A Toll-receptor map underlies structural brain plasticity
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.
Data availability
All data generated or analysed during this study are included in the manuscript and supporting files.
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Author details
Funding
Biotechnology and Biological Sciences Research Council (BB/P004997/1)
- Alicia Hidalgo
Biotechnology and Biological Sciences Research Council (BB/R017034/1)
- Alicia Hidalgo
EU Marie Curie-Sklodowska Fellowship (NPN)
- Jill S Wentzell
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Hugo J Bellen, Baylor College of Medicine, United States
Version history
- Received: October 14, 2019
- Accepted: February 12, 2020
- Accepted Manuscript published: February 18, 2020 (version 1)
- Version of Record published: March 17, 2020 (version 2)
Copyright
© 2020, Li et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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