Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN 55455, USA.
Science. 2009 Dec 4;326(5958):1403-5. doi: 10.1126/science.1176450.
Holometabolous insects undergo complete metamorphosis to become sexually mature adults. Metamorphosis is initiated by brain-derived prothoracicotropic hormone (PTTH), which stimulates the production of the molting hormone ecdysone via an incompletely defined signaling pathway. Here we demonstrate that Torso, a receptor tyrosine kinase that regulates embryonic terminal cell fate in Drosophila, is the PTTH receptor. Trunk, the embryonic Torso ligand, is related to PTTH, and ectopic expression of PTTH in the embryo partially rescues trunk mutants. In larvae, torso is expressed specifically in the prothoracic gland (PG), and its loss phenocopies the removal of PTTH. The activation of Torso by PTTH stimulates extracellular signal-regulated kinase (ERK) phosphorylation, and the loss of ERK in the PG phenocopies the loss of PTTH and Torso. We conclude that PTTH initiates metamorphosis by activation of the Torso/ERK pathway.
完全变态的昆虫经历完全变态,成为性成熟的成虫。变态由脑源性前胸腺激素 (PTTH) 启动,后者通过不完全定义的信号通路刺激蜕皮激素的产生。在这里,我们证明了 Torso,一种在果蝇中调节胚胎末端细胞命运的受体酪氨酸激酶,是 PTTH 受体。Trunk,胚胎 Torso 配体,与 PTTH 有关,胚胎中异位表达 PTTH 部分挽救了 trunk 突变体。在幼虫中,torso 特异性表达于前胸腺 (PG),其缺失表型类似于 PTTH 的缺失。PTTH 通过激活 Torso 来刺激细胞外信号调节激酶 (ERK) 的磷酸化,而 PG 中 ERK 的缺失类似于 PTTH 和 Torso 的缺失。我们得出结论,PTTH 通过激活 Torso/ERK 途径启动变态。