APA
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Sasaki, S., Mori, D., Toyo-oka, K., Chen, A., Garrett-Beal, L., Muramatsu, M., … Hirotsune, S. (2005). Complete Loss of Ndel1 Results in Neuronal Migration Defects and Early Embryonic Lethality. Molecular and Cellular Biology, 25(17), 7812–7827.
Chicago/Turabian
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Sasaki, Shinji, D. Mori, K. Toyo-oka, Amy Chen, L. Garrett-Beal, M. Muramatsu, S. Miyagawa, et al. “Complete Loss of Ndel1 Results in Neuronal Migration Defects and Early Embryonic Lethality.” Molecular and Cellular Biology 25, no. 17 (2005): 7812–7827.
MLA
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Sasaki, Shinji, et al. “Complete Loss of Ndel1 Results in Neuronal Migration Defects and Early Embryonic Lethality.” Molecular and Cellular Biology, vol. 25, no. 17, 2005, pp. 7812–27.
BibTeX Click to copy
@article{shinji2005a,
title = {Complete Loss of Ndel1 Results in Neuronal Migration Defects and Early Embryonic Lethality},
year = {2005},
issue = {17},
journal = {Molecular and Cellular Biology},
pages = {7812-7827},
volume = {25},
author = {Sasaki, Shinji and Mori, D. and Toyo-oka, K. and Chen, Amy and Garrett-Beal, L. and Muramatsu, M. and Miyagawa, S. and Hiraiwa, N. and Yoshiki, A. and Wynshaw-Boris, A. and Hirotsune, S.}
}
ABSTRACT Regulation of cytoplasmic dynein and microtubule dynamics is crucial for both mitotic cell division and neuronal migration. NDEL1 was identified as a protein interacting with LIS1, the protein product of a gene mutated in the lissencephaly. To elucidate NDEL1 function in vivo, we generated null and hypomorphic alleles of Ndel1 in mice by targeted gene disruption. Ndel1 −/− mice were embryonic lethal at the peri-implantation stage like null mutants of Lis1 and cytoplasmic dynein heavy chain. In addition, Ndel1 −/− blastocysts failed to grow in culture and exhibited a cell proliferation defect in inner cell mass. Although Ndel1 +/− mice displayed no obvious phenotypes, further reduction of NDEL1 by making null/hypomorph compound heterozygotes (Ndel1 cko/− ) resulted in histological defects consistent with mild neuronal migration defects. Double Lis1 cko/+ -Ndel1 +/− mice or Lis1 +/− -Ndel1 +/− mice displayed more severe neuronal migration defects than Lis1 cko/+ -Ndel1 +/ + mice or Lis1 +/− -Ndel1 +/+ mice, respectively. We demonstrated distinct abnormalities in microtubule organization and similar defects in the distribution of β-COP-positive vesicles (to assess dynein function) between Ndel1 or Lis1-null MEFs, as well as similar neuronal migration defects in Ndel1- or Lis1-null granule cells. Rescue of these defects in mouse embryonic fibroblasts and granule cells by overexpressing LIS1, NDEL1, or NDE1 suggest that NDEL1, LIS1, and NDE1 act in a common pathway to regulate dynein but each has distinct roles in the regulation of microtubule organization and neuronal migration.
