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Dictyostelium myosin IK is involved in the maintenance of cortical tension and affects motility and phagocytosis

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Schwarz,  Eva C.
Department of Molecular Cell Research, Max Planck Institute for Medical Research, Max Planck Society;

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Neuhaus,  Eva Maria
Department of Molecular Cell Research, Max Planck Institute for Medical Research, Max Planck Society;

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Kistler,  Claudia
Department of Biomedical Optics, Max Planck Institute for Medical Research, Max Planck Society;

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Henkel,  Andreas Wolfram
Department of Biomedical Optics, Max Planck Institute for Medical Research, Max Planck Society;

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Soldati,  Thierry
Department of Biomedical Optics, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Schwarz, E. C., Neuhaus, E. M., Kistler, C., Henkel, A. W., & Soldati, T. (2000). Dictyostelium myosin IK is involved in the maintenance of cortical tension and affects motility and phagocytosis. Journal of Cell Science, 113, 621-633. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/10652255.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0027-A9BC-F
Abstract
Dictyostelium discoideum myosin Ik (MyoK) is a novel type of myosin distinguished by a remarkable architecture. MyoK is related to class I myosins but lacks a cargo-binding tail domain and carries an insertion in a surface loop suggested to modulate motor velocity. This insertion shows similarity to a secondary actin-binding site present in the tail of some class I myosins, and indeed a GST-loop construct binds actin. Probably as a consequence, binding of MyoK to actin was not only ATP- but also salt-dependent. Moreover, as both binding sites reside within its motor domain and carry potential sites of regulation, MyoK might represent a new form of actin crosslinker. MyoK was distributed in the cytoplasm with a significant enrichment in dynamic regions of the cortex. Absence of MyoK resulted in a drop of cortical tension whereas overexpression led to significantly increased tension. Absence and overexpression of MyoK dramatically affected the cortical actin cytoskeleton and resulted in reduced initial rates of phagocytosis. Cells lacking MyoK showed excessive ruffling, mostly in the form of large lamellipodia, accompanied by a thicker basal actin cortex. At early stages of development, aggregation of myoK null cells was slowed due to reduced motility. Altogether, the data indicate a distinctive role for MyoK in the maintenance and dynamics of the cell cortex.