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Amoeboid T lymphocytes require the septin cytoskeleton for cortical integrity and persistent motility.

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.

SUBMITTER: Tooley AJ

PROVIDER: S-EPMC3777658 | biostudies-literature | 2009 Jan

REPOSITORIES: biostudies-literature

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Amoeboid T lymphocytes require the septin cytoskeleton for cortical integrity and persistent motility.

Tooley Aaron J AJ Gilden Julia J Jacobelli Jordan J Beemiller Peter P Trimble William S WS Kinoshita Makoto M Krummel Matthew F MF

Nature cell biology 20081130 1

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. Pharmacologicall ...[more]

PMID: 19043408

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