| |||||||||||
- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
- Terms of Use
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
Former Names B6.Cg-Tg(Syn1-Cre)671Jxm (Changed: 15-DEC-04 ) Type Congenic; Mutant Strain; Transgenic; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Donating Investigator Jamey Marth, University of California at San Diego Description
These transgenic mice express Cre recombinase under the direction of a synapsin promoter. Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Recombinase activity is detected in neuronal cells by embryonic day 12.5.Development
A transgenic construct containing a Cre recombinase gene under the direction of a synapsin promoter was injected into fertilized B6;CBAF1 mouse eggs. Founder animals were bred to wildtype C57BL/6NHsd mice.
Control Information
| Control | ||
|---|---|---|
| Noncarrier | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying other alleles of cre
View Strains carrying other alleles of cre (162 strains)
Additional Web Information
Introduction to Cre-lox technology
JAX® NOTES, Summer 2001; 482. Cre Transgenic Strains for Conditional Mutagenesis.
Phenotype
Phenotype Information
This mouse can be used to support research in many areas including:
cre relatedNeurobiology Research
Cre-lox System
Cre Recombinase expression in neural tissue
Research Tools
Cre-lox System
Cre Recombinase Expression
Genetics Research
Mutagenesis and Transgenesis: Cre-lox System
Neurobiology Research
Research Tools
Cre-lox System
Genetics Research
Mutagenesis and Transgenesis: Cre-lox System
Genes & Alleles
Gene & Allele Information
| Allele Symbol | Tg(Syn1-cre)671Jxm | ||
|---|---|---|---|
| Allele Name | transgene insertion 671, Jamey Marth | ||
| Allele Type | Transgenic (Cre/Flp) | ||
| Common Name(s) | Syn-cre; SynI-Cre; | ||
| Mutation Made By | Jamey Marth, University of California at San Diego | ||
| Strain of Origin | (C57BL/6 x CBA)F2 | ||
| Site of Expression | neuronal cells by embryonic day 12.5 | ||
| Expressed Gene | cre, cre recombinase, bacteriophage P1 | ||
| Cre recombinase is an enzyme derived from the bacteriophage P1 that specifically recognizes loxP sites. Cre has been shown to effectively mediate the excision of DNA located between loxP sites. After the excision event, the DNA ends recombine leaving a single loxP site in place of the intervening sequence. | |||
| Promoter | Syn1, synapsin I, rat | ||
| Gene Symbol and Name | Tg(Syn1-cre)671Jxm, transgene insertion 671, Jamey Marth | ||
| Chromosome | UN | ||
| Gene Common Name(s) | Syn-cre; SynI-Cre; | ||
| Driver Note | Syn1 | ||
| General Note | Homozygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. | ||
| Molecular Note | This transgene expresses Cre recombinase under the control of a rat synapsin I promoter. Cre recombinase activity is detected in neuronal cells, including brain, spinal cord and DRGs, as early as E12.5, as well as in neurons in adult. [MGI Ref ID J:68558] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Generic Cre Melt Curve Analysis, Melt Curve Analysis
Generic Cre, Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References
Selected Reference(s)
Zhu Y; Romero MI; Ghosh P; Ye Z; Charnay P; Rushing EJ; Marth JD; Parada LF. 2001. Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain. Genes Dev 15(7):859-76. [PubMed: 11297510] [MGI Ref ID J:68558]
Additional References
Mori H; Hanada R; Hanada T; Aki D; Mashima R; Nishinakamura H; Torisu T; Chien KR; Yasukawa H; Yoshimura A. 2004. Socs3 deficiency in the brain elevates leptin sensitivity and confers resistance to diet-induced obesity. Nat Med 10(7):739-43. [PubMed: 15208705] [MGI Ref ID J:91796]
