All Phenotypes Tg(Syn1-cre)671Jxm MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Tg(Syn1-cre)671Jxm
transgene insertion 671, Jamey Marth
MGI:2176055

Summary

43 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Bcl7a^tm1Ban/Bcl7a^tm1Ban Bcl7b^tm1Ban/Bcl7b^tm1Ban Tg(Syn1-cre)671Jxm/0	B6.Cg-Bcl7a^tm1Ban Bcl7b^tm1Ban Tg(Syn1-cre)671Jxm	MGI:6361930
cn2	Bcl7a^tm1Ban/Bcl7a^tm1Ban Tg(Syn1-cre)671Jxm/0	B6.Cg-Bcl7a^tm1Ban Tg(Syn1-cre)671Jxm	MGI:6361928
cn3	Npc1^m1N/Npc1^tm1.1Apl Tg(Syn1-cre)671Jxm/0	B6J.Cg-Npc1^m1N/Npc1^tm1.1Apl Tg(Syn1-cre)671Jxm	MGI:5925346
cn4	Socs3^tm1Ayos/Socs3^tm1Ayos Tg(Syn1-cre)671Jxm/0	involves: 129 * C57BL/6	MGI:3051642
cn5	Slc12a6^tm1Garo/Slc12a6^tm1Garo Tg(Syn1-cre)671Jxm/0	involves: 129 * C57BL/6 * CBA	MGI:5318542
cn6	Lepr^tm1.1Chua/Lepr^tm1.1Chua Tg(Syn1-cre)671Jxm/0	involves: 129 * C57BL/6 * CBA	MGI:3837371
cn7	Gabrb3^tm2.1Geh/Gabrb3^tm2.1Geh Tg(Syn1-cre)671Jxm/?	involves: 129 * C57BL/6 * CBA * SJL	MGI:3767261
cn8	Coasy^tm1.1Vtr/Coasy^tm1.1Vtr Tg(Syn1-cre)671Jxm/0	involves: 129 * C57BL/6N * CBA	MGI:6491890
cn9	Slc6a9^tm1Veul/Slc6a9^tm1Veul Tg(Syn1-cre)671Jxm/?	involves: 129P2/OlaHsd * C57BL/6 * CBA	MGI:4818488
cn10	Lepr^tm1Rck/Lepr^tm1.1Rck Tg(Syn1-cre)671Jxm/0	involves: 129P2/OlaHsd * C57BL/6 * CBA	MGI:2176782
cn11	Actb^tm1(INSR)Dac/Actb^tm1(INSR)Dac Insr^tm1Dac/Insr^tm1Dac Tg(Syn1-cre)671Jxm/?	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA	MGI:4831155
cn12	Ogt^tm1Gwh/Y Tg(Syn1-cre)671Jxm/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA	MGI:3841626
cn13	Nf1^tm1Par/Nf1^tm1Par Tg(Syn1-cre)671Jxm/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA	MGI:2176767
cn14	Kif5a^tm1Gsn/Kif5a^tm2Gsn Tg(Syn1-cre)671Jxm/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA	MGI:2656905
cn15	Fig4^tm1.1Mm/Fig4^tm1.1Mm Tg(Syn1-cre)671Jxm/?	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA	MGI:5431086
cn16	Ogt^tm1Gwh/Ogt^tm1Gwh Tg(Syn1-cre)671Jxm/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA	MGI:3841627
cn17	Ntf3^tm1Esm/Ntf3^tm1Esm Tg(Syn1-cre)671Jxm/0	involves: 129S1/Sv * C57BL/6 * CBA	MGI:2653303
cn18	Slc1a2^tm1.1Pros/Slc1a2^tm1.1Pros Tg(Syn1-cre)671Jxm/0	involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6	MGI:5771813
cn19	Slc38a1^tm1.1Ttaka/Slc38a1^tm1.1Ttaka Tsc1^tm1Djk/Tsc1⁺ Tg(Syn1-cre)671Jxm/0	involves: 129S4/SvJae * C57BL/6 * C57BL/6NCrlj * CBA * CBA/JNCrlj	MGI:6441084
cn20	Tsc1^tm1Djk/Tsc1^tm1Djk Tg(Syn1-cre)671Jxm/0	involves: 129S4/SvJae * C57BL/6 * CBA	MGI:3802618
cn21	Tsc1^tm1Djk/Tsc1^tm1.1Djk Tg(Syn1-cre)671Jxm/0	involves: 129S4/SvJae * C57BL/6 * CBA	MGI:3802545
cn22	Kif5a^tm1.2Noh/Kif5a^tm1.2Noh Tg(Syn1-cre)671Jxm/0	involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * CBA	MGI:5495663
cn23	Lrp1^tm2Her/Lrp1^tm2Her Tg(Syn1-cre)671Jxm/0	involves: 129S7/SvEvBrd * C57BL/6 * CBA	MGI:4943558
cn24	Atr^tm1Bal/Atr^tm2Bal Tg(Syn1-cre)671Jxm/0	involves: 129S/SvEv * 129S2/SvPas * C57BL/6 * CBA	MGI:3717477
cn25	Ntrk2^tm1Jom/Ntrk2⁺ Tg(Syn1-cre)671Jxm/0	involves: 129/Sv * C57BL/6 * ICR	MGI:3051975
cn26	Ntrk2^tm1Jom/Ntrk2^tm1Jom Tg(Syn1-cre)671Jxm/0	involves: 129/Sv * C57BL/6 * ICR	MGI:3051974
cn27	Bdnf^tm3Jae/Bdnf^tm3Jae Tg(Syn1-cre)671Jxm/0	involves: 129/Sv * C57BL/6 * ICR	MGI:3051973
cn28	Nkx2-1^tm2Shk/Nkx2-1^tm2Shk Tg(Syn1-cre)671Jxm/0	involves: 129X1/SvJ * C57BL/6 * CBA	MGI:4367245
cn29	Pqbp1^tm1.1Hiok/Pqbp1⁺ Tg(Syn1-cre)671Jxm/0	involves: C57BL/6 * C57BL/6J	MGI:6474222
cn30	Pqbp1^tm1.1Hiok/Y Tg(Syn1-cre)671Jxm/0	involves: C57BL/6 * C57BL/6J	MGI:6474221
cn31	Clstn3^{tm1c(EUCOMM)Hmgu}/Clstn3^{tm1c(EUCOMM)Hmgu} Tg(Syn1-cre)671Jxm/0	involves: C57BL/6 * C57BL/6N * CBA * SJL	MGI:6454088
cn32	Slc38a1^tm1.1Ttaka/Slc38a1^tm1.1Ttaka Tg(Syn1-cre)671Jxm/0	involves: C57BL/6 * C57BL/6NCrlj * CBA * CBA/JNCrlj	MGI:6441082
cn33	Prkar2b^tm3Gsm/Prkar2b^tm2Gsm Tg(Syn1-cre)671Jxm/0	involves: C57BL/6 * CBA	MGI:5515333
cn34	Tg(Syn1-cre)671Jxm/0 Ubqln1^tm1.1Hmw/Ubqln1^tm1.1Hmw	involves: C57BL/6 * CBA	MGI:5576880
cn35	Plrg1^tm2Jcbr/Plrg1^tm2Jcbr Tg(Syn1-cre)671Jxm/0	involves: C57BL/6 * CBA	MGI:3848250
cn36	Sema3f^tm1.1Ddg/Sema3f^tm1.2Ddg Tg(Syn1-cre)671Jxm/0	involves: C57BL/6 * CBA	MGI:2670688
cn37	Sema3f^tm1.1Ddg/Sema3f^tm1.1Ddg Tg(Syn1-cre)671Jxm/0	involves: C57BL/6 * CBA	MGI:2670683
cn38	Gt(ROSA)26Sor^{tm1(CAG-EGFP/Vamp2)Ggc}/Gt(ROSA)26Sor⁺ Tg(Syn1-cre)671Jxm/0	involves: C57BL/6 * CBA	MGI:5564784
cn39	Hgs^tm2Tkh/Hgs^tm2Tkh Tg(Syn1-cre)671Jxm/0	involves: C57BL/6 * CBA * SJL	MGI:3818706
cn40	Tg(ACTB-NOTCH1)1Shn/0 Tg(Syn1-cre)671Jxm/0	involves: C57BL/6J	MGI:3044599
cn41	S1pr1^tm1Jch/S1pr1^tm1Jch Tg(Syn1-cre)671Jxm/?	involves: C57BL/6J * CBA	MGI:4939154
cn42	Depdc5^{tm1c(EUCOMM)Hmgu}/Depdc5⁺ Tg(Syn1-cre)671Jxm/0	involves: C57BL/6N * CBA	MGI:6154994
cn43	Depdc5^{tm1c(EUCOMM)Hmgu}/Depdc5^{tm1c(EUCOMM)Hmgu} Tg(Syn1-cre)671Jxm/0	involves: C57BL/6N * CBA	MGI:6154993

