Increased insulin/insulin growth factor signaling advances the onset of metamorphosis in Drosophila

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 insul...

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Published inPloS one Vol. 4; no. 4; p. e5072
Main Authors Walkiewicz, Magdalena A, Stern, Michael
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 07.04.2009
Public Library of Science (PLoS)
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Summary: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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Conceived and designed the experiments: MAW MS. Performed the experiments: MAW MS. Analyzed the data: MAW MS. Wrote the paper: MS.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0005072