Fig 1. Endoreplication-associated SC growth in mated male Drosophila is regulated by hormone-independent EcR signalling.

(A) Schematic showing model of growth regulation in Drosophila SCs, as measured by nuclear growth². Growth in virgin males is controlled by hormone-dependent EcR signalling, which itself is stimulated by BMP signalling involving the ligand Decapentaplegic (Dpp) and the BMP type I receptor Thick Veins (Tkv) and inhibited by the transcriptional repressor Dad. After mating, 25% of cells endoreplicate and grow via an EcR-mediated mechanism that does not require hormone. The remaining 75% of cells also increase their growth, and most of this growth also appears to involve hormone-independent EcR signalling under the control of autocrine BMP signalling stimulated by increased secretion during mating. (B) Schematic describing key features of the cell cycle transitions and the roles of CycD, Rb, E2F1 and CycE in driving cells into S phase. Rb is a negative regulator of the cell cycle. In its active form, Rb binds to the E2F1 transcription factor and inhibits its activity. When Rb is inactivated by hyperphosphorylation, E2F1 transcribes genes, including CycE. CycD/cdk4/6 mediates events that occur in early G1-phase (including Rb/E2F1 regulation) and CycE/cdk2 is required for initiating the G1/S transition via a negative feedback loop that inhibits Rb activity, while Cyclin A (CycA)/cdk2, CycA/cdk1 and Cyclin B (CycB/cdk1) are involved in driving cells through the rest of the cell cycle.