Juvenile hormone reveals mosaic developmental programs in the metamorphosing optic lobe of Drosophila melanogaster.

Lynn M Riddiford,James W Truman,Aljoscha Nern

doi:10.1242/bio.034025

Lynn M Riddiford, James W Truman + Show 1 more

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https://doi.org/10.1242/bio.034025

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Abstract

ABSTRACTThe development of the adult optic lobe (OL) of Drosophila melanogaster is directed by a wave of ingrowth of the photoreceptors over a 2-day period at the outset of metamorphosis, which is accompanied by the appearance of the pupal-specific transcription factor Broad-Z3 (Br-Z3) and expression of early drivers in OL neurons. During this time, there are pulses of ecdysteroids that time the metamorphic events. At the outset, the transient appearance of juvenile hormone (JH) prevents precocious development of the OL caused by the ecdysteroid peak that initiates pupariation, but the artificial maintenance of JH after this time misdirects subsequent development. Axon ingrowth, Br-Z3 appearance and the expression of early drivers were unaffected, but aspects of later development such as the dendritic expansion of the lamina monopolar neurons and the expression of late drivers were suppressed. This effect of the exogenous JH mimic (JHM) pyriproxifen is lost by 24 h after pupariation. Part of this effect of JHM is due to its suppression of the appearance of ecdysone receptor EcR-B1 that occurs after pupation and during early adult development.

Highlights

In insects, ecdysone causes molting and metamorphosis and juvenile hormone (JH) prevents metamorphosis and is critical for the normal growth and development of the immature stage (Nijhout, 1995; Truman et al, 2006)
The neuropils are organized into discrete lamina cartridges and medulla columns that are organized around sets of photoreceptors
The photoreceptors R1-R6 terminate in the lamina cartridges, while R7 and R8 extend into the medulla columns

Summary

Introduction

Ecdysone (a steroid hormone) causes molting and metamorphosis and juvenile hormone (JH) (a sesquiterpenoid hormone) prevents metamorphosis and is critical for the normal growth and development of the immature stage (Nijhout, 1995; Truman et al, 2006). In most insects larval cells are reprogrammed for metamorphosis by ecdysone acting in the absence of JH (Riddiford, 1994). In Drosophila larval cells die except in the nervous system and the Malpighian tubules, and the adult is formed from imaginal discs and imaginal precursor cells (Fristrom and Fristrom, 1993). Drosophila larvae are mosaic in terms of their sensitivity to JH. For example, the imaginal discs are insensitive to JH, whereas the abdominal histoblasts that make the adult cuticle are sensitive (Postlethwait, 1974; Zhou and Riddiford, 2002). The Janelia Research Campus, Howard Hughes Medical Institute, 19700 Helix Drive, Ashburn, VA 20147, USA. *Present address: Friday Harbor Laboratories, University of Washington, Friday Harbor, WA 98250, USA The Janelia Research Campus, Howard Hughes Medical Institute, 19700 Helix Drive, Ashburn, VA 20147, USA. *Present address: Friday Harbor Laboratories, University of Washington, Friday Harbor, WA 98250, USA

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