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. 2014 Apr 16;5:147. doi: 10.3389/fphys.2014.00147

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Copyright © 2014 Sato-Miyata, Muramatsu, Funakoshi, Tsuda and Aigaki.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Genetic manipulation of InR/Akt1/PI3K modifies the dilp2-induced lethality. Relative viability of the sd > dilp2 flies was determined in combination with loss of function mutations in InR, Akt1, or PI3K, which are components of the insulin/IGF signaling pathway. dilp2- induced semi-lethality was markedly improved by reduction of InR or Akt1, but enhanced by reduction of PTEN (A). Relative viability of the sd > dilp2 flies in combination with loss-of-function mutations in Tor and S6K (B). The Tor/S6K pathway may not contribute to mediating the semi- lethality of dilp2-overexpressing flies. Student t-test was performed to analyze statistical significance. ^*p < 0.05, ^**p < 0.01.