Ecdysone regulates Drosophila wing disc size via a TORC1 dependent mechanism

During development, organs grow to achieve a size necessary for their function; how final organ size is sensed to trigger growth arrest, however, remains unclear. Here the authors show that Drosophila wing disc size is determined by the hormone ecdysone through a TORC1-dependent mechanism. Most cells in a developing organ stop proliferating when the organ reaches a correct, final size. The underlying molecular mechanisms are not understood. We find that in Drosophila the hormone ecdysone controls wing disc size. To study how ecdysone affects wing size, we inhibit endogenous ecdysone synthesis and feed larvae exogenous ecdysone in a dose-controlled manner. For any given ecdysone dose, discs stop proliferating at a particular size, with higher doses enabling discs to reach larger sizes. Termination of proliferation coincides with a drop in TORC1, but not Dpp or Yki signaling. Reactivating TORC1 bypasses the termination of proliferation, indicating that TORC1 is a main downstream effector causing proliferation termination at the maximal ecdysone-dependent size. Experimental manipulation of Dpp or Yki signaling can bypass proliferation termination in hinge and notum regions, but not the pouch, suggesting that the mechanisms regulating proliferation termination may be distinct in different disc regions.

Automated summary

The size of Drosophila wing discs is determined by the hormone ecdysone through a TORC1-dependent mechanism, with most cells stopping proliferation when the organ reaches the correct size. Reactivation of TORC1 can bypass the termination of proliferation, indicating its role as a main effector in regulating growth arrest at the maximal ecdysone-dependent size. Manipulation of Dpp or Yki signaling can affect proliferation termination in different regions of the wing disc.