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Strain Name:

B6CBACa Aw-J/A-Aifm1Hq/J

Stock Number:

000501

Availability:

Repository- Live

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General Terms and Conditions

Former Name      B6CBACa Aw-J/A-Pdcd8Hq/J    (Changed: 20-NOV-06 )
      B6CBACa-Aw-J/A-Hq    (Changed: 15-DEC-04 )
      B6CBACa-Aw-J/A-Pdcd8Hq    (Changed: 15-DEC-04 )
Genes & Alleles   Aw-J;   Aifm1;   Aifm1Hq;   a;

Product Information

Strain Details

Type JAX® GEMM® Strain - Mutant Strain
Additional information on JAX® GEMM® Strains.
Type JAX® GEMM® Strain - Spontaneous Mutation
Specieslaboratory mouse
Generation(N15F1p)+N15 (21-JAN-08)

Appearance
white bellied agouti or agouti, balding, small, ataxic
Related Genotype: Aw-J/? or A/A, Aifm1Hq/Y male or Aifm1Hq/Aifm1Hq female

white bellied agouti or agouti, possible patchy fur
Related Genotype: Aw-J/? or A/A, Aifm1Hq/+ female

Strain Description
Harlequin mice exhibit paucity of fur resulting in near baldness in hemizygous males and homozygous females. Heterozygous females have a patchy absence of hair that is not always obvious, since the degree of hair loss is notably less than 50%. Homozygotes and hemizygous males weigh less than heterozygous or wild type controls. Ataxia is noticeable by 5 months and progresses as the mice age. Initially the ataxia manifests itself as a side-to-side, unsteady gait with a lateral tremor visible at rest. A delayed cerebellar cortical atrophy has been characterized in these mutants, with an apoptotic loss of granule cells beginning at 4 months of age and a necrotic loss of Purkinje cells occurring subsequently. The granule cells re-enter the cell cycle, but the Purkinje cells do not, supporting the postulate that inappropriate cell cycle re-entry of terminally differentiated neurons can induce apoptosis. Cell loss is greater in the caudal lobules of the cerebellum and is extensive by 9 to 11 months of age. Retinal degeneration is found beginning with ganglion and amacrine cell loss in the ganglion cell layer at 3 months of age, and progresses with cell loss in the inner and outer nuclear layers and reduction of rod and cone ERG responses at 4 months of age. By 10 months, the rod and cone ERG responses are gone, and at 11 months of age there isapparent cell loss in all layers of the retina. No cerebellar or retinal abnormalities were found in heterozygous females. Catalase activity and expression and total glutathione levels are increased in the cerebella of mutant mice, but not in other brain regions, and lipid hydroperoxidases are increased in brain and heart tissue. Primary granule cell cultures, but not cortical cultures, from harlequin mice show increased sensitivity to peroxide. Hemizygous males, homozygous females and hemizygous females are all viable and fertile. (Barber 1971; Falconer and Isaacson 1972; Bronson et al., 1990; Klein et al., 2002.)

Mammalian Phenotype Terms assigned by genotype

Aifm1Hq/Aifm1+

        B6CBACa-Aw-J/A
  • skin/coat/nails phenotype
  • partial hair loss (MGI Ref ID J:79052)
    • patchy irregular hair loss
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype (MGI Ref ID J:79052)
    • heterozygotes are normal with respect to ataxia
  • nervous system phenotype
  • *normal* nervous system phenotype (MGI Ref ID J:79052)
    • no loss of granule cells seen to 26 months of age

