. Author manuscript; available in PMC: 2015 Jun 1.

Published in final edited form as: Circ Cardiovasc Genet. 2014 May 13;7(3):257–265. doi: 10.1161/CIRCGENETICS.113.000455

Table 1.

Phenotypes of NMII-B knockout and R709C mutant Mice

	Brain	Heart	Body Wall
B⁺/B⁺, B⁺/B-, B⁺/B^R709CN	None	None	None
B-/B-	Hydrocephalus, Abnormal neuronal migration, Disruption of neuroepithelial cell adhesion	Defect in cardiac myocyte cytokinesis, Decreased proliferation or early exit from mitosis of cardiac myocytes, Double outlet of right ventricle, Ventricular septal defect	None
B^R709CN/B^R709CN	Hydrocephalus, Abnormal neuronal migration, Disruption of neuroepithelial cell adhesion, Delayed cerebellum development	Defect in cardiac myocyte cytokinesis, Decreased proliferation and early exit from mitosis of cardiac myocytes, Double outlet of right ventricle, Ventricular septal defect	None
B⁺/B^R709C	None	None	Omphalocele (50%), Diaphragmatic herniation
B^R709C/B^R709C	Abnormal neuronal migration	Decreased proliferation and early exit from mitosis of cardiac myocytes, Double outlet of right ventricle, Ventricular septal defect, Defects in fusion and remodeling of the endocardiac cushions, Ectopia cordis (50%).	Cleft palate, Split lower sternum, Omphalocele, Diaphragmatic herniation

We have analyzed at least 10 mice for each genotype. The phenotypes seen in mutant mice are 100% penetrant except as indicated.