Signal transduction - Actin, cofilin and cognition

Patients with Williams syndrome have defects in visuo-spatial cognition (a failure to integrate parts into a whole) that are linked to deletion of the gene that encodes LIM kinase-1 (LIMK-1). The reasons for this are becoming clearer with the identification of a molecular target for LIMK-1. It turns out that this enzyme phosphorylates cofilin, which is essential for the turnover of actin filaments. Such turnover may be implicated in axon guidance, and could explain why high levels of LIMK-1 are found in neurons.