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First published online 30 May 2006
doi: 10.1242/dev.02427
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1 Howard Hughes Medical Institute, Waksman Institute and Department of Molecular
Biology and Biochemistry, Rutgers The State University of New Jersey,
Piscataway, NJ 08854, USA.
2 Waksman Institute, Rutgers The State University of New Jersey, Piscataway, NJ
08854, USA.
3 Department of Biology, Texas A&M University, College Station, TX
77843-3258, USA.
¶ Author for correspondence (e-mail: irvine{at}waksman.rutgers.edu)
Accepted 4 May 2006
The dachs gene was first identified almost a century ago based on its requirements for appendage growth, but has been relatively little studied. Here, we describe the phenotypes of strong dachs mutations, report the cloning of the dachs gene, characterize the localization of Dachs protein, and investigate the relationship between Dachs and the Fat pathway. Mutation of dachs reduces, but does not abolish, the growth of legs and wings. dachs encodes an unconventional myosin that preferentially localizes to the membrane of imaginal disc cells. dachs mutations suppress the effects of fat mutations on gene expression, cell affinity and growth in imaginal discs. Dachs protein localization is influenced by Fat, Four-jointed and Dachsous, consistent with its genetic placement downstream of fat. However, dachs mutations have only mild tissue polarity phenotypes, and only partially suppress the tissue polarity defects of fat mutants. Our results implicate Dachs as a crucial downstream component of a Fat signaling pathway that influences growth, affinity and gene expression during development.
Key words: Dachs, Myosin, Leg, Wing, fat, Growth, Protocadherin, Drosophila
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