Abstract

In both vertebrates and insects, developmental transition from the juvenile stage to adulthood is regulated by steroid hormones. In insects, the steroid hormone, 20-hydroxyecdysone (20E), elicits metamorphosis, thus promoting this transition, while the sesquiterpenoid juvenile hormone (JH) antagonizes 20E signaling to prevent precocious metamorphosis during the larval stages. However, not much is known about the mechanisms involved in cross-talk between these two hormones. In this study, we discovered that in the ring gland (RG) of Drosophila larvae, JH and 20E control each other’s biosynthesis. JH induces expression of a Krüppel-like transcription factor gene Kr-h1 in the prothoracic gland (PG), a portion of the RG that produces the 20E precursor ecdysone. By reducing both steroidogenesis autoregulation and PG size, high levels of Kr-h1 in the PG inhibit ecdysteriod biosynthesis, thus maintaining juvenile status. JH biosynthesis is prevented by 20E in the corpus allatum, the other portion of the RG that produces JH, to ensure the occurrence of metamorphosis. Hence, antagonistic actions of JH and 20E within the RG determine developmental transitions in Drosophila. Our study proposes a mechanism of cross-talk between the two major hormones in the regulation of insect metamorphosis.

Document Type

Article

Publication Date

1-2-2018

Notes/Citation Information

Published in PNAS, v. 115, no. 1, p. 139-144.

Copyright © 2017 the Author(s). Published by PNAS.

This open access article is distributed under Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND).

Digital Object Identifier (DOI)

https://doi.org/10.1073/pnas.1716897115

Funding Information

This study was supported by the National Science Foundation of China (Grant 31620103917), the National Key Research and Development Program of China (Grant 2016YFD0101900), the Chinese Academy of Sciences (Grant 173176001000162007), and the National Science Foundation of China (Grants 31330072 and 31572325) (to S. Li).

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This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1716897115/-/DCSupplemental.

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