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

Daiji Sakata, Hiroyuki Taniguchi, Shingo Yasuda, Aki Adachi-Morishima, Yoko Hamazaki, Rika Nakayama, Takashi Miki, Nagahiro Minato, Shuh Narumiya

Research output: Contribution to journalArticlepeer-review

109 Citations (Scopus)


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. JEM

Original languageEnglish
Pages (from-to)2031-2038
Number of pages8
JournalJournal of Experimental Medicine
Issue number9
Publication statusPublished - Sept 3 2007
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology


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