Article abstract
Nature Cell Biology 11, 17 - 26 (2008)
Published online: 30 November 2008 | doi:10.1038/ncb1808
Amoeboid T lymphocytes require the septin cytoskeleton for cortical integrity and persistent motility
Aaron J. Tooley1,4, Julia Gilden1,4, Jordan Jacobelli1, Peter Beemiller1, William S. Trimble2, Makoto Kinoshita3 & Matthew F. Krummel1
Abstract
The systems that refine actomyosin forces during motility remain poorly understood. Septins assemble on the T-cell cortex and are enriched at the mid-zone in filaments. Septin knockdown causes membrane blebbing, excess leading-edge protrusions and lengthening of the trailing-edge uropod. The associated loss of rigidity permits motility, but cells become uncoordinated and poorly persistent. This also relieves a previously unrecognized restriction to migration through small pores. Pharmacologically rigidifying cells counteracts this effect, and relieving cytoskeletal rigidity synergizes with septin depletion. These data suggest that septins tune actomyosin forces during motility and probably regulate lymphocyte trafficking in confined tissues.
- The Department of Pathology, University of California, San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143-0511, USA.
- Program in Cell Biology, Hospital for Sick Children and Department of Biochemistry, University of Toronto, 555 University Avenue, Toronto, M5G 1X8, Canada.
- Biochemistry and Cell Biology Unit, HMRO, Kyoto University Graduate School of Medicine, Yoshida Konoe, Sakyo, Kyoto 606-8501, Japan.
- These authors contributed equally to this work.
Correspondence to: Matthew F. Krummel1 e-mail: matthew.krummel@ucsf.edu
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