Strain Name:

B6EiC3Sn a/A-Cacnb4lh/J

Stock Number:

000504

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Availability:

Cryopreserved - Ready for recovery

Description

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

Strain Information

Type Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
GenerationN27
Generation Definitions

Appearance
black, ataxic
Related Genotype: a/a Cacnb4lh/Cacnb4lh

agouti, ataxic
Related Genotype: A/? Cacnb4lh/Cacnb4lh

black, unaffected
Related Genotype: a/a Cacnb4lh/+ or a/a +/?

agouti, unaffected
Related Genotype: A/? Cacnb4lh/+ or A/? +/?

Description
Mice homozygous for the lethargic spontaneous mutation (Cacnb4lh) are first recognizable at 15 days by their lethargic behavior with gait instability and occasional seizures. The seizures resemble human petit mal seizures. No pathological changes were found in the CNS or in skeletal muscles, but peripheral motor nerves show reduced conduction velocity and prolonged distal latency. There is early thymic involution at 3 to 4 weeks in Cacnb4lh homozygotes, accompanied by decreased lymphocyte count, decreased cell-mediated immunity, and increased levels of serum IgG1. The defects in the immune system tend to disappear by 2 months of age in mice that survive. In addition to neurological and immunological defects, homozygous lethargic mice show pituitary-adrenal hypercorticism. Homozygotes are smaller and weaker than their normal littermates and often die before 2 months old. Survivors of both sexes may breed, but their reproductivity is low.

Control Information

  Control
   Untyped from the colony
 
  Considerations for Choosing Controls

Related Strains

View Strains carrying   A     (18 strains)

Strains carrying other alleles of Cacnb4
004951   C3HeB/FeJ-Cacnb4lh-3J/GrsrJ
008626   STOCK Cacnb4lh-2J/LetJ
View Strains carrying other alleles of Cacnb4     (2 strains)

