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The ribosome is critical for all aspects of cell growth due to its essential role in protein synthesis. Paradoxically, many Ribosomal proteins (Rps) act as tumour suppressors in  Drosophila  and vertebrates. To examine how reductions in  Rps  could lead to tissue overgrowth, we took advantage of the observation that an  RpS6  mutant dominantly suppresses the small rough eye phenotype in a  cyclin E  hypomorphic mutant ( cycE JP  ). We demonstrated that the suppression of  cycE JP   by the  RpS6  mutant is not a consequence of restoring CycE protein levels or activity in the eye imaginal tissue. Rather, the use of  UAS-RpS6  RNAi transgenics revealed that the suppression of  cycE JP   is exerted via a mechanism extrinsic to the eye, whereby reduced Rp levels in the prothoracic gland decreases the activity of ecdysone, the steroid hormone, delaying developmental timing and hence allowing time for tissue and organ overgrowth. These data provide for the first time a rationale to explain the counter-intuitive organ overgrowth phenotypes observed for certain members of the  Minute  class of  Drosophila Rp  mutants. They also demonstrate how  Rp  mutants can affect growth and development cell non-autonomously.

Drosophila Ribosomal Protein Mutants Control Tissue Growth Non-Autonomously via Effects on the Prothoracic Gland and Ecdysone