The actin-based molecular motors of the myosin family are encoded by multiple genes. Mammals possess two genes encoding long-tailed "amoeboid" Myo1e and Myo1f forms. Kim et al. now find that Myo1f negatively regulates the activity of neutrophils, the immune cells that engulf and kill bacteria. Myo1f did not directly influence phagocytic activity or the intracellular oxidative burst in these cells that eventually kills bacteria. However, cells from mice lacking Myo1f had reduced motility and increased adhesion caused by exocytosis of integrin-containing granules upon neutrophil stimulation. Myo1f deficiency also led to increased susceptibility to bacterial infection. Thus, Myo1f regulates the host response to infection by ensuring mobility of phagocytic cells through the modulation of integrin-dependent adhesion.
S. V. Kim, W. Z. Mehal, X. Dong, V. Heinrich, M. Pypaert, I. Mellman, M. Dembo, M. S. Mooseker, D. Wu, R. A. Flavell, Modulation of cell adhesion and motility in the immune system by Myo1f. Science 314, 136-139 (2006). [Abstract] [Full Text]