Allelic Composition	Bcl7a^tm1Ban/Bcl7a^tm1Ban Bcl7b^tm1Ban/Bcl7b^tm1Ban Tg(Syn1-cre)671Jxm/0
Genetic Background	B6.Cg-Bcl7a^tm1Ban Bcl7b^tm1Ban Tg(Syn1-cre)671Jxm

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl7a^tm1Ban mutation (0 available); any Bcl7a mutation (27 available)
Bcl7b^tm1Ban mutation (0 available); any Bcl7b mutation (75 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

behavior/neurological phenotype ( J:279171 )

N	• no defects in spatial learning are detected

impaired coordination ( J:279171 )

• on a rotarod

impaired swimming ( J:279171 )

• decrease in swim speeding and increased floating behavior

nervous system

abnormal Purkinje cell dendrite morphology ( J:279171 )

• complexity of the arbor is significantly reduced, but is similar to mutant mice wild-type for Bcl7b

• however, the number and alignment of Purkinje neurons is similar to controls

growth/size/body

decreased body weight ( J:279171 )

• mild reduction

Allelic Composition	Bcl7a^tm1Ban/Bcl7a^tm1Ban Tg(Syn1-cre)671Jxm/0
Genetic Background	B6.Cg-Bcl7a^tm1Ban Tg(Syn1-cre)671Jxm

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl7a^tm1Ban mutation (0 available); any Bcl7a mutation (27 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

behavior/neurological phenotype ( J:279171 )

N	• no defects in spatial learning are detected in a Morris water maze

impaired coordination ( J:279171 )

• shorter latency to fall off a rotarod and fail to improve performance with training

impaired swimming ( J:279171 )

• decrease in swim speeding and slightly increased floating behavior

abnormal gait ( J:279171 )

• slightly abnormal with increased front paw stand duration and stride length and reduced paw overlap

nervous system

abnormal Purkinje cell dendrite morphology ( J:279171 )

• complexity of the arbor is significantly reduced

• however, the number and alignment of Purkinje neurons is similar to controls

growth/size/body

decreased body weight ( J:279171 )

• decrease in body weight is seen at 6 months of age

Allelic Composition	Npc1^m1N/Npc1^tm1.1Apl Tg(Syn1-cre)671Jxm/0
Genetic Background	B6J.Cg-Npc1^m1N/Npc1^tm1.1Apl Tg(Syn1-cre)671Jxm

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Npc1^m1N mutation (3 available); any Npc1 mutation (74 available)
Npc1^tm1.1Apl mutation (0 available); any Npc1 mutation (74 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:176888 )

• mice show early death, with an average lifespan of 105 days

nervous system

microgliosis ( J:176888 )

• mice show activated microglia in many brain regions

increased brain cholesterol level ( J:176888 )

astrocytosis ( J:176888 )

• mice show activated astrocytes in many brain regions

abnormal axon morphology ( J:176888 )

• mice show severe axonal pathology

axonal spheroids ( J:176888 )

• mice exhibit frequent axonal spheroids in the brainstem

demyelination ( J:176888 )

• mice show loss of myelinated fibers in the corpus callosum

behavior/neurological

impaired balance ( J:176888 )

• mice develop motor deficits in the balance beam

impaired coordination ( J:176888 )

• mice develop motor deficits in the rotarod

growth/size/body

weight loss ( J:176888 )

• mice exhibit progressive weight loss

hematopoietic system

microgliosis ( J:176888 )

• mice show activated microglia in many brain regions

homeostasis/metabolism

increased brain cholesterol level ( J:176888 )

immune system

microgliosis ( J:176888 )

• mice show activated microglia in many brain regions

Allelic Composition	Socs3^tm1Ayos/Socs3^tm1Ayos Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129 * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Socs3^tm1Ayos mutation (2 available); any Socs3 mutation (22 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

adipose tissue

decreased body fat mass ( J:91796 )

• on a high fat diet total fat weight and individual fat pad weights increase less in mutants compared to wild-type mice

behavior/neurological

abnormal food intake ( J:91796 )

• food intake is decreased on a high fat diet compared to wild-type mice on the same diet

growth/size/body

decreased body fat mass ( J:91796 )

• on a high fat diet total fat weight and individual fat pad weights increase less in mutants compared to wild-type mice

decreased body weight ( J:91796 )

• on a high fat diet mutants gain less weight

homeostasis/metabolism

decreased circulating free fatty acids level ( J:91796 )

• after 22 weeks on a high fat diet plasma free fatty acid levels are significantly lower in mutants

decreased circulating triglyceride level ( J:91796 )

• after 22 weeks on a high fat diet triglyceride levels are significantly lower in mutants

improved glucose tolerance ( J:91796 )

• glucose clearance is significantly faster in mutants compared to wild-type mice

increased insulin sensitivity ( J:91796 )

• on a high fat diet mutants do not develop insulin resistance

increased response to leptin ( J:91796 )

• leptin treatment induces a greater decrease in food intake in mutants compared to wild-type mice

• treatment with leptin induces greater weight loss in mutants

Allelic Composition	Slc12a6^tm1Garo/Slc12a6^tm1Garo Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129 * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc12a6^tm1Garo mutation (1 available); any Slc12a6 mutation (120 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

reproductive system

infertility ( J:183239 )

• unable to successfully breed

nervous system

abnormal nervous system morphology ( J:183239 )

• progressive peripheral neuropathy starting at 3-4 weeks of age

increased brain weight ( J:183239 )

• at 2 months of age

decreased corpus callosum size ( J:183239 )

• hypoplastic with a small but significant decrease in length

abnormal axon morphology ( J:183239 )

• axon swelling in sciatic nerves

abnormal sciatic nerve morphology ( J:183239 )

