Modulation of cell adhesion and motility in the immune system by Myo1f

Science. 2006 Oct 6;314(5796):136-9. doi: 10.1126/science.1131920.

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

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • CD18 Antigens / metabolism
  • Cell Adhesion*
  • Cell Degranulation
  • Cell Movement*
  • Chemotaxis, Leukocyte
  • Colony Count, Microbial
  • Cytoplasmic Granules / metabolism
  • Exocytosis
  • Immunity, Innate*
  • Ligands
  • Listeria monocytogenes / growth & development
  • Listeriosis / immunology*
  • Listeriosis / microbiology
  • Mice
  • Mice, Knockout
  • Myosin Type I / deficiency
  • Myosin Type I / genetics
  • Myosin Type I / physiology*
  • N-Formylmethionine Leucyl-Phenylalanine
  • Neutrophil Activation
  • Neutrophils / immunology
  • Neutrophils / physiology*

Substances

  • Actins
  • CD18 Antigens
  • Ligands
  • Myo1f protein, mouse
  • N-Formylmethionine Leucyl-Phenylalanine
  • Myosin Type I