Structural abnormalities develop in the brain after ablation of the gene encoding nonmuscle myosin II-B heavy chain

Ablation of nonmuscle myosin heavy chain II-B (NMHC-B) in mice results in s evere hydrocephalus with enlargement of the lateral and third ventricles. A ll B*/B* mice died either during embryonic development or on the day of bir th (PO). Neurons cultured from superior cervical ganglia of B*/B* mice betw een embryonic day (E) 18 and P0 showed decreased rates of neurite outgrowth , and their growth cones had a distinctive narrow morphology compared with those from normal mice. Serial sections of E12.5, E13.5, and E15 mouse brai ns identified developmental defects in the ventricular neuroepithelium. On E12.5, disruption of the coherent ventricular surface and disordered cell m igration of neuroepithelial and differentiated cells were seen at various p oints in the ventricular walls. These abnormalities resulted in the formati on of rosettes in various regions of the brain and spinal cord. On E13.5 an d E15, disruption of the ventricular surface and aberrant protrusions of ne ural cells into the ventricles became more prominent. By E18.5 and P0, the defects in cells lining the ventricular wall resulted in an obstructive hyd rocephalus due to stenosis or occlusion of the third ventricle and cerebral aqueduct. These defects may be caused by abnormalities in the cell adhesiv e properties of neuroepithelial cells and suggest that NMHC-B is essential for both early and late developmental processes in the mammalian brain. Pub lished 2001 Wiley-Liss, inc.(dagger).