Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Stock; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse   Donating Investigator Dr. Thomas C. Sudhof,   Stanford University School of Medicine

Appearance
black
Related Genotype: a/a

Description
Mice homozygous for the Syt1^tm1Sud targeted mutation die 1-2 days after birth. Homozygous mutant mice show an impaired synchronous, fast Ca²⁺-dependent neurotransmitter release.

Control Information

	Control
	Wild-type from the colony
	101045 B6129SF2/J	(approximate)
Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Syt1

006385	B6;129P2-Syt1tm3Sud/J
006386	B6;129P2-Syt1tm5Sud/J
006387	B6;129P2-Syt1tm6Sud/J

View Strains carrying other alleles of Syt1     (3 strains)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Syt1^tm1Sud/Syt1^tm1Sud

        involves: 129S4/SvJae

• mortality/aging
• complete postnatal lethality
  • homozygous animals become weak and die within 48 hours of birth   (MGI Ref ID J:21602)
• nervous system phenotype
• *normal* nervous system phenotype   (MGI Ref ID J:171203)
• • abnormal neuron physiology
    • calcium-stimulated fast release of synaptic vesicles is delayed compared to in control neurons   (MGI Ref ID J:167753)
    • synaptic vesicle slow release induced by calcium uncaging in the presence of hypertonic sucrose solution is delayed compared to in control neurons   (MGI Ref ID J:167753)
  • abnormal synaptic transmission
    • defects in synchronous synaptic transmission is not restored by Otof over-expression   (MGI Ref ID J:171203)
    • however, Otof over-expression increases asynchronous release   (MGI Ref ID J:171203)
  • • abnormal CNS synaptic transmission
      • cultured mutant hippocampal neurons exhibit greatly decreased postsynaptic responses evoked by whole-cell patch clamping compared to controls   (MGI Ref ID J:21602)
      • the fast, synchronous, Ca2+ dependent phase of neurotransmitter release is affected, while the spontaneous release of neurotransmitters is unaffected   (MGI Ref ID J:21602)
    • • abnormal excitatory postsynaptic currents
        • excitatory postsynaptic current amplitudes are reduced compared to in control mice   (MGI Ref ID J:167753)
        • hippocampal neurons exhibit decreased mean excitatory postsynaptic current (EPSC) amplitude that cannot be rescued by Otof over-expression   (MGI Ref ID J:171203)
        • mean EPSC integral is rescued by Otof over-expression   (MGI Ref ID J:171203)
      • abnormal inhibitory postsynaptic currents
        • inhibitions of postsynaptic currents (IPSCs) is impaired slightly similar to in Syt2^tm1Sud homozygotes   (MGI Ref ID J:122459)
      • abnormal miniature excitatory postsynaptic currents
        • miniature excitatory postsynaptic current is slightly increased by Otof over-expression   (MGI Ref ID J:171203)
    • abnormal neurotransmitter secretion
      • the fast, synchronous, Ca2+ dependent phase of neurotransmitter release is affected, while the spontaneous release of neurotransmitters is unaffected   (MGI Ref ID J:21602)
• behavior/neurological phenotype
• abnormal suckling behavior
  • homozygotes do not suckle; no milk is seen in stomachs and these mice are rejected by their mothers   (MGI Ref ID J:21602)
• endocrine/exocrine gland phenotype
• abnormal adrenal gland physiology
  • adrenal chromaffin cells exhibit reduced exocytosis compared with wild-type mice that cannot be rescued by Otof over-expression   (MGI Ref ID J:171203)

View Research Applications

Research Applications

This mouse can be used to support research in many areas including:

Syt1^tm1Sud related

Neurobiology Research
Neurotransmitter Receptor and Synaptic Vesicle Defects

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Syt1tm1Sud
Allele Name		targeted mutation 1, Thomas C Sudhof
Allele Type		Targeted (knock-out)
Common Name(s)		Syt-;
Mutation Made By		Dr. Thomas Sudhof,   Stanford University School of Medicine
Strain of Origin		129S4/SvJae
ES Cell Line Name		J1
ES Cell Line Strain		129S4/SvJae
Gene Symbol and Name		Syt1, synaptotagmin I
Chromosome		10
Gene Common Name(s)		AW124717; G630098F17Rik; P65; RIKEN cDNA G630098F17 gene; SVP65; SYT; expressed sequence AW124717;
Molecular Note		A 5' portion of the exon encoding amino acids 270 through 308 and the preceding intron were replaced with a neomycin selection cassette. In addition to the coding sequence, the intron acceptor site was deleted. Lysates derived from the brains of homozygous mice were shown to contain less than 5% of the amount of a truncated form of the encoded protein compared to controls by immunoblotting. [MGI Ref ID J:21602]

Genotyping

Genotyping Information

Genotyping Protocols

Syt1^tm1Sud, Separated PCR
NEOTD (Generic Neo), Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Geppert M; Goda Y; Hammer RE; Li C; Rosahl TW; Stevens CF; Sudhof TC. 1994. Synaptotagmin I: a major Ca2+ sensor for transmitter release at a central synapse. Cell 79(4):717-27. [PubMed: 7954835]  [MGI Ref ID J:21602]

