The cut locus of Drosophila encodes a homeodomain protein (Cut) that controls cell fates in several embryonic and adult tissues. In this application, experiments are proposed that characterize the role of cut during oogenesis, a developmental system in which many changes in cellular physiology occur and is amenable to molecular and genetic manipulation. Preliminary mosaic analysis using the FLP/FRT system and analysis of hypomorphic combinations of cut alleles has shown that decreased cut expression results in altered organization of the germline-derived cells and eventual degradation of follicles. Conversely, ectopic Cut protein expression results in follicles that contain too many germline-derived cells, and later disrupts formation of the dorsal cuticle in progeny of these females. Thus, consistent with its biphasic expression pattern in the ovary, cut appears to a formation of follicles in early stages, and maternal Cut expression influences pattern formation during embryogenesis. Presumably, this is accomplished by influencing cell fate choices and/or by influencing patterns of gene expression. The role of cut in the formation of individual follicles will be determined by examining effects of altered Cut expression on specific follicle cell fates. interactions between cut and genes that pro similar oogenic disruptions when mutated will be examined. The maternal contribution of cut will be determined by examining the effects of altered maternal Cut expression on the expression of genes that are involved in dorsal-central axis formation. To address the molecular mechanisms responsible for these effects, differential display will be used to isolate gene products that are regulated by Cut during oogenesis. These studies will provide insights into the role of the cut locus in influencing gene expression patterns and cell fate choices.
Jackson, S M; Berg, C A (1999) Soma-to-germline interactions during Drosophila oogenesis are influenced by dose-sensitive interactions between cut and the genes cappuccino, ovarian tumor and agnostic. Genetics 153:289-303 |