Active fluctuations of cytoplasmic actomyosin networks facilitate dynein-driven transport.

Abstract

Inside cells, molecular motors transport cargo through a highly crowded cytoplasmic environment. While such an environment is assumed to hinder transport, its precise effect remains unclear. Here, we investigated how the dynamics of cytoplasmic environments affect dynein-driven transport in <i>C. elegans</i> early embryos. In living embryos, we found that an artificial dynein-cargo complex exhibited significantly faster transport than <i>in vitro</i>, indicating an active acceleration mechanism <i>in vivo</i>. By altering the activity of actomyosin networks, we found that dynein-driven transport was accelerated by actomyosin-driven cytoplasmic fluctuations, with speed increasing upon myosin upregulation and decreasing upon its depletion. Furthermore, <i>in vitro</i> force measurements of dynein suggest that the asymmetric force response to random forces, generated by fluctuating dynamics of actomyosin networks, may contribute to acceleration. This study provides insights into a regulatory mechanism of molecular motors within fluctuating cytoplasm, harnessing cytoplasmic fluctuations to enhance transport efficiency in a highly crowded environment.