Regulation of Drosophila behavior by
neuropeptides and the circadian clock
Circadian control of adult eclosion
The final ecdysis to the adult, also called eclosion, is controlled by the circadian clock, which restricts emergence to a specific window of time. This “gating” of emergence depends on the activity of the central circadian pacemaker in the brain and on that of a peripheral clock located in the prothoracic gland (PG), which produces the molting hormone, ecdysone. We have recently shown that central brain clock neurons (in magenta) communicate with the PG clock by transmitting time information to PTTH neurons (in green) via the neuropeptide sNPF; the PTTH neurons in turn communicate with the PG via the PTTH neuropeptide, acting on its receptor encoded by the torso gene (see Selcho et al. (2017). Nature Comm 8:15563; doi: 10.1038/ncomms15563).
Our lab uses Drosophila to investigate how neuropeptides and the circadian clock regulate animal behavior. Much of our work focuses on ecdysis, the behavior used by all insects to shed the remains of the old exoskeleton at the end of every molt. Ecdysis is controlled by a number of neuropeptides and hormones, which regulate the precise order and timing of the different ecdysial behavioral subroutines. Two key neuropeptides are Ecdysis Triggering Hormone (ETH) and Eclosion Hormone (EH). The ecdysial sequence in triggered by the release of ETH, but we have recently shown that the response of the nervous system to ETH depends on a number of interacting neuropeptides downstream of ETH, including EH, CCAP (Crustacean cardioactive peptide), and bursicon (Kruger et al. 2015. Development 142, 4279-4287. doi: 10.1242/dev.126995; Mena et al. 2016. Elife 5: e19686. doi: 10.7554/eLife.19686).
Neuropeptide control of ecdysis behavior
Degenerate control of ecdysis by neuropeptides CCAP and PBURS.
Failures at the ecdysis to the pupal stage cause the head to remain in the thorax and the wings and legs to be short (white arrow and black arrowheads in C and D, respectively). (A) Flies mutant for CCAP expressed normal adult morphology. By contrast, flies mutant for pburs (B) showed abnormalities at pupal ecdysis a well as in adult post-ecdysis (e.g., in wing inflation). Interestingly, animals mutant for CCAP and pburs (C) showed a complete failure at pupal ecdysis, expressing defects that were more severe than those expressed by either mutant alone. (D) Pharate control fly, showing a normal head, and normal wing and leg extension. Lahr et al., (2012) J Neurosci. 32:6819-29. doi: 10.1523/JNEUROSCI.5301-11.2012.
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