• axon degeneration, hypomyelination and axon swelling in sciatic nerves

axon degeneration ( J:183239 )

• in sciatic nerves

demyelination ( J:183239 )

• hypomyelination in sciatic nerves

behavior/neurological

limb grasping ( J:183239 )

• by 3-4 weeks of age

impaired coordination ( J:183239 )

abnormal locomotor behavior ( J:183239 )

• severe locomotor deficiencies

• deficiencies become more severe after 8 months of age

increased locomotor activity ( J:183239 )

• significant increase in the total distance traveled and the number of movement bouts at 5 months of age

decreased chemical nociceptive threshold ( J:183239 )

• significantly less sensitive in a formalin test of spontaneous chemical/inflammatory pain

growth/size/body

decreased body weight ( J:183239 )

• at 2 months of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
agenesis of the corpus callosum with peripheral neuropathy		DOID:0090003	OMIM:218000	J:183239

Allelic Composition	Lepr^tm1.1Chua/Lepr^tm1.1Chua Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129 * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lepr^tm1.1Chua mutation (1 available); any Lepr mutation (122 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

increased insulin secretion ( J:145998 )

decreased circulating adrenaline level ( J:145998 )

decreased circulating noradrenaline level ( J:145998 )

endocrine/exocrine glands

increased insulin secretion ( J:145998 )

nervous system

abnormal sympathetic nervous system physiology ( J:145998 )

• sympathetic tone, as measured by Ucp1 expression and levels of epinephrine and norepinephrine, is low compared to in wild-type mice

• however, treatment with isoproterenol increases sympathetic tone

Allelic Composition	Gabrb3^tm2.1Geh/Gabrb3^tm2.1Geh Tg(Syn1-cre)671Jxm/?
Genetic Background	involves: 129 * C57BL/6 * CBA * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gabrb3^tm2.1Geh mutation (1 available); any Gabrb3 mutation (33 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

postnatal lethality, incomplete penetrance ( J:127877 )

• born at expected Mendelian frequency

• no cleft palate found

• about 61% died before weaning, many within a few days after birth

behavior/neurological

behavior/neurological phenotype ( J:127877 )

N	• homozygous mice that survived beyond weaning were normal and fertile • unlike global knockout, they did not display foot clasping behavior, hyperactivity, seizures, or tremors

impaired behavioral response to xenobiotic ( J:127877 )

• less sensitive to the sedative/hypnotic effects of etomidate

Allelic Composition	Coasy^tm1.1Vtr/Coasy^tm1.1Vtr Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129 * C57BL/6N * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Coasy^tm1.1Vtr mutation (0 available); any Coasy mutation (15 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

impaired righting response ( J:299154 )

dystonia ( J:299154 )

• dystonia-like movements with flexing or prolonged stiff extension of the limbs and tail rigidity

abnormal tail movements ( J:299154 )

• tail rigidity

positive geotaxis ( J:299154 )

cellular

abnormal mitochondrial physiology ( J:299154 )

• impairment of pyruvate-dependent mitochondrial respiration in the brain

growth/size/body

decreased body weight ( J:299154 )

• starting at P8

postnatal growth retardation ( J:299154 )

• starting at P8

homeostasis/metabolism

abnormal calcium level ( J:299154 )

• increased in the brain

increased brain iron level ( J:299154 )

abnormal magnesium level ( J:299154 )

• increased in the brain

mortality/aging

premature death ( J:299154 )

• mice were euthanized around P13 for compassionate reasons

muscle

dystonia ( J:299154 )

• dystonia-like movements with flexing or prolonged stiff extension of the limbs and tail rigidity

nervous system

nervous system phenotype ( J:299154 )

N	• forebrains exhibit normal troughs and no astrocytosis, neuroinflammation, neuronal loss or intracellular inclusion

increased brain iron level ( J:299154 )

decreased brain weight ( J:299154 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
neurodegeneration with brain iron accumulation 6		DOID:0110740	OMIM:615643	J:299154

Allelic Composition	Slc6a9^tm1Veul/Slc6a9^tm1Veul Tg(Syn1-cre)671Jxm/?
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc6a9^tm1Veul mutation (0 available); any Slc6a9 mutation (24 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

muscle

muscle phenotype ( J:161993 )

N	• no hypotonia

behavior/neurological

behavior/neurological phenotype ( J:161993 )

N	• no motor defects seen in open field or rotarod tests

nervous system

abnormal neuron physiology ( J:161993 )

• GlyT1 specific uptake of glycine by hippocampal membranes is reduced 50%

Allelic Composition	Lepr^tm1Rck/Lepr^tm1.1Rck Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lepr^tm1.1Rck mutation (1 available); any Lepr mutation (122 available)
Lepr^tm1Rck mutation (1 available); any Lepr mutation (122 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

adipose tissue

increased total body fat amount ( J:72241 )

growth/size/body

abnormal body composition ( J:72241 )

• increased adipose tissue mass and decreased lean tissue mass

increased body weight ( J:72241 )

• observed after 5 weeks of age

homeostasis/metabolism

hyperglycemia ( J:72241 )

• 2.3 fold greater plasma glucose levels in females compared to littermates; males normal

increased circulating insulin level ( J:72241 )

• hyperinsulinemia; 6 fold greater plasma insulin levels in males and 16.1 fold greater levels in females compared to littermates

increased circulating leptin level ( J:72241 )

• 5.8 fold greater in males and 8.3 fold greater in females compared to littermates

liver/biliary system

hepatic steatosis ( J:72241 )

• enlarged liver due to fatty deposits

Allelic Composition	Actb^tm1(INSR)Dac/Actb^tm1(INSR)Dac Insr^tm1Dac/Insr^tm1Dac Tg(Syn1-cre)671Jxm/?
Genetic Background	involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Actb^tm1(INSR)Dac mutation (0 available); any Actb mutation (53 available)
Insr^tm1Dac mutation (2 available); any Insr mutation (95 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:91350 )

• die between 6 and 8 weeks

homeostasis/metabolism

increased circulating glucose level ( J:91350 )

• diabetic in one week

increased circulating insulin level ( J:91350 )

• extremely elevated

Allelic Composition	Ogt^tm1Gwh/Y Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ogt^tm1Gwh mutation (2 available); any Ogt mutation (12 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

postnatal lethality, complete penetrance ( J:93112 )

• none survive for more than 10 days

prenatal lethality, incomplete penetrance ( J:93112 )

• found at only about 50% of the expected frequency

behavior/neurological

abnormal suckling behavior ( J:93112 )

• rarely nurse

abnormal locomotor behavior ( J:93112 )

• fail to develop normal locomotor activity

growth/size/body

decreased fetal size ( J:93112 )

Allelic Composition	Nf1^tm1Par/Nf1^tm1Par Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nf1^tm1Par mutation (4 available); any Nf1 mutation (161 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

decreased body weight ( J:68558 )

• body weight and size are about 50% of normal

postnatal growth retardation ( J:68558 )

• 3-4 days after birth, mice begin to exhibit growth retardation that is sustained into adulthood

nervous system

decreased forebrain size ( J:68558 )

• forebrain, but not the rest of the brain, is reduced in size, however mice exhibit normal neuronal development

abnormal cerebral cortex morphology ( J:68558 )

• increase in cell density in the cerebral cortex, often resulting in less apparent lamination

thin cerebral cortex ( J:68558 )

