Abstract：
:Communication between neurons involves presynaptic neurotransmitter release which can be evoked by action potentials or occur spontaneously as a result of stochastic vesicle fusion. The Ca2+-binding double C2 proteins Doc2a and -b were implicated in spontaneous and asynchronous evoked release, but the mechanism remains unclear. Here, we compared wildtype Doc2b with two Ca2+ binding site mutants named DN and 6A, previously classified as gain- and loss-of-function mutants. They carry the substitutions D218,220N or D163,218,220,303,357,359A respectively. We found that both mutants bound phospholipids at low Ca2+ concentrations and were membrane-associated in resting neurons, thus mimicking a Ca2+-activated state. Their overexpression in hippocampal primary cultured neurons had similar effects on spontaneous and evoked release, inducing high mEPSC frequencies and increased short-term depression. Together, these data suggest that the DN and 6A mutants both act as gain-of-function mutants at resting conditions.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Bourgeois-Jaarsma Q,Verhage M,Groffen AJdoi
10.1038/s41598-019-50684-1subject
Has Abstractpub_date
2019-10-08 00:00:00pages
14408issue
1issn
2045-2322pii
10.1038/s41598-019-50684-1journal_volume
9pub_type
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