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Mutational analysis of the Guanine Nucleotide Exchange Factor C3G in Drosophila melanogaster reveals a role for C3G in larval muscle development.
(English)Manuscript (Other academic)
URN: urn:nbn:se:umu:diva-22150OAI: diva2:212877
Available from: 2009-04-24 Created: 2009-04-24 Last updated: 2010-01-14Bibliographically approved
In thesis
1. Midgut and muscle development in Drosophila melanogaster
Open this publication in new window or tab >>Midgut and muscle development in Drosophila melanogaster
2009 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The fully developed and functional Drosophila midgut comprises two layers, the visceral mesoderm and the endoderm. The visceral muscle of the midgut is formed by the fusion of founder cells with fusion competent cells to form the muscle syncytia. The specification of these cells and thus the fusion and the formation of the midgut muscle is dependent on the  Receptor tyrosine kinase (RTK) Alk (Loren et al., 2003). The endoderm underlies the visceral muscle and is formed from cells that originate from the anterior and the posterior parts of the embryo. These cells use the visceral mesoderm as a substrate for their migration. Using Alk mutant animals, we have studied endoderm migration during embryonic development. While the initial migration of the endoderm is not affected in the absence of the visceral mesoderm, we observe that the later dorsal-ventral endodermal migration does not take place.

The development of the visceral muscle and its dependence on the endoderm is poorly understood.  We have analysed gürtelchen (gurt) mutant animals, originally identified in a genetic screen for mutations affecting visceral muscle formation. Gurt mutants are so named due to their belt-like phenotype of the visceral muscle (gürtelchen is German for belt). Mapping of the genomic locus identified gurt as a mutation in a previously described gene - huckebein (hkb) which is known to have an important function in endoderm development. Gurt (hkb) mutants were used to further study the interaction between the endoderm and the visceral muscle during development. The initial specification of founder cells and fusion competent myoblasts as well as fusion events are unaffected in gurt (hkb) mutants, however, the elongation and stretching of the visceral muscle does not proceed as normal. Moreover, ablation of the visceral mesoderm disrupts endoderm migration, while ablation of the endoderm results in a delayed disruption of visceral muscle formation.

Signaling between the two tissues was investigated in detail. Since Alk is a critical player in visceral muscle development, we employed Alk mutant embryos for this task. In addition to the role of Alk in specifying the founder cells and initiating the visceral muscle fusion, we have shown that Alk mediated signaling has a role in the induction of the midgut constriction process by regulating dpp expression in the developing embryonic gut.

 Finally, we wished to identify genes in the founder cells/fusion competent myoblasts that might be regulated by Alk. C3G is a gunaine nucleotide exchange factor expressed in the visceral muscle founder cells. Deletion of the Drosophila C3G locus resulted in the generation of null mutants in C3G which are viable, but display decreased longevity, fitness and are semi-lethal. Further analysis of C3G mutants indicated that C3G is essential for normal larval musculature development, in part by regulating integrin localization at muscle attachment sites.

Place, publisher, year, edition, pages
Umeå: Department of molecular biology, 2009. 59 p.
Umeå University medical dissertations, ISSN 0346-6612 ; 1264
Drosophila, visceral mesoderm, endoderm, somatic muscles, Alk, C3G
National Category
Cell and Molecular Biology
Research subject
Molecular Biology
urn:nbn:se:umu:diva-22137 (URN)978-91-7264-782-4 (ISBN)
Institutionen för molekylärbiologi (Medicinska fakulteten), 901 87, Umeå
Public defence
2009-05-20, Major Groove, byggnad 6L, Institutionen för Molekylärbiologi, 13:00 (English)
Available from: 2009-04-28 Created: 2009-04-24 Last updated: 2011-09-01Bibliographically approved

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