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. Author manuscript; available in PMC: 2020 Aug 1.
Published in final edited form as: Curr Opin Neurobiol. 2019 Jan 25;57:17–25. doi: 10.1016/j.conb.2018.12.011

Figure 4.

Figure 4.

Model for relief of autoinhibition by calcium and DAG. Cartoon of the canonical Unc13 with C1-C2B module interacting with the plasma membrane (PM) via C2B-PIP2 interactions. This module also interacts with the MUN domain, stabilizing an inhibited state that corresponds to low release probability (Pv). Elevated calcium and DAG drive membrane translocation of the C1-C2B module thereby relieving autoinhibition and enhancing release probability. This may correspond to a super-primed state. Substitution of a conserved proline in the C2B-MUN Linker (blue “P”) destabilizes the inhibited state and has been associated with severe neurological disorders [71,72].