Updated 26 May 2009

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Name/ Symbol Strain Name Transgene/ Promoter and Regulatory Elements Genetic Background Behavioral  Phenotype Neurological  Characteristics Patents/  Availability Primary Citation β-Synuclein Symbol: bSYN Posted 05/26/09 B6.129-Sncbtm1Sud/J Introduced loxP sites on either side of exon 2 (residues 1-41)/bred with mice expressing cre, thus removing floxed exon 2 /(129X1/SvJ x 129S1/Sv)F1-Kitl +-derived R1-ES cells. Origin: (129X1/SvJ x 129S1/Sv)F1-Kitl<+>. Generation: N5pN1. Backcrossed: C57BL/6. Homozygous mice are viable, normal in size and do not display any gross physical or behavioral abnormalities, but breed very poorly. When bred to a strain expressing Cre recombinase, this mutant mouse strain may be useful in studies of presynaptic proteins and synaptic vesicles. The Jackson Lab, cryopreserved, Stock #008133. Use of mice by companies or for-profit entities requires a license prior to shipping. Chandra et al., 2004 α/β-Synuclein ko Symbol: aSYN-bSYN Posted 05/26/09 B6;129-Sncatm1Sud Sncbtm1.1Sud/J First mutation SNCA gene: first coding exon (residues 1-40), deleted via homologous recombination/electroporated into 129P2/OlaHsd ?derived E14.1 ES cells/injected into C57BL/6 blastocysts/crossed with C57BL/6 mice. Second mutation SNCB gene stock # 8133. Mice carrying the independent targeted mutation genes were intercrossed to generate animals with both mutations. Origin: 129P2/OlaHsd/ (129X1/SvJ x 129S1/Sv)F1-Kitl<+>. Generation: N?+N1F7 (16-Apr-09). Homozygous mice are viable and fertile and do not display any gross physical or behavioral abnormalities. Overall brain morphology and structure normal. Dopamine levels in the mice decreased by ~20 percent, but dopamine uptake and release from isolated nerve terminals is normal. Serotonin levels are unchanged. The Jackson Lab, available, stock #006390. Use of mice by companies or for-profit entities requires a license prior to shipping. Chandra et al., 2004 α-Synuclein (A53T mutation) Line 53 Symbol: aSYN Posted 05/26/09 B6.Cg-Tg(THY1-SNCA*A53T)M53Sud/J/J Mouse SNCA (synuclein, alpha) gene/human THY1 (thymus cell antigen 1, theta) promoter. Origin: unknown. Generation: N5+F2 (02-Jan-09). Hemizygous mice are viable and fertile. Hind limb paralysis due to loss of motor neurons and a resting tremor seen ~6 months. Parkinson-like phenotype upon aging. Cell death in the spinal cord (extensive) and brain. No Lewy body-like pathology. The Jackson Lab, available, stock #008135. Use of mice by companies or for-profit entities requires a license prior to shipping. Chandra et al., 2005 α-Synuclein (huA30P mutation) Line M30 Symbol: aSYN Posted 05/26/09 B6.Cg-Tg(THY1-SNCA*A30P)M30Sud/J/J Human A30P mutant SNCA (synuclein, alpha) gene/human THY1 (thymus cell antigen 1, theta) promoter/injected into B6SJLF1/J embryos, backcrossed ~10 times to C57BL/6. Origin: (C57BL/6J x SJL/J)F1. Generation: N11+F (15-Jan-09). Hind limb mobility problems and a resting tremor phenotype at 10 months due to a loss of motor neurons. Mice live 14 months. Expression of the transgene is fivefold higher in the brain and 10-fold higher in the spinal cord. No Lewy body-like pathology. The Jackson Lab, available, stock #008473. Use of mice by companies or for-profit entities requires a license prior to shipping. Chandra et al., 2005 Tg(THY1-SNCA)1Sud Symbol: aSYN Posted 05/26/09 C57BL/6-Tg(THY1-SNCA)1Sud/J/J HuSNCA gene/THY1 promoter. Generation: N?pN1. Hemizygotes are viable and fertile; mice show onset of motorneuron disease at ~5-6 months. Levels of expression show a 5-fold increase in the brain and a 10-fold increase in the spinal cord. The Jackson Lab, cryopreserved, stock #008389. Use of mice by companies or for-profit entities requires a license prior to shipping. Chandra et al., 2005 α-SYN ko Symbol: aSYN Posted 05/26/09 B6;129X1-Sncatm1Rosl/J PGK-neo cassette used to delete exons 1 and 2 (aa 1-41)/phosphoglycerate 1 promoter/RW-4 ES cells/injected into C57BL/6 blastocysts. Origin: 129X1/SvJ. Generation: [F8p]+F7 (24-Dec-08). Homozygous null mice are viable, fertile, normal in size and do not display any gross abnormalities. No gene product detected in brain tissue. A wildtype complement of dopamine neurons, fibers and synaptic terminals is present and the overall brain architecture appears intact. There is a reduction in total striatal dopamine. Available The Jackson Lab, stock #003692. Use of mice by companies or for-profit entities requires a license prior to shipping. Abeliovich et al., 2000 α-Synuclein, M1m Symbol: aSYN Posted 05/26/09 STOCK Tg(THY1-Snca)M1mSud/J Mouse Snca (synuclein, alpha) cDNA/ mouse Thy1 (thymus cell antigen 1, theta) promoter/ insertion M1m. Origin: unknown. Generation: N?