Growing evidence suggests that some molecular regulatory pathways dictating cell fate are associated with the cell cycle machinery; however, the molecular connections remain unclear. Because the ability of Drosophila ovaries to create mature oocytes depends on a well-characterized population of germline stem cells (GSCs), the proliferative ability of GSCs must be tightly regulated. GSCs therefore serve as an exceptional model for study of cell cycle control in stem cells. The GSC cell cycle has been previously characterized by monitoring the morphology of the fusome, a germline-specific organelle that changes morphology during the cell cycle. To more precisely understand GSC cell cycle regulation, we characterized the Fluorescence Ubiquitin Cell Cycle Indicator (FUCCI) system in GSCs, which utilizes degradable versions of E2f1::GFP and CycB::RFP to fluorescently label cells in each phase of the cell cycle. We found that the FUCCI system faithfully labeled GSC cell cycle phases consistent with somatic cell types, but must be used in combination with fusome morphology for most accurate cell cycle assessment. Importantly, we found that E2f1::GFP expression mirrors that of Cyclin E, previously demonstrated to control GSC fate independently of proliferation. In contrast to Cyclin E mutants, however, loss of E2f1 has only minor effects on maintenance of the GSC fate. Additionally, GSC proliferation and maintenance appear to be largely independent of degradation of E2f1, as stabilizing E2f1 expression throughout the cell cycle results neither in major loss of GSCs nor obvious increases in cell death. Our data suggest that repression of E2f1 activity in GSCs may instead be more highly controlled by Rb and/or the repressor E2f2. We are currently investigating the role of E2f2 in this context. Our data also further emphasizes that cell cycle-independent roles of Cyclin E regulate maintenance of the GSC fate. These findings provide further insight into the regulation of the balance between maintaining cell fate and proliferation in GSCs, with broad implications on other asymmetrically dividing cells.