCAR and Arp2/3 mutations result in a reduction in the amount of cortical filamentous actin and the disruption of dynamically regulated actin structures. Remarkably, the single Drosophila WASp homologue, Wasp, is largely dispensable for these numerous Arp2/3-dependent functions, whereas SCAR does not contribute to cell fate decisions in which Wasp and Arp2/3 play an essential role. These results identify SCAR as a major component of Arp2/3-dependent cell morphology during Drosophila development and demonstrate that the Arp2/3 complex can govern distinct cell biological events in response to SCAR and Wasp regulation.

Alternate JournalJ. Cell Biol.