ABSTRACT
Gonad formation requires specific interactions between germ cells and specialized somatic cells, along with the elaborate morphogenetic movements of these cells to create an ovary or testis. We have identified mutations in the fear of intimacy (foi) gene that cause defects in the formation of the embryonic gonad in Drosophila. foi is of particular interest because it affects gonad formation without affecting gonad cell identity, and is therefore specifically required for the morphogenesis of this organ. foi is also required for tracheal branch fusion during tracheal development. E-cadherin/shotgun is similarly required for both gonad coalescence and tracheal branch fusion, suggesting that E-cadherin and FOI cooperate to mediate these processes. foi encodes a member of a novel family of transmembrane proteins that includes the closely related human protein LIV1. Our findings that FOI is a cell-surface protein required in the mesoderm for gonad morphogenesis shed light on the function of this new family of proteins and on the molecular mechanisms of organogenesis.
Subject(s)
Drosophila Proteins/genetics , Drosophila/embryology , Drosophila/genetics , Genes, Insect , Membrane Proteins/genetics , Ovary/embryology , Testis/embryology , Animals , Cadherins/physiology , Drosophila Proteins/physiology , Female , Gene Expression Regulation, Developmental , Humans , Male , Membrane Proteins/physiology , Mutation , Phenotype , Trachea/embryologyABSTRACT
Drosophila germ cell migration is directed by attractive and repulsive guidance cues. We have identified a novel gene, slow as molasses (slam), which is required for germ cell migration. In slam zygotic mutants, germ cells fail to transit off the midgut into the mesoderm. We show that slam is required at this stage in parallel to HMG Coenzyme A reductase, a previously identified germ cell migration gene. Removal of both zygotic and maternal slam results in an earlier defect: a failure to form a cellular blastoderm. Consistent with this phenotype, we found that slam is one of the earliest genes to be transcribed in the embryo, and Slam protein localizes to the growing basal-lateral membrane during blastoderm formation, but Slam is not detected during later stages of embryogenesis. Because slam RNA and protein are expressed earlier than the time when we observe defects in germ cell migration, we propose that Slam is required for the localization of a signal to the basal side of blastoderm cells that is needed later in the posterior midgut to guide germ cells.