Author
Li, GuiyiForero, 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
Affiliation
Univ Arizona, Coll Sci, NeurosciIssue Date
2020-02-18
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ELIFE SCIENCES PUBLICATIONS LTDCitation
eLife 2020;9:e52743Journal
ELIFERights
Copyright © Li et al. This article is distributed under the terms of the Creative Commons Attribution License.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.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.Note
Open access journalISSN
2050-084XPubMed ID
32066523Version
Final published versionae974a485f413a2113503eed53cd6c53
10.7554/eLife.52743
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Except where otherwise noted, this item's license is described as Copyright © Li et al. This article is distributed under the terms of the Creative Commons Attribution License.
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