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Science 6 October 2006:
Vol. 314. no. 5796, pp. 136 - 139
DOI: 10.1126/science.1131920

Reports

Modulation of Cell Adhesion and Motility in the Immune System by Myo1f

Sangwon V. Kim,1* Wajahat Z. Mehal,1,3 Xuemei Dong,6 Volkmar Heinrich,7{dagger} Marc Pypaert,4,5 Ira Mellman,4,5 Micah Dembo,7 Mark S. Mooseker,4,8 Dianqing Wu,6{ddagger} Richard A. Flavell1,2§

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 ß2 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.

1 Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
2 Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA.
3 Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT 06520, USA.
4 Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06520, USA.
5 Ludwig Institute for Cancer Research, Yale University School of Medicine, New Haven, CT 06520, USA.
6 Department of Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, CT 06030, USA.
7 Department of Biomedical Engineering, Boston University, Boston, MA 02215, USA.
8 Departments of Molecular, Cellular and Developmental Biology, and Department of Pathology, Yale University, New Haven, CT 06511, USA.

* Present address: Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.

{dagger} Present address: Department of Biomedical Engineering, University of California Davis, Davis, CA 95616, USA.

{ddagger} Present address: Vascular Biology and Transplantation Program and Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, USA.

§ To whom correspondence should be addressed. E-mail: richard.flavell{at}yale.edu

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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Identification of an Evolutionarily Conserved Transcriptional Signature of CD8 Memory Differentiation That Is Shared by T and B Cells.
W. N. Haining, B. L. Ebert, A. Subrmanian, E. J. Wherry, Q. Eichbaum, J. W. Evans, R. Mak, S. Rivoli, J. Pretz, J. Angelosanto, et al. (2008)
J. Immunol. 181, 1859-1868
   Abstract »    Full Text »    PDF »
Tonic protein kinase A activity maintains inactive {beta}2 integrins in unstimulated neutrophils by reducing myosin light-chain phosphorylation: role of myosin light-chain kinase and Rho kinase.
C. D. Chilcoat, Y. Sharief, and S. L. Jones (2008)
J. Leukoc. Biol. 83, 964-971
   Abstract »    Full Text »    PDF »



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Science. ISSN 0036-8075 (print), 1095-9203 (online)