Abstract
How steroid hormones shape animal growth remains poorly understood. In Drosophila, the main steroid hormone, ecdysone, limits systemic growth during juvenile development. Here we show that ecdysone controls animal growth rate by specifically acting on the fat body, an organ that retains endocrine and storage functions of the vertebrate liver and fat. We demonstrate that fat body-targeted loss of function of the Ecdysone receptor (EcR) increases dMyc expression and its cellular functions such as ribosome biogenesis. Moreover, changing dMyc levels in this tissue is sufficient to affect animal growth rate. Finally, the growth increase induced by silencing EcR in the fat body is suppressed by cosilencing dMyc. In conclusion, the present work reveals an unexpected function of dMyc in the systemic control of growth in response to steroid hormone signaling.
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