Gene: Dmel\Syt1
Syt, synaptotagmin, synaptotagmin I, Syt I, SytI
calcium sensor in synaptic vesicle fusion - functions during exocytosis - functions as the fast calcium sensor for neurotransmitter release at synapses
Please see the JBrowse view of Dmel\Syt1 for information on other features
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Gene model reviewed during 5.53
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Gene model reviewed during 5.45
Gene model reviewed during 5.55
Gene model reviewed during 6.19
6.5, 4.0 (northern blot)
7.0, 4.5, 2.18 (longest cDNA)
69 (kD)
474 (aa)
Homodimer or homotrimer (Potential). Identified in a complex with Syn and nwk (PubMed:29568072). Interacts with StnA and StnB via its second C2 domain. This interaction may mediate its retrieval from the plasma membrane, thereby facilitating the internalization of multiple synaptic vesicles from the plasma membrane.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Syt1 using the Feature Mapper tool.
Comment: reference states 12-20 hr AEL
Comment: reference states >8-12 hr AEL
Syt1 transcripts are first detected in 12-15hr embryos on northern blots and are detected at all subsequent stages tested. The are enriched in adult head relative to adult body.
Syt1 transcripts are first detected in embryos at stage 13 and are detected throughout the CNS and PNS. In adults, transcripts are detected in the cell bodies of the CNS in both the brain and in the thoracic ganglia.
The 4.5 kb syt transcript first appears between 8 and 12 hours of embryogenesis, and is expressed throughout development.
The 7.0 kb syt transcript is first detected at 12 to 20 hours of embryogenesis, and is expressed throughout development.
Syt1 transcript is detected only in neuronal cells. All peripheral nervous system (PNS) neurons, and most (if not all) central nervous system (CNS) neurons express Syt1 transcript. The first Syt1 transcripts in the CNS are detected in late stage 13 embryos, in the ventral nerve cord in a few cells per segment. This expression increases and intensifies by stage 14. In stage 15 embryos, Syt1 transcript is detected in the supraoesophageal and suboesophageal ganglia, as well as in a subset of PNS neurons. At stage 17, Syt1 transcript is abundant in both the CNS and PNS.
On Northern blots, two transcripts of 4.5 and 7.0 kb are observed in adult head extracts with a Syt1 probe. No transcript is seen in 0-4 hour embryos and in third instar larvae.
In the adult prothorax and neck, Syt1 immunoreactivity is observed in the type I boutons of motor neurons innervating the ventral cervical muscles, prothoracic sternal anterior rotator muscle 31, and prothoracic sternal adductor muscle 33, and in the type II boutons of motorneurons innervating ventral cervical muscle 27 and prothoracic sternal anterior rotator muscle 31. Type II boutons on muscle 31 that are along the cuticle lack Syt1 immunoreactivity.
Syt1 protein is detected in the neuropil of the adult brain. It is observed in the synapse-rich regions in the lamina, the medulla, and the lobula. Staining is also observed in the neuropil in embryonic sections. In larvae, staining is observed at the neuromuscular junctions where it is tightly confined to the nerve terminals.
Immunocytochemical staining of whole mount embryos shows that Syt1 protein is rapidly transported to synapses and localizes to synaptic contact sites. In stage 14 embryos, the cell bodies of central nervous system neurons are transiently labeled. At stage 15, Syt1 protein is in the dorsal portion of the ventral nerve cord and in the brain. At stage 16, the longitudinal tracts of the central nervous system, motor neurons, and parts of the peripheral nervous system are stained. At stage 17, staining localizes to the longitudinal tracts of the central nervous system and to synapses in the body wall musculature. During larval development, Syt1 protein continues to be detected in neuromuscular junctions. Synaptic terminals in both type I and type II junctions stain. In the adult, Syt1 is detected in synapses of the adult head neuropil including those in the antennal lobes and the visual lamina.
GBrowse - Visual display of RNA-Seq signals
View Dmel\Syt1 in GBrowse 2
2-7
2-6.2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
polyclonal
Source for identity of: Syt1 syt
Source for merge of: syt l(2)k05909
FlyBase Curator comment: 'syt' has been renamed 'Syt1' to be in accordance with the FlyBase nomenclature rules, and to maintain consistency and clarity in the nomenclature of the Synaptotagmin gene family.
Ca[2+] binding by the C[[2]]B domain of Syt1 is required at intact synapses.
Mutation of a poly-lysine motif in Syt1 alters vesicle size but not endocytic rate, whereas mutation of calcium-coordinating aspartate residues alters endocytic rate but not vesicle size.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
The same H3 residues of the syt gene product that mediate Ca2+ channel inhibition also govern SNARE complexes through increased complex stability/assembly.
syt can facilitate SNARE complex formation in vitro.
A mutation that deletes the C2B domain of syt disrupts clathrin AP-2 binding and endocytosis. In contrast, a mutation that blocks Ca2+-triggered conformational changes in C2B and diminishes Ca2+-triggered syt protein oligomerisation results in a postdocking defect in neurotransmitter release and a decrease in SNARE assembly.
Identified with: GH17619 <up>FlyBase curator comment: EST subsequently found to be chimeric</up>.
The syt gene product is a negative regulator of synaptic vesicle fusion and may act as a calcium-sensor and/or component of the vesicle docking machinery.
Neuromuscular transmission persists in the absence of syt.
syt is a negative regulator of vesicle fusion and acts to increase the efficiency of excitation-secretion coupling during synaptic transmission.
Reduced levels of syt result in a substantial alteration in synaptic function in the eye and at larval neuromuscular junctions. Decreased neurotransmitter release causes smaller evoked synaptic potentials. The frequency, but not the size, of spontaneous quantal events is simultaneously increased. There is no detectable morphological change in the arborisation of the synapse. The increased frequency of spontaneous events is sufficient to deplete significantly the vesicle supply and thereby account for reduced transmission.
syt is required for hatching and locomotion of first instar larvae.
The defects caused by various mutant combinations of syt alleles that produce adult progeny vary from severe uncoordination and death to subtle behavioural defects affecting flight and fertility.
Genetic and electrophysiological evidence demonstrates that syt forms a multimeric complex that can function as a clamp in vivo. Upon nerve stimulation and calcium influx all synaptotagmin mutants dramatically decrease the ability of calcium to promote release, suggesting that syt plays a key role in activation of synaptic vesicle fusion.
Synaptotagmin is one of the major integral proteins of synaptic vesicles, postulated to dock vesicles to their release sites, act as the Ca2+ sensor for release and be a fusion protein during exocytosis. Mutant alleles isolated demonstrate that synaptotagmin is not required for synaptic transmission.
syt plays a key role in Ca2+ activation of neurotransmitter release: mutant analysis indicates the existence of separate pathways for evoked and spontaneous neurotransmitter release.
Identification: Isolated from a cDNA library using rat synaptotagmin probes under low stringency conditions.
