| First Author | Nakanishi K | Year | 2019 |
| Journal | Cereb Cortex | Volume | 29 |
| Issue | 9 | Pages | 3738-3751 |
| PubMed ID | 30307479 | Mgi Jnum | J:296732 |
| Mgi Id | MGI:6469792 | Doi | 10.1093/cercor/bhy253 |
| Citation | Nakanishi K, et al. (2019) Isozyme-Specific Role of SAD-A in Neuronal Migration During Development of Cerebral Cortex. Cereb Cortex 29(9):3738-3751 |
| abstractText | 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. |
