DLin-7 Is Required in Postsynaptic Lamina Neurons to Prevent Light-Induced Photoreceptor Degeneration in Drosophila
Current Biology. 2013-07-01; 23(14): 1349-1354
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1. Curr Biol. 2013 Jul 22;23(14):1349-54. doi: 10.1016/j.cub.2013.05.060. Epub 2013
DLin-7 is required in postsynaptic lamina neurons to prevent light-induced
photoreceptor degeneration in Drosophila.
Soukup SF(1), Pocha SM, Yuan M, Knust E.
(1)Max Planck Institute of Molecular Cell Biology and Genetics,
Pfotenhauerstrasse 108, 01307 Dresden, Germany.
Inherited retinal degeneration in humans is caused by mutations in a wide
spectrum of genes that regulate photoreceptor development and homeostasis. Many
of these genes are structurally and functionally conserved in Drosophila, making
the fly eye an ideal system in which to study the cellular and molecular basis of
blindness. DLin-7, the ortholog of vertebrate MALS/Veli, is a core component of
the evolutionarily conserved Crumbs complex. Mutations in any core member of the
Crb complex lead to retinal degeneration in Drosophila. Strikingly, mutations in
the human ortholog, CRB1, result in retinitis pigmentosa 12 (RP12) and Leber
congenital amaurosis, two severe retinal dystrophies. Unlike Crumbs, DLin-7 is
expressed not only in photoreceptor cells but also in postsynaptic lamina
neurons. Here, we show that DLin-7 is required in postsynaptic neurons, but not
in photoreceptors such as Crumbs, to prevent light-dependent retinal
degeneration. At the photoreceptor synapse, DLin-7 acts as part of a conserved
DLin-7/CASK/DlgS97 complex required to control the number of capitate projections
and active zones, important specializations in the photoreceptor synapse that are
essential for proper neurotransmission. These results are the first to
demonstrate that a postsynaptically acting protein prevents light-dependent
photoreceptor degeneration and describe a novel, Crumbs-independent mechanism for
Copyright © 2013 Elsevier Ltd. All rights reserved.
PMID: 23850283 [Indexed for MEDLINE]