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doi: 10.1242/dev.00972


Development 131, 743-754 (2004)
Published by The Company of Biologists 2004


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Myoblast determination in the somatic and visceral mesoderm depends on Notch signalling as well as on milliways(miliAlk) as receptor for Jeb signalling

Christiana Stute1, Kristina Schimmelpfeng2,*, Renate Renkawitz-Pohl1, Ruth H. Palmer3 and Anne Holz4,{dagger}

1 Philipps-Universität Marburg, Fachbereich Biologie, Zoologie/Entwicklungsbiologie, Karl-von-Frisch-Strasse, 35039 Marburg, Germany
2 Institut für Neuro- und Verhaltensbiologie, Westfälische Wilhelms-Universität Münster, Badestrasse 9, 48149 Münster, Germany
3 Umeå Center for Molecular Pathogenesis, Building 6L, Umeå University, S-90187, Sweden
4 Institut für Allgemeine und Spezielle Zoologie, Allgemeine Zoologie und Entwicklungsbiologie, Justus-Liebig-Universität Gießen, Stephanstraße 24, 35390 Gießen, Germany

{dagger} Author for correspondence (e-mail: anne.holz{at}allzool.bio.uni-giessen.de)

Accepted 7 November 2003

The visceral muscles of the Drosophila midgut consist of syncytia and arise by fusion of founder and fusion-competent myoblasts, as described for the somatic muscles. A single-step fusion results in the formation of binucleate circular midgut muscles, whereas a multiple-step fusion process produces the longitudinal muscles. A prerequisite for muscle fusion is the establishment of myoblast diversity in the mesoderm prior to the fusion process itself. We provide evidence for a role of Notch signalling during establishment of the different cell types in the visceral mesoderm, demonstrating that the basic mechanism underlying the segregation of somatic muscle founder cells is also conserved during visceral founder cell determination.

Searching for genes involved in the determination and differentiation of the different visceral cell types, we identified two independent mutations causing loss of visceral midgut muscles. In both of these mutants visceral muscle founder cells are missing and the visceral mesoderm consists of fusion-competent myoblasts only. Thus, no fusion occurs resulting in a complete disruption of visceral myogenesis. Subsequent characterisation of the mutations revealed that they are novel alleles of jelly belly (jeb) and the Drosophila Alk homologue named milliways (miliAlk). We show that the process of founder cell determination in the visceral mesoderm depends on Jeb signalling via the Milliways/Alk receptor.

Moreover, we demonstrate that in the somatic mesoderm determination of the opposite cell type, the fusion-competent myoblasts, also depends on Jeb and Alk, revealing different roles for Jeb signalling in specifying myoblast diversity. This novel mechanism uncovers a crosstalk between somatic and visceral mesoderm leading not only to the determination of different cell types but also maintains the separation of mesodermal tissues, the somatic and splanchnic mesoderm.

Key words: Drosophila, Myogenesis, Visceral and Somatic muscles, Founder cells, Fusion-competent cells, Myoblast fusion, Notch, Delta, lethal of scute, jelly belly, Alk, RTK signalling




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