Mirth Christen Kerry, Riddiford Lynn M
Department of Biology, University of Washington, Seattle, WA 98195, USA.
Bioessays. 2007 Apr;29(4):344-55. doi: 10.1002/bies.20552.
Size control depends on both the regulation of growth rate and the control over when to stop growing. Studies of Drosophila melanogaster have shown that insulin and Target of Rapamycin (TOR) pathways play principal roles in controlling nutrition-dependent growth rates. A TOR-mediated nutrient sensor in the fat body detects nutrient availability, and regulates insulin signaling in peripheral tissues, which in turn controls larval growth rates. After larvae initiate metamorphosis, growth stops. For growth to stop at the correct time, larvae need to surpass a critical weight. Recently, it was found that the insulin-dependent growth of the prothoracic gland is involved in assessing when critical weight has been reached. Furthermore, mutations in DHR4, a repressor of ecdysone signaling, reduce critical weight and adult size. Thus, the mechanisms that control growth rates converge on those assessing size to ensure that the larvae attain the appropriate size at metamorphosis.
体型控制既取决于生长速率的调节,也取决于对何时停止生长的控制。对黑腹果蝇的研究表明,胰岛素和雷帕霉素靶蛋白(TOR)信号通路在控制营养依赖型生长速率方面发挥着主要作用。脂肪体中由TOR介导的营养传感器检测营养物质的可利用性,并调节外周组织中的胰岛素信号传导,进而控制幼虫的生长速率。幼虫开始变态后,生长停止。为了在正确的时间停止生长,幼虫需要超过一个临界体重。最近发现,前胸腺的胰岛素依赖性生长参与评估何时达到临界体重。此外,蜕皮激素信号转导的抑制因子DHR4发生突变会降低临界体重和成虫体型。因此,控制生长速率的机制与评估体型的机制相互汇聚,以确保幼虫在变态时达到合适的体型。