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Open syntaxin overcomes synaptic transmission defects in diverse C. elegans exocytosis mutants
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Summary
Assembly of SNARE complexes that mediate neurotransmitter release requires opening of a ‘closed’ conformation of UNC-64/syntaxin. Rescue of
unc-13/Munc13
phenotypes by overexpressed open UNC-64/syntaxin suggested a specific function of UNC-13/Munc13 in opening UNC-64/ syntaxin. Here, we revisit the effects of open
unc-64
/syntaxin by generating knockin (KI) worms. The KI animals exhibited enhanced spontaneous and evoked exocytosis compared to wild-type animals. Unexpectedly, the open syntaxin KI partially suppressed exocytosis defects of various mutants, including
snt-1
/synaptotagmin,
unc-2/
P/Q/N-type Ca
2+
channel alpha-subunit, and
unc-31/
CAPS in addition to
unc-13/
Munc13 and
unc-10/
RIM, and enhanced exocytosis in
tom-1/
Tomosyn mutants. However, open syntaxin aggravated the defects of
unc-18/
Munc18 mutants. Correspondingly, open syntaxin partially bypasses the requirement of Munc13 but not Munc18 for liposome fusion. Our results show that facilitating opening of syntaxin enhances exocytosis in a wide range of genetic backgrounds, and may provide a general means to enhance synaptic transmission in normal and disease states.
Title: Open syntaxin overcomes synaptic transmission defects in diverse
C. elegans
exocytosis mutants
Description:
Summary
Assembly of SNARE complexes that mediate neurotransmitter release requires opening of a ‘closed’ conformation of UNC-64/syntaxin.
Rescue of
unc-13/Munc13
phenotypes by overexpressed open UNC-64/syntaxin suggested a specific function of UNC-13/Munc13 in opening UNC-64/ syntaxin.
Here, we revisit the effects of open
unc-64
/syntaxin by generating knockin (KI) worms.
The KI animals exhibited enhanced spontaneous and evoked exocytosis compared to wild-type animals.
Unexpectedly, the open syntaxin KI partially suppressed exocytosis defects of various mutants, including
snt-1
/synaptotagmin,
unc-2/
P/Q/N-type Ca
2+
channel alpha-subunit, and
unc-31/
CAPS in addition to
unc-13/
Munc13 and
unc-10/
RIM, and enhanced exocytosis in
tom-1/
Tomosyn mutants.
However, open syntaxin aggravated the defects of
unc-18/
Munc18 mutants.
Correspondingly, open syntaxin partially bypasses the requirement of Munc13 but not Munc18 for liposome fusion.
Our results show that facilitating opening of syntaxin enhances exocytosis in a wide range of genetic backgrounds, and may provide a general means to enhance synaptic transmission in normal and disease states.
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