Aifm1Hq/Aifm1Hq

        B6CBACa-Aw-J/A
  • skin/coat/nails phenotype
  • partial hair loss (MGI Ref ID J:79052)
    • described as nearly bald
  • behavior/neurological phenotype
  • abnormal motor capabilities/coordination/movement (MGI Ref ID J:79052)
    • abnormal gait (MGI Ref ID J:79052)
      • side by side unsteady gait at 5 months of age
      • marked lateral swaying when moving and at rest by 9 months of age
    • ataxia (MGI Ref ID J:79052)
      • age of onset is approximately 5 months of age
      • mild
      • truncal ataxia by 9 months
    • tremors (MGI Ref ID J:79052)
      • age of onset is approximately 5 months
      • a perceptible lateral tremor at rest by 9 months of age
  • pharmacologically induced seizures (MGI Ref ID J:98103)
    • mice are protected against CA3 region damage at both 4 and 7 days after kainic acid induced stage 4 seizures although some cell damage is observed
  • nervous system phenotype
  • abnormal cerebellar cortex morphology (MGI Ref ID J:78983)
    • Purkinje cell degeneration (MGI Ref ID J:79052)
      • described as mild and patchy in the folia, but extensive in the floccular lobes in mice 5-8 months of age
      • Purkinje cell loss occurs later than granule cell loss
      • cell loss apparently due to necrosis
      • many Purkinje cells are dead by 7 months of age
    • abnormal cerebellar granule layer (MGI Ref ID J:79052)
      • no reduction in the folia but extensive loss in the floccular lobes in mice 5-8 months of age
      • losses are preferentially from the caudal vermis and hemispheres
      • most caudal granule cells are lost by 12 months
      • abnormal granule neuron (MGI Ref ID J:78983)
        • pyknotic granule cell nuclei at 4 months of age
        • apoptotic granule cells seen at 4 months of age
  • amacrine cell degeneration (MGI Ref ID J:78983)
    • cell loss is seen in the ganglion layer after about 3 months of age
  • decreased susceptibility to neuronal excitotoxicity (MGI Ref ID J:98103)
    • resistant to cell death induced by glutamate, NMDA, and kainic acid
  • pharmacologically induced seizures (MGI Ref ID J:98103)
    • mice are protected against CA3 region damage at both 4 and 7 days after kainic acid induced stage 4 seizures although some cell damage is observed
  • retinal ganglion cell degeneration (MGI Ref ID J:78983)
    • ganglion cell loss is seen after about 3 months of age
  • small cerebellum (MGI Ref ID J:78983)
    • cerebellum normal before 3 months
    • much smaller at 7 months
  • vision/eye phenotype
  • abnormal eye electrophysiology (MGI Ref ID J:78983)
    • both rod and cone ERG are diminished by 4 months of age
    • ERG responses are completely abolished by 10 months of age
  • amacrine cell degeneration (MGI Ref ID J:78983)
    • cell loss is seen in the ganglion layer after about 3 months of age
  • retinal degeneration (MGI Ref ID J:78983)
    • onset of retinal degeneration is after 3 months of age
    • cell loss is seen in all layers of the retina by 11 months
  • retinal ganglion cell degeneration (MGI Ref ID J:78983)
    • ganglion cell loss is seen after about 3 months of age
  • thin retinal inner plexiform layer (MGI Ref ID J:78983)
    • thinning by 11 months
  • thin retinal outer plexiform layer (MGI Ref ID J:78983)
    • thinning by 11 months
  • cellular phenotype
  • abnormal mitosis (MGI Ref ID J:78983)
    • cerebellar granule cells and retina cells re-enter the cell cycle with greater frequency than in controls
