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The aim of this dissertation was to analyse factors that are involved in the determination of the founder and fusion competent myoblasts (FCM) in the visceral mesoderm of Drosophila melanogaster as well as to establish a GAL4-driver line for the expression in the FCM. As a prerequisite for the establishment of the GAL4-driver line the promoter region of sticks and stones was analysed. A fragment of 4.5 kb upstream of the transcription start site of sns was found to be sufficient to get the full expression pattern. This fragment was ligated in a newly generated GAL4-vector.
To analyse the mechanisms that are involved in the cell determination in the visceral mesoderm two different approaches were undertaken. First, it was investigated if the processes that are involved in the determination in the somatic mesoderm also play a role in the visceral mesoderm. In the former Notch is mainly involved in the selection of the muscle precursor cells from a group of lethal of scute expressing cells in a process called lateral inhibition. The obtained results show that also in the visceral mesoderm Notch is involved in the determination of the founder cells. Furthermore, lethal of scute seems to be important for this process, as shown by RNAi experiments and analysis of mutants. Other factors that are known to be involved in the precursor selection in the somatic mesoderm did not seem to have an effect in the visceral mesoderm. Therefore, Notch seems to act through an alternative pathway in this tissue.
Secondly, a collection of EMS-mutagenised flies was screened to obtain new factors that are involved in the development of the visceral mesoderm. Hereby eight mutants were identified which can be subdivided into three groups. In mutants of the first group the visceral mesoderm consists only of FCM and is no longer detectable after stage 11. The mutants of the second group establish a normal band of the visceral mesoderm in stage 11, but later on it does not surround the midgut. In the mutants of the third group no visceral mesoderm is detectable at any stage. Genetic analysis of the mutants of the first group showed that they are new allels of Jelly belly, which is secreted from the somatic mesoderm and the Receptor Tyrosin Kinase Alk, which is expressed in the visceral mesoderm. It could be shown that Jelly belly and Alk act together in the same pathway. In addition to the loss of founder cells in the visceral mesoderm both mutants showed a specific loss of FCM in the somatic mesoderm. The lacking FCM were replaced by the FCM of the visceral mesoderm, which differentiated normally. The newly identified Alk-mediated Jeb-signalling pathway therefore seems responsible for the determination of the visceral founder and the somatic FCM.