A collaborative project between the Forscher (MCDB) and Kaczmarek (Pharmacology) labs at Yale have revealed the mechanisms by which mutations in the Kv3.3 potassium channel cause neurodegeneration. Interestingly, the C-terminus of the channel protein recruits Arp2/3 to the plasma membrane to form a stable actin network that slows the rate of channel closing. Mutations in the Kv3.3 channel that occur in human patients impairs Arp2/3 recruitment, resulting in defective actin networks in neuronal cells derived from human induced pluripotent stem cells. This work highlights a novel mechanism by which the cytoskeleton regulates ion channels and provides novel targets for neuronal degeneration.
Link to publication: http://www.ncbi.nlm.nih.gov/pubmed/26997484
Link to comment in Dev. Cell on our paper: http://dx.doi.org/10.1016/j.devcel.2016.03.014