• about 20% reduction in coritcal thickness

astrocytosis ( J:68558 )

• mice display astrogliosis in various brain regions, however do not develop neuronal degeneration or microgliosis

behavior/neurological

abnormal learning/memory/conditioning ( J:68558 )

• mice display severe learning disability

neoplasm

neoplasm ( J:68558 )

N	• no evidence of tumors; optic gliomas, astrocytomas, or neurofibroma are not observed

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
neurofibromatosis 1		DOID:0111253	OMIM:162200	J:68558

Allelic Composition	Kif5a^tm1Gsn/Kif5a^tm2Gsn Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kif5a^tm1Gsn mutation (1 available); any Kif5a mutation (55 available)
Kif5a^tm2Gsn mutation (1 available); any Kif5a mutation (55 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

lethality at weaning, incomplete penetrance ( J:82911 )

• 72% of mutant mice die of seizures at ~3 weeks of age, between P15 and P25

premature death ( J:82911 )

• the remaining ~28% (8 of 29) of mutant mice survived to >3 months of age; one died at 3 months, one at 4 months, and another at 5.5 months, while the rest were sacrified at 5.5, 7, and 8 months

growth/size/body

decreased body size ( J:82911 )

• by 2-3 weeks of age, mutant mice are obviously smaller than control littermates

decreased body weight ( J:82911 )

• at 3 weeks of age, mutant body weight is only ~50% of control weight

behavior/neurological

tremors ( J:82911 )

• at 3 weeks of age, mutant mice frequently display a tremor, although their posture is relatively normal

• all mutant mice surviving to >5 months of age, develop tremors while walking

impaired coordination ( J:82911 )

• at 3 weeks of age, mutant mice fall off the rotarod more frequently than control mice

abnormal posture ( J:82911 )

• all mutant mice surviving to >5 months of age develop abnormal hindlimb posture at rest

• however, a relatively normal posture is observed until ~5 months of age

hindlimb paralysis ( J:82911 )

• mutant mice surviving to >5 months of age develop a partial hindlimb paralysis

sporadic seizures ( J:82911 )

• 72% of mutant mice die from spontaneous seizures lasting 20-30 seconds

• repetitive seizures and stress-induced seizures are also observed

nervous system

sporadic seizures ( J:82911 )

• 72% of mutant mice die from spontaneous seizures lasting 20-30 seconds

• repetitive seizures and stress-induced seizures are also observed

axon degeneration ( J:82911 )

• mutant mice surviving to >5 months of age display a striking degeneration of sensory axons within L5 lumbar dorsal roots along with numerous profiles of myelin debris

• at 3 weeks of age, mutants show a ~14% loss of sensory axon numbers within L5 dorsal roots, with a preferrential (60%) loss of large caliber sensory axons (>3 m in diameter) but no significant loss of small caliber axons

• by 5.5 months of age, mutants exhibit a ~12% loss of motor axons and a profound 36% loss of sensory axons; again, sensory and motor axon loss is most severe for large caliber axons (>4 m), and loss of ventral root axons is not as profound as that observed in the dorsal root

• at 5.5 months of age, the peak of the distribution of the diameter of large caliber axons in the ventral root shifts from 7-7.5 m in controls to 5.5-6 m in mutants

• in the dorsal roots, severe axon loss is noted in sensory axons with calibers >2 m, with complete loss of the largest sensory axons (>7 m), but no loss of small caliber sensory axons (<1.5 m)

abnormal axonal transport ( J:82911 )

• at 3 weeks of age, mutant mice show a a specific deficit in the slow axonal transport of neurofilaments, as evidenced by the accumulation of NF subunits (NF-H, NF-L, and NF-M) and peripherin in the cell bodies of DRG sensory neurons

• however, no obvious changes in the amounts of NF-H, NF-M, NF-L, or peripherin are detected in the brain and sciatic nerve of mutant mice

• in addition, fast axonal transport appears to be intact, as markers of several fast axonal transport pathways (APP, Rab3, and synaptophysin) appeared unchanged in the DRG and in sciatic nerve ligation experiments

homeostasis/metabolism

abnormal protein level ( J:82911 )

• at 3 weeks of age, mutant mice display a striking accumulation of neurofilament (NF) subunits (NF-H, NF-L, and NF-M) and peripherin in the cell bodies of dorsal root ganglion (DRG) sensory neurons, due to a specific deficit in slow axonal transport of NFs

• neurofilament accumulation in the DRG is accompanied by a significant decrease in the number of large caliber sensory axons

• betaIII-tubulin is unchanged in younger animals, but displays behavior indicative of defective transport in some older mutant mice

• notably, accumulation of NF subunit levels in the DRG is not accompanied by obvious reductions in the sciatic nerve

Allelic Composition	Fig4^tm1.1Mm/Fig4^tm1.1Mm Tg(Syn1-cre)671Jxm/?
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fig4^tm1.1Mm mutation (0 available); any Fig4 mutation (52 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:185989 )

• survival to 5 months of age but severely weakened

behavior/neurological

abnormal motor capabilities/coordination/movement ( J:185989 )

• severe movement disorder by 30 days of age

limb grasping ( J:185989 )

• both forelimb and hind limb clasping in tail suspension tests at 3 months of age

nervous system

astrocytosis ( J:185989 )

• low level of astrocyte dysfunction

spongiform encephalopathy ( J:185989 )

• in deep layers of cortex, cerebellar nuclei, hippocampus, brainstem, and dorsal root ganglia

growth/size/body

decreased body weight ( J:185989 )

• body weight reductions are modest, weights of about 17g

integument

integument phenotype ( J:185989 )

N	• normal coat color (not diluted)

Allelic Composition	Ogt^tm1Gwh/Ogt^tm1Gwh Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ogt^tm1Gwh mutation (2 available); any Ogt mutation (12 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

postnatal lethality, complete penetrance ( J:93112 )

• none survive for more than 10 days

behavior/neurological

abnormal suckling behavior ( J:93112 )

• rarely nurse

abnormal locomotor behavior ( J:93112 )

• fail to develop normal locomotor activity

growth/size/body

decreased fetal size ( J:93112 )

Allelic Composition	Ntf3^tm1Esm/Ntf3^tm1Esm Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129S1/Sv * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ntf3^tm1Esm mutation (0 available); any Ntf3 mutation (24 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

nervous system phenotype ( J:82354 )

N	• mutants exhibit normal synaptic transmission, with no differences in paired-pulse facilitation, post-tetanic potentiation, or long-term potentiation

Allelic Composition	Slc1a2^tm1.1Pros/Slc1a2^tm1.1Pros Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc1a2^tm1.1Pros mutation (1 available); any Slc1a2 mutation (40 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal synaptic physiology ( J:221590 )

• at 14-19 weeks of age, the synaptosomal glutamate uptake capacity (Vmax) is reduced by ~40% relative to wild-type controls

• uptake of D-[3H]aspartate into crude forebrain synaptosomes is reduced by ~49% relative to controls

• however, both the GLT-1 protein and glutamate uptake activity that could be solubilized and reconstituted in liposomes are unaffected

mortality/aging

mortality/aging ( J:221590 )

N	• mice exhibit normal survival up to 70 weeks of age

growth/size/body

growth/size/body region phenotype ( J:221590 )

N	• mice exhibit normal weight gain up to 24 weeks of age

behavior/neurological

behavior/neurological phenotype ( J:221590 )

