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First published online September 1, 2004
doi: 10.1242/10.1242/dev.01309



1 Philipps-Universität Marburg, Fachbereich Biologie, Entwicklungsbiologie,
Karl-von-Frisch Strasse 8, 35043 Marburg, Germany
2 Philipps-Universität Marburg, Fachbereich Biologie, Spezielle Zoologie,
Karl-von-Frisch Strasse 8, 35043 Marburg, Germany
3 Institut für Neuround Verhaltensbiologie, Westfälische
Wilhelms-Universität Münster, Badestrasse 9, 48149 Münster,
Germany
Author for correspondence (e-mail:
renkawit{at}staff.uni-marburg.de)
Accepted 9 June 2004
Drosophila myoblast fusion proceeds in two steps. The first one gives rise to small syncytia, the muscle precursor cells, which then recruit further fusion competent myoblasts to reach the final muscle size. We have identified Kette as an essential component for myoblast fusion. In kette mutants, founder cells and fusion-competent myoblasts are determined correctly and overcome the very first fusion. But then, at the precursor cell stage, fusion is interrupted. At the ultrastructural level, fusion is characterised by cell-cell recognition, alignment, formation of prefusion complexes, electron dense plaques and membrane breakdown. In kette mutants, electron dense plaques of aberrant length accumulate and fusion is interrupted owing to a complete failure of membrane breakdown. Furthermore, we show that kette interacts genetically with blown fuse (blow) which is known to be required to proceed from prefusion complexes to the formation of the electron dense plaques. Interestingly, a surplus of Kette can replace Blow function during myogenesis. We propose a model in which Dumbfounded/Sticks and stones-dependent cell adhesion is mediated over Rolling Pebbles, Myoblast city, Crk, Blown fuse and Kette, and thus induces membrane fusion.
Key words: Myoblast fusion, Attachment, Prefusion complex, Electron dense plaque kette, blow, rols, sns, mbc, crk
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