Autocrine regulation of ecdysone synthesis by β3-octopamine receptor in the prothoracic gland is essential for Drosophila metamorphosis

Yuya Ohhara, Yuko Shimada-Niwa, Ryusuke Niwa, Yasunari Kayashima, Yoshiki Hayashi, Kazutaka Akagi, Hitoshi Ueda, Kimiko Yamakawa-Kobayashi, Satoru Kobayashi

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

In Drosophila, pulsed production of the steroid hormone ecdysone plays a pivotal role in developmental transitions such as metamorphosis. Ecdysone production is regulated in the prothoracic gland (PG) by prothoracicotropic hormone (PTTH) and insulin-like peptides (Ilps). Here, we show that monoaminergic autocrine regulation of ecdysone biosynthesis in the PG is essential for metamorphosis. PG-specific knockdown of a monoamine G protein-coupled receptor, β3-octopamine receptor (Octβ3R), resulted in arrested metamorphosis due to lack of ecdysone. Knockdown of tyramine biosynthesis genes expressed in the PG caused similar defects in ecdysone production and metamorphosis. Moreover, PTTH and Ilps signaling were impaired by Octβ3R knockdown in the PG, and activation of these signaling pathways rescued the defect in metamorphosis. Thus, monoaminergic autocrine signaling in the PG regulates ecdysone biogenesis in a coordinated fashion on activation by PTTH and Ilps. We propose that monoaminergic autocrine signaling acts downstream of a body size checkpoint that allows metamorphosis to occur when nutrients are sufficiently abundant.

Original languageEnglish
Pages (from-to)1452-1457
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume112
Issue number5
DOIs
Publication statusPublished - Feb 3 2015

Keywords

  • Drosophila
  • Ecdysone
  • Metamorphosis
  • Monoamine
  • Prothoracic gland

ASJC Scopus subject areas

  • General

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