    • number of cycling cells in the cerebellum and retina increase through 7 months and then declines
  • increased cellular sensitivity to hydrogen peroxide (MGI Ref ID J:78983)
    • granule cells of the cerebellum in culture show increased sensitivity to hydrogen peroxide
  • oxidative stress (MGI Ref ID J:78983)
    • increased sensitivity of the cerebellum to oxidative stress
    • catalase activity increased in the cerebellum at 1 and 3 months of age
    • oxidative damage to mitochondria of the cerebellar granular layer and the ganglion layer of the retina
    • slightly increased as a result of transverse aortic banding
  • life span-post-weaning/aging
  • abnormal induced morbidity/mortality (MGI Ref ID J:110278)
    • significantly reduced survival at both 1 and 4 weeks after transverse aortic banding
  • cardiovascular system phenotype
  • abnormal cardiovascular system morphology (MGI Ref ID J:110278)
    • cardiac hypertrophy (MGI Ref ID J:110278)
      • hypertrophy due to transverse aorting banding is twice as great as is seen in controls
    • dilated left ventricle (MGI Ref ID J:110278)
      • increased left ventricular internal diameter relative to controls as a result of transverse aortic banding
    • increased cardiomyocyte apoptosis (MGI Ref ID J:110278)
      • greatly increased levels of both apoptosis and necrosis in myocytes after transverse aortic banding
  • abnormal cardiovascular system physiology (MGI Ref ID J:110278)
    • abnormal myocardial fiber physiology (MGI Ref ID J:110278)
      • cardiomyocytes more prone to die in response to exposure to hydrogen peroxide
    • altered response to myocardial infarction (MGI Ref ID J:110278)
      • increased sensitivity to ischemia/reperfusion injury
      • over 80% fail to survive 30minutes of left anterior descending artery occlusion followed by 2 to 24 hours of reperfusion
      • increased infarction size (MGI Ref ID J:110278)
        • experimental infarction size is increased by 50% over controls in 2 month old animals and by 78% in 6 month old animals
        • apoptosis in viable muscle cells is also increased
    • decreased cardiac muscle contractility (MGI Ref ID J:110278)
      • deterioration of cardiac contractility as a result of transverse aortic banding
  • muscle phenotype
  • decreased cardiac muscle contractility (MGI Ref ID J:110278)
    • deterioration of cardiac contractility as a result of transverse aortic banding
  • increased cardiomyocyte apoptosis (MGI Ref ID J:110278)
    • greatly increased levels of both apoptosis and necrosis in myocytes after transverse aortic banding
  • homeostasis/metabolism phenotype
  • altered response to myocardial infarction (MGI Ref ID J:110278)
    • increased sensitivity to ischemia/reperfusion injury
    • over 80% fail to survive 30minutes of left anterior descending artery occlusion followed by 2 to 24 hours of reperfusion
    • increased infarction size (MGI Ref ID J:110278)
      • experimental infarction size is increased by 50% over controls in 2 month old animals and by 78% in 6 month old animals
      • apoptosis in viable muscle cells is also increased
  • decreased susceptibility to neuronal excitotoxicity (MGI Ref ID J:98103)
    • resistant to cell death induced by glutamate, NMDA, and kainic acid
  • pharmacologically induced seizures (MGI Ref ID J:98103)
    • mice are protected against CA3 region damage at both 4 and 7 days after kainic acid induced stage 4 seizures although some cell damage is observed

