Abstract
This article reports the production of an EP-element insertion library with more than 3,700 unique target sites within the Drosophila melanogaster genome and its use to systematically identify genes that affect embryonic muscle pattern formation. We designed a UAS/GAL4 system to drive GAL4-responsive expression of the EP-targeted genes in developing apodeme cells to which migrating myotubes finally attach and in an intrasegmental pattern of cells that serve myotubes as a migration substrate on their way towards the apodemes. The results suggest that misexpression of more than 1.5% of the Drosophila genes can interfere with proper myotube guidance and/or muscle attachment. In addition to factors already known to participate in these processes, we identified a number of enzymes that participate in the synthesis or modification of protein carbohydrate side chains and in Ubiquitin modifications and/or the Ubiquitin-dependent degradation of proteins, suggesting that these processes are relevant for muscle pattern formation.
Highlights
Whole genome sequences of many animals are known, including those of Caenorhabditis elegans, human, mouse, and Drosophila melanogaster
In addition to providing a most valuable tool for the Drosophila community of researchers, the results provide a framework for a detailed analysis of the gene network and insight into molecular mechanisms underlying embryonic muscle pattern formation
We identified a series of genes whose activity impairs muscle pattern formation when misexpressed in a defined pattern of epidermal cells that represent the migration substrate and/or the attachment sites for the outgrowing myotubes and muscle fibers
Summary
Whole genome sequences of many animals are known, including those of Caenorhabditis elegans, human, mouse, and Drosophila melanogaster (see for example [1,2,3,4]). In order to perform a large-scale gain-of-function screen for gene activities that interfere with D. melanogaster muscle pattern formation during embryogenesis, we designed a GAL4-driver that allowed the misexpression of EP-targeted genes in presumptive apodeme precursors at the segment border and in an ectopic array of intrasegmental cell rows within the epidermis of the embryo. The identification of a subset of transmembrane proteins in which two out of four proteins (Sdc and Toll) are already known to participate in muscle pattern formation [25,28] provides trust that other identified genes that code for membrane associated and secreted factors with unknown functions may take part in the process. Our results show that sdc-dependent Slit signaling serves as a muscle attractant during a late phase of muscle guidance [19], since abnormal muscle elongations are observed in fully developed but unhatched sdc mutant larvae (Figure 4C and 4F)
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