Abstract

Ablation of nonmuscle myosin (NM) II-B and II-C in mice results in a defect in cardiac myocyte karyokinesis. More than 90% of the double knockout cardiac myocytes demonstrate defects in chromatid segregation and mitotic spindle formation. The requirement for NM II in karyokinesis is demonstrated in both the intact heart and in HL-1 atrial myocytes in culture

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