Stimulation of ribosome biogenesis is a conserved mechanism of growth control. Studies in yeast and cell culture have shown how ribosome synthesis controls cell growth. However, less is known about how ribosome synthesis promotes body growth and development. I have been exploring this issue by studying the Minutes. These are a class of dominant ribosomal protein (RP) mutants that exhibit a characteristic delay in larval development – a phenotype classically thought to be due to an overall reduction in ribosome numbers and protein synthesis. However, when I examined rpS13/+ Minutes I saw little or no change in either global ribosome numbers or in protein synthesis rates, when compared to wild-type controls. Instead, I found evidence of a cell type-specific function for rpS13/+ in the control of larval development. Termination of the larval period is controlled by a pulse of secretion of the steroid hormone ecdysone from the prothoracic gland (PG) in response to signals from specific CNS neurons and imaginal tissues as well as environmental factors. I found that rpS13/+ animals had a delayed ecdysone pulse as seen by delayed expression of spookier and phantom, two enzymes which are required for ecdysone synthesis in the PG. Ecdysone (20HE) feeding also partially reversed the delay in development, suggesting a specific role for RpS13 in the neuroendocrine circuit that controls ecdysone. To test this, I used the GAL4/UAS system to see if tissue selective expression of RpS13 could rescue the delayed development seen in rps13/+ animals. Expression in imaginal tissues or the PG had no effect. However, re-expression of RpS13 in a subset of serotonergic (5-HT) neurons that project to the PG to control ecdysone production, reversed the delay in development in rpS13/+ animals by ~40%. I found that while the growth and development of 5-HT neuronal projections to the PG were normal, these neurons showed a defect in secretion in rpS13/+ animals. Moreover, I found overexpressing synaptic vesicle proteins in these neurons was sufficient to partially reverse the delay in development seen in three different Minute mutants (rpS13/+, rpS24/+, rpS26/+). These results suggest that the delayed organismal development in Rp/+ animals is explained in part by defective neuronal secretion, and they point to a specific role for serotonergic ribosomal function in the neuroendocrine control of Drosophila development.