Aifm1Hq/Y

        B6CBACa-Aw-J/A
  • skin/coat/nails phenotype
  • partial hair loss (MGI Ref ID J:79052)
    • described as nearly bald
  • behavior/neurological phenotype
  • abnormal motor capabilities/coordination/movement (MGI Ref ID J:79052)
    • abnormal gait (MGI Ref ID J:79052)
      • side by side unsteady gait at 5 months of age
      • marked lateral swaying when moving and at rest by 9 months of age
    • ataxia (MGI Ref ID J:79052)
      • age of onset is approximately 5 months of age
      • mild
      • truncal ataxia by 9 months
    • tremors (MGI Ref ID J:79052)
      • age of onset is approximately 5 months
      • a perceptible lateral tremor at rest by 9 months of age
  • pharmacologically induced seizures (MGI Ref ID J:98103)
    • mice are protected against CA3 region damage at both 4 and 7 days after kainic acid induced stage 4 seizures although some cell damage is observed
  • nervous system phenotype
  • abnormal cerebellar cortex morphology (MGI Ref ID J:78983)
    • Purkinje cell degeneration (MGI Ref ID J:78983)
      • Purkinje cell loss occurs later than granule cell loss
      • cell loss apparently due to necrosis
      • many Purkinje cells are dead by 7 months of age
      • described as mild and patchy in the folia, but extensive in the floccular lobes in mice 5-8 months of age
    • abnormal cerebellar granule layer (MGI Ref ID J:78983)
      • losses are preferentially from the caudal vermis and hemispheres
      • most caudal granule cells are lost by 12 months
      • no reduction in the folia but extensive loss in the floccular lobes in mice 5-8 months of age
      • abnormal granule neuron (MGI Ref ID J:78983)
        • pyknotic granule cell nuclei at 4 months of age
        • apoptotic granule cells seen at 4 months of age
  • amacrine cell degeneration (MGI Ref ID J:78983)
    • cell loss is seen in the ganglion layer after 3 months of age
  • decreased susceptibility to neuronal excitotoxicity (MGI Ref ID J:98103)
    • resistant to cell death induced by glutamate, NMDA, and kainic acid
  • pharmacologically induced seizures (MGI Ref ID J:98103)
    • mice are protected against CA3 region damage at both 4 and 7 days after kainic acid induced stage 4 seizures although some cell damage is observed
  • retinal ganglion cell degeneration (MGI Ref ID J:78983)
    • ganglion cell loss is seen after about 3 months of age
  • small cerebellum (MGI Ref ID J:78983)
    • much smaller at 7 months
    • cerebellum normal before 3 months
  • vision/eye phenotype
  • abnormal eye electrophysiology (MGI Ref ID J:78983)
    • both rod and cone ERG are diminished by 4 months of age
    • ERG responses are completely abolished by 10 months of age
  • amacrine cell degeneration (MGI Ref ID J:78983)
    • cell loss is seen in the ganglion layer after 3 months of age
  • retinal degeneration (MGI Ref ID J:78983)
    • onset of retinal degeneration is after 3 months of age
    • cell loss is seen in all layers of the retina by 11 months
  • retinal ganglion cell degeneration (MGI Ref ID J:78983)
    • ganglion cell loss is seen after about 3 months of age
  • thin retinal inner plexiform layer (MGI Ref ID J:78983)
    • thinning by 11 months
  • thin retinal outer plexiform layer (MGI Ref ID J:78983)
    • thinning by 11 months
  • cellular phenotype
  • abnormal mitosis (MGI Ref ID J:78983)
    • cerebellar granule cells and retina cells re-enter the cell cycle with greater frequency than in controls
    • number of cycling cells in the cerebellum and retina increase through 7 months and then declines
  • increased cellular sensitivity to hydrogen peroxide (MGI Ref ID J:78983)
    • granule cells of the cerebellum in culture show increased sensitivity to hydrogen peroxide
  • oxidative stress (MGI Ref ID J:78983)
    • increased sensitivity of the cerebellum to oxidative stress
    • catalase activity increased in the cerebellum at 1 and 3 months of age
    • oxidative damage to mitochondria of the cerebellar granular layer and the ganglion layer of the retina
    • slightly increased as a result of transverse aortic banding
  • life span-post-weaning/aging
  • abnormal induced morbidity/mortality (MGI Ref ID J:110278)
    • significantly reduced survival at both 1 and 4 weeks after transverse aortic banding
  • cardiovascular system phenotype
  • abnormal cardiovascular system morphology (MGI Ref ID J:110278)
    • cardiac hypertrophy (MGI Ref ID J:110278)
      • hypertrophy due to transverse aorting banding is twice as great as is seen in controls
    • dilated left ventricle (MGI Ref ID J:110278)
      • increased left ventricular internal diameter relative to controls as a result of transverse aortic banding
    • increased cardiomyocyte apoptosis (MGI Ref ID J:110278)
      • greatly increased levels of both apoptosis and necrosis in myocytes after transverse aortic banding
  • abnormal cardiovascular system physiology (MGI Ref ID J:110278)
    • abnormal myocardial fiber physiology (MGI Ref ID J:110278)
      • cardiomyocytes more prone to die in response to exposure to hydrogen peroxide
    • altered response to myocardial infarction (MGI Ref ID J:110278)
      • increased sensitivity to ischemia/reperfusion injury
      • over 80% fail to survive 30minutes of left anterior descending artery occlusion followed by 2 to 24 hours of reperfusion
      • increased infarction size (MGI Ref ID J:110278)
        • experimental infarction size is increased by 50% over controls in 2 month old animals and by 78% in 6 month old animals
        • apoptosis in viable muscle cells is also increased
    • decreased cardiac muscle contractility (MGI Ref ID J:110278)
      • deterioration of cardiac contractility as a result of transverse aortic banding
  • muscle phenotype
  • decreased cardiac muscle contractility (MGI Ref ID J:110278)
    • deterioration of cardiac contractility as a result of transverse aortic banding
  • increased cardiomyocyte apoptosis (MGI Ref ID J:110278)
    • greatly increased levels of both apoptosis and necrosis in myocytes after transverse aortic banding
  • homeostasis/metabolism phenotype
  • altered response to myocardial infarction (MGI Ref ID J:110278)
    • increased sensitivity to ischemia/reperfusion injury
    • over 80% fail to survive 30minutes of left anterior descending artery occlusion followed by 2 to 24 hours of reperfusion
    • increased infarction size (MGI Ref ID J:110278)
      • experimental infarction size is increased by 50% over controls in 2 month old animals and by 78% in 6 month old animals
      • apoptosis in viable muscle cells is also increased
  • decreased susceptibility to neuronal excitotoxicity (MGI Ref ID J:98103)
    • resistant to cell death induced by glutamate, NMDA, and kainic acid
  • pharmacologically induced seizures (MGI Ref ID J:98103)
    • mice are protected against CA3 region damage at both 4 and 7 days after kainic acid induced stage 4 seizures although some cell damage is observed

