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1. Cell Rep. 2018 Aug 7;24(6):1389-1396. doi: 10.1016/j.celrep.2018.07.012.
Pitpnc1a Regulates Zebrafish Sleep and Wake Behavior through Modulation of
Insulin-like Growth Factor Signaling.
Ashlin TG(1), Blunsom NJ(1), Ghosh M(2), Cockcroft S(3), Rihel J(4).
(1)Department of Neuroscience, Physiology and Pharmacology, University College
London, London WC1E 6BT, UK.
(2)Department of Cell and Developmental Biology, University College London,
London WC1E 6BT, UK.
(3)Department of Neuroscience, Physiology and Pharmacology, University College
London, London WC1E 6BT, UK. Electronic address: .
(4)Department of Cell and Developmental Biology, University College London,
London WC1E 6BT, UK. Electronic address: .
The lipid transporters of the phosphatidylinositol transfer protein (PITP) family
dictate phosphoinositide compartmentalization, and specific phosphoinositides
play crucial roles in signaling cascades, membrane traffic, ion channel
regulation, and actin dynamics. Although PITPs are enriched in the brain, their
physiological functions in neuronal signaling pathways in vivo remain ill
defined. We describe a CRISPR/Cas9-generated zebrafish mutant in a
brain-specific, conserved class II PITP member, pitpnc1a. Zebrafish pitpnc1a
mutants are healthy but display widespread aberrant neuronal activity and
increased wakefulness across the day-night cycle. The loss of Pitpnc1a increases
insulin-like growth factor (IGF) signaling in the brain, and inhibition of IGF
pathways is sufficient to rescue both neuronal and behavioral hyperactivity in
pitpnc1a mutants. We propose that Pitpnc1a-expressing neurons alter behavior via
modification of neuro-modulatory IGF that acts on downstream wake-promoting
Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.