N	• at 12-52 weeks of age, mice show no significant differences in total SHIRPA scores relative to control mice • no spontaneous clinical seizures are observed • no electrographic seizures are detected by scalp or tethered EEG recordings

Allelic Composition	Slc38a1^tm1.1Ttaka/Slc38a1^tm1.1Ttaka Tsc1^tm1Djk/Tsc1⁺ Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129S4/SvJae * C57BL/6 * C57BL/6NCrlj * CBA * CBA/JNCrlj

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc38a1^tm1.1Ttaka mutation (0 available); any Slc38a1 mutation (32 available)
Tg(Syn1-cre)671Jxm mutation (1 available)
Tsc1^tm1Djk mutation (2 available); any Tsc1 mutation (71 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

nervous system phenotype ( J:288818 )

N	• normal susceptibility to ischemic brain injury after applying middle cerebral artery occlusion (MCAO)

Allelic Composition	Tsc1^tm1Djk/Tsc1^tm1Djk Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129S4/SvJae * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Syn1-cre)671Jxm mutation (1 available)
Tsc1^tm1Djk mutation (2 available); any Tsc1 mutation (71 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:121858 )

• clinical features, survival, and brain pathology are stated to be identical to that of Tsc1^tm1Djk Tsc1^tm1.1Djk Tg(Syn1-cre)671Jxm conditional mutants; however no data are presented

growth/size/body

abnormal body size ( J:121858 )

nervous system

abnormal nervous system morphology ( J:121858 )

abnormal nervous system physiology ( J:121858 )

behavior/neurological

abnormal behavior ( J:121858 )

Allelic Composition	Tsc1^tm1Djk/Tsc1^tm1.1Djk Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129S4/SvJae * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Syn1-cre)671Jxm mutation (1 available)
Tsc1^tm1.1Djk mutation (1 available); any Tsc1 mutation (71 available)
Tsc1^tm1Djk mutation (2 available); any Tsc1 mutation (71 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:121858 , J:136366 )

• median survival of 35 days, with no survivors beyond 65 days (J:121858)

• mice treated with rapamycin or RAD001 (mTOR inhibitor) show 90-100% survival to 80 days of age compared to median survival of 33 days for untreated mutants (J:136366)

• discontinuation of drug treatment at P30 results in clinical symptom improvement for 1-2 weeks followed by clinical deterioration and death at 79 days for rapamycin-treated and 77 days for RAD001-treated mutants (J:136366)

growth/size/body

slow postnatal weight gain ( J:121858 )

• after P5 until death, mutants fail to gain weight at same rate as controls; average maximum weight is 10 grams

nervous system

seizures ( J:121858 )

• mice develop clinical seizures, spontaneous and some provoked in most part by physical simulation; both types of seizures are mild or severe

• severe seizures are characterized by brief behavioral arrest, followed by several seconds of clonic activity, followed by tonic extensor posturing of trunk and limbs for 15-45 seconds

• after P21, suspension by the tail results in gentle spinning leading severe seizure activity, followed by bradycardia and death

sporadic seizures ( J:121858 )

• only mild seizures occur spontaneously, characterized by brief myoclonic jerking of head and torso

abnormal brain morphology ( J:121858 )

• enlarged cells are seen outside cerebral cortex, in other parts of brain including thalamus, hypothalamus and brainstem

• no increased cell loss or degeneration is observed in regions containing anomalous enlarged cells

increased brain weight ( J:136366 )

• brain weight to body weight ratio is significantly greater (2.4-fold) in mutants compared to wild-type; with rapamycin/RAD001 treatment, difference from control is significantly reduced but still observed

abnormal dentate gyrus morphology ( J:121858 )

• enlarged cells are observed in hilus

abnormal hippocampus pyramidal cell layer ( J:121858 )

• enlarged cells are seen throughout pyramidal cell layer, particularly in CA3 region

abnormal hippocampus region morphology ( J:121858 )

• enlarged ectopic cells are seen outside the CA1-CA3 fields in stratum oriens and stratum radiatum

abnormal cerebral cortex morphology ( J:121858 , J:136366 )

• laminar organization is less distinct than in the 6 cortical layers of controls (J:121858)

• unusually large cells are observed in all six layers in mutants, particularly in layer V; layer of enlarged cells is seen at gray-white matter border throughout cerebral cortex at P21 (J:121858)

• mutants display subset of enlarged pS6-positive cells at base of cortex and in cortical layer V; drug treatment results in marked reduction in size of enlarged cells (J:136366)

• mild cortical disorganization is observed in mutants with or without rapamycin treatment (J:136366)

abnormal neocortex morphology ( J:121858 )

• contains some enlarged cells

abnormal neuron morphology ( J:121858 , J:136366 )

• Nissl bodies and filamentous aggregates are often detected in enlarged neurons, prominently in brainstem but rarely in enlarged cortical cells (J:121858)

• some neurons are aberrantly localized outside primary pyramidal cell layers; ectopic neurons are isolated, not organized into clusters or columns (J:121858)

• some neurons in somatosensory cortex show 60% increase in soma size relative to controls (J:121858)

• many pyramidal neurons demonstrate dysplastic features including increased size and thicker dendritic arbors compared to control neurons (J:121858)

• population of neurons in lateral somatosensory cortex are considerably enlarged compared with those in controls; size is significantly reduced after drug treatment (from 1.8-fold to 1.2-fold), but effect reverses when treatment is stopped (J:136366)

• in somatosensory cortex, layer V neurons often have major dendrites extending tangentially and diagonally to the pia, in contrast to control neurons which mainly have long apical dendrite oriented directly toward pial surface; rapamycin treatment initiated at P7 does not significantly decrease abnormally oriented dendrite percentage (J:136366)

abnormal neuron differentiation ( J:121858 )

• in mutant brains, neurons appear to be still actively growing after P14-21, whereas wild-type neurons have stopped growing

• this may result in the hypomyelination, due to secondary myelination failure

abnormal dendrite morphology ( J:136366 )

• in hippocampal neuron cultures, neuronal dendritic spine density is reduced >20% compared to controls

• with rapamycin treatment, spine density is marginally increased; spine length however is increased 9% compared to treated and untreated controls or untreated mutants

abnormal myelination ( J:121858 , J:136366 )

• hypomyelination is observed in brains of mutants (J:121858)

• oligodendrocyte number and distribution appears similar to wild-type (J:121858)

• myelination particularly in cortex is impaired due to decreased myelin production by oligodendrocytes; rapamycin treatment works to restore myelination throughout brain with greatest improvement in cortex and hippocampus (J:136366)

abnormal brain wave pattern ( J:121858 )

• mice aged P21-48 display 3 types of electrographic abnormalities: short spike bursts observed in all mice examined, occasionally spontaneous period of desynchronization with electrodecrement and at low incidence, frequent high-amplitude sharp waves

• interictal (seizure) 1-2 second bursts of high-amplitude 7-8 hertz spikes are observed with high frequency compared with controls; these are without obvious clinical correlate

behavior/neurological

abnormal involuntary movement ( J:136366 )

• clasping behavior and tremor are significantly ameliorated by rapamycin/RAD001 treatment relative to untreated animals at 30, 60, and 100 days postnatal

increased startle reflex ( J:121858 )

• apparent by P10

limb grasping ( J:121858 )

• display posterior limb-clasping behavior when lifted by tail

tremors ( J:121858 )

