| Here we examined the requirement of the C2A polylysine motif for Syt 1 interaction with the cardiac Cav1 . 2 ( L type ) and the neuronal Cav2 . 3 ( R type ) voltage gated Ca2+ channels , two channels required for neurotransmission . ^^^ We find that the C2A polylysine motif presents a critical interaction surface with Cav1 . 2 and Cav2 . 3 since truncated Syt 1 containing a mutated motif ( Syt 1 * 1 264 ) was ineffective at modifying the channel kinetics . ^^^ Mutating the polylysine motif also abolished C2A binding to Lc 753 893 , the cytosolic interacting domain of Syt 1 at Cav1 . 2 1 subunit . ^^^ |