Strains carrying other alleles of a
002655   Mus pahari/EiJ
000251   AEJ.Cg-ae +/a Gdf5bp-H/J
000202   AEJ/Gn-bd/J
000199   AEJ/GnLeJ
000433   B10.C-H3c H13? A/(28NX)SnJ
000427   B10.CE-H13b Aw/(30NX)SnJ
000423   B10.KR-H13? A/SnJ
000420   B10.LP-H13b Aw/Sn
000477   B10.PA-Bloc1s6pa H3e at/SnJ
000419   B10.UW-H3b we Pax1un at/SnJ
003879   B10;TFLe-a/a T Itpr3tf/+ Itpr3tf/J
001538   B6 x B6C3Sn a/A-T(1;9)27H/J
000916   B6 x B6C3Sn a/A-T(5;12)31H/J
000602   B6 x B6C3Sn a/A-T(8;16)17H/J
000593   B6 x B6CBCa Aw-J/A-Grid2Lc T(2;6)7Ca MitfMi-wh/J
000502   B6 x B6CBCa Aw-J/A-Myo5aflr Gnb5flr/J
000599   B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J
003759   B6 x B6EiC3Sn a/A-T(10;16)232Dn/J
002071   B6 x B6EiC3Sn a/A-T(11;17)202Dn/J
002113   B6 x B6EiC3Sn a/A-T(11A2;16B3)238Dn/J
002068   B6 x B6EiC3Sn a/A-T(11B1;16B5)233Dn/J
002069   B6 x B6EiC3Sn a/A-T(14E4or5;16B5)225Dn/J
001926   B6 x B6EiC3Sn a/A-T(15;16)198Dn/J
001832   B6 x B6EiC3Sn a/A-T(15E;16B1)60Dn/J
003758   B6 x B6EiC3Sn a/A-T(16C3-4;17A2)65Dn/J
001833   B6 x B6EiC3Sn a/A-T(1C2;16C3)45Dn/J
001903   B6 x B6EiC3Sn a/A-T(6F;18C)57Dn/J
001535   B6 x B6EiC3Sn a/A-T(8A4;12D1)69Dn/J
001831   B6 x B6EiC3Sn a/A-T(8C3;16B5)164Dn/J
000618   B6 x FSB/GnEi a/a Ctslfs/J
000577   B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J
000601   B6 x STOCK a/a T(7;18)50H/J
000592   B6 x STOCK T(2;4)13H a/J
002016   B6(Cg)-Aw-J EdaTa-6J Chr YB6-Sxr/EiJ
000600   B6-Gpi1b x B6CBCa Aw-J/A-T(7;15)9H Gpi1a/J
000769   B6.C/(HZ18)By-at-44J/J
000203   B6.C3-Aiy/a/J
000017   B6.C3-Avy/J
001572   B6.C3-am-J/J
001809   B6.Cg-Aw-J EdaTa-6J +/+ ArTfm/J
000552   B6.Cg-Aw-J EdaTa-6J Sxr
001730   B6.Cg-Aw-J EdaTa-6J Sxrb Hya-/J
000841   B6.Cg-Aw-J EdaTa-By/J
000021   B6.Cg-Ay/J
100409   B6129PF1/J-Aw-J/Aw
014608   B6;129S1-a Kitlsl-24J/GrsrJ
000231   B6;C3Fe a/a-Csf1op/J
004200   B6;CBACa Aw-J/A-Npr2cn-2J/GrsrJ
000785   B6;D2-a Ces1ce/EiJ
000505   B6C3 Aw-J/A-Bloc1s5mu/J
000604   B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J
001750   B6C3Fe a/a-Eif3cXs-J/J
002807   B6C3Fe a/a-Meox2fla/J
000506   B6C3Fe a/a-Qkqk-v/J
000224   B6C3Fe a/a-Scyl1mdf/J
003020   B6C3Fe a/a-Zdhhc21dep/J
001037   B6C3Fe a/a-Agtpbp1pcd/J
000221   B6C3Fe a/a-Alx4lst-J/J
002062   B6C3Fe a/a-Atp7aMo-8J/J
001756   B6C3Fe a/a-Cacng2stg/J
001815   B6C3Fe a/a-Col1a2oim/J
000209   B6C3Fe a/a-Dh/J
000211   B6C3Fe a/a-Dstdt-J/J
000210   B6C3Fe a/a-Edardl-J/J
000207   B6C3Fe a/a-Edaraddcr/J
000182   B6C3Fe a/a-Eef1a2wst/J
001278   B6C3Fe a/a-Glra1spd/J
000241   B6C3Fe a/a-Glrbspa/J
002875   B6C3Fe a/a-Hoxd13spdh/J
000304   B6C3Fe a/a-Krt71Ca Scn8amed-J/J
000226   B6C3Fe a/a-Largemyd/J
000636   B6C3Fe a/a-Lmx1adr-J/J
001280   B6C3Fe a/a-Lse/J
001573   B6C3Fe a/a-MitfMi/J
001035   B6C3Fe a/a-Napahyh/J
000181   B6C3Fe a/a-Otogtwt/J
000278   B6C3Fe a/a-Papss2bm Hps1ep Hps6ru/J
000205   B6C3Fe a/a-Papss2bm/J
002078   B6C3Fe a/a-Pcdh15av-2J/J
000246   B6C3Fe a/a-Pitpnavb/J
001430   B6C3Fe a/a-Ptch1mes/J
000235   B6C3Fe a/a-Relnrl/J
000237   B6C3Fe a/a-Rorasg/J
000290   B6C3Fe a/a-Sox10Dom/J
000230   B6C3Fe a/a-Tcirg1oc/J
003612   B6C3Fe a/a-Trak1hyrt/J
001512   B6C3Fe a/a-Ttnmdm/J
001607   B6C3Fe a/a-Unc5crcm/J
000005   B6C3Fe a/a-Wc/J
000243   B6C3Fe a/a-Wnt1sw/J
000248   B6C3Fe a/a-Xpl/J
000624   B6C3Fe a/a-anx/J
008044   B6C3Fe a/a-bpck/J
002018   B6C3Fe a/a-din/J
002339   B6C3Fe a/a-nma/J
000240   B6C3Fe a/a-soc/J
000063   B6C3Fe a/a-sy/J
001055   B6C3Fe a/a-tip/J
000245   B6C3Fe a/a-tn/J
000065   B6C3Fe a/a-we Pax1un at/J
000296   B6C3Fe-a/a Hoxa13Hd Mcoln3Va-J/J
000019   B6C3Fe-a/a-Itpr1opt/J
001022   B6C3FeF1/J a/a
000314   B6CBACa Aw-J/A-EdaTa/J-XO
000501   B6CBACa Aw-J/A-Aifm1Hq/J
001046   B6CBACa Aw-J/A-Grid2Lc/J
000500   B6CBACa Aw-J/A-Gs/J
002703   B6CBACa Aw-J/A-Hydinhy3/J
000247   B6CBACa Aw-J/A-Kcnj6wv/J
000287   B6CBACa Aw-J/A-Plp1jp EdaTa/J
000515   B6CBACa Aw-J/A-SfnEr/J
000242   B6CBACa Aw-J/A-spc/J
000288   B6CBACa Aw-J/A-we a Mafbkr/J
001201   B6CBACaF1/J-Aw-J/A
006450   B6EiC3 a/A-Vss/GrsrJ
000971   B6EiC3 a/A-Och/J
000551   B6EiC3 a/A-Tbx15de-H/J
000557   B6EiC3-+ a/LnpUl A/J
000503   B6EiC3Sn a/A-Gy/J
001811   B6EiC3Sn a/A-Otcspf-ash/J
002343   B6EiC3Sn a/A-Otcspf/J
000391   B6EiC3Sn a/A-Pax6Sey-Dey/J
001923   B6EiC3Sn a/A-Ts(417)2Lws TimT(4;17)3Lws/J
001875   B6EiC3SnF1/J
000638   C3FeB6 A/Aw-J-Sptbn4qv-J/J
000200   C3FeB6 A/Aw-J-Ankank/J
001203   C3FeB6F1/J A/Aw-J
000225   C3FeLe.B6 a/a-Ptpn6me/J
000198   C3FeLe.B6-a/J
000291   C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J
001272   C3H/HeSnJ-Ahvy/J
000099   C3HeB/FeJ-Avy/J
001886   C3HeB/FeJLe a/a-gnd/J
000338   C57BL/6J Aw-J-EdaTa-6J/J
000584   C57BL/6J-+ T(1;2)5Ca/a +/J
000258   C57BL/6J-Ai/a/J
000774   C57BL/6J-Asy/a/J
000569   C57BL/6J-Aw-J-EdaTa +/+ ArTfm/J
000051   C57BL/6J-Aw-J/J
000055   C57BL/6J-at-33J/J
000070   C57BL/6J-atd/J
000284   CWD/LeJ
000670   DBA/1J
000671   DBA/2J
001057   HPT/LeJ
000260   JGBF/LeJ
002468   KK.Cg-Ay/J
000262   LS/LeJ
000265   MY/HuLeJ
000308   SSL/LeJ
001427   STOCK Aw us/J
000994   STOCK a Myo5ad Mregdsu/J
000064   STOCK a Tyrp1b Pmelsi/J
002238   STOCK a Tyrp1b shmy/J
001433   STOCK a skt/J
000579   STOCK a tp/J
000319   STOCK a us/J
002648   STOCK a/a Cln6nclf/J
000302   STOCK a/a MitfMi-wh +/+ Itpr1opt/J
000286   STOCK a/a Myo5ad fd/+ +/J
000281   STOCK a/a Tmem79ma Flgft/J
000206   STOCK a/a Tyrc-h/J
001432   STOCK a/a Tyrp1b Ndc1sks/Tyrp1b +/J
000312   STOCK stb + a/+ Fignfi a/J
000596   STOCK T(2;11)30H/+ x AEJ-a Gdf5bp-H/J or A/J-a Gdf5bp-J/J
000970   STOCK T(2;16)28H A/T(2;16)28H a/J
000590   STOCK T(2;4)1Sn a/J
000594   STOCK T(2;8)26H a/T(2;8)26H a Tyrp1+/Tyrp1b/J
000623   TR/DiEiJ
View Strains carrying other alleles of a     (169 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Epilepsy, Idiopathic Generalized, Susceptibility to, 9; EIG9   (CACNB4)
Episodic Ataxia, Type 5; EA5   (CACNB4)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Cacnb4lh/Cacnb4lh