• progressive high-frequency trunk and limb tremor apparent by P10

abnormal limb posture ( J:121858 )

• at death, usually in third to fifth postnatal week, mice are found with extensor posture of fore- and hindlimbs

hunched posture ( J:121858 )

• develops by by third or fourth postnatal week

straub tail ( J:121858 )

• tail dorsiflexion is exhibited

decreased locomotor activity ( J:121858 )

• mice show progressive decline in activity with limited mobility by third or fourth postnatal week

hyperactivity ( J:121858 )

• apparent by P10

seizures ( J:121858 )

• mice develop clinical seizures, spontaneous and some provoked in most part by physical simulation; both types of seizures are mild or severe

• severe seizures are characterized by brief behavioral arrest, followed by several seconds of clonic activity, followed by tonic extensor posturing of trunk and limbs for 15-45 seconds

• after P21, suspension by the tail results in gentle spinning leading severe seizure activity, followed by bradycardia and death

sporadic seizures ( J:121858 )

• only mild seizures occur spontaneously, characterized by brief myoclonic jerking of head and torso

skeleton

abnormal spine curvature ( J:136366 )

• kyphosis is significantly improved in rapamycin/RAD001-treated mice compared with untreated mutants

cellular

abnormal neuron differentiation ( J:121858 )

• in mutant brains, neurons appear to be still actively growing after P14-21, whereas wild-type neurons have stopped growing

• this may result in the hypomyelination, due to secondary myelination failure

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
tuberous sclerosis		DOID:13515	OMIM:PS191100	J:136366

Allelic Composition	Kif5a^tm1.2Noh/Kif5a^tm1.2Noh Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kif5a^tm1.2Noh mutation (0 available); any Kif5a mutation (55 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

postnatal lethality, complete penetrance ( J:197666 )

• mice die at approximately 3 weeks postnatally

nervous system

nervous system phenotype ( J:197666 )

N	• mice exhibit normal brain histology

seizures ( J:197666 )

• mice exhibit epileptic electroencephalography (EEG) and reduced EEG power during rest and locomotive states compared with control mice

abnormal GABA-mediated receptor currents ( J:197666 )

• impaired neurotransmission in the hippocampus with abnormal post-Golgi GABA receptor trafficking and localization

decreased miniature inhibitory postsynaptic current amplitude ( J:197666 )

• reduced mean amplitude with a shift to smaller amplitudes

• however, miniature inhibitory postsynaptic currents frequency, rise time and decay time are normal

growth/size/body

postnatal growth retardation ( J:197666 )

behavior/neurological

seizures ( J:197666 )

• mice exhibit epileptic electroencephalography (EEG) and reduced EEG power during rest and locomotive states compared with control mice

Allelic Composition	Lrp1^tm2Her/Lrp1^tm2Her Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129S7/SvEvBrd * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lrp1^tm2Her mutation (0 available); any Lrp1 mutation (211 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:93329 )

• die around 9 months of age

reproductive system

reduced fertility ( J:93329 )

• greatly reduced fertility

behavior/neurological

increased food intake ( J:93329 )

• adults eat more compared to wild-type controls

limb grasping ( J:93329 )

tremors ( J:93329 )

• a constant muscle tremor develops by 3 weeks of age

impaired limb coordination ( J:93329 )

• mild

weakness ( J:93329 )

• pronounced hind limb weakness, unable to stand on their hind legs

abnormal posture ( J:93329 )

• develop dystonic posturing over time

abnormal limb posture ( J:93329 )

• over time increased plantar flexion of the feet occurs, with asymmetric involvement in some mice

abnormal gait ( J:93329 )

• waddling gait

• step width increases in relation to step length

hyperactivity ( J:93329 )

• general hyperactivity combined with increased voluntary movement, detectable by 3 weeks of age

skeleton

kyphosis ( J:93329 )

• increased thoracic kyphosis develops over time

growth/size/body

postnatal growth retardation ( J:93329 )

• initially similar in size and weight to wild-type controls but gradually fall behind in their growth rate

adipose tissue

decreased total body fat amount ( J:93329 )

• adults are leaner than wild-type controls

homeostasis/metabolism

hypoglycemia ( J:93329 )

decreased circulating insulin level ( J:93329 )

nervous system

nervous system phenotype ( J:93329 )

N	• no histological defects in brain morphology are detected • electroencephalographic and electromyographic studies confirmed the tremor but did not detect any abnormalities in neuro- or neuromuscular transmission • no abnormalities in hippocampal long term potentiation are detected

Allelic Composition	Atr^tm1Bal/Atr^tm2Bal Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129S/SvEv * 129S2/SvPas * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atr^tm1Bal mutation (1 available); any Atr mutation (133 available)
Atr^tm2Bal mutation (1 available); any Atr mutation (133 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

behavior/neurological phenotype ( J:123200 )

N	• tamoxifen-treated mice do not show any significant differences from controls in circadian activity, strength, motor coordination, anxiety-like behavior, learning or memory

Allelic Composition	Ntrk2^tm1Jom/Ntrk2⁺ Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129/Sv * C57BL/6 * ICR

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ntrk2^tm1Jom mutation (0 available); any Ntrk2 mutation (66 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

decreased kindling response ( J:91467 )

• a modest inhibition of kindling development is seen with an increased number of stimulations required to induce the third consecutive class 4 or class 5 seizure

nervous system

decreased kindling response ( J:91467 )

• a modest inhibition of kindling development is seen with an increased number of stimulations required to induce the third consecutive class 4 or class 5 seizure

Allelic Composition	Ntrk2^tm1Jom/Ntrk2^tm1Jom Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129/Sv * C57BL/6 * ICR

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ntrk2^tm1Jom mutation (0 available); any Ntrk2 mutation (66 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

decreased kindling response ( J:91467 )

• kindling could not be induced even after 48 to 50 stimulations and an increase in the current required to induce the initial electrographic seizure is seen

• electroconvulsive shock can induce tonic-clonic seizures (the behavioral endpoint of kindling) in mutants

nervous system

decreased kindling response ( J:91467 )

• kindling could not be induced even after 48 to 50 stimulations and an increase in the current required to induce the initial electrographic seizure is seen

• electroconvulsive shock can induce tonic-clonic seizures (the behavioral endpoint of kindling) in mutants

Allelic Composition	Bdnf^tm3Jae/Bdnf^tm3Jae Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129/Sv * C57BL/6 * ICR

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bdnf^tm3Jae mutation (2 available); any Bdnf mutation (42 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

abnormal kindling response ( J:91467 )

• an increased number of stimulations are required to initiate kindling behavior, however once initiated progression through subsequent classes of kindling is the same as in wild-type mice and no increase in the current required to induce the initial electrographic seizure is seen

nervous system

abnormal kindling response ( J:91467 )

Allelic Composition	Nkx2-1^tm2Shk/Nkx2-1^tm2Shk Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: 129X1/SvJ * C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nkx2-1^tm2Shk mutation (0 available); any Nkx2-1 mutation (24 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

early reproductive senescence ( J:116686 )

• female mutants exhibit a shorter reproductive span than control females, with 50% of mutant dams ceasing to deliver pups by 6-9 months of age

reproductive system

early reproductive senescence ( J:116686 )

• female mutants exhibit a shorter reproductive span than control females, with 50% of mutant dams ceasing to deliver pups by 6-9 months of age

delayed sexual maturation ( J:116686 )

