A toll-receptor map underlies structural brain plasticity

Guiyi Li, Manuel G. Forero, Jill Wentzell, Ilgim Durmus, Reinhard Wolf, Niki Anthoney, Mieczyslaw Parker, Ruiying Jiang, Jacob Hasenauer, Nicholas Strausfeld, Martin Heisenberg, Alicia Hidalgo

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


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.

Original languageEnglish (US)
Article numbere52743
StatePublished - Feb 2020


  • Apoptosis
  • Brain
  • Cell death
  • Cell proliferation
  • Cell survival
  • Deadpan
  • Drosophila
  • JNK
  • MyD88
  • NFκB
  • Neurodegeneration
  • Neurogenesis
  • Neuron
  • Neuronal activity
  • Progenitor cell
  • Quiescence
  • Sarm
  • Structural plasticity
  • TLR
  • Toll
  • Weckle
  • Yorkie

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)


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