کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10956895 | 1099462 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Synaptotagmin mutants Y311N and K326/327A alter the calcium dependence of neurotransmission
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
Synaptotagmin I, a calcium-binding synaptic vesicle protein, is thought to act as the calcium sensor for fast neurotransmission, but what synaptotagmin I does, upon binding calcium, to trigger exocytosis is still unknown. To begin to examine the role of synaptotagmin I's interactions with calcium-dependent binding partners, three mutant versions of synaptotagmin I reported to affect calcium-dependent self-oligomerization (Y311N, K327A, and K326/327A) were expressed in cultured mouse hippocampal neurons lacking endogenous synaptotagmin I, and effects on neurotransmission were evaluated by comparison with transmission rescued by wild-type synaptotagmin I. All three mutants reduced transmitter release. To separate effects on calcium binding from effects on calcium-dependent oligomerization, we measured the calcium dependence of exocytosis for two of the mutants. Both showed apparent calcium affinity much lower than wild-type, a reduction sufficient to account for the neurotransmission defects. We conclude that self-oligomerization is unlikely to play any significant role in triggering synaptic vesicle exocytosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Neuroscience - Volume 29, Issue 3, July 2005, Pages 462-470
Journal: Molecular and Cellular Neuroscience - Volume 29, Issue 3, July 2005, Pages 462-470
نویسندگان
Catherine R. Borden, Charles F. Stevens, Jane M. Sullivan, Yongling Zhu,