+N1F2 (28-Jan-09). Backcrossed: C57BL/6. Mice hemizygous for this transgene are viable and fertile and do not display any gross physical or behavioral abnormalities, even upon aging. *Normal* nervous system phenotype, mice do not develop motoneuron disease. Available The Jackson Lab, stock #008132. Use of mice by companies or for-profit entities requires a license prior to shipping. Chandra et al., 2005 A53T αsynuclein PRP transgenic-/- (See JAX datasheet) Symbol: SNCA Updated 3/16/09 B6;C3-Tg(Prnp-SNCA*A53T)83Vle/J Mouse Prnp, prion protein promoter/ human α-synuclein A53T mutation cDNA /B6C3H mouse eggs. Origin: C57BL/6 x C3H; Designation: Line 83. Generation: N?+N7F4 (01-Jan-09). Homozygous mice are viable, fertile and normal in size. By 16 months display severe motor phenotype. Lax grooming, weight loss and diminished mobility precede movement impairment, partial limb paralysis, trembling and inability to stand. 8 to 12 months widely distributed α-synuclein inclusions, with dense accumulation in the spinal cord, brainstem, cerebellum and thalamus. This parallels the onset of the motor impairment phenotype. Axons and myelin sheaths exhibit progressive ultrastructural degeneration. Available The Jackson Lab: Stock 004479. Use by companies or for-profit entities requires a license prior to shipping. Giasson et al., 2002 Alpha Synuclein   Human alpha-synuclein cDNA with A53T mutation/ Thy1 gene promoter C57BL/6 An early-onset (>3 weeks of age) and a progressive decline of motor function caused by severe degeneration of neuromuscular junctions. Increased levels of a-synuclein protein in brain found in neurons throughout the telencephalon, brainstem, and spinal cord. Also showed astrocytic gliosis and microglial activation. Many of the cells showed diffuse perikaryal a-synuclein staining. Intense staining with the Campbell-Switzer pyridine silver, a routine and sensitive method used to detect Lewy-type changes in human brain tissue. Unpatented van der Putten H et al., 2000; Sommer B et al., 2000 (PLP)-h[wt] αSYN Symbol: αSYN Updated 4/14/05   Human wt αSYN / proteolipid protein promoter (PLP)/injected into C57BL/6 DBA/2 fertilized eggs. Origin: C57BL/6. Backcross generation N7   Transgenic SYN was detected in brain white matter and oligodendrocytes, detergent insoluble. Hyperphosphorylation at S129 of SYN in the tg mice. Contact Philipp Kahle at pkahle@pbm.med.uni-muenchen.de Kahle et al., 2002 (TH)-h[A30P] SYN Symbol: αSYN Posted 7/9/04   human mutant [A30P] SYN sequence was cloned into a cassette with 4.5-kb 5' flanking DNA from rat TH gene promotor/Injected DBA X C57BL/6 eggs. Origin: C57BL/6; Backcrossed to 4 generations No motor disability Tg mice showed somal and neuritic accumulation of transgenic A30P SYN in TH-positive neurones in the substantia nigra. No difference in the number of TH-positive neurones or concentrations of catecholamines between tg mice and non-tg littermates. Contact Philipp Kahle at pkahle@pbm.med.uni-muenchen.de Rathke-Hartlieb et al., 2001 (Thy1)-h[A30P] SYN Updated 4/14/05   The amplified human [wt]Alpha-SYN-coding sequence with A30P mutation/ neuron specific Thy1 promoter Backcrossed N > 8 generations C57BL/6J, (2002) No overt motor abnormalities to 1 year of age. Shows age-gene-dose dependent lethal locomotor deterioration along with Lewy pathology. Mutant hα-SYN found in synapses, and positive neurites exhibit Lewy body characteristics. Shows age- and gene dose- dependent development of Lewy pathology. Unpatented Contact: Philipp Kahle Kahle et al., 2000 (Thy1)-h[wt] αSYN Updated 11/4/03   human wild-type α-SYN cDNA C57BL/6 None listed. hα-SYN initially undetectable but then increased to plateau at 1 month, expression was 3 fold of endogenous α-SYN. Abnormal Tg α-syn-positive neurites were seen. Tg α-syn found in detergent-insoluble tissue fractions. Contact: Philipp Kahle Kahle et al., 2001