This review highlights the role of ROCK protein kinase in regulating stress fibre formation and actomyosin contractility in non-muscle cells.
ROCK centrality in stress fibre control suggests candidate targets for vascular contractility disorders; leaves open validation in disease models.
Animal cell movement is effected through a combination of protrusive and contractile events. Non-muscle cells contain stress fibres - bundles of actomyosin that are the major mediators of cell contraction and that can be compared to the highly organised actomyosin arrays of muscle cells. Recent studies have defined regulatory mechanisms that control stress fibre formation, placing the ROCK protein kinase at the centre of a complex signalling network controlling actomyosin contractility and stress fibre assembly. As we uncover the details of stress fibre construction, it is becoming clear that different categories of stress fibres exist. Some of these structures are less suited for cell motility and more suited to static contraction. In keeping with this, many specialised contractile cell types use stress fibres to remodel tissues and extracellular matrix.
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Stéphanie Pellegrin (2007) studied this question.
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