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Strain Name:

B6C3Fe a/a-Relnrl/J

Stock Number:

000235

Availability:

Repository- Live

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General Terms and Conditions

Former Name      B6C3Fe-a/a-Relnrl/+    (Changed: 15-DEC-04 )
Genes & Alleles   Reln;   Relnrl;   a;

Product Information

Strain Details

Type JAX® GEMM® Strain - Mutant Strain
Additional information on JAX® GEMM® Strains.
Type JAX® GEMM® Strain - Spontaneous Mutation
Mating SystemBackcross-Intercross         (Female x Male)
TJL Breeding Summary: homozygote x B6C3FeF1 a/a then heterozygote x heterozygote
Specieslaboratory mouse
GenerationN62 (23-JAN-08)

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

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

Strain Description
Mice homozygous for the reeler (Relnrl) mutation exhibit an ataxic gait, dystonic posture and tremors starting around 2 weeks of age. These mutants are incapable of maintaining their hindquarters upright and often fall over during locomotor activity. Moreover, viability and fertility are greatly reduced, especially when the gene is carried on an inbred genetic background. Heterozygotes are visually indistinguishable from wildtype controls. Neuropathies characteristic of Relnrl/Relnrl mutants include a failure of neuronal layer formation in laminated brain regions during development. Neuronal positioning is abnormal within cerebellar, cerebral and hippocampal cortices. The behavioral phenotype is primarily attributed to the severe hypoplasia of the cerebellum, which lacks foliation. Here, there are reduced numbers of granule and Purkinje cells and these cells are aberrantly dispersed among the layers. In the Reln-deficient neocortex, neurons normally destined to migrate past the subplate remain confined to deeper nuclei, thus ablating normal cortical layer formation. Similarly, pyramidal and granule cells of the developing hippocampus are scattered throughout the hippocampal tracts causing gross disorganization. RELN is required for normal spinal cord formation since migration of sympathetic preganglionic neurons in the intermediolateral column becomes disrupted in developing Relnrl/Relnrl mice. While somatic motor neurons and cholinergic interneurons are positioned normally in the Relnrl/Relnrl spinal cord, parasympathetic and sympathetic preganglionic neurons migrate medially past their normal destinations, indicating that RELN may act in a cell-specific manner. Neurons are also found abnormally positioned in the facial nucleus, inferior olivary complex, and mesencephalic trigeminal nucleus of affected reeler mutants. A RELN deficiency additionally results in an alteration in the structure and function of retinal synaptic circuitry. There is a reduction in the number of rod bipolar cells and physiologic responsiveness is compromised. Specifically, electroretinography analysis demonstrated a reduction in rod b-wave amplitudes. RELN may also play a role in the development of immune function since T-cell and macrophage function are suppressed in Relnrl/Relnrl mutants. Taken together, the data suggest that RELN functions in the extracellular matrix as a patterning signal for postmitotic neuronal migration along radial glial cell pathways. It may alternatively function to modulate neuron-neuron adhesivity and/or stability. Severe defects in neuronal cell migration underlie general lissencephalic disorders that affect humans. Therefore, the reeler mice may serve as a murine model for such neuronal ectopia disorders. Additionally, mice heterozygous for the Relnrl mutation are currently being pursued as a model for dopamine-related pathophysiological disorders such as schizophrenia. These Relnrl/+ mice exhibit a reduction in 1) the number of tryrosine hydroxylase-immunoreactive cell bodies, 2) tyrosine hydroxylase and dopamine transporter immunoreactivity, 3) tyrosine hydroxylase and D2 dopamine receptor mRNA levels in the mesolimbic dopamine system, and 4) oxytocin receptors in the piriform cortex, neocortex, retrosplenial cortex and certain regions of the hippocampus (reviewed by Rice and Curran, 2001, D'Arcangelo and Curran, 1998, and Hatten, 1999; Falconer, 1951; Soriano et al., 1997; Hunter-Schaedle, 1997; Caviness and Rakic, 1978; Caviness, 1982; Caviness et al., 1972; Rice et al., 2001; Yip et al., 2000; Phelps et al., 2002; Ballmaier et al., 2002; Liu et al., 2005).

