Abstract
Mutation of the Src64 gene of Drosophila results in ovarian ring canal defects and reduced female fertility. We used a dosage-sensitive modifier screen to search for downstream components of the SRC64 signaling pathway. We show that mutations affecting Tec29, an essential gene encoding a member of the Tec family of protein tyrosine kinases, dominantly enhance the Src64 ring canal phenotype. Loss of Tec29 function in the female germline results in a phenotype strikingly similar to that caused by the loss of Src64 function. In each case, the ring canals are reduced in size and phosphotyrosine content. We further demonstrate that TEC29 localizes to the ring canal, and this subcellular localization requires Src64 function. These data suggest that TEC29 is a downstream target of SRC64, and that regulating TEC29 localization during ring canal growth may be a crucial SRC64 function.