Tg(Syn1-cre)671Jxm relatedCai J; Chen Y; Cai WH; Hurlock EC; Wu H; Kernie SG; Parada LF; Lu QR. 2007. A crucial role for Olig2 in white matter astrocyte development. Development 134(10):1887-99. [PubMed: 17428828] [MGI Ref ID J:121422]
Cohen P; Zhao C; Cai X; Montez JM; Rohani SC; Feinstein P; Mombaerts P; Friedman JM. 2001. Selective deletion of leptin receptor in neurons leads to obesity. J Clin Invest 108(8):1113-21. [PubMed: 11602618] [MGI Ref ID J:72241]
Corbetta S; Gualdoni S; Ciceri G; Monari M; Zuccaro E; Tybulewicz VL; de Curtis I. 2009. Essential role of Rac1 and Rac3 GTPases in neuronal development. FASEB J 23(5):1347-57. [PubMed: 19126596] [MGI Ref ID J:148225]
Cui Y; Costa RM; Murphy GG; Elgersma Y; Zhu Y; Gutmann DH; Parada LF; Mody I; Silva AJ. 2008. Neurofibromin regulation of ERK signaling modulates GABA release and learning. Cell 135(3):549-60. [PubMed: 18984165] [MGI Ref ID J:147614]
DeFalco J; Tomishima M; Liu H; Zhao C; Cai X; Marth JD; Enquist L; Friedman JM. 2001. Virus-assisted mapping of neural inputs to a feeding center in the hypothalamus. Science 291(5513):2608-13. [PubMed: 11283374] [MGI Ref ID J:68414]
Di Nardo A; Kramvis I; Cho N; Sadowski A; Meikle L; Kwiatkowski DJ; Sahin M. 2009. Tuberous sclerosis complex activity is required to control neuronal stress responses in an mTOR-dependent manner. J Neurosci 29(18):5926-37. [PubMed: 19420259] [MGI Ref ID J:148479]
Ferguson C; Hardy SL; Werner DF; Hileman SM; Delorey TM; Homanics GE. 2007. New insight into the role of the beta3 subunit of the GABAA-R in development, behavior, body weight regulation, and anesthesia revealed by conditional gene knockout. BMC Neurosci 8:85. [PubMed: 17927825] [MGI Ref ID J:127877]
Hasue F; Kuwaki T; Kisanuki YY; Yanagisawa M; Moriya H; Fukuda Y; Shimoyama M. 2005. Increased sensitivity to acute and persistent pain in neuron-specific endothelin-1 knockout mice. Neuroscience 130(2):349-58. [PubMed: 15664691] [MGI Ref ID J:95930]
He XP; Kotloski R; Nef S; Luikart BW; Parada LF; McNamara JO. 2004. Conditional deletion of TrkB but not BDNF prevents epileptogenesis in the kindling model. Neuron 43(1):31-42. [PubMed: 15233915] [MGI Ref ID J:91467]
Hinoi E; Gao N; Jung DY; Yadav V; Yoshizawa T; Myers MG Jr; Chua SC Jr; Kim JK; Kaestner KH; Karsenty G. 2008. The sympathetic tone mediates leptin's inhibition of insulin secretion by modulating osteocalcin bioactivity. J Cell Biol 183(7):1235-42. [PubMed: 19103808] [MGI Ref ID J:145998]
Huang YZ; Pan E; Xiong ZQ; McNamara JO. 2008. Zinc-mediated transactivation of TrkB potentiates the hippocampal mossy fiber-CA3 pyramid synapse. Neuron 57(4):546-58. [PubMed: 18304484] [MGI Ref ID J:135687]
Kleinridders A; Pogoda HM; Irlenbusch S; Smyth N; Koncz C; Hammerschmidt M; Bruning JC. 2009. PLRG1 is an essential regulator of cell proliferation and apoptosis during vertebrate development and tissue homeostasis. Mol Cell Biol 29(11):3173-85. [PubMed: 19307306] [MGI Ref ID J:149153]
Li Y; Lim S; Hoffman D; Aspenstrom P; Federoff HJ; Rempe DA. 2009. HUMMR, a hypoxia- and HIF-1alpha-inducible protein, alters mitochondrial distribution and transport. J Cell Biol 185(6):1065-81. [PubMed: 19528298] [MGI Ref ID J:150420]
Li Y; Luikart BW; Birnbaum S; Chen J; Kwon CH; Kernie SG; Bassel-Duby R; Parada LF. 2008. TrkB regulates hippocampal neurogenesis and governs sensitivity to antidepressive treatment. Neuron 59(3):399-412. [PubMed: 18701066] [MGI Ref ID J:147252]
