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. 2009 Apr 10;5(4):e1000452. doi: 10.1371/journal.pgen.1000452

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This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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Three proposed system states are depicted, reflecting the balance between kinase signaling and transcriptional feedback suppression: reproductive mode, in which kinase signaling predominates, activated via the insulin/IGF-1 receptor (DAF-2, here labeled Ins-R); longevity mode, wherein FOXO (DAF-16) prevails and suppresses kinase transcription; and hyperlongevity mode—in which switching between the first two modes is blocked, thus strongly favoring survival but with no possibility of resuming reproduction. State transitions are normally triggered by signaling modulators (e.g., insulin-like peptides [12] or SIR-2/14-3-3 complex [77]), to which age-1(mg44)-F2 mutants (“hyperlongevity” state) cannot respond.