The Journal of Experimental Medicine
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Published online August 6, 2007
doi:10.1084/jem.20062647
The Journal of Experimental Medicine, Vol. 204, No. 9, 2031-2038
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Sakata et al.
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BRIEF DEFINITIVE REPORT

 Impaired T lymphocyte trafficking in mice deficient in an actin-nucleating protein, mDia1

Daiji Sakata1, Hiroyuki Taniguchi1,2, Shingo Yasuda1,2, Aki Adachi-Morishima1, Yoko Hamazaki3, Rika Nakayama4, Takashi Miki1, Nagahiro Minato3, and Shuh Narumiya1

1 Department of Pharmacology, 2 Horizontal Medical Research Organization, and 3 Department of Immunology and Cell Biology, Kyoto University Faculty of Medicine, Kyoto 606-8501, Japan
4 Laboratory for Animal Resources and Genetic Engineering, Center for Developmental Biology, RIKEN Kobe Institute, Kobe 650-0047, Japan

CORRESPONDENCE Shuh Narumiya: snaru{at}mfour.med.kyoto-u.ac.jp

Trafficking of immune cells is controlled by directed migration of relevant cells toward chemotactic signals. Actin cytoskeleton undergoes continuous remodeling and serves as machinery for cell migration. The mDia family of formins and the Wiskott-Aldrich syndrome protein (WASP)–Arp2/3 system are two major actin nucleating–polymerizing systems in mammalian cells, with the former producing long straight actin filaments and the latter producing branched actin meshwork. Although much is known about the latter, the physiological functions of mDia proteins are unclear. We generated mice deficient in one mDia isoform, mDia1. Although mDia1–/– mice were born and developed without apparent abnormality, mDia1–/– T lymphocytes exhibited impaired trafficking to secondary lymphoid organs in vivo and showed reduced chemotaxis, little actin filament formation, and impaired polarity in response to chemotactic stimuli in vitro. Similarly, mDia1–/– thymocytes showed reduced chemotaxis and impaired egression from the thymus. These results suggest that mDia1 plays a distinct role in chemotaxis in T lymphocyte trafficking.

D. Sakata, H. Taniguchi, and S. Yasuda contributed equally to this work.


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