Regulation and targets of Mal-D during border cell migration in Drosophila melanogaster oogenesis

Abstract

Border cells, a group of specialized follicle cells that commit collective migration during the oogenesis of Drosophila, constitute a useful migration model. Previous work in our laboratory by Kalman Somogyi identified Mal-D, a transcriptional co-activator of DSRF, is important for border cell migration. mal-D mutation causes decrease of F-Actin levels and loss of cellular integrity in border cells. Moreover Mal-D was found to accumulate in the nucleus of some border cells while the cluster is migrating and only if the cluster is migrating. A suggested mechanism was that the border cells receive a migration related signal, such as an increase of cellular tension and send Mal-D to the nucleus. The first part of my project was to understand how Mal-D is regulated by the migration. In order to visualize subcellular distribution of Mal-D I generated a tagged version of the endogenous protein by using homologous recombination. Analysis of subcellular distribution of Mal-D with this tool showed that the increase in nuclear levels of Mal-D in migrating cells is the result of an overall increase in the level of Mal-D protein and not redistribution of a fixed amount of protein. Furthermore I identified that mutations in Profilin or DSRF affect the nuclear levels of Mal-D. In the second part of my project I focused on the targets of Mal-D. I isolated border cell mutant for Mal-D or wild-type, and I compared their gene expression profiles by using microarrays.