Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12313/2123
Title: A Toll-receptor map underlies structural brain plasticity
Authors: Li, Guiyi
Forero, Manuel G.
Wentzell, Jill S.
Durmus, Ilgim
Wolf, Reinhard
Anthoney, Niki C.
Parker, Mieczyslaw
Jiang, Ruiying
Hasenauer, Jacob
Strausfeld, Nicholas James
Heisenberg, Martin
Hidalgo, Alicia
Keywords: D. melanogaster
Drosophila
MyD88
Toll
Yorkie
Adult progenitor cells
Adult neurogenesis
Brain
Critical period
Neurodegeneration
Neuron
Neuronal activity
Neuroscience
Quiescence
Tructural plasticity
Wek
Issue Date: 18-Feb-2020
Publisher: eLife
Citation: Li G, Forero MG, Wentzell JS, et al. A Toll-receptor map underlies structural brain plasticity. Elife. 2020;9:e52743. Published 2020 Feb 18. doi:10.7554/eLife.52743
Abstract: Experience alters brain structure, but the underlying mechanism remained unknown. Structural plasticity reveals that brain function is encoded in generative changes to cells that compete with destructive processes driving neurodegeneration. At an adult critical period, experience increases fiber number and brain size in Drosophila. Here, we asked if Toll receptors are involved. Tolls demarcate a map of brain anatomical domains. Focusing on Toll-2, loss of function caused apoptosis, neurite atrophy and impaired behaviour. Toll-2 gain of function and neuronal activity at the critical period increased cell number. Toll-2 induced cycling of adult progenitor cells via a novel pathway, that antagonized MyD88-dependent quiescence, and engaged Weckle and Yorkie downstream. Constant knock-down of multiple Tolls synergistically reduced brain size. Conditional over-expression of Toll-2 and wek at the adult critical period increased brain size. Through their topographic distribution, Toll receptors regulate neuronal number and brain size, modulating structural plasticity in the adult brain.
URI: https://pubmed.ncbi.nlm.nih.gov/32066523/
ISSN: 2050-084X
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