期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 112, 期 5, 页码 1452-1457出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1414966112
关键词
Drosophila; ecdysone; monoamine; prothoracic gland; metamorphosis
资金
- Japan Society for the Promotion of Science (JSPS)
- Ministry of Education, Culture, Sport, Science and Technology of Japan
- PRESTO/JST
- Inamori Foundation
- Naito Foundation
- JSPS fellowships
- Grants-in-Aid for Scientific Research [12J40063] Funding Source: KAKEN
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, beta 3-octopamine receptor (Oct beta 3R), 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 Oct beta 3R 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.
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