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Fig. 1. Actin stress fibre structure. (A) Gerbil fibroma cell stained for non-muscle myosin (red) and  -actinin (green) reveals the periodic banding of these components on actin stress fibres. Reproduced with kind permission from (Peterson et al., 2004 ). (B) Models of stress fibre structure and contractility. Sarcomeric stress fibres have blocks of actin filaments of alternating polarity and bands of interdigitating non-muscle myosin. The structure is held together by -actinin and also crosslinked by non-muscle myosin. On contraction (right), myosin slides between the filaments, pulling them towards each other and closing the gap. In stress fibres with uniform polarity, myosin would not be able to cause contraction. In these structures myosin might be instead able to move along the filaments towards the plus (barbed) end. If this myosin was attached to cargo, transport towards the focal contact would occur. Whether the double-headed non-muscle myosin is able to perform this role is unknown, but single-headed myosins are known to be able to transport cargo along actin filaments. Ventral stress fibres show graded polarity and are formed by two fibres of uniform polarity joining at their minus (pointed) ends. Contraction of these structures could occur by myosin driving invasion of filaments in the central region into each bundle. The difference between this form of contraction and the sarcomeric model is that actin filaments become interleaved, which should give rise to mixed polarity of the bundle at the central region. Such contraction would require displacement of -actinin. (C) U2OS osteosarcoma cells stained for F-actin, displaying the three categories of actin stress fibres (dorsal, red; arcs, yellow; ventral, green). Reproduced with kind permission from (Hotulainen and Lappalainen, 2006). (D) Model of stress fibre formation. Dorsal stress fibres arise from focal contacts at the cell periphery and elongate up through the cell to join transverse arcs at the cell surface. Two dorsal stress fibres may meet at a transverse arc and draw down to the bottom of the cell to form a ventral stress fibre. This model is adapted from (Hotulainen and Lappalainen, 2006).
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catalytic subunit and the regulatory MBS (MYPT) subunit. Inhibition of myosin phosphatase activity downstream of RhoA increases MLC phosphorylation and hence increases actomyosin contractility. ROCK activity is inhibited by the Rho GTPase RhoE and by the small GTPases Rad and Gem.