Mammalian Phenotype Terms assigned by genotype

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

Relnrl/Reln+

        involves: BALB/c
  • nervous system phenotype
  • *normal* nervous system phenotype (J:42417)
    • cerebellum is normally foliated and qualitatively indistinguishable from that of wild type controls
    • Purkinje cell degeneration (J:42417)
      • males, but not females, have a 16% reduction in the number of Purkinje cells at 3 months of age and a 24% reduction at 16 months of age with the loss occurring throughout the mediolateral extento of the cerebellum
    • decreased Purkinje cell number (J:42417)
    • small cerebellum (J:42417)
      • males, but not females, have reduction in overall cross-sectional area of the cerebella at 3 and 16 months of age

Relnrl/Relnrl

        Background Not Specified
  • lethality-postnatal
  • lethality at weaning (J:13038)
    • many die at around 3 weeks of age, although delaying weaning and providing moist food prolongs life
  • growth/size phenotype
  • decreased body size (J:13038)
    • often smaller at around 15 days of age
  • postnatal growth retardation (J:13038)
  • behavior/neurological phenotype
  • abnormal gait (J:13038)
    • when standing still, hindquaters sway slowly from side to side and when walking, swaying is accentuated and the mutant falls over on its side, however righting is easily achieved
    • exhibit some improvement with age as some adults are able to run without falling over, however legs are kept further apart
  • hypoactivity (J:13038)
    • reduction in activity is identifiable at 15 days of age
  • impaired balance (J:13038)
    • unable to keep hindquaters upright and when walking or running, frequently fall over on their sides
  • tremors (J:13038)
    • a slight tremor of the foot is usually seen when the mutants fall and a more generalized tremor is sometimes seen when the mutant is excited and active
  • reproductive system phenotype
  • male infertility (J:13038)
  • reduced female fertility (J:13038)
    • majority of females are sterile
  • skin/coat/nails phenotype
  • disheveled coat (J:13038)
    • fur of adults exhibits an unkempt appearance

Relnrl/Relnrl

        C3.Cg-Relnrl
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype (J:5312)
    • mutants on a C57BL/6J background crossed to C3H/HeJ to the N7 generation only show mild behavioral/neurological disabilities compared to mutants on a C57BL/6J background, and are able to right themselves and remain active
    • ataxia (J:5312)
      • at around 4 weeks of age, develop a more moderate ataxia during ambulation than on a C57BL/6J background
  • life span-post-weaning/aging
  • premature death (J:5312)
    • 80% die by 40 days of age, the rest survive and are in normal health, indicating increased vitality than on a C57BL/6J background
  • growth/size phenotype
  • postnatal growth retardation (J:5312)
    • growth retardation is much less severe than on a C57BL/6J background
    • postnatal slow weight gain (J:5312)
      • exhibit normal weight gain during the first 2 weeks of life, then growth decreases in the third week but weight gain resumes after weaning, although at a slower rate so that by 60 days, they are still growing but weight is less than 70% of wild type
  • digestive/alimentary phenotype
  • diarrhea (J:5312)
    • more than half of the mutants lost during the 20- to 30-day interval die as a consequence of diarrhea
  • nervous system phenotype
  • abnormal cerebral cortex morphology (J:12728)
    • the ascending glial fiber gives rise to 3 or less terminal branches (compared to 3-5 or more in wild type) within the superplate (SP) rather than the pleriform zone (PZ)
    • at the lower margin of the cortex, cells are frequently found bunched close one upon the other with substantial overlap of radially adjacent cells and the leading processes of these cells are abnormally short and blunt
    • extent of contact between the somatic surfaces of postmigratory neurons and the surfaces of the radial glial fibers is substantially greater than in wild type indicating abnormal adhesions between the postmigratory cells and the radial glial fibers
    • abnormal stratification in cerebral cortex (J:12728)
  • abnormal entorhinal cortex morphology (J:5312)
    • the entorhinal cortex exhibits an outer zone of tangentially oriented polymorphic cells in the superficial plane normally given to an external plexiform layer
    • a wide inner zone of larger cells in the entorhinal cortex is cytologically similar to the outer large cell layers of the normal
  • abnormal hippocampus morphology (J:5312)
    • abnormal dentate gyrus morphology (J:5312)
      • many granule cells of the dentate gyrus are scattered through the hilus and are intermixed with large cells of CA4
    • abnormal hippocampus CA1 region morphology (J:5312)
      • CA1 has two separate cellular laminae
    • abnormal hippocampus CA2 region morphology (J:5312)
      • CA2 is subluxed away from its junction with CA1
  • abnormal neuronal migration (J:12728)
    • different classes of neurons take their orgin from the ependymal layer at the normal time but migrate abnormally and come to rest in abnormal relations to each other
    • migratory ascent along the radial glial fibers (RGF) proceeds normally as the cell crosses the IZ but is blocked upon encounter with postmigratory neurons within the cortex
  • abnormal olfactory cortex morphology (J:5312)
    • the piriform cortex is composed of an outer polymorphic and inner large cell zone, resembling the deep polymorphic and overlying pyramidal zones of wild type
    • immediately subjacent to the lateral olfactory tract, the outer polymorphic zone is attenuated
  • abnormal sensory neuron innervation (J:5312)
    • fiber bundles course from the olfactory crus in aberrant superficial relation to the lateral olfactory tract and join the main mass of the anterior commissure at a more caudal level

