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RESEARCH PAPER
1 European Neuroscience Institute Göttingen, Max-Planck-Society, 37073 Göttingen, Germany; 2 Department of Neuro and Sensory Physiology, Medical School, University of Göttingen, 37073 Göttingen, Germany; 3 Institute for Physiological Chemistry, University of Tübingen, 72076 Tübingen, Germany; 4 Max-Planck-Institute for Biophysical Chemistry, 37077 Göttingen, Germany
During Drosophila embryogenesis, developing muscles extend growth-conelike structures to navigate toward specific epidermal attachment sites. Here, we show that the homolog of Glutamate ReceptorInteracting Proteins (DGrip) acts as a key component of proper muscle guidance. Mutations in dgrip impair patterning of ventral longitudinal muscles (VLMs), whereas lateral transverse muscles (LTMs) that attach to intrasegmental attachment sites develop normally. Myoblast fusion, stabilization of muscle contacts, and general muscle function are not impaired in the absence of DGrip. Instead, the proper formation of cellular extensions during guidance fails in dgrip mutant VLMs. DGrip protein concentrates at the ends of VLMs while these muscles guide toward segment border attachment sites. Conversely, LTMs overexpressing DGrip form ectopic cellular extensions that can cause attachment of these muscles to other muscles at segment borders. Our data suggest that DGrip participates in the reception of an attractive signal that emanates from the epidermal attachment sites to direct the motility of developing muscles. This dgrip phenotype should be valuable to study mechanistic principles of Grip function.
[Keywords: dgrip; muscle; muscle guidance; Glutamate ReceptorInteracting Protein; Drosophila]
Received October 4, 2003; revised version accepted November 26, 2003.
5 These authors contributed equally to this work.
6 Corresponding author. E-MAIL ssigris{at}gwdg.de; FAX 49-551-3912346.
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