Key result
Bni1 drives elongation of randomly oriented actin cables in unpolarized cells, whereas Bnr1 and Bni1 mediate slower polymerization in polarized cells, with Myo2 acting as a motor for cable motility.
Identifies molecular mechanisms for the regulation of actin cable dynamics in yeast, suggesting fast actin reorganization is necessary for cell polarization fidelity.
Does not inform clinical practice; hypothesis-generating for actin dynamics in mammalian cell polarization.
Cell morphogenesis requires complex and rapid reorganization of the actin cytoskeleton. The budding yeast Saccharomyces cerevisiae is an invaluable model system for studying molecular mechanisms driving actin dynamics. Actin cables in yeast are formin-generated linear actin arrays that serve as tracks for directed intracellular transport by type V myosins. Cables are constantly reorganized throughout the cell cycle but the molecular basis for such dynamics remains poorly understood. By combining total internal reflection microscopy, quantitative image analyses and genetic manipulations we identify kinetically distinct subpopulations of cables that are differentially driven by formins and myosin. Bni1 drives elongation of randomly oriented actin cables in unpolarized cells, whereas both formins Bnr1 and Bni1 mediate slower polymerization of cables in polarized cells. Type V myosin Myo2 surprisingly acts as a motor for translational cable motility along the cell cortex. During polarization, cells change from fast to slow cable dynamics through spatio-temporal regulation of Bni1, Bnr1 and Myo2. In summary, we identify molecular mechanisms for the regulation of cable dynamics and suggest that fast actin reorganization is necessary for fidelity of cell polarization.
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Yu et al. (2011) studied Cell morphogenesis in budding yeast. Genetic manipulations of formins and myosin V was evaluated on Actin cable dynamics (elongation and motility). Bni1 drives elongation of randomly oriented actin cables in unpolarized cells, whereas Bnr1 and Bni1 mediate slower polymerization in polarized cells, with Myo2 acting as a motor for cable motility.
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