| Literature DB >> 32066523 |
Guiyi Li1,2, Manuel G Forero3, Jill S Wentzell1, Ilgim Durmus1, Reinhard Wolf2, Niki C Anthoney1, Mieczyslaw Parker1, Ruiying Jiang1, Jacob Hasenauer1, Nicholas James Strausfeld2,4, Martin Heisenberg2, Alicia Hidalgo1.
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.Entities:
Keywords: D. melanogaster; Drosophila; MyD88; Toll; Yorkie; adul progenitor cells; adult neurogenesis; brain; critical period; neurodegeneration; neuron; neuronal activity; neuroscience; quiescence; structural plasticity; wek
Mesh:
Substances:
Year: 2020 PMID: 32066523 PMCID: PMC7077983 DOI: 10.7554/eLife.52743
Source DB: PubMed Journal: Elife ISSN: 2050-084X Impact factor: 8.140