NULL MUTATIONS OF VERTEBRATE NONMUSCLE MYOSIN HEAVY CHAINS

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Previous work from this laboratory demonstrated that ablation of the nonmuscle myosin II-B heavy chain (NMHC-B) in mice resulted in a cardiac ventricular septal defect and abnormalities of the aortic outflow tract. These B-/B- mice all demonstrated hydrocephalus and died in utero or just after birth (PO). Analysis of brains from E12.5, E13.5 and E15 mice identified developmental defects in the ventricular neuroepithelium. On E12.5, disruption of the cells lining the ventricular surface along with abnormal migration of the neuroepithelial cells was seen in parts of the ventricular wall. Identification of mitotic cells outside of the ventricular surface layer was consistent with an abnormality in interkinetic nuclear migration. On E13.5 and E15, there was a protrusion of cells into the ventricle and on E18.5 and PO, the defects in the ependymal cell layer resulted in stenosis of the cerebal aqueduct or obstruction of the fourth ventricle. Immunofluorescence staining using antibodies to NMHC-B as well as gamma-catenin showed localization of both epitopes to the ventricular surface. These findings raise the possibility that the defects observed in the brain may be related to an alteration in the adhesive properties of the cells.