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

Aifm1Hq/Aifm1Hq

        involves: CF1
  • skin/coat/nails phenotype
  • partial hair loss (MGI Ref ID J:15073)
    • mice have bald patches of varying extend and distribution
  • growth/size phenotype
  • decreased body weight (MGI Ref ID J:15073)
    • adults are about 1/3 the weight of controls

Aifm1Hq/Y

        involves: CF1
  • skin/coat/nails phenotype
  • partial hair loss (MGI Ref ID J:15073)
    • mice have bald patches of varying extend and distribution
  • growth/size phenotype
  • decreased body weight (MGI Ref ID J:15073)
    • adults are about 1/3 the weight of controls

Gene & Allele Details

Allele Symbol Aw-J
Allele Name white bellied agouti Jackson
Common Name(s) AWJ;
Strain of OriginC57BL/6J
Gene Symbol and Name a, nonagouti
Chromosome 2
Gene Common Name(s) AGSW; AGTI; AGTIL; ASP; As; MGC126092; MGC126093; SHEP9; agouti; agouti signal protein; agouti suppressor;
 
Allele Symbol Aifm1Hq
Allele Name harlequin
Common Name(s) Hq;
Strain of OriginCF1
Gene Symbol and Name Aifm1, apoptosis-inducing factor, mitochondrion-associated 1
Chromosome X
Gene Common Name(s) AIF; AIFsh2; Hq; MGC111425; PDCD8; Pdcd8; apoptosis-inducing factor; harlequin; programmed cell death 8;
General Note Although initial reports were that ataxia was more severe in males than females, later unpublished reports indicate that there is no significant difference in severity of the ataxia phenotype between hemizygous males and homozygous females (S. Ackerman, personal communication)
Molecular Note The harlequin mutation is an ecotropic proviral insertion at the Pdcd8 gene. This insertion leads to an 80% decrease in transcipt and protein levels, relative to wild type controls. [MGI Ref ID J:78983]

Control Information

  Allele   Control
 Aifm1Hq  Wild-type from the colony
 
  Considerations for Choosing Controls

Genotyping Protocols

Aw-J
Aifm1Hq

Colony Maintenance

Breeding & HusbandryComments: Hq/Y males need to stay with their mothers an extra week or more because they are too small to wean at 3 weeks.
Diet Information LabDiet® 5K52/5K67

Related Strains

View Strains carrying   Aw-J     (31 strains)

