Key result
Synthetic myofilaments fragment and compact membrane-bound actin by generating ~20 pN of compressive force.
Why the study?
Little is known about the interaction between individual myofilaments and membrane-bound actin filaments during cell cortex remodeling.
Single myofilaments can generate sufficient force (~20 pN) to buckle and break membrane-bound actin filaments, which may contribute to actin turnover and cortex reorganization during cytokinesis.
May inform cytoskeletal models in dividing cells; leaves open relevance to cardiac myocyte actin turnover.
Cell cortex remodeling during cell division is a result of myofilament-driven contractility of the cortical membrane-bound actin meshwork. Little is known about the interaction between individual myofilaments and membrane-bound actin filaments. Here we reconstituted a minimal actin cortex to directly visualize the action of individual myofilaments on membrane-bound actin filaments using TIRF microscopy. We show that synthetic myofilaments fragment and compact membrane-bound actin while processively moving along actin filaments. We propose a mechanism by which tension builds up between the ends of myofilaments, resulting in compressive stress exerted to single actin filaments, causing their buckling and breakage. Modeling of this mechanism revealed that sufficient force (∼20 pN) can be generated by single myofilaments to buckle and break actin filaments. This mechanism of filament fragmentation and compaction may contribute to actin turnover and cortex reorganization during cytokinesis.DOI:http://dx.doi.org/10.7554/eLife.00116.001.
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Vogel et al. (2013) studied this question. Synthetic myofilaments was evaluated on Actin filament buckling and breakage. Synthetic myofilaments fragment and compact membrane-bound actin by generating sufficient compressive force (~20 pN) to cause filament buckling and breakage.
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