Coupling Neuropeptide Levels to Structural Plasticity in Drosophila Clock Neurons.
Current Biology. 2020-08-01; 30(16): 3154-3166.e4
DOI: 10.1016/j.cub.2020.06.009
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Herrero A(1), Yoshii T(2), Ispizua JI(1), Colque C(1), Veenstra JA(3), Muraro NI(1), Ceriani MF(4).
Author information:
(1)Laboratorio de Genética del Comportamiento, Fundación Instituto Leloir, IIB-BA
CONICET, Av. Patricias Argentinas 435, 1405 Buenos Aires, Argentina.
(2)Graduate School of Natural Science and Technology, Okayama University, Okayama
700-8530, Japan.
(3)INCIA UMR 5287 CNRS, Université de Bordeaux, allée Geoffroy St Hillaire, CS
50023, 33 615 Pessac Cedex, France.
(4)Laboratorio de Genética del Comportamiento, Fundación Instituto Leloir, IIB-BA
CONICET, Av. Patricias Argentinas 435, 1405 Buenos Aires, Argentina. Electronic
address: .
We have previously reported that pigment dispersing factor (PDF) neurons, which
are essential in the control of rest-activity cycles in Drosophila, undergo
circadian remodeling of their axonal projections, a phenomenon called circadian
structural plasticity. Axonal arborizations display higher complexity during the
day and become simpler at night, and this remodeling involves changes in the
degree of connectivity. This phenomenon depends on the clock present within the
ventrolateral neurons (LNvs) as well as in glia. In this work, we characterize in
detail the contribution of the PDF neuropeptide to structural plasticity at
different times across the day. Using diverse genetic strategies to temporally
restrict its downregulation, we demonstrate that even subtle alterations to PDF
cycling at the dorsal protocerebrum correlate with impaired remodeling,
underscoring its relevance for the characteristic morning spread; PDF released
from the small LNvs (sLNvs) and the large LNvs (lLNvs) contribute to the process.
Moreover, forced depolarization recruits activity-dependent mechanisms to mediate
growth only at night, overcoming the restriction imposed by the clock on membrane
excitability. Interestingly, the active process of terminal remodeling requires
PDF receptor (PDFR) signaling acting locally through the cyclic-nucleotide-gated
channel ion channel subunit A (CNGA). Thus, clock-dependent PDF signaling shapes
the connectivity of these essential clock neurons on daily basis.
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