論文

査読有り 最終著者 責任著者 国際誌
2021年7月20日

Oscillation of Cdc20-APC/C-mediated CAMDI stability is critical for cortical neuron migration.

The Journal of biological chemistry
  • Shohei Okuda
  • ,
  • Mariko Sato
  • ,
  • Saho Kato
  • ,
  • Shun Nagashima
  • ,
  • Ryoko Inatome
  • ,
  • Shigeru Yanagi
  • ,
  • Toshifumi Fukuda

297
2
開始ページ
100986
終了ページ
100986
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.jbc.2021.100986

Radial migration during cortical development is required for formation of the six-layered structure of the mammalian cortex. Defective migration of neurons is linked to several developmental disorders such as autism and schizophrenia. A unique swollen structure called the dilation is formed in migrating neurons and is required for movement of the centrosome and nucleus. However, the detailed molecular mechanism by which this dilation forms is unclear. We report that CAMDI, a gene whose deletion is associated with psychiatric-behavior, is degraded by Cdc20-APC/C cell-cycle machinery after centrosome migration into the dilation in mouse brain development. We also show that CAMDI is restabilized in the dilation until the centrosome enters the dilation, at which point it is once again immediately destabilized. CAMDI degradation is carried out by binding to Cdc20-APC/C via the destruction box (D-box) degron of CAMDI. CAMDI D-box mutant overexpression inhibits dilation formation and neuronal cell migration via maintaining the stabilized state of CAMDI. These results indicate that CAMDI is a substrate of the Cdc20-APC/C system and that the oscillatory regulation of CAMDI protein correlates with dilation formation for proper cortical migration.

リンク情報
DOI
https://doi.org/10.1016/j.jbc.2021.100986
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/34298015
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8353494
ID情報
  • DOI : 10.1016/j.jbc.2021.100986
  • PubMed ID : 34298015
  • PubMed Central 記事ID : PMC8353494

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