        B6EiC3Sn a/A-Cacnb4lh/J
  • immune system phenotype
  • abnormal CD4-positive, alpha-beta T cell physiology
    • initial peak and plateau calcium responses are attenuated compared to in wild-type mice   (MGI Ref ID J:115345)
  • abnormal Peyer's patch germinal center morphology
    • absent   (MGI Ref ID J:5281)
  • abnormal interleukin secretion
    • IL-4 production is reduced   (MGI Ref ID J:115345)
    • decreased interleukin-2 secretion
      • TCR-mediated IL-2 production is partially inhibited   (MGI Ref ID J:115345)
  • abnormal lymph node morphology
    • between 18 and 35 days of age, mice exhibit fewer lymphatic follicles compared to wild-type mice   (MGI Ref ID J:5281)
    • enlarged lymph nodes
      • mice older than 5 months exhibit enlarged lymph nodes compared to wild-type mice   (MGI Ref ID J:5281)
  • abnormal thymus corticomedullary boundary morphology
    • the boundary between the cortex and medulla is not visible as in wild-type mice   (MGI Ref ID J:5281)
  • abnormal thymus development
    • mice undergo thymus involution   (MGI Ref ID J:5281)
  • decreased Peyer's patch number   (MGI Ref ID J:5281)
  • decreased interferon-gamma secretion   (MGI Ref ID J:115345)
  • decreased lymphocyte cell number
    • in the thymus and spleen   (MGI Ref ID J:5281)
    • decreased double-positive T cell number
      • in mice older than 2 weeks of age when the onset of neuropathy occurs   (MGI Ref ID J:115345)
      • however, prior to 2 weeks of age mice exhibit normal T cell development   (MGI Ref ID J:115345)
  • small Peyer's patches   (MGI Ref ID J:5281)
  • small spleen
    • between 15 days and 10 months of age   (MGI Ref ID J:5281)
  • small thymus
    • between 26 and 40 days of age   (MGI Ref ID J:5281)
  • growth/size/body phenotype
  • cachexia
    • between 26 and 40 days of age   (MGI Ref ID J:5281)
  • digestive/alimentary phenotype
  • diarrhea
    • between 26 and 40 days of age   (MGI Ref ID J:5281)
  • vision/eye phenotype
  • *normal* vision/eye phenotype
    • both a- and b-waves appear normal in mutant mice   (MGI Ref ID J:80080)
    • histological analysis indicates that retinal morphology is normal   (MGI Ref ID J:80080)
    • abnormal eye electrophysiology
      • electroretinograms generated by retinal pigment epithelial cells are reduced compared to in wild-type mice   (MGI Ref ID J:136113)
      • maximum amplitude of the light peak is reduced and overall sensitivity is decreased compared to in wild-type mice   (MGI Ref ID J:136113)
  • hematopoietic system phenotype
  • abnormal CD4-positive, alpha-beta T cell physiology
    • initial peak and plateau calcium responses are attenuated compared to in wild-type mice   (MGI Ref ID J:115345)
  • abnormal thymus corticomedullary boundary morphology
    • the boundary between the cortex and medulla is not visible as in wild-type mice   (MGI Ref ID J:5281)
  • abnormal thymus development
    • mice undergo thymus involution   (MGI Ref ID J:5281)
  • decreased lymphocyte cell number
    • in the thymus and spleen   (MGI Ref ID J:5281)
    • decreased double-positive T cell number
      • in mice older than 2 weeks of age when the onset of neuropathy occurs   (MGI Ref ID J:115345)
      • however, prior to 2 weeks of age mice exhibit normal T cell development   (MGI Ref ID J:115345)
  • small spleen
    • between 15 days and 10 months of age   (MGI Ref ID J:5281)
  • small thymus
    • between 26 and 40 days of age   (MGI Ref ID J:5281)
  • endocrine/exocrine gland phenotype
  • abnormal thymus corticomedullary boundary morphology
    • the boundary between the cortex and medulla is not visible as in wild-type mice   (MGI Ref ID J:5281)
  • abnormal thymus development
    • mice undergo thymus involution   (MGI Ref ID J:5281)
  • small thymus
    • between 26 and 40 days of age   (MGI Ref ID J:5281)

