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Signal transduction

Actin, cofilin and cognition

Nature volume 393, pages 739–740 (1998)Cite this article

Patients with Williams syndrome, a multi-gene deletion syndrome, suffer from mild mental retardation and vascular disease. They also have defects in visuo-spatial cognition — a failure to integrate parts into a whole — that are linked to deletion of the gene that codes for LIM-kinase 1 (LIMK-1)1. Consistent with this cognitive defect, large amounts of LIMK-1 are expressed in neurons2, yet its molecular targets have remained elusive until now. On pages 805 and pages 809 of this issue, however, Arber et al.3 and Yang et al.4 report that LIMK-1 phosphorylates cofilin, an essential protein that is required for turnover of actin filaments.

During cell movements such as neuron outgrowth or leukocyte chemotaxis, actin filaments must be organized into a dense, dynamic meshwork. This forms at the leading edge of a cell, where actin polymerization drives forward movement, and it usually takes the form of thin sheets (lamellipodia) or spikes (filopodia). Cell movement is a dynamic process, and actin at the leading edge of the cell must be continuously depolymerized and then repolymerized to produce this movement5. Actin depolymerization limits the length of lamellipodia and enables the actin subunits to be recycled for further rounds of polymerization.

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Figure 1: Model for Rac-induced changes in actin dynamics to form a lamellipodium, based on the findings of Arber et al.3 and Yang et al.4.

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Authors and Affiliations

  1. The Department of Biochemistry, University of California at San Francisco, 513 Parnassus Avenue, San Francisco, 94143, California, USA

    Jody Rosenblatt

  2. The Department of Cell Biology, Harvard Medical School, Room C517, 240 Longwood Avenue, Boston, 02115, MassachusettsM, USA

    Timothy J. Mitchison

Authors
  1. Jody Rosenblatt
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  2. Timothy J. Mitchison
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Rosenblatt, J., Mitchison, T. Actin, cofilin and cognition. Nature 393, 739–740 (1998). https://doi.org/10.1038/31597

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