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# Characterization ofstalled, a grooming mutant that interacts with laminin

Abstract (Summary)
A molecular and genetic dissection of the stalled grooming mutant was performed to characterize a gene which may be necessary for the assembly of the pupal and adult nervous system of Drosophila melanogaster. To determine whether the grooming deficit observed in stalled resulted from disrupting the development of the sensory nervous system, afferent projections were examined in stalled using two P (Gal4) lines as markers of subsets of femoral chordotonal neurons. These lines were isolated in a screen of P (Gal4) enhancer trap lines to identify those which label distinct subsets of sensory neurons and their afferent projections in the pupal and adult nervous system (Chapter 1). In addition, afferent projections from the posterior tactile neurons were examined in stalled mutants using the en-lacZ marker line. Because the stalled P element insertion site was mapped to the 67C region of the third chromosome (as was the laminin $\gamma$ gene), it was of interest to determine whether stalled had identified $laminin\ \gamma$ since it has been demonstrated that the laminin plays roles during neuronal development. It was possible that stalled would interact with $laminin\ \alpha$ as a result of identifying the $laminin\ \gamma$ gene. Therefore, a genetic analysis was performed by combining stalled with the $laminin\ \alpha$ mutant and examining projections from different classes of sensory receptors in the single and double mutants. It was found that the interaction with stalled and $laminin\ \alpha$ was required for the proper development of at least two classes of sensory receptors (Chapter 3). Therefore, molecular characterization of stalled was performed to determine if stalled had identified the $laminin\ \gamma$ gene. Northern analysis demonstrated that the expression of $laminin\ \gamma$ was decreased in stalled and the $stalled\sp{e71}$ hypomorph. However, mapping experiments demonstrated that the stalled P element insertion site was 20-60 kilobases downstream of $laminin\ \gamma$. Taken together, these results suggest that stalled has identified an enhancer of the $laminin\ \gamma$ gene such that the amount of the laminin heterotrimeric complex is reduced in the $laminin\alpha;stld$ double mutants. This results in significant effects on the development of at least two distinct classes of sensory afferent projections.
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