Increased insulin/insulin growth factor signaling advances the onset of metamorphosis in Drosophila.
Increased insulin/insulin growth factor signaling advances the onset of metamorphosis in Drosophila.
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DOI：
10.1371/journal.pone.0005072
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发表时间：
2009
期刊：
影响因子：
3.7
通讯作者：
Stern M
中科院分区：
文献类型：
--
作者：
Walkiewicz MA;Stern M
达到特定体型引发发育过渡到成年期(例如青春期或变态)的机制还不完全清楚。在果蝇中，变态是由前胸腺(PG)的蜕皮激素合成触发的，而生长速度是由胰岛素/胰岛素生长因子信号(IIS)加速的。转基因诱导的PG内IIS的主要效应分子PI3K的激活通过早熟蜕皮酮的合成促进了变态的开始，增加了IIS通过PI3K在PG中激活而触发变态的可能性。在这里，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增加了幼虫的生长速度，也加快了变态的开始，变态伴随着早熟蜕皮激素合成和至少一个蜕皮激素生物合成基因的转录增加。我们的观察结果表明，IIS受IPC中PKA途径活性的调节。此外，结合以前的发现，我们的观察结果与这样一种可能性是一致的，即在果蝇中，获得特定的身体尺寸通过IIS介导的PI3K激活触发变态，从而在PG中合成蜕皮激素。
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.
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