• female mutants display delayed puberty, defined as the age at which the first ovulation takes place, relative to control females

• however, the onset of vaginal opening is normal relative to control littemates

• reproductive defects are associated with reduced hypothalamic expression of genes critical for sexual development and deregulation of a gene involved in restraining puberty

delayed estrous cycle ( J:116686 )

• female mutants show a significantly delayed initiation of cyclicity relative to control females

• however, no differences in body weight gain are observed over a 240-day period relative to control females

abnormal ovulation ( J:116686 )

• female mutants deliver their first litter ~2 weeks later than control females, consistent with a 10-day delay in first ovulation assessed by the age at first estrus

• however, mating behavior appears unaffected

prolonged estrous cycle ( J:116686 )

• the length of the first estrous cycle is nearly three times longer than in wild-type controls

• subsequent estrous cycles are slightly longer in duration (5-6 days) relative to cycles in control littermates (4-5 days)

reduced female fertility ( J:116686 )

• 50% of female mutants fail to become pregnant by 6-9 months of age, whereas >90% of control females reproduce normally at this age

• mutant dams produce fewer pups than control dams in a 1-year period

• the total number of litters produced by each mutant dam every 90 days is reduced by ~50% by 3 months of age

• however, pups born to mutant females appear normal and show normal birth weights relative to controls

behavior/neurological

behavior/neurological phenotype ( J:116686 )

N	• adult mutant exhibit normal novel object recognition as well as normal learning and memory, as assessed by the water maze and passive avoidance tests, indicating that basal forebrain cholinergic neuronal function is essentially intact

decreased exploration in new environment ( J:116686 )

• adult mutants exhibit reduced novel location recognition relative to wild-type mice

• however, novel object recognition remains intact relative to wild-type mice

increased anxiety-related response ( J:116686 )

• unexpectedly, adult mutants display higher, instead of lower, measures of anxiety than wild-type mice in the elevated zero maze test

enhanced coordination ( J:116686 )

• at 14 months of age, adult mutants are able to stay longer on the rotarod than wild-type mice

increased locomotor activity ( J:116686 )

• unexpectedly, adult mutants exhibit higher, rather than lower, locomotor activity than age-matched wild-type controls in the open field test

nervous system

nervous system phenotype ( J:116686 )

N	• no extrapyramidal deficits associated with basal ganglia dysfunction are observed • mutants display normal basal ganglia/hypothalamic morphology relative to control littermates

Allelic Composition	Pqbp1^tm1.1Hiok/Pqbp1⁺ Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6 * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pqbp1^tm1.1Hiok mutation (0 available); any Pqbp1 mutation (4 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

nervous system phenotype ( J:279053 )

N	• at 2 months of age, females exhibit no microcephaly as shown by normal brain size/weight relative to control mice

Allelic Composition	Pqbp1^tm1.1Hiok/Y Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6 * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pqbp1^tm1.1Hiok mutation (0 available); any Pqbp1 mutation (4 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

nervous system phenotype ( J:279053 )

N	• at 2 months of age, males exhibit no microcephaly as shown by normal brain size/weight relative to control mice

abnormal neuron morphology ( J:279053 )

• at P90, two-photon microscopy revealed a reduction in single-cell volume of a neuron (retrosplenial dysgranular cortex, layer V) relative to controls

• however, total dendrite length is normal

Allelic Composition	Clstn3^{tm1c(EUCOMM)Hmgu}/Clstn3^{tm1c(EUCOMM)Hmgu} Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6 * C57BL/6N * CBA * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Clstn3^{tm1c(EUCOMM)Hmgu} mutation (0 available); any Clstn3 mutation (66 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

adipose tissue

decreased bone marrow adipose tissue amount ( J:293885 )

• reduced bone marrow volume

growth/size/body

decreased body mass index ( J:293885 )

• from age 6 weeks on normal chow

limbs/digits/tail

limbs/digits/tail phenotype ( J:293885 )

N	• normal volume fraction, thickness, number, and separation of trabecular bone in distal metaphysis

skeleton

decreased bone marrow adipose tissue amount ( J:293885 )

• reduced bone marrow volume

decreased compact bone mass ( J:293885 )

• at distal metaphysis and midshaft regions of femur

• normal cortical bone thickness

Allelic Composition	Slc38a1^tm1.1Ttaka/Slc38a1^tm1.1Ttaka Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6 * C57BL/6NCrlj * CBA * CBA/JNCrlj

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc38a1^tm1.1Ttaka mutation (0 available); any Slc38a1 mutation (32 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

decreased susceptibility to ischemic brain injury ( J:288818 )

• after applying middle cerebral artery occlusion (MCAO)

decreased cerebral infarct size ( J:288818 )

• as judged from smaller NeuN- or MAP2-negative area after applying middle cerebral artery occlusion (MCAO)

nervous system

decreased susceptibility to ischemic brain injury ( J:288818 )

• after applying middle cerebral artery occlusion (MCAO)

decreased cerebral infarct size ( J:288818 )

• as judged from smaller NeuN- or MAP2-negative area after applying middle cerebral artery occlusion (MCAO)

Allelic Composition	Prkar2b^tm3Gsm/Prkar2b^tm2Gsm Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prkar2b^tm2Gsm mutation (1 available); any Prkar2b mutation (27 available)
Prkar2b^tm3Gsm mutation (0 available); any Prkar2b mutation (27 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

behavior/neurological phenotype ( J:196157 )

N	• locomotor behavior restored to normal

growth/size/body

growth/size/body region phenotype ( J:196157 )

N	• body weight restored to normal

adipose tissue

adipose tissue phenotype ( J:196157 )

N	• major fat pads are comparable to controls

Allelic Composition	Tg(Syn1-cre)671Jxm/0 Ubqln1^tm1.1Hmw/Ubqln1^tm1.1Hmw
Genetic Background	involves: C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Syn1-cre)671Jxm mutation (1 available)
Ubqln1^tm1.1Hmw mutation (0 available); any Ubqln1 mutation (24 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal response to CNS ischemic injury ( J:206930 )

• slower recovery of motor function after ischemic injury

increased cerebral infarct size ( J:206930 )

• increased ischemia/reperfusion-caused brain injury in 2 months old animals

abnormal brain morphology ( J:206930 )

• increased accumulation of ubiquitinated-proteins

homeostasis/metabolism

abnormal response to CNS ischemic injury ( J:206930 )

• slower recovery of motor function after ischemic injury

increased cerebral infarct size ( J:206930 )

• increased ischemia/reperfusion-caused brain injury in 2 months old animals

Allelic Composition	Plrg1^tm2Jcbr/Plrg1^tm2Jcbr Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plrg1^tm2Jcbr mutation (0 available); any Plrg1 mutation (17 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

postnatal lethality, complete penetrance ( J:149153 )

• survival at P3 is 25% compared to 88% for wild-type mice

• all mice die by P9

nervous system

increased neuron apoptosis ( J:149153 )

cellular

increased neuron apoptosis ( J:149153 )

Allelic Composition	Sema3f^tm1.1Ddg/Sema3f^tm1.2Ddg Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sema3f^tm1.1Ddg mutation (1 available); any Sema3f mutation (41 available)
Sema3f^tm1.2Ddg mutation (0 available); any Sema3f mutation (41 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal axon fasciculation ( J:84687 )