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Cacnb4lh/Cacnb4lh

        involves: BALB/cGn * C3H/HeSnJ * C57BL/6JEi
  • nervous system phenotype
  • *normal* nervous system phenotype
    • synaptic electrophysiology including neurotransmitter release and end plate potentials, as well as responses to channel inhibitors is not different from wild-type NMJs   (MGI Ref ID J:121463)
    • abnormal CNS synaptic transmission
      • peak current densities of low voltage-activated (LVA) calcium channels in thalamocortical neurons at membrane potential of -50 mV are increased by 51% compared to control   (MGI Ref ID J:106959)
      • peak current densities of high voltage calcium channels (HVA) in TC neurons are similar to wild-type   (MGI Ref ID J:106959)
    • abnormal brain wave pattern
      • EEG of saline-treated mice display frequent polyspike discharges   (MGI Ref ID J:79139)
      • mice exhibit bilaterally synchronous electrographic bursts (seizures) that last 1.5 s with a frequency of 127 per hour   (MGI Ref ID J:1484)
    • abnormal motor neuron morphology
      • synaptic electrophysiology including neurotransmitter release and end plate potentials, as well as responses to channel inhibitors is not different from wild-type NMJs   (MGI Ref ID J:121463)
    • abnormal neuromuscular synapse morphology
      • neuromuscular junction area (area staining for acetylcholine receptors) in ~38% smaller relative to wild-type mice (277 um2 vs 446 um2)   (MGI Ref ID J:121463)
    • seizures
      • mice exhibit absence seizures   (MGI Ref ID J:1484)
      • seizures are increased by treatment with GAB agonists and decreased by treatment with GABA antagonists   (MGI Ref ID J:1484)
      • clonic seizures
        • mice have attacks with clonic movements of the limbs most apparent at 4 weeks of age   (MGI Ref ID J:79139)
      • tonic seizures
        • mice show periods of tonic extension or retraction of the limbs at 4 weeks of age   (MGI Ref ID J:79139)
  • behavior/neurological phenotype
  • abnormal motor capabilities/coordination/movement
    • transient periods of severe motor disability are superimposed on the more minor abnormalities   (MGI Ref ID J:79139)
    • abnormal posture
      • mice show periods of abnormal flexion or extension of the trunk most apparent at 4 weeks of age   (MGI Ref ID J:79139)
    • ataxia
      • mice show wide stance, imprecise limb placement, poor timing and interlimb coordination, and a staggering gait, all characteristic of ataxia   (MGI Ref ID J:79139)
    • circling
      • mice display circling, becoming less frequent by 5-6 weeks of age   (MGI Ref ID J:79139)
    • hypoactivity
      • mice show transient periods of reduced locomotor activity when tested in photocell chambers   (MGI Ref ID J:79139)
    • impaired coordination
      • mice perform very poorly in rotarod tests, falling off the rod whereas wild-type remain on for ~length of test   (MGI Ref ID J:79139)
    • impaired righting response
      • mice tend to fall and are unable to regain upright position, becoming less frequent by 5-6 weeks of age   (MGI Ref ID J:79139)
  • impaired behavioral response to xenobiotic
    • phenytoin and carbamazepine fail to reduce seizure frequency   (MGI Ref ID J:1484)
  • seizures
    • mice exhibit absence seizures   (MGI Ref ID J:1484)
    • seizures are increased by treatment with GAB agonists and decreased by treatment with GABA antagonists   (MGI Ref ID J:1484)
    • clonic seizures
      • mice have attacks with clonic movements of the limbs most apparent at 4 weeks of age   (MGI Ref ID J:79139)
    • tonic seizures
      • mice show periods of tonic extension or retraction of the limbs at 4 weeks of age   (MGI Ref ID J:79139)
  • muscle phenotype
  • muscle spasm
    • mice display facial twitching, becoming less prominent by 5-6 weeks of age   (MGI Ref ID J:79139)

Cacnb4lh/Cacnb4lh

        BALB/cGn-Cacnb4lh
  • mortality/aging
  • premature death
    • mice exhibit high mortality rates between 3 and 4 weeks of age   (MGI Ref ID J:12166)
  • reproductive system phenotype
  • absent corpus luteum   (MGI Ref ID J:12166)
  • reduced fertility
    • mice exhibit reduced reproductivity   (MGI Ref ID J:12166)
  • immune system phenotype
  • abnormal thymus development
    • mice undergo thymus involution   (MGI Ref ID J:12166)
  • increased length of allograft survival
    • between 15 to 30 days of age, mice fail to reject skin grafts as wild-type mice do   (MGI Ref ID J:5766)
    • however, by 45 days of age graft rejection is normal   (MGI Ref ID J:5766)
  • nervous system phenotype
  • pituitary gland hyperplasia
    • pituitary glands exhibit an increase in cellular population density compared to in wild-type pituitaries   (MGI Ref ID J:12166)
  • behavior/neurological phenotype
  • abnormal behavior
    • mice sit up with front feet contracted for several minutes   (MGI Ref ID J:28465)
    • abnormal fear/anxiety-related behavior
      • mice appear nervous   (MGI Ref ID J:28465)
    • abnormal locomotor activation
      • mice exhibit difficulty in moving forward and make long pauses between movements, often hunch the back and raise first the front foot then the hind foot   (MGI Ref ID J:28465)
  • endocrine/exocrine gland phenotype
  • abnormal thymus development
    • mice undergo thymus involution   (MGI Ref ID J:12166)
  • absent corpus luteum   (MGI Ref ID J:12166)
  • pituitary gland hyperplasia
    • pituitary glands exhibit an increase in cellular population density compared to in wild-type pituitaries   (MGI Ref ID J:12166)
  • growth/size/body phenotype
  • postnatal growth retardation   (MGI Ref ID J:12166)
  • hematopoietic system phenotype
  • abnormal thymus development
    • mice undergo thymus involution   (MGI Ref ID J:12166)

