Non-muscle myosin IIA and IIB have separate but linked mechanical roles in mediating lamellipodia extension and actin network remodeling during cell spreading.
Distinguishes myosin IIA/IIB roles in motility; extends cell biology insights but leaves open relevance to cardiovascular models.
Non-muscle myosin II role has been implicated in the extension of lamellipodia, a critical step in the initiation of directed cell migration, invasion and other cellular processes, but the mechanistic details are limited to driving retrograde actin filaments. The present study reveals distinct localization of myosin IIA and IIB with an unexpected opposite mechanical roles in mediating lamellipodia extension during spreading. Attachment of cells to matrix is impaired in the absence of either isoforms, but differential regulation of focal contacts formation occurs in myosin IIA^-^; and IIB^-^; cells. Spreading cells expressing both isoforms display an organized actin network consisting of retrograde filaments, arcs and central filaments. Loss of actin arcs and central filaments occurs upon depletion of either myosin IIA or IIB, but myosin IIB^-^; cells displayed long parallel actin filaments elongated from cell edge. From these studies, a model for myosin IIA and IIB with separate, but linked mechanical roles in mediating lamellipodia extension is developed.
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Venkaiah Betapudi (2009) studied this question.
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