• the anterior limb of the anterior commissure is defasciculated

abnormal hippocampus development ( J:84687 )

• 2 of 3 mutants exhibit improper development of the infrapyramidal tract

abnormal innervation ( J:84687 )

• most axons of the anterior limb of the anterior commissure cross the midline aberrantly and axons of the infrapyramidal tract extend beyond the stratum oriens of CA3

• however, no defects in stria terminalis targeting

abnormal nervous system tract morphology ( J:84687 )

• 2 of 3 mutants exhibit an infrapyramidal tract defect in which axons extend far into the stratum oriens of CA3, beyond the level at which they normally turn dorsally into the stratum radiatum

abnormal anterior commissure morphology ( J:84687 )

• the anterior limb of the anterior commissure is reduced and defasciculated

• although a small number of axons of the anterior commissure decussate properly, most axons cross the midline aberrantly as smaller tightly bundled fascicles

cellular

abnormal axon fasciculation ( J:84687 )

• the anterior limb of the anterior commissure is defasciculated

Allelic Composition	Sema3f^tm1.1Ddg/Sema3f^tm1.1Ddg Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Sema3f^tm1.1Ddg mutation (1 available); any Sema3f mutation (41 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal axon fasciculation ( J:84687 )

• the anterior limb of the anterior commissure is defasciculated

abnormal hippocampus development ( J:84687 )

• 1 of 5 mutants exhibit improper development of the infrapyramidal tract

abnormal innervation ( J:84687 )

• most axons of the anterior limb of the anterior commissure cross the midline aberrantly and axons of the infrapyramidal tract extend beyond the stratum oriens of CA3

• however, no defects in stria terminalis targeting

abnormal nervous system tract morphology ( J:84687 )

• 1 of 5 mutants exhibit an infrapyramidal tract defect in which axons extend far into the stratum oriens of CA3, beyond the level at which they normally turn dorsally into the stratum radiatum

abnormal anterior commissure morphology ( J:84687 )

• the anterior limb of the anterior commissure is reduced and defasciculated

• although a small number of axons of the anterior commissure decussate properly, most axons cross the midline aberrantly as smaller tightly bundled fascicles

cellular

abnormal axon fasciculation ( J:84687 )

• the anterior limb of the anterior commissure is defasciculated

Allelic Composition	Gt(ROSA)26Sor^{tm1(CAG-EGFP/Vamp2)Ggc}/Gt(ROSA)26Sor⁺ Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6 * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^{tm1(CAG-EGFP/Vamp2)Ggc} mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

normal phenotype

no abnormal phenotype detected ( J:206865 )

• mice are phenotypically indistinguishable from control littermates

Allelic Composition	Hgs^tm2Tkh/Hgs^tm2Tkh Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6 * CBA * SJL

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hgs^tm2Tkh mutation (0 available); any Hgs mutation (40 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

reproductive system

infertility ( J:141391 )

nervous system

increased neuron apoptosis ( J:141391 )

• the number of neurons undergoing apoptosis in the CA3 region is increased compared to in wild-type mice

abnormal hippocampus pyramidal cell morphology ( J:141391 )

• at 5 weeks of age, mice exhibit a loss of pyramidal neurons in the CA3 region that progressively worsens with age unlike in wild-type mice

• however, the numbers of pyramidal cells in the CA1 region and mossy fiber attachments are normal

• pyramidal neuron loss is due to increased apoptosis of cells

behavior/neurological

impaired passive avoidance behavior ( J:141391 )

• mice exhibit a reduced latency to entering in a dark box compared to wild-type mice in a passive avoidance test

behavioral despair ( J:141391 )

• mice exhibit increased time immobilized during a swim test despite normal muscle strength

decreased vertical activity ( J:141391 )

growth/size/body

postnatal growth retardation ( J:141391 )

• begining at 3 weeks

slow postnatal weight gain ( J:141391 )

• by 8 weeks of age, mice cease to gain weight unlike wild-type mice

cellular

increased neuron apoptosis ( J:141391 )

• the number of neurons undergoing apoptosis in the CA3 region is increased compared to in wild-type mice

Allelic Composition	Tg(ACTB-NOTCH1)1Shn/0 Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(ACTB-NOTCH1)1Shn mutation (1 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cellular

cellular phenotype ( J:90392 )

N	• no increase in apoptosis is seen at E13.5 in the telencephalon of double transgenic mice

Allelic Composition	S1pr1^tm1Jch/S1pr1^tm1Jch Tg(Syn1-cre)671Jxm/?
Genetic Background	involves: C57BL/6J * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
S1pr1^tm1Jch mutation (0 available); any S1pr1 mutation (32 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

immune system phenotype ( J:168824 )

N	• response to Experimental Autoimmune Encephalitis induced by Myelin Oligodendrocyte Glycoprotein is similar to controls

Allelic Composition	Depdc5^{tm1c(EUCOMM)Hmgu}/Depdc5⁺ Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6N * CBA

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Depdc5^{tm1c(EUCOMM)Hmgu} mutation (3 available); any Depdc5 mutation (120 available)
Tg(Syn1-cre)671Jxm mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

decreased body weight ( J:260943 )

• in male, but not female, mice after 3 months of age

Allelic Composition	Depdc5^{tm1c(EUCOMM)Hmgu}/Depdc5^{tm1c(EUCOMM)Hmgu} Tg(Syn1-cre)671Jxm/0
Genetic Background	involves: C57BL/6N * CBA

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

decreased susceptibility to xenobiotic induced morbidity/mortality ( J:260943 )

• following PTZ-induced seizures

premature death ( J:260943 )

• median survival is 115 days with no mice surviving past 175 days with no wounds or major pathology to explain sudden death

nervous system

seizures ( J:260943 )

• in three mice without detection of electroclinical seizures

increased susceptibility to pharmacologically induced seizures ( J:260943 )

• shorter latency to seizures induced by PTZ and increased death

• however, duration of seizures is normal

tonic seizures ( J:260943 )

• in two mice

tonic-clonic seizures ( J:260943 )

• in one mouse

increased brain size ( J:260943 )

• median survival is 115 days with no mice surviving past 175 days with no wounds or major pathology to explain sudden death

astrocytosis ( J:260943 )

abnormal dendrite morphology ( J:260943 )

• thicker and disorganized in layer V cortical neurons

neuron hypertrophy ( J:260943 )

• enlarged and dysplastic neurons with abnormal cytoplasmic accumulation

behavior/neurological

behavior/neurological phenotype ( J:260943 )

N	• unlike constitutive knock-out mice, conditional knock-out mice do not exhibit a hunchback phenotype

limb grasping ( J:260943 )

• hindlimb clasping after 60 days of age

seizures ( J:260943 )

• in three mice without detection of electroclinical seizures

increased susceptibility to pharmacologically induced seizures ( J:260943 )

• shorter latency to seizures induced by PTZ and increased death

• however, duration of seizures is normal

tonic seizures ( J:260943 )

• in two mice

tonic-clonic seizures ( J:260943 )

• in one mouse

growth/size/body

decreased body weight ( J:260943 )

• in male, but not female, mice from the time of weaning and persisting through adulthood

megacephaly ( J:260943 )

homeostasis/metabolism

decreased susceptibility to xenobiotic induced morbidity/mortality ( J:260943 )

• following PTZ-induced seizures

skeleton

increased compact bone thickness ( J:260943 )

• with decreased neuronal density in deep layers

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