Cacnb4lh/Cacnb4lh

        involves: BALB/cGn
  • behavior/neurological phenotype
  • abnormal gait
    • at 14 to 16 days of age, mice exhibit a mild gait instability   (MGI Ref ID J:28466)
  • convulsive seizures
    • mice exhibit clonic and/or tonic seizures   (MGI Ref ID J:28466)
    • excitement during seizure worsens the severity of the seizure   (MGI Ref ID J:28466)
    • however, gentle handling quells the seizures until released   (MGI Ref ID J:28466)
    • sometimes mice exhibit a Jacksonian march during seizures   (MGI Ref ID J:28466)
  • lethargy
    • when removed from a swim test mice exhibit slowed responses with hindlimbs appearing weak and he animal unable to ascend a 45 degree incline for 10 to 15 minutes   (MGI Ref ID J:28466)
  • nervous system phenotype
  • abnormal nerve conduction
    • mice exhibit adult motor nerve conduction velocities at 3 months of again instead of 5 as in wild-type mice   (MGI Ref ID J:6556)
    • decreased nerve conduction velocity
      • peripheral motor nerves exhibit reduced conduction velocity and prolonged distal latency   (MGI Ref ID J:6556)
  • convulsive seizures
    • mice exhibit clonic and/or tonic seizures   (MGI Ref ID J:28466)
    • excitement during seizure worsens the severity of the seizure   (MGI Ref ID J:28466)
    • however, gentle handling quells the seizures until released   (MGI Ref ID J:28466)
    • sometimes mice exhibit a Jacksonian march during seizures   (MGI Ref ID J:28466)
  • immune system phenotype
  • increased IgG1 level   (MGI Ref ID J:5883)
  • hematopoietic system phenotype
  • increased IgG1 level   (MGI Ref ID J:5883)
View Research Applications

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

Cacnb4lh related

Cell Biology Research
Channel and Transporter Defects
      calcium

Endocrine Deficiency Research
Adrenal Cortex Defects
Hypothalamus/Pituitary Defects

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency Associated with Other Defects

Internal/Organ Research
Adrenal Cortex Defects

Neurobiology Research
Ataxia (Movement) Defects
Channel and Transporter Defects
      calcium
Epilepsy

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol A
Allele Name wild-type agouti
Allele Type Spontaneous
Common Name(s) dark-bellied agouti;
Strain of Originvarious
Gene Symbol and Name a, nonagouti
Chromosome 2
Gene Common Name(s) ASP; As; agouti; agouti signal protein; agouti suppressor;
General Note The A allele is usually regarded as a wild-type allele. The C3H and CBA mouse sublines are homozygous for agouti. Hairs are black with a subapical yellow band. This black-yellow-black pattern is referred to as agouti. The general appearance is yellowish brown, slightly lighter on the belly than on the back.
Molecular Note This allele, often referred to as wild-type, comprises a novel 131 amino acid protein encoded in a gene comprising four exons, three coding, spanning 18kb. Unique changes in this gene account for all other alleles that have been molecularly characterized. The expression of this allele is almost always dominant to other alleles of this gene. [MGI Ref ID J:3523]
 
Allele Symbol Cacnb4lh
Allele Name lethargic
Allele Type Spontaneous
Common Name(s) beta4lh; lh;
Strain of OriginBALB/cGn
Gene Symbol and Name Cacnb4, calcium channel, voltage-dependent, beta 4 subunit
Chromosome 2
Gene Common Name(s) 3110038O15Rik; CAB4; CACNLB4; Cchb4; EA5; EIG9; EJM; EJM4; EJM6; RIKEN cDNA 3110038O15 gene; calcium channel, B4 subunit; lethargic; lh;
Molecular Note A four bp insertion that disrupts the consensus 5' splice site of intron A/B was identified. Reduced levels of transcripts are produced from this allele and are present at approximately 20% of the normal levels in homozygous mice. [MGI Ref ID J:38214]

Genotyping

Genotyping Information

Genotyping Protocols

Cacnb4lh, Restriction Enzyme Digest


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Burgess DL; Jones JM; Meisler MH; Noebels JL. 1997. Mutation of the Ca2+ channel beta subunit gene Cchb4 is associated with ataxia and seizures in the lethargic (lh) mouse. Cell 88(3):385-92. [PubMed: 9039265]  [MGI Ref ID J:38214]

Additional References

Dung HC; Swigart RH. 1972. Histo-pathologic observations of the nervous and lymphoid tissues of lethargic mutant mice. Tex Rep Biol Med 30(1):23-39. [PubMed: 5037658]  [MGI Ref ID J:5281]

Lin FH; Cao Z; Hosford DA. 1993. Increased number of GABAB receptors in the lethargic (lh/lh) mouse model of absence epilepsy. Brain Res 608(1):101-6. [PubMed: 8388308]  [MGI Ref ID J:4388]

A related

Blewitt ME; Vickaryous NK; Hemley SJ; Ashe A; Bruxner TJ; Preis JI; Arkell R; Whitelaw E. 2005. An N-ethyl-N-nitrosourea screen for genes involved in variegation in the mouse. Proc Natl Acad Sci U S A 102(21):7629-34. [PubMed: 15890782]  [MGI Ref ID J:99816]

Bultman SJ; Michaud EJ; Woychik RP. 1992. Molecular characterization of the mouse agouti locus. Cell 71(7):1195-204. [PubMed: 1473152]  [MGI Ref ID J:3523]

