Brain size is controlled by the mammalian target of rapamycin (mTOR) in mice

Woo Yang Kim

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The number of neurons in the brain is mostly determined by neural progenitor proliferation and neurogenesis during embryonic development. Increase in postnatal brain size is largely dependent on cellular volume changes. The mammalian target of rapamycin (mTOR) signaling has been associated with cell proliferation and size determination in a variety of cell types. The role of mTOR signaling in neural development has been increasingly pursued due to its association with neurodevelopmental disorders and cancers. Surprisingly, however, there has been lack of in vivo genetic evidence that defines mTOR functions in neural progenitors during progenitor self-renewal and subsequent brain formation. Here, we discuss our recent evidence that mTOR signaling is required for the establishment of normal brain size during development. Mice lacking mTOR show smaller brain and reduced numbers of neural progenitors and neurons. Additionally, mTOR interacts with the Wnt signaling pathway in the control of neural progenitors. Our study establishes the mTOR signal as a key regulator of an evolutionarily conserved cascade that is responsible for vertebrate brain size.

Original languageEnglish (US)
Article numbere994377
JournalCommunicative and Integrative Biology
Volume8
Issue number1
DOIs
StatePublished - 2015

Fingerprint

Sirolimus
brain
mice
Brain
neurons
neurogenesis
neurodevelopment
Neurons
Wnt Signaling Pathway
Neurogenesis
Cell Size
cell proliferation
embryogenesis
Embryonic Development
Vertebrates
vertebrates
Cell Proliferation
neoplasms
Neoplasms
cells

Keywords

  • Brain size
  • GSK-3
  • mTOR
  • Neural progenitor
  • Neurogenesis

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)

Cite this

Brain size is controlled by the mammalian target of rapamycin (mTOR) in mice. / Kim, Woo Yang.

In: Communicative and Integrative Biology, Vol. 8, No. 1, e994377, 2015.

Research output: Contribution to journalArticle

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