Abstract
Although class I myosins are known to play a wide range of roles, the physiological function of long-tailed class I myosins in vertebrates remains elusive. We demonstrated that one of these proteins, Myo1f, is expressed predominantly in the mammalian immune system. Cells from Myo1f-deficient mice exhibited abnormally increased adhesion and reduced motility, resulting from augmented exocytosis of beta2 integrin-containing granules. Also, the cortical actin that co-localizes with Myo1f was reduced in Myo1f-deficient cells. In vivo, Myo1f-deficient mice showed increased susceptibility to infection by Listeria monocytogenes and an impaired neutrophil response. Thus, Myo1f directs immune cell motility and innate host defense against infection.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Actins / metabolism
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Animals
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CD18 Antigens / metabolism
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Cell Adhesion*
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Cell Degranulation
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Cell Movement*
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Chemotaxis, Leukocyte
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Colony Count, Microbial
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Cytoplasmic Granules / metabolism
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Exocytosis
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Immunity, Innate*
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Ligands
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Listeria monocytogenes / growth & development
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Listeriosis / immunology*
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Listeriosis / microbiology
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Mice
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Mice, Knockout
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Myosin Type I / deficiency
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Myosin Type I / genetics
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Myosin Type I / physiology*
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N-Formylmethionine Leucyl-Phenylalanine
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Neutrophil Activation
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Neutrophils / immunology
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Neutrophils / physiology*
Substances
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Actins
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CD18 Antigens
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Ligands
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Myo1f protein, mouse
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N-Formylmethionine Leucyl-Phenylalanine
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Myosin Type I