2019年8月14日
Isozyme-Specific Role of SAD-A in Neuronal Migration During Development of Cerebral Cortex.
Cerebral cortex (New York, N.Y. : 1991)
- 巻
- 29
- 号
- 9
- 開始ページ
- 3738
- 終了ページ
- 3751
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1093/cercor/bhy253
- 出版者・発行元
- Oxford University Press ({OUP})
SAD kinases regulate presynaptic vesicle clustering and neuronal polarization. A previous report demonstrated that Sada-/- and Sadb-/- double-mutant mice showed perinatal lethality with a severe defect in axon/dendrite differentiation, but their single mutants did not. These results indicated that they were functionally redundant. Surprisingly, we show that on a C57BL/6N background, SAD-A is essential for cortical development whereas SAD-B is dispensable. Sada-/- mice died within a few days after birth. Their cortical lamination pattern was disorganized and radial migration of cortical neurons was perturbed. Birth date analyses with BrdU and in utero electroporation using pCAG-EGFP vector showed a delayed migration of cortical neurons to the pial surface in Sada-/- mice. Time-lapse imaging of these mice confirmed slow migration velocity in the cortical plate. While the neurites of hippocampal neurons in Sada-/- mice could ultimately differentiate in culture to form axons and dendrites, the average length of their axons was shorter than that of the wild type. Thus, analysis on a different genetic background than that used initially revealed a nonredundant role for SAD-A in neuronal migration and differentiation.
- リンク情報
- ID情報
-
- DOI : 10.1093/cercor/bhy253
- ISSN : 1047-3211
- ORCIDのPut Code : 51515083
- PubMed ID : 30307479
- PubMed Central 記事ID : PMC7335017