We have sought to define the developmental and cellular roles played by differential expression of distinct β-tubulins. Drosophila β3-tubulin (β3) is a structurally divergent isoform transiently expressed during midembryogenesis. Severe β3 mutations cause larval lethality resulting from failed gut function and consequent starvation. However, mutant larvae also display behavioral abnormalities consistent with defective sensory perception, We identified embryonic β3 expression in several previously undefined sites, including different types of sensory organs. We conclude that abnormalities in foraging behavior and photoresponsiveness exhibited by prelethal mutant larvae reflect defective β3 function in the embryo during development of chordotonal and other mechanosensory organs and of Bolwig's organ and nerve. We show that microtubule organization in the cap cells of chordotonal organs is altered in mutant larvae. Thus transient zygotic β3 expression has permanent consequences for the architecture of the cap cell microtubule cytoskeleton in the larval sensilla, even when β3 is no longer present. Our data provide a link between the microtubule cytoskeleton in embryogenesis and the behavioral phenotype manifested as defective proprioreception at the larval stage.
|Original language||English (US)|
|Number of pages||11|
|State||Published - May 22 2001|
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