Published 18 February 2002. doi:10.1083/jcb1564iti4
© The Rockefeller University Press,
0021-9525/2002/2/586-a $5.00
The Journal of Cell Biology, Volume 156, Number 4, February 18, 2002 586-a-586
Activating actin
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Actin (green) separates embryonic fly nuclei imperfectly in a SCAR mutant (bottom).
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On page 677, Hudson and Cooley characterize Drosophila melanogaster strains with defects in the evolutionarily conserved actin nucleation factor Arp2/3. The work provides significant new insights into the specificity of Arp2/3 activity.During Drosophila egg development, intercellular connections called ring canals form between nurse cells and developing oocytes, allowing cytoplasm from the nurse cells to flow into the oocytes. These processes require at least three distinct types of actin structures: contractile actin to squeeze cytoplasmic contents, actin to keep ring canals open, and bundles of actin filaments that position the nucleus and stop it from clogging the ring canals. Similar actin bundles are also seen during metamorphosis, when the growth of bristles on the pupal epithelium requires hexagonally packed bundles of actin filaments.
In the new work, Hudson and Cooley found that flies with defective Arp2/3 complexes exhibit specific flaws in the formation of the loosely organized actin filaments in ring canals, and that Arp2/3 components are localized to the ring canals. However, the mutants are still able to form parallel actin filament bundles in nurse cells and epithelial bristles, suggesting that other factors are required for actin nucleation in these structures. The authors are now using their Drosophila system to try to identify these factors.
In addition to defects in oogenesis, Arp2/3-deficient flies exhibit several other developmental phenotypes, and on page 689, Zallen et al. build on the results of Hudson and Cooley to dissect the activities of two Arp2/3 activators. Previous work has shown that members of the WASp-Scar/WAVE family of proteins can regulate Arp2/3 activity, and that the two main branches of this protein family, WASp and Scar/WAVE, are highly conserved. Mutations in SCAR, which encodes the only Drosophila Scar/WAVE subfamily protein, cause flaws in oogenesis and several other developmental processes that are strikingly similar to some of the phenotypes seen in Arp2/3 complex mutants. Mutants in the single WASp homologue in the fly undergo apparently normal oogenesis, but display defects in the Arp2/3-dependent process of asymmetric cell division in neural lineages, indicating that SCAR and Wasp induce distinct cellular activities of Arp2/3 during development. 
Alan W. Dove
alanwdove{at}earthlink.net
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