Ma L; Reis G; Parada LF; Schuman EM. 1999. Neuronal NT-3 is not required for synaptic transmission or long-term potentiation in area CA1 of the adult rat hippocampus. Learn Mem 6(3):267-75. [PubMed: 10492008] [MGI Ref ID J:82354]
Mastronardi C; Smiley GG; Raber J; Kusakabe T; Kawaguchi A; Matagne V; Dietzel A; Heger S; Mungenast AE; Cabrera R; Kimura S; Ojeda SR. 2006. Deletion of the Ttf1 gene in differentiated neurons disrupts female reproduction without impairing basal ganglia function. J Neurosci 26(51):13167-79. [PubMed: 17182767] [MGI Ref ID J:116686]
May P; Rohlmann A; Bock HH; Zurhove K; Marth JD; Schomburg ED; Noebels JL; Beffert U; Sweatt JD; Weeber EJ; Herz J. 2004. Neuronal LRP1 Functionally Associates with Postsynaptic Proteins and Is Required for Normal Motor Function in Mice. Mol Cell Biol 24(20):8872-83. [PubMed: 15456862] [MGI Ref ID J:93329]
Meikle L; Pollizzi K; Egnor A; Kramvis I; Lane H; Sahin M; Kwiatkowski DJ. 2008. Response of a neuronal model of tuberous sclerosis to mammalian target of rapamycin (mTOR) inhibitors: effects on mTORC1 and Akt signaling lead to improved survival and function. J Neurosci 28(21):5422-32. [PubMed: 18495876] [MGI Ref ID J:136366]
Meikle L; Talos DM; Onda H; Pollizzi K; Rotenberg A; Sahin M; Jensen FE; Kwiatkowski DJ. 2007. A mouse model of tuberous sclerosis: neuronal loss of Tsc1 causes dysplastic and ectopic neurons, reduced myelination, seizure activity, and limited survival. J Neurosci 27(21):5546-58. [PubMed: 17522300] [MGI Ref ID J:121858]
Mori H; Hanada R; Hanada T; Aki D; Mashima R; Nishinakamura H; Torisu T; Chien KR; Yasukawa H; Yoshimura A. 2004. Socs3 deficiency in the brain elevates leptin sensitivity and confers resistance to diet-induced obesity. Nat Med 10(7):739-43. [PubMed: 15208705] [MGI Ref ID J:91796]
O'Donnell N; Zachara NE; Hart GW; Marth JD. 2004. Ogt-dependent X-chromosome-linked protein glycosylation is a requisite modification in somatic cell function and embryo viability. Mol Cell Biol 24(4):1680-90. [PubMed: 14749383] [MGI Ref ID J:93112]
Ramanan N; Shen Y; Sarsfield S; Lemberger T; Schutz G; Linden DJ; Ginty DD. 2005. SRF mediates activity-induced gene expression and synaptic plasticity but not neuronal viability. Nat Neurosci 8(6):759-67. [PubMed: 15880109] [MGI Ref ID J:99232]
Rempe D; Vangeison G; Hamilton J; Li Y; Jepson M; Federoff HJ. 2006. Synapsin I Cre transgene expression in male mice produces germline recombination in progeny. Genesis 44(1):44-9. [PubMed: 16419044] [MGI Ref ID J:105271]
Romero MI; Lin L; Lush ME; Lei L; Parada LF; Zhu Y. 2007. Deletion of Nf1 in neurons induces increased axon collateral branching after dorsal root injury. J Neurosci 27(8):2124-34. [PubMed: 17314307] [MGI Ref ID J:118374]
Ruzankina Y; Pinzon-Guzman C; Asare A; Ong T; Pontano L; Cotsarelis G; Zediak VP; Velez M; Bhandoola A; Brown EJ. 2007. Deletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss. Cell Stem Cell 1(1):113-26. [PubMed: 18371340] [MGI Ref ID J:123200]
Sahay A; Molliver ME; Ginty DD; Kolodkin AL. 2003. Semaphorin 3F is critical for development of limbic system circuitry and is required in neurons for selective CNS axon guidance events. J Neurosci 23(17):6671-80. [PubMed: 12890759] [MGI Ref ID J:84687]
Shi Y; Yadav VK; Suda N; Liu XS; Guo XE; Myers MG Jr; Karsenty G. 2008. Dissociation of the neuronal regulation of bone mass and energy metabolism by leptin in vivo. Proc Natl Acad Sci U S A 105(51):20529-33. [PubMed: 19074282] [MGI Ref ID J:142673]
Smith KM; Ohkubo Y; Maragnoli ME; Rasin MR; Schwartz ML; Sestan N; Vaccarino FM. 2006. Midline radial glia translocation and corpus callosum formation require FGF signaling. Nat Neurosci 9(6):787-97. [PubMed: 16715082] [MGI Ref ID J:110263]
