This work has studied the role of complexin in regulated
exocytosis, a key mechanism underlies hormone and neurotransmitter
release and understanding of which will help to design therapeutic
interventions in a lot of neuronal diseases or endocrine diseases.
The work here systematically dissects the vesicle stages leading up
to exocytosis using a knockout-rescue strategy in a mammalian model
system. The work shows that adrenal chromaffin cells from CPX II
knockout mice exhibit a markedly diminished readily releasable
vesicle pool, while showing no change in the kinetics of fusion
pore dilation or morphological vesicle docking. Overexpression of
wildtype CPX II but not of SNARE-binding-deficient mutants --
restores the size of the readily releasable pool in knockout cells,
and in wildtype cells it markedly enlarges the readily releasable
pool. These results suggest that CPXs prime vesicles for exocytosis
and, therefore, are positive regulators of Ca2 -triggered
exocytosis.
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