Walkiewicz Magdalena A, Stern Michael
Department of Biochemistry and Cell Biology, Rice University, Houston, Texas, United States of America.
PLoS One. 2009;4(4):e5072. doi: 10.1371/journal.pone.0005072. Epub 2009 Apr 7.
Mechanisms by which attainment of specific body sizes trigger developmental transitions to adulthood (e.g. puberty or metamorphosis) are incompletely understood. In Drosophila, metamorphosis is triggered by ecdysone synthesis from the prothoracic gland (PG), whereas growth rate is increased by insulin/insulin growth factor signalling (IIS). Transgene-induced activation of PI3K, the major effector of IIS, within the PG advances the onset of metamorphosis via precocious ecdysone synthesis, raising the possibility that IIS triggers metamorphosis via PI3K activation in the PG. Here we show that blocking the protein kinase A (PKA) pathway in the insulin producing cells (IPCs) increases IIS. This increased IIS increases larval growth rate and also advances the onset of metamorphosis, which is accompanied by precocious ecdysone synthesis and increased transcription of at least one ecdysone biosynthetic gene. Our observations suggest that IIS is regulated by PKA pathway activity in the IPCs. In addition, taken together with previous findings, our observations are consistent with the possibility that, in Drosophila, attainment of a specific body size triggers metamorphosis via the IIS-mediated activation of PI3K and hence ecdysone synthesis in the PG.
特定体型的达成引发向成年期发育转变（如青春期或变态）的机制尚未完全明了。在果蝇中，变态由前胸腺（PG）合成蜕皮激素触发，而生长速率则通过胰岛素/胰岛素生长因子信号传导（IIS）提高。转基因诱导PG内IIS的主要效应器PI3K激活，通过早熟的蜕皮激素合成提前变态的起始，这增加了IIS通过激活PG中的PI3K触发变态的可能性。在此我们表明，阻断胰岛素产生细胞（IPC）中的蛋白激酶A（PKA）途径会增加IIS。这种增加的IIS提高了幼虫生长速率，也提前了变态的起始，伴随有早熟的蜕皮激素合成以及至少一个蜕皮激素生物合成基因转录的增加。我们的观察结果表明，IIS受IPC中PKA途径活性的调节。此外，结合先前的研究结果，我们的观察结果与以下可能性一致：在果蝇中，特定体型的达成通过IIS介导的PI3K激活从而PG中的蜕皮激素合成触发变态。
