期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2015
卷号：112
期号：5
页码：1452-1457
DOI：10.1073/pnas.1414966112
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：SignificanceMetamorphosis is an important biological process by which animals alter their body structures to become sexually mature adults. We discovered that tyramine signaling through the {beta}3-octopamine receptor plays an essential role in producing the steroid hormone ecdysone, which is critical for metamorphosis. Based on our observations, we propose that monoamine signaling acts downstream of a body size checkpoint that allows metamorphosis to occur only when a critical body weight is attained during larval development and nutrients are sufficiently abundant. This work also provides a new perspective on an evolutionarily conserved monoaminergic regulation of steroid hormone production during developmental transitions such as metamorphosis. This study provides a new understanding of how metamorphosis is coordinately regulated by nutritional conditions and developmental timing. 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.