Tamai K; Toyoshima M; Tanaka N; Yamamoto N; Owada Y; Kiyonari H; Murata K; Ueno Y; Ono M; Shimosegawa T; Yaegashi N; Watanabe M; Sugamura K. 2008. Loss of hrs in the central nervous system causes accumulation of ubiquitinated proteins and neurodegeneration. Am J Pathol 173(6):1806-17. [PubMed: 19008375] [MGI Ref ID J:141391]
Xia CH; Roberts EA; Her LS; Liu X; Williams DS; Cleveland DW; Goldstein LS. 2003. Abnormal neurofilament transport caused by targeted disruption of neuronal kinesin heavy chain KIF5A. J Cell Biol 161(1):55-66. [PubMed: 12682084] [MGI Ref ID J:82911]
Yang X; Klein R; Tian X; Cheng HT; Kopan R; Shen J. 2004. Notch activation induces apoptosis in neural progenitor cells through a p53-dependent pathway. Dev Biol 269(1):81-94. [PubMed: 15081359] [MGI Ref ID J:90392]
Ye Z; Marth JD. 2004. N-glycan branching requirement in neuronal and postnatal viability. Glycobiology 14(6):547-58. [PubMed: 15044398] [MGI Ref ID J:94770]
Zhu Y; Harada T; Liu L; Lush ME; Guignard F; Harada C; Burns DK; Bajenaru ML; Gutmann DH; Parada LF. 2005. Inactivation of NF1 in CNS causes increased glial progenitor proliferation and optic glioma formation. Development 132(24):5577-88. [PubMed: 16314489] [MGI Ref ID J:104342]
Health & husbandry
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.
Health & Colony Maintenance Information
Colony Maintenance
Breeding & Husbandry This strain originated on a B6;CBAF1 background and has been backcrossed to wildtype C57BL/6NHsd mice for at least 5 generations. Coat color expected from breeding:Black
Purchasing information
Pricing, Supply Level & Notes, Controls, General Terms & Conditions
Pricing
| Pricing for USA, Canada and Mexico shipping destinations |
|
Animals Provided
Price (US dollars $) Cryorecovery Fee $1900.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Additional Supply Details
| Pricing for International shipping destinations |
|
Animals Provided
Price (US dollars $) Cryorecovery Fee $2470.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Additional Supply Details
|
|
|
Supply Details
| Standard Supply | Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information. |
|---|---|
| Supply Notes |
|
Control Information
| Control | ||
|---|---|---|
| Noncarrier | ||
| Considerations for Choosing Controls | ||
| USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| International - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
Payment Terms and Conditions
Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.
See Terms of Use tab for General Terms and Conditions
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.Ordering and Purchasing Information
Purchasing Information
JAX® Mice Orders
Surgical Services
Contact Information
Orders & Technical Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form
Terms of Use
Terms of Use
General Terms and Conditions
Contact information
General inquiries
Contracts Administration
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
JAX® Mice, Products & Services Conditions of Use
"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.No Warranty
MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.
In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.
No Liability
In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. In purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.
MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.
The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.
Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.