Ass through the blastoderm prior to PMG specification seem to migrate

Ass through the blastoderm prior to PMG specification seem to migrate correctly to the gonad, which would not be expected if passing through the blastoderm were the consequence of a partially penetrant migration phenotype. This suggests that tre1 germ cells are defective in a migratory Drosophila GPCR in Germ Cell Migration consequence, these germ cells also remained associated with the PMG. Expression of wild-type Rho1 had no effect on germ cell migration . The fact that a dominant-negative form of Rho1 caused a similar migration defect as that observed in tre1 mutant embryos and that expression of other GTPases either showed no or a different migration defect strongly suggest that Tre1-dependent XAV-939 web transepithelial migration is mediated by Rho GTPase in germ cells. Discussion We have identified a novel Drosophila GPCR, Tre1, that is required for transepithelial migration of germ cells through the PMG epithelium. tre1 RNA is expressed in germ cells, and tre1 acts cell autonomously in germ cells. Transmigration of germ cells through the PMG epithelium is the first active stage of germ cell migration, and specific mutations had previously not been identified for this step. Tre1 GPCR function specifically affects this stage, as “pioneer”tre1 germ cells that bypass the requirement for transepithelial migration through the PMG are motile and can follow other, lateracting migratory cues. These results suggest that GPCRs play an important role in transepithelial migration of germ cells and lead us to speculate that Tre1 might function in a manner equivalent to the chemokine receptors required for transepithelial migration of leukocytes. step that allows them to pass through the PMG epithelium, but that they are otherwise motile and able to respond to other guidance signals to reach the gonad. Tre1 and Directed Transepithelial Cell Migration Previous models for transgut migration of germ cells relied on the study of wild-type germ cell migration and analysis of mutants that affect PMG specification. Most of these observations– TG100 115 web including the fact that the midgut epithelium reorganizes independently of germ cells, that genes that disrupt PMG specification block germ cell transgut migration, and that either retarded or precocious germ cells would transmigrate the gut in accord with gut PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19858355 morphology–were compatible with a passive model. In this model, germ cells would pass through the gut merely as a consequence of the reorganization of the gut epithelium. Furthermore, this model would predict that, except for their ability to be motile, germ cells would not require any specific functions to pass the midgut epithelium. In contrast, our analysis of tre1 gene function demonstrates that the Tre1 GPCR acts in germ cells to specifically promote transepithelial migration. Thus, alternative models have to be considered in which gut rearrangements, while being a prerequisite for transgut migration, would not be sufficient to trigger the migration event per se. One possibility is that Tre1 mediates the initial interactions between germ cells and PMG cells, which may facilitate the passage of germ cells. Alternatively, Tre1 may mediate the directed migration of germ cells through the PMG. According to this latter model, migration may be directed by the expression of a ligand on the basal side of the midgut. Both attractant and repellant guidance signals for germ cells have already been identified in Drosophila. The gonadal mesoderm produces an attractant mediat.Ass through the blastoderm prior to PMG specification seem to migrate correctly to the gonad, which would not be expected if passing through the blastoderm were the consequence of a partially penetrant migration phenotype. This suggests that tre1 germ cells are defective in a migratory Drosophila GPCR in Germ Cell Migration consequence, these germ cells also remained associated with the PMG. Expression of wild-type Rho1 had no effect on germ cell migration . The fact that a dominant-negative form of Rho1 caused a similar migration defect as that observed in tre1 mutant embryos and that expression of other GTPases either showed no or a different migration defect strongly suggest that Tre1-dependent transepithelial migration is mediated by Rho GTPase in germ cells. Discussion We have identified a novel Drosophila GPCR, Tre1, that is required for transepithelial migration of germ cells through the PMG epithelium. tre1 RNA is expressed in germ cells, and tre1 acts cell autonomously in germ cells. Transmigration of germ cells through the PMG epithelium is the first active stage of germ cell migration, and specific mutations had previously not been identified for this step. Tre1 GPCR function specifically affects this stage, as “pioneer”tre1 germ cells that bypass the requirement for transepithelial migration through the PMG are motile and can follow other, lateracting migratory cues. These results suggest that GPCRs play an important role in transepithelial migration of germ cells and lead us to speculate that Tre1 might function in a manner equivalent to the chemokine receptors required for transepithelial migration of leukocytes. step that allows them to pass through the PMG epithelium, but that they are otherwise motile and able to respond to other guidance signals to reach the gonad. Tre1 and Directed Transepithelial Cell Migration Previous models for transgut migration of germ cells relied on the study of wild-type germ cell migration and analysis of mutants that affect PMG specification. Most of these observations– including the fact that the midgut epithelium reorganizes independently of germ cells, that genes that disrupt PMG specification block germ cell transgut migration, and that either retarded or precocious germ cells would transmigrate the gut in accord with gut PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19858355 morphology–were compatible with a passive model. In this model, germ cells would pass through the gut merely as a consequence of the reorganization of the gut epithelium. Furthermore, this model would predict that, except for their ability to be motile, germ cells would not require any specific functions to pass the midgut epithelium. In contrast, our analysis of tre1 gene function demonstrates that the Tre1 GPCR acts in germ cells to specifically promote transepithelial migration. Thus, alternative models have to be considered in which gut rearrangements, while being a prerequisite for transgut migration, would not be sufficient to trigger the migration event per se. One possibility is that Tre1 mediates the initial interactions between germ cells and PMG cells, which may facilitate the passage of germ cells. Alternatively, Tre1 may mediate the directed migration of germ cells through the PMG. According to this latter model, migration may be directed by the expression of a ligand on the basal side of the midgut. Both attractant and repellant guidance signals for germ cells have already been identified in Drosophila. The gonadal mesoderm produces an attractant mediat.