Relnrl/Relnrl

        B6.Cg-Relnrl
  • behavior/neurological phenotype
  • abnormal gait (J:5312)
    • legs tend to splay on smooth hard surfaces
  • ataxia (J:5312)
    • show ataxic gait beginning at P13 that is more severe than on a C3H/HeJ background
  • hypoactivity (J:5312)
    • general level of activity begins to decrease during the third week of life unlike on a C3H/HeJ background in which activity is normal
  • impaired righting response (J:5312)
    • if turned on the side, mutants on a C57BL/6J background kick all legs futilely in unison and may not be able to right themselves without assistance, a phenotype not seen on the C3H/HeJ background
  • tremors (J:5312)
    • show rapid unsustained low amplitude tremor of the body when walking starting at P13 that is not readily observed on a C3H/HeJ background
  • life span-post-weaning/aging
  • premature death (J:5312)
    • all die by 30 days of age, earlier than on a C3H/HeJ background
  • growth/size phenotype
  • decreased body weight (J:5312)
    • attain maximum weight by the end of the second week of life, then growth ceases during the third week and mutants remain smaller thereafter
  • postnatal growth retardation (J:5312)
    • growth retardation is more severe than on a C3H/HeJ background
  • reproductive system phenotype
  • infertility (J:5312)
    • mutants on a C57BL/6J background do not breed while those on a C3H/HeJ background are fertile
  • nervous system phenotype
  • abnormal entorhinal cortex morphology (J:5312)
    • the entorhinal cortex exhibits an outer zone of tangentially oriented polymorphic cells in the superficial plane normally given to an external plexiform layer
    • a wide inner zone of larger cells in the entorhinal cortex is cytologically similar to the outer large cell layers of the normal
  • abnormal hippocampus morphology (J:5312)
    • abnormal dentate gyrus morphology (J:5312)
      • many granule cells of the dentate gyrus are scattered through the hilus and are intermixed with large cells of CA4
    • abnormal hippocampus CA1 region morphology (J:5312)
      • CA1 has two separate cellular laminae
    • abnormal hippocampus CA2 region morphology (J:5312)
      • CA2 is subluxed away from its junction with CA1
  • abnormal olfactory cortex morphology (J:5312)
    • the piriform cortex is composed of an outer polymorphic and inner large cell zone, resembling the deep polymorphic and overlying pyramidal zones of wild type
    • immediately subjacent to the lateral olfactory tract, the outer polymorphic zone is attenuated
  • abnormal sensory neuron innervation (J:5312)
    • fiber bundles course from the olfactory crus in aberrant superficial relation to the lateral olfactory tract and join the main mass of the anterior commissure at a more caudal level

