GSBS Student Publications


Cortical actin turnover during cytokinesis requires myosin II

Student Author(s)

Minakshi Guha

GSBS Program

Cancer Biology

UMMS Affiliation

Department of Physiology



Document Type


Medical Subject Headings

Actins; Animals; Calcium-Calmodulin-Dependent Protein Kinases; Cells, Cultured; Cytokinesis; Fluorescence Recovery After Photobleaching; Heterocyclic Compounds with 4 or More Rings; Myosin Type II; Protein Transport; Protozoan Proteins; Quinolinium Compounds; Rats


Cell and Developmental Biology | Life Sciences | Medicine and Health Sciences


The involvement of myosin II in cytokinesis has been demonstrated with microinjection, genetic, and pharmacological approaches; however, the exact role of myosin II in cell division remains poorly understood. To address this question, we treated dividing normal rat kidney (NRK) cells with blebbistatin, a potent inhibitor of the nonmuscle myosin II ATPase. Blebbistatin caused a strong inhibition of cytokinesis but no detectable effect on the equatorial localization of actin or myosin. However, whereas these filaments dissociated from the equator in control cells during late cytokinesis, they persisted in blebbistatin-treated cells over an extended period of time. The accumulation of equatorial actin was caused by the inhibition of actin filament turnover, as suggested by a 2-fold increase in recovery half-time after fluorescence photobleaching. Local release of blebbistatin at the equator caused localized accumulation of equatorial actin and inhibition of cytokinesis, consistent with the function of myosin II along the furrow. However, treatment of the polar region also caused a high frequency of abnormal cytokinesis, suggesting that myosin II may play a second, global role. Our observations indicate that myosin II ATPase is not required for the assembly of equatorial cortex during cytokinesis but is essential for its subsequent turnover and remodeling.

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Citation: Curr Biol. 2005 Apr 26;15(8):732-6. Link to article on publisher's site

DOI of Published Version


Related Resources

Link to article in PubMed

Journal Title

Current biology : CB

PubMed ID