Institute of Developmental Biology and Cancer, University of Nice-Sophia Antipolis, CNRS, Parc Valrose, 06108 Nice, France.
Dev Cell. 2010 Jun 15;18(6):1012-21. doi: 10.1016/j.devcel.2010.05.007.
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.
类固醇激素如何塑造动物生长仍然知之甚少。在果蝇中，主要的类固醇激素蜕皮激素在幼年发育期间限制全身生长。在这里，我们表明蜕皮激素通过特异性作用于脂肪体来控制动物的生长速度，脂肪体是一个保留脊椎动物肝脏和脂肪内分泌和储存功能的器官。我们证明，脂肪体靶向的蜕皮激素受体 (EcR) 功能丧失会增加 dMyc 的表达及其细胞功能，如核糖体生物发生。此外，改变该组织中的 dMyc 水平足以影响动物的生长速度。最后，脂肪体中 EcR 的沉默引起的生长增加被 dMyc 的共沉默所抑制。总之，本工作揭示了 dMyc 在类固醇激素信号响应中对全身生长控制的意外功能。