Strains carrying other alleles of a
003301   (C57BL/6J x C3H-Eya1bor)F1/J
000251   AEJ.Cg-ae +/a Gdf5bp-H/J
000202   AEJ/Gn-bd/J
000199   AEJ/GnLeJ
000427   B10.CE-H13b Aw/(30NX)SnJ
000420   B10.LP-H13b Aw/Sn
000477   B10.PA-Pldnpa H3e at/SnJ
000419   B10.UW-H3b we Pax1un at/SnJ
003879   B10;TFLe-a/a T tf/+ tf/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
002083   B6 x B6EiC3 a/A-T(7;16)235Dn/J
000507   B6 x B6EiC3 a/A-Otcspf/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
000769   B6.C/(HZ18)By-at-44J/J
000001   B6.C3 A/a Mgrn1md/J
000203   B6.C3-Aiy/a/J
000017   B6.C3Fe-Avy/J
000628   B6.CE-A Amy1b Amy2b/J
005505   B6.Cg-Ay Slc7a11sut/LmLlp
000021   B6.Cg-Ay/J
001572   B6.Cg-am-J/J
004200   B6;CBACa Aw-J/A-Npr2cn-2J/J
000785   B6;D2-a Es1e/J
000604   B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J
002807   B6C3Fe a/a-Meox2fla/J
000224   B6C3Fe a/a-Scyl1mdf/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
000231   B6C3Fe a/a-Csf1op/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
000506   B6C3Fe a/a-Qkqk/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
001750   B6C3Fe a/a-XsJ/J
000624   B6C3Fe a/a-anx/J
003020   B6C3Fe a/a-dep/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
001752   B6CBCa Aw-J/A-T(7;15)9H/J
000971   B6EiC3 a/A-Och/J
000551   B6EiC3 a/A-Tbx15de-H/J
006450   B6EiC3 a/A-Vss/J
000557   B6EiC3-+ a/LnpUl A/J
000504   B6EiC3Sn a/A-Cacnb4lh/J
000553   B6EiC3Sn a/A-Egfrwa2 Wnt3avt/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
001924   B6EiC3Sn a/A-Ts(1716)65Dn
001923   B6EiC3Sn a/A-Ts(417)2Lws Tim/J
000200   C3FeB6 A/Aw-J-Ankank/J
000638   C3FeB6 A/Aw-J-Spnb4qv-J/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
000584   C57BL/6J-+ T(1;2)5Ca/a +/J
000258   C57BL/6J-Ai/a/J
000774   C57BL/6J-Asy/a/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
000283   LT.CAST-A/J
000265   MY/HuLeJ
000308   SSL/LeJ
001759   STOCK A Tyrc Sha/J
001427   STOCK Aw us/J
000994   STOCK a Myo5ad Mregdsu/J
000064   STOCK a Tyrp1b Sisi/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
000317   STOCK a/a Egfrwa2/J
000302   STOCK a/a MitfMi-wh +/+ Itpr1opt/J
000286   STOCK a/a Myo5ad fd/+ +/J
000206   STOCK a/a Tyrc-h/J
001432   STOCK a/a Tyrp1b sks/Tyrp1b +/J
000281   STOCK a/a ma ft/ma ft/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     (138 strains)

Additional Web Information

Genetic Quality Control Annual Report
JAX® NOTES, Winter 2002; 488. Jackson Laboratory Scientist Identifies Gene Implicated in Oxidative Stress and Neurodegeneration.

Animal Health Reports

Room Number           FGB29

Research Applications

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

Aifm1Hq related

Apoptosis Research
Endogenous Regulators

Cardiovascular Research

Cell Biology Research
Cell Cycle Regulation

Dermatology Research
Skin and Hair Texture Defects

Developmental Biology Research
Eye Defects
Growth Defects

Neurobiology Research
Cerebellar Defects (Purkinje cell defect)
Neurodegeneration
Tremor Defects

Sensorineural Research
Eye Defects
Retinal Degeneration

References

Selected Reference(s)

Klein JA; Longo-Guess CM; Rossmann MP; Seburn KL; Hurd RE; Frankel WN; Bronson RT; Ackerman SL. 2002. The harlequin mouse mutation downregulates apoptosis-inducing factor. Nature 419(6905):367-74. [PubMed: 12353028]  [MGI Ref ID J:78983]

Additional References

Price and Supply Information

Strain Name: B6CBACa Aw-J/A-Aifm1Hq/J
Stock Number: 000501

Price Details

IMPORTANT NOTE: Prices are based on shipping destination. To view prices, select your shipping destination.

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Supply Details

Standard SupplyRepository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of ~nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within 48 hours of order placement.
Supply Notes Usually shipped between four and eight weeks of age.
Genomic DNA is available for this strain from the Mouse DNA Resource.
LicensingSee General Terms and Conditions below  
Control InformationView Control Information in Strain Details.

General Terms and Conditions

View JAX® Mice & Services Conditions of Use.

The Jackson Laboratory's Genotype Promise

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

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Contact Information
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Fax: 207.288.6150
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