|  Help  |  About  |  Contact Us

Publication : Loss of cell adhesion causes hydrocephalus in nonmuscle myosin II-B-ablated and mutated mice.

First Author  Ma X Year  2007
Journal  Mol Biol Cell Volume  18
Issue  6 Pages  2305-12
PubMed ID  17429076 Mgi Jnum  J:127463
Mgi Id  MGI:3763786 Doi  10.1091/mbc.E07-01-0073
Citation  Ma X, et al. (2007) Loss of cell adhesion causes hydrocephalus in nonmuscle myosin II-B-ablated and mutated mice. Mol Biol Cell 18(6):2305-12
abstractText  Ablation of nonmuscle myosin (NM) II-B in mice during embryonic development leads to marked enlargement of the cerebral ventricles and destruction of brain tissue, due to hydrocephalus. We have identified a transient mesh-like structure present at the apical border of cells lining the spinal canal of mice during development. This structure, which only contains the II-B isoform of NM, also contains beta-catenin and N-cadherin, consistent with a role in cell adhesion. Ablation of NM II-B or replacement of NM II-B with decreased amounts of a mutant (R709C), motor-impaired NM II-B in mice results in collapse of the mesh-like structure and loss of cell adhesion. This permits the underlying neuroepithelial cells to invade the spinal canal and obstruct cerebral spinal fluid flow. These defects in the CNS of NM II-B-ablated mice seem to be the cause of hydrocephalus. Interestingly, the mesh-like structure and patency of the spinal canal can be restored by increasing expression of the motor-impaired NM II-B, which also rescues hydrocephalus. However, the mutant isoform cannot completely rescue neuronal cell migration. These studies show that the scaffolding properties of NM II-B play an important role in cell adhesion, thereby preventing hydrocephalus during mouse brain development.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

3 Authors

13 Bio Entities

0 Expression