Bundschuh VG; Madry M. 1988. [atwp mutation in an albino mouse substrain (AB/Hum-1)] Z Versuchstierkd 31(6):249-54. [PubMed: 3227730]  [MGI Ref ID J:16568]

Cota CD; Liu RR; Sumberac TM; Jung S; Vencato D; Millet YH; Gunn TM. 2008. Genetic and phenotypic studies of the dark-like mutant mouse. Genesis 46(10):562-73. [PubMed: 18821597]  [MGI Ref ID J:143333]

Czyzyk TA; Sikorski MA; Yang L; McKnight GS. 2008. Disruption of the RIIbeta subunit of PKA reverses the obesity syndrome of Agouti lethal yellow mice. Proc Natl Acad Sci U S A 105(1):276-81. [PubMed: 18172198]  [MGI Ref ID J:131039]

Dickie MM. 1969. Mutations at the agouti locus in the mouse. J Hered 60(1):20-5. [PubMed: 5798139]  [MGI Ref ID J:30922]

Dry FW. 1928. The agouti coloration of the mouse (Mus Musculus) and the rat (Mus Norvegicus). J Genet 20:131-144.  [MGI Ref ID J:46318]

Dunn LC. 1945. A New Eye Color Mutant in the Mouse with Asymmetrical Expression. Proc Natl Acad Sci U S A 31(11):343-6. [PubMed: 16578176]  [MGI Ref ID J:13122]

Galbraith DB; Wolff GL; Brewer NL. 1979. Tissue microenvironment and the genetic control of hair pigment patterns in mice Dev Genet 1(2):167-179.  [MGI Ref ID J:156092]

Green EL. 1968. . In: Handbook on Genetically Standardized Jax Mice. The Jackson Laboratory, Bar Harbor, ME.  [MGI Ref ID J:36414]

Guido V; and The Mouse Mutant Resource (MMR) at The Jackson Laboratory. 2002. Two new mutations of white bellied agouti, w-46J and w-47J MGI Direct Data Submission :.  [MGI Ref ID J:77218]

Jackson IJ; Budd PS; Keighren M; McKie L. 2007. Humanized MC1R transgenic mice reveal human specific receptor function. Hum Mol Genet 16(19):2341-8. [PubMed: 17652101]  [MGI Ref ID J:129904]

Kelly EM. 1957. Beige, bg Mouse News Lett 16:36.  [MGI Ref ID J:29744]

Mather K; North SB. 1940. Umbrous: a case of dominance modification in mice. J Genet 40:229-41.  [MGI Ref ID J:280]

MouseBookTM. 2005. Information obtained from MouseBook<sup>TM</sup>, Medical Research Council Mammalian Genetics Unit, Harwell, UK. Unpublished :.  [MGI Ref ID J:169366]

Perry WL; Copeland NG; Jenkins NA. 1994. The molecular basis for dominant yellow agouti coat color mutations. Bioessays 16(10):705-7. [PubMed: 7980472]  [MGI Ref ID J:21244]

Phillips RJS. 1966. A cis-trans position effect at the A locus of the house mouse. Genetics 54(2):485-95. [PubMed: 5968639]  [MGI Ref ID J:5027]

Quevedo WC Jr.; Chase HB. 1958. An analysis of the light mutation of coat color in mice. J Morphol 102:329-345.  [MGI Ref ID J:13094]

Silvers WK. 1979. The Coat Colors of Mice; A Model for Mammalian Gene Action and Interaction. In: The Coat Colors of Mice. Springer-Verlag, New York.  [MGI Ref ID J:78801]

Siracusa LD; Washburn LL; Swing DA; Argeson AC; Jenkins NA; Copeland NG. 1995. Hypervariable yellow (Ahvy), a new murine agouti mutation: Ahvy displays the largest variation in coat color phenotypes of all known agouti alleles. J Hered 86(2):121-8. [PubMed: 7751596]  [MGI Ref ID J:24247]

Cacnb4lh related

Aizawa M; Ito Y; Fukuda H. 1997. Pharmacological profiles of generalized absence seizures in lethargic, stargazer and gamma-hydroxybutyrate-treated model mice. Neurosci Res 29(1):17-25. [PubMed: 9293489]  [MGI Ref ID J:43226]

Badou A; Basavappa S; Desai R; Peng YQ; Matza D; Mehal WZ; Kaczmarek LK; Boulpaep EL; Flavell RA. 2005. Requirement of voltage-gated calcium channel beta4 subunit for T lymphocyte functions. Science 307(5706):117-21. [PubMed: 15637280]  [MGI Ref ID J:95687]

Badou A; Jha MK; Matza D; Mehal WZ; Freichel M; Flockerzi V; Flavell RA. 2006. Critical role for the beta regulatory subunits of Cav channels in T lymphocyte function. Proc Natl Acad Sci U S A 103(42):15529-34. [PubMed: 17028169]  [MGI Ref ID J:115345]

Ball SL; Powers PA; Shin HS; Morgans CW; Peachey NS; Gregg RG. 2002. Role of the beta(2) subunit of voltage-dependent calcium channels in the retinal outer plexiform layer. Invest Ophthalmol Vis Sci 43(5):1595-603. [PubMed: 11980879]  [MGI Ref ID J:80080]

Burgess DL; Biddlecome GH; McDonough SI; Diaz ME; Zilinski CA; Bean BP; Campbell KP; Noebels JL. 1999. beta subunit reshuffling modifies N- and P/Q-type Ca2+ channel subunit compositions in lethargic mouse brain. Mol Cell Neurosci 13(4):293-311. [PubMed: 10328888]  [MGI Ref ID J:57712]

