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Correction for 'A bioenergetic mechanism for amoeboid-like cell motility profiles tested in a microfluidic electrotaxis assay' by Hagit Peretz-Soroka et al., Integr. Biol., 2017, DOI: .

The amoeboid-like cell motility is known to be driven by the acidic enzymatic hydrolysis of ATP in the actin-myosin system. However, the electro-mechano-chemical coupling, whereby the free energy of ATP hydrolysis is transformed into the power of electrically polarized cell movement, is poorly understood. Previous experimental studies showed that actin filaments motion, cytoplasmic streaming, and muscle contraction can be reconstituted under actin-activated ATP hydrolysis by soluble non-filamentous myosin fragments. Thus, biological motility was demonstrated in the absence of a continuous protein network. These results lead to an integrative conceptual model for cell motility, which advocates an active role played by intracellular proton currents and cytoplasmic streaming (iPC-CS). In this model, we propose that protons and fluid currents develop intracellular electric polarization and pressure gradients, which generate an electro-hydrodynamic mode of amoeboid motion. Such energetic proton currents and active streaming are considered to be mainly driven by stereospecific ATP hydrolysis through myosin heads along oriented actin filaments. Key predictions of this model are supported by microscopy visualization and in-depth sub-population analysis of purified human neutrophils using a microfluidic electrotaxis assay. Three distinct phases in cell motility profiles, morphology, and cytoplasmic streaming in response to physiological ranges of chemoattractant stimulation and electric field application are revealed. Our results support an intrinsic electric dipole formation linked to different patterns of cytoplasmic streaming, which can be explained by the iPC-CS model. Collectively, this alternative biophysical mechanism of cell motility provides new insights into bioenergetics with relevance to potential new biomedical applications.

Chemotaxis is a classic mechanism for guiding cell migration and an important topic in both fundamental cell biology and health sciences. Neutrophils are a widely used model to study eukaryotic cell migration and neutrophil chemotaxis itself can lead to protective or harmful immune actions to the body. While much has been learnt from past research about how neutrophils effectively navigate through a chemoattractant gradient, many interesting questions remain unclear. For example, while it is tempting to model neutrophil chemotaxis using the well-established biased random walk theory, the experimental proof was challenged by the cell's highly persistent migrating nature. A special experimental design is required to test the key predictions from the random walk model. Another question that has interested the cell migration community for decades concerns the existence of chemotactic memory and its underlying mechanism. Although chemotactic memory has been suggested in various studies, a clear quantitative experimental demonstration will improve our understanding of the migratory memory effect. Motivated by these questions, we developed a microfluidic cell migration assay (so-called dual-docking chip or D 2 -Chip) that can test both the biased random walk model and the memory effect for neutrophil chemotaxis on a single chip enabled by multi-region gradient generation and dual-region cell alignment. Our results provide experimental support for the biased random walk model and chemotactic memory for neutrophil chemotaxis. Quantitative data analyses provide new insights into neutrophil chemotaxis and memory by making connections to entropic disorder, cell morphology and oscillating migratory response.