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Vol. 16, Issue 2, 891-901, February 2005

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EB1 Is Essential during Drosophila Development and Plays a Crucial Role in the Integrity of Chordotonal Mechanosensory Organs

Sarah L. Elliott ^* , C. Fiona Cullen ^*, Nicola Wrobel ^* , Maurice J. Kernan , and Hiroyuki Ohkura ^* ||

^* Wellcome Trust Centre for Cell Biology, Institute of Cell Biology, School of Biological Sciences, The University of Edinburgh, Edinburgh EH9 3JR, United Kingdom; Department of Neurobiology and Behavior, The State University of New York at Stony Brook, Stony Brook, NY 11794

Submitted July 27, 2004; Revised November 22, 2004; Accepted November 28, 2004
Monitoring Editor: Lawrence Goldstein

EB1 is a conserved microtubule plus end tracking protein considered to play crucial roles in microtubule organization and the interaction of microtubules with the cell cortex. Despite intense studies carried out in yeast and cultured cells, the role of EB1 in multicellular systems remains to be elucidated. Here, we describe the first genetic study of EB1 in developing animals. We show that one of the multiple Drosophila EB1 homologues, DmEB1, is ubiquitously expressed and has essential functions during development. Hypomorphic DmEB1 mutants show neuromuscular defects, including flightlessness and uncoordinated movement, without any general cell division defects. These defects can be partly explained by the malfunction of the chordotonal mechanosensory organs. In fact, electrophysiological measurements indicated that the auditory chordotonal organs show a reduced response to sound stimuli. The internal organization of the chordotonal organs also is affected in the mutant. Consistently, DmEB1 is enriched in those regions important for the structure and function of the organs. Therefore, DmEB1 plays a crucial role in the functional and structural integrity of the chordotonal mechanosensory organs in Drosophila.

The online version of this article contains supplemental material at MBC Online (http://www.molbiolcell.org).

Present address: Department of Biological Sciences, Stanford University, Stanford, CA 94305

Present address: Medical School, The University of Edinburgh, Edinburgh EH8 9AG, United Kingdom

^|| Corresponding author. E-mail address: h.ohkura{at}ed.ac.uk.

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