Caddick SJ; Wang C; Fletcher CF; Jenkins NA; Copeland NG; Hosford DA. 1999. Excitatory but not inhibitory synaptic transmission is reduced in lethargic (Cacnb4(lh)) and tottering (Cacna1atg) mouse thalami. J Neurophysiol 81(5):2066-74. [PubMed: 10322048]  [MGI Ref ID J:56225]

Cope DW; Di Giovanni G; Fyson SJ; Orban G; Errington AC; Lorincz ML; Gould TM; Carter DA; Crunelli V. 2009. Enhanced tonic GABAA inhibition in typical absence epilepsy. Nat Med 15(12):1392-8. [PubMed: 19966779]  [MGI Ref ID J:155872]

Devanagondi R; Egami K; LeDoux MS; Hess EJ; Jinnah HA. 2007. Neuroanatomical substrates for paroxysmal dyskinesia in lethargic mice. Neurobiol Dis 27(3):249-57. [PubMed: 17561408]  [MGI Ref ID J:134825]

Dickie MM. 1964. Lethargic (lh) Mouse News Lett 30:31.  [MGI Ref ID J:28465]

Dung HC. 1981. 2. Lethargic mice. In: Immunologic Defects in Laboratory Animals. Plenum Press.  [MGI Ref ID J:28475]

Dung HC. 1977. Deficiency in the thymus-dependent immunity in lethargic mutant mice. Transplantation 23(1):39-43. [PubMed: 13525]  [MGI Ref ID J:5766]

Dung HC. 1975. Growth retardation, high mortality, and low reproductivity of neurological mutant mice. Anat Rec 181:347-348 (Abstr.).  [MGI Ref ID J:12166]

Dung HC; Lawson RL; Stevens M. 1977. A study of the increased serum level of IgG1 in 'lethargic' mice combined with a depressed thymus-dependent lymphoid system. J Immunogenet 4(4):287-93. [PubMed: 410895]  [MGI Ref ID J:5883]

Dung HC; Swigart RH. 1972. Histo-pathologic observations of the nervous and lymphoid tissues of lethargic mutant mice. Tex Rep Biol Med 30(1):23-39. [PubMed: 5037658]  [MGI Ref ID J:5281]

Herring JM; Dung HC; Yoo JH; Yu J. 1981. Chronological studies of peripheral motor nerve conduction in lethargic mice. Electromyogr Clin Neurophysiol 21(2-3):121-34. [PubMed: 7261997]  [MGI Ref ID J:6556]

Hosford DA; Clark S; Cao Z; Wilson WA Jr; Lin FH; Morrisett RA; Huin A. 1992. The role of GABAB receptor activation in absence seizures of lethargic (lh/lh) mice. Science 257(5068):398-401. [PubMed: 1321503]  [MGI Ref ID J:1484]

Hosford DA; Lin FH; Kraemer DL; Cao Z; Wang Y; Wilson JT Jr. 1995. Neural network of structures in which GABAB receptors regulate absence seizures in the lethargic (lh/lh) mouse model. J Neurosci 15(11):7367-76. [PubMed: 7472490]  [MGI Ref ID J:29786]

Hosford DA; Wang Y; Liu CC; Snead OC 3rd. 1995. Characterization of the antiabsence effects of SCH 50911, a GABA-B receptor antagonist, in the lethargic mouse, gamma-hydroxybutyrate, and pentylenetetrazole models. J Pharmacol Exp Ther 274(3):1399-403. [PubMed: 7562514]  [MGI Ref ID J:30226]

Ishige K; Ito Y; Fukuda H. 1999. Characterization of absence seizure-dependent cyclic AMP responsive element-and activator protein 1 DNA-binding activities in lethargic (lh/lh) mice. Neurosci Lett 262(1):53-6. [PubMed: 10076871]  [MGI Ref ID J:56009]

Kaja S; Todorov B; van de Ven RC; Ferrari MD; Frants RR; van den Maagdenberg AM; Plomp JJ. 2007. Redundancy of Cav2.1 channel accessory subunits in transmitter release at the mouse neuromuscular junction. Brain Res 1143:92-101. [PubMed: 17320843]  [MGI Ref ID J:121463]

Khan Z; Jinnah HA. 2002. Paroxysmal dyskinesias in the lethargic mouse mutant. J Neurosci 22(18):8193-200. [PubMed: 12223573]  [MGI Ref ID J:79139]

Lin F; Barun S; Lutz CM; Wang Y; Hosford DA. 1999. Decreased (45)Ca(2)(+) uptake in P/Q-type calcium channels in homozygous lethargic (Cacnb4lh) mice is associated with increased beta3 and decreased beta4 calcium channel subunit mRNA expression. Brain Res Mol Brain Res 71(1):1-10. [PubMed: 10407181]  [MGI Ref ID J:56507]

Lin F; Wang Y; Hosford DA. 1999. Age-related relationship between mRNA expression of GABA(B) receptors and calcium channel beta4 subunits in cacnb4lh mice. Brain Res Mol Brain Res 71(1):131-5. [PubMed: 10407196]  [MGI Ref ID J:109316]

Lin FH; Cao Z; Hosford DA. 1993. Increased number of GABAB receptors in the lethargic (lh/lh) mouse model of absence epilepsy. Brain Res 608(1):101-6. [PubMed: 8388308]  [MGI Ref ID J:4388]

Lin FH; Lin S; Wang Y; Hosford DA. 1999. Glutamate decarboxylase isoforms in thalamic nuclei in lethargic mouse model of absence seizures. Brain Res Mol Brain Res 71(1):127-30. [PubMed: 10407195]  [MGI Ref ID J:109317]