Additional References

Syt1^tm1Sud related

Beurg M; Michalski N; Safieddine S; Bouleau Y; Schneggenburger R; Chapman ER; Petit C; Dulon D. 2010. Control of exocytosis by synaptotagmins and otoferlin in auditory hair cells. J Neurosci 30(40):13281-90. [PubMed: 20926654]  [MGI Ref ID J:165099]

Burgalossi A; Jung S; Meyer G; Jockusch WJ; Jahn O; Taschenberger H; O'Connor VM; Nishiki T; Takahashi M; Brose N; Rhee JS. 2010. SNARE protein recycling by alphaSNAP and betaSNAP supports synaptic vesicle priming. Neuron 68(3):473-87. [PubMed: 21040848]  [MGI Ref ID J:167753]

Dong M; Tepp WH; Liu H; Johnson EA; Chapman ER. 2007. Mechanism of botulinum neurotoxin B and G entry into hippocampal neurons. J Cell Biol 179(7):1511-22. [PubMed: 18158333]  [MGI Ref ID J:135458]

Han W; Rhee JS; Maximov A; Lin W; Hammer RE; Rosenmund C; Sudhof TC. 2005. C-terminal ECFP fusion impairs synaptotagmin 1 function: crowding out synaptotagmin 1. J Biol Chem 280(6):5089-100. [PubMed: 15561725]  [MGI Ref ID J:105052]

Kerr AM; Reisinger E; Jonas P. 2008. Differential dependence of phasic transmitter release on synaptotagmin 1 at GABAergic and glutamatergic hippocampal synapses. Proc Natl Acad Sci U S A 105(40):15581-6. [PubMed: 18832148]  [MGI Ref ID J:143451]

Maximov A; Sudhof TC. 2005. Autonomous function of synaptotagmin 1 in triggering synchronous release independent of asynchronous release. Neuron 48(4):547-54. [PubMed: 16301172]  [MGI Ref ID J:107600]

Nicholson-Tomishima K; Ryan TA. 2004. Kinetic efficiency of endocytosis at mammalian CNS synapses requires synaptotagmin I. Proc Natl Acad Sci U S A 101(47):16648-52. [PubMed: 15492212]  [MGI Ref ID J:94470]

Nishiki T; Augustine GJ. 2004. Synaptotagmin I synchronizes transmitter release in mouse hippocampal neurons. J Neurosci 24(27):6127-32. [PubMed: 15240804]  [MGI Ref ID J:97274]

Reisinger E; Bresee C; Neef J; Nair R; Reuter K; Bulankina A; Nouvian R; Koch M; Buckers J; Kastrup L; Roux I; Petit C; Hell SW; Brose N; Rhee JS; Kugler S; Brigande JV; Moser T. 2011. Probing the Functional Equivalence of Otoferlin and Synaptotagmin 1 in Exocytosis. J Neurosci 31(13):4886-4895. [PubMed: 21451027]  [MGI Ref ID J:171203]

Schonn JS; Maximov A; Lao Y; Sudhof TC; Sorensen JB. 2008. Synaptotagmin-1 and -7 are functionally overlapping Ca2+ sensors for exocytosis in adrenal chromaffin cells. Proc Natl Acad Sci U S A :. [PubMed: 18308932]  [MGI Ref ID J:131424]

Shin OH; Rhee JS; Tang J; Sugita S; Rosenmund C; Sudhof TC. 2003. Sr2+ binding to the Ca2+ binding site of the synaptotagmin 1 C2B domain triggers fast exocytosis without stimulating SNARE interactions. Neuron 37(1):99-108. [PubMed: 12526776]  [MGI Ref ID J:89486]

Shin OH; Xu J; Rizo J; Sudhof TC. 2009. Differential but convergent functions of Ca2+ binding to synaptotagmin-1 C2 domains mediate neurotransmitter release. Proc Natl Acad Sci U S A 106(38):16469-74. [PubMed: 19805322]  [MGI Ref ID J:153229]

Voets T; Moser T; Lund PE; Chow RH; Geppert M; Sudhof TC; Neher E. 2001. Intracellular calcium dependence of large dense-core vesicle exocytosis in the absence of synaptotagmin I. Proc Natl Acad Sci U S A 98(20):11680-5. [PubMed: 11562488]  [MGI Ref ID J:126394]

Xu J; Mashimo T; Sudhof TC. 2007. Synaptotagmin-1, -2, and -9: Ca(2+) sensors for fast release that specify distinct presynaptic properties in subsets of neurons. Neuron 54(4):567-81. [PubMed: 17521570]  [MGI Ref ID J:122459]

Xu J; Pang ZP; Shin OH; Sudhof TC. 2009. Synaptotagmin-1 functions as a Ca2+ sensor for spontaneous release. Nat Neurosci 12(6):759-66. [PubMed: 19412166]  [MGI Ref ID J:161265]

Yao J; Gaffaney JD; Kwon SE; Chapman ER. 2011. Doc2 is a Ca2+ sensor required for asynchronous neurotransmitter release. Cell 147(3):666-77. [PubMed: 22036572]  [MGI Ref ID J:178686]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Diet Information	LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

General Supply Notes

• Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

	Control
	Wild-type from the colony
	101045 B6129SF2/J	(approximate)
Considerations for Choosing Controls
Control Pricing Information for Genetically Engineered Mutant Strains.

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX^® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX^® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX^® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.

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