Linked Life Data

8100740

Source:http://linkedlifedata.com/resource/pubmed/id/8100740

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1993-8-12
pubmed:abstractText
Synaptotagmin is one of the major integral membrane proteins of synaptic vesicles. It has been postulated to dock vesicles to their release sites, to act as the Ca2+ sensor for the release process, and to be a fusion protein during exocytosis. To clarify the function of this protein, we have undertaken a genetic analysis of the synaptotagmin gene in Drosophila. We have identified five lethal alleles of synaptotagmin, at least one of which lacks detectable protein. Surprisingly, however, many embryos homozygous for this null allele hatch and, as larvae, crawl, feed, and respond to stimuli. Electrophysiological recordings in embryonic cultures confirmed that synaptic transmission persists in the null allele. Therefore, synaptotagmin is not absolutely required for the regulated exocytosis of synaptic vesicles. The lethality of synaptotagmin in late first instar larvae is probably due to a perturbation of transmission that leaves the main apparatus for vesicle docking and fusion intact.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0092-8674
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
73
pubmed:geneSymbol
syt
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1281-90
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Synaptic transmission persists in synaptotagmin mutants of Drosophila.
pubmed:affiliation
Department of Molecular and Cellular Physiology, Stanford University Medical Center, California 94305-5426.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't