Actin, cofilin and cognition

摘要

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). Consistent with this cognitive defect, large amounts of LIMK-1 are expressed in neurons, yet its molecular targets have remained elusive until now. On pages 805 and 809 of this issue, however, Arbe'r et al. and Yang et aV report that LIMK-1 phosphorylates cofilin, an essential protein that is required for turnover of actin filaments.