Lin FH; Wang Y; Lin S; Cao Z; Hosford DA. 1995. GABAB receptor-mediated effects in synaptosomes of lethargic (lh/lh) mice. J Neurochem 65(5):2087-95. [PubMed: 7595494]  [MGI Ref ID J:29347]

Marmorstein LY; Wu J; McLaughlin P; Yocom J; Karl MO; Neussert R; Wimmers S; Stanton JB; Gregg RG; Strauss O; Peachey NS; Marmorstein AD. 2006. The light peak of the electroretinogram is dependent on voltage-gated calcium channels and antagonized by bestrophin (best-1). J Gen Physiol 127(5):577-89. [PubMed: 16636205]  [MGI Ref ID J:136113]

McEnery MW; Copeland TD; Vance CL. 1998. Altered expression and assembly of N-type calcium channel alpha1B and beta subunits in epileptic lethargic (lh/lh) mouse. J Biol Chem 273(34):21435-8. [PubMed: 9705268]  [MGI Ref ID J:49244]

Qian J; Noebels JL. 2000. Presynaptic Ca(2+) influx at a mouse central synapse with Ca(2+) channel subunit mutations. J Neurosci 20(1):163-70. [PubMed: 10627593]  [MGI Ref ID J:120572]

Sidman RL; Green MC; Appel SH. 1965. Lethargic, lh, recessive. In: Catalog of the Neurological Mutants of the Mouse. Harvard University Press.  [MGI Ref ID J:28466]

Song I; Kim D; Choi S; Sun M; Kim Y; Shin HS. 2004. Role of the alpha1G T-type calcium channel in spontaneous absence seizures in mutant mice. J Neurosci 24(22):5249-57. [PubMed: 15175395]  [MGI Ref ID J:96913]

Tadmouri A; Kiyonaka S; Barbado M; Rousset M; Fablet K; Sawamura S; Bahembera E; Pernet-Gallay K; Arnoult C; Miki T; Sadoul K; Gory-Faure S; Lambrecht C; Lesage F; Akiyama S; Khochbin S; Baulande S; Janssens V; Andrieux A; Dolmetsch R; Ronjat M; Mori Y; De Waard M. 2012. Cacnb4 directly couples electrical activity to gene expression, a process defective in juvenile epilepsy. EMBO J 31(18):3730-44. [PubMed: 22892567]  [MGI Ref ID J:188568]

Zhang Y; Mori M; Burgess DL; Noebels JL. 2002. Mutations in high-voltage-activated calcium channel genes stimulate low-voltage-activated currents in mouse thalamic relay neurons. J Neurosci 22(15):6362-71. [PubMed: 12151514]  [MGI Ref ID J:106959]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

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

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3300.00
Animals Provided

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.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery of Strains Needing Progeny Testing
    At least two untested males and two untested females (two pairs) will be recovered (eight or more mice is typical). The total number of animals provided, their gender and genotype will vary. Untested animals typically are available to ship between 10 and 14 weeks from the date of your order. If the first recovery attempt is unsuccessful, a second recovery will be done, extending the overall recovery time to approximately 25 weeks. Progeny testing is required to identify the genotype of mice of this strain, as a genotyping assay is not available. This type of testing involves breeding the recovered animals and assessing the phenotype of the offspring in order to identify animals carrying the mutation of interest. We can perform the progeny testing for you as a service or we can ship all recovered animals to you for progeny testing at your facility. If you perform the progeny testing, there is no guarantee that a carrier will be identified. If we perform progeny testing as a service, additional breeding time will be required. In this case, when a male and female (one pair) are identified that carry the mutation, they and their offspring will be shipped. Delivery time for strains requiring progeny testing often exceeds 25 weeks and may take 12 months or more due to the difficulties in breeding some strains. The progeny testing cost is in addition to the recovery cost and is based on the number of boxes used and the time taken to produce the mice identified as carrying the mutation.
    Please note that identified pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation.

    Please contact Customer Service for more information on the cost of progeny testing for a strain, tel: 1-800-422-6423 or 1-207-288-5845 (from any location). The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
    Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $4290.00
Animals Provided

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.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery of Strains Needing Progeny Testing
    At least two untested males and two untested females (two pairs) will be recovered (eight or more mice is typical). The total number of animals provided, their gender and genotype will vary. Untested animals typically are available to ship between 10 and 14 weeks from the date of your order. If the first recovery attempt is unsuccessful, a second recovery will be done, extending the overall recovery time to approximately 25 weeks. Progeny testing is required to identify the genotype of mice of this strain, as a genotyping assay is not available. This type of testing involves breeding the recovered animals and assessing the phenotype of the offspring in order to identify animals carrying the mutation of interest. We can perform the progeny testing for you as a service or we can ship all recovered animals to you for progeny testing at your facility. If you perform the progeny testing, there is no guarantee that a carrier will be identified. If we perform progeny testing as a service, additional breeding time will be required. In this case, when a male and female (one pair) are identified that carry the mutation, they and their offspring will be shipped. Delivery time for strains requiring progeny testing often exceeds 25 weeks and may take 12 months or more due to the difficulties in breeding some strains. The progeny testing cost is in addition to the recovery cost and is based on the number of boxes used and the time taken to produce the mice identified as carrying the mutation.
    Please note that identified pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation.

    Please contact Customer Service for more information on the cost of progeny testing for a strain, tel: 1-800-422-6423 or 1-207-288-5845 (from any location). The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
    Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

General Supply Notes

  • View the complete collection of spontaneous mutants in the Mouse Mutant Resource.

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