Rings of actin (green) around synaptic vesicle clusters are lost when talin cannot bind PIPKIγ (right).
Synapses are specialized sites of cell adhesion that were recently shown to hold talin. Talin interacts with PIPKIγ, a PI(4,5)P2-producing enzyme, which in turn regulates talin and other actin regulatory proteins. The importance of this interaction is now shown at synapses, where PI(4,5)P2 also controls clathrin coat dynamics.
The authors interfered with talin–PIPKIγ interactions in the axons of giant lamprey neurons. The interference inhibited the recycling of synaptic vesicles on the presynaptic side. Clathrin-coated pits formed but did not bud off the plasma membrane. These changes were associated with reduced synaptic actin networks. The defects are probably due to low levels of PI(4,5)P2 resulting from a block in PIPKIγ recruitment to the membrane. The same lab has also recently shown genetically that PI(4,5)P2 is necessary for synaptic vesicle trafficking (Di Paolo et al. Nature. 431:415–422).
As PIP2 production is up-regulated by neuronal depolarization, the authors are now studying how the talin-PIPKIγ interaction is affected by the firing of synapses. 
