ArticleGenetics2008
A random mutagenesis approach to isolate dominant-negative yeast sec1 mutants reveals a functional role for domain 3a in yeast and mammalian Sec1/Munc18 proteins.
Article in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 46 citations in OpenAlex.
- Article
- Article
- In Silico identification of angiotensin-converting enzyme inhibitory peptides from MRJP1.PloS one · 2020Article
- SNARE zippering requires activation by SNARE-like peptides in Sec1/Munc18 proteins.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Extension of Helix 12 in Munc18-1 Induces Vesicle Priming.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- SEC-uring membrane fusion: a sneak peek at SNARE-complex assembly driven by Sec1-Munc18 proteins.Nature structural & molecular biology · 2015Article
- An extended helical conformation in domain 3a of Munc18-1 provides a template for SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complex assembly.The Journal of biological chemistry · 2014Article
- Syntaxin binding mechanism and disease-causing mutations in Munc18-2.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Article
- Insight into the role of Ca2+-binding protein 5 in vesicle exocytosis.Investigative ophthalmology & visual science · 2011Article
- Munc18-1 domain-1 controls vesicle docking and secretion by interacting with syntaxin-1 and chaperoning it to the plasma membrane.Molecular biology of the cell · 2011Article
- Structure-function study of mammalian Munc18-1 and C. elegans UNC-18 implicates domain 3b in the regulation of exocytosis.PloS one · 2011Article
- Possible roles for Munc18-1 domain 3a and Syntaxin1 N-peptide and C-terminal anchor in SNARE complex formation.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Evidence for an interaction between Golli and STIM1 in store-operated calcium entry.The Biochemical journal · 2010Article
- The SM protein Vps33 and the t-SNARE H(abc) domain promote fusion pore opening.Nature structural & molecular biology · 2010Article
- I-TASSER: a unified platform for automated protein structure and function prediction.Nature protocols · 2010Article
- Protein structure prediction: when is it useful?Current opinion in structural biology · 2009Review
- UNC-18 modulates ethanol sensitivity in Caenorhabditis elegans.Molecular biology of the cell · 2009Article
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9 authors at 1 institution in 1 country.
Funding
Abstract
SNAP receptor (SNARE) and Sec1/Munc18 (SM) proteins are required for all intracellular membrane fusion events. SNAREs are widely believed to drive the fusion process, but the function of SM proteins remains unclear. To shed light on this, we screened for dominant-negative mutants of yeast Sec1 by random mutagenesis of a GAL1-regulated SEC1 plasmid. Mutants were identified on the basis of galactose-inducible growth arrest and inhibition of invertase secretion. This effect of dominant-negative sec1 was suppressed by overexpression of the vesicle (v)-SNAREs, Snc1 and Snc2, but not the target (t)-SNAREs, Sec9 and Sso2. The mutations isolated in Sec1 clustered in a hotspot within domain 3a, with F361 mutated in four different mutants. To test if this region was generally involved in SM protein function, the F361-equivalent residue in mammalian Munc18-1 (Y337) was mutated. Overexpression of the Munc18-1 Y337L mutant in bovine chromaffin cells inhibited the release kinetics of individual exocytosis events. The Y337L mutation impaired binding of Munc18-1 to the neuronal SNARE complex, but did not affect its binary interaction with syntaxin1a. Taken together, these data suggest that domain 3a of SM proteins has a functionally important role in membrane fusion. Furthermore, this approach of screening for dominant-negative mutants in yeast may be useful for other conserved proteins, to identify functionally important domains in their mammalian homologs.
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