Gene & Allele Details

Allele Symbol Relnrl
Allele Name reeler
Common Name(s) rl; rl-; rlJ;
Strain of Origin"snowy-bellied" stock and unspecified inbred strain
Gene Symbol and Name Reln, reelin
Chromosome 5
Gene Common Name(s) PRO1598; RL; Reelen; reeler; rl;
General Note Relnrl, reeler, recessive. The reeler mutation was identified by Falconer (J:13038) as a spontaneous mutation in a mildly inbred stock. Reeler homozygotes are unable to keep their hindquarters upright and frequently fall over on their sides when walking or running. Viability and fertility are much reduced, particularly when the gene is on an inbred genetic background, but viability is greatly improved on a hybrid background, and an occasional female or rarely a male may breed (J:5312). Healthyreeler mice have fairly normal behavior except for difficulties in locomotion (J:5359). The neuropathology of Relnrl/Relnrl mice has been studied very extensively. These studies were summarized and critically reviewed by Goffinet (J:12281). Briefly, the cerebellum is greatly reduced in size, and the typical organization and lamination of the cerebellar cortex, the cerebral cortex, and the hippocampus are altered. Abnormal arrangement of neurons is also seen in other brain structures. Autoradiographic studies of development of the cerebral cortex in reelers have shown that the different classes of neurons take their origin from the ependymal layer at the normal time but migrate abnormally and come to rest in abnormal relations to each other (J:12728). The earliest cortical neurons may be overly adhesive and may block migration of later neurons (J:26896). The abnormal arrangement of neurons in other parts of the brain is the result of a similar abnormal pattern of migration. In spite of abnormal location of the neurons and also their greatly reduced number in the cerebellum, relatively normal cell connections are established. Chimeras produced by fusion between Relnrl/Relnrl and +/+ embryos indicated that factorsextrinsic to the abnormally positioned Purkinje cells were defective in reeler (J:15345).
Molecular Note This allele comprises, minimally, a 150 kd deletion between D5Mit61 and D5Mit72. [J:24458]
 
Allele Symbol a
Allele Name nonagouti

Control Information

  Allele   Control
 Relnrl  Untyped from the colony
 
  Considerations for Choosing Controls

Colony Maintenance

Diet Information LabDiet® 5K52/5K67

Related Strains

Strains carrying   a allele
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
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
000001   B6.C3 A/a Mgrn1md/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
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
000296   B6C3Fe-a/a Hoxa13Hd Mcoln3Va-J/J
000019   B6C3Fe-a/a-Itpr1opt/J
001022   B6C3FeF1/J a/a
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
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
000225   C3FeLe.B6 a/a-Ptpn6me/J
000198   C3FeLe.B6-a/J
000291   C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J
001886   C3HeB/FeJLe a/a-gnd/J
000584   C57BL/6J-+ T(1;2)5Ca/a +/J
000284   CWD/LeJ
001057   HPT/LeJ
000260   JGBF/LeJ
000265   MY/HuLeJ
000308   SSL/LeJ
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   a     (100 strains)

Strains carrying other alleles of Reln
005250   B6;129S2-Relnrl-4J/J
005744   C57BL/6J-Relnrl-6J/J
007892   C57BL/6J-Relnrl-7J/J
View Strains carrying other alleles of Reln     (3 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
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
002083   B6 x B6EiC3 a/A-T(7;16)235Dn/J
000507   B6 x B6EiC3 a/A-Otcspf/J
002016   B6(Cg)-Aw-J EdaTa-6J Chr YB6-Sxr/EiJ
000552   B6-Aw-J-EdaTa-6J.Cg-Sxr
001730   B6-Aw-J-EdaTa-6J.Cg-Sxrb Hya-/J
000841   B6-Aw-J.CBy-EdaTa-By/J
001809   B6-Aw-J.Cg-EdaTa-6J +/+ ArTfm/J
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.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
100409   B6129PF1/J-Aw-J/Aw
004200   B6;CBACa Aw-J/A-Npr2cn-2J/J
000505   B6C3 Aw-J/A-Mutedmu/J
000604   B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J
000065   B6C3Fe a/a-we Pax1un at/J
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
001752   B6CBCa Aw-J/A-T(7;15)9H/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
001811   B6EiC3Sn a/A-Otcspf-ash/J
002343   B6EiC3Sn a/A-Otcspf/J
001923   B6EiC3Sn a/A-Ts(417)2Lws Tim/J
000200   C3FeB6 A/Aw-J-Ankank/J
000638   C3FeB6 A/Aw-J-Spnb4qv-J/J
001203   C3FeB6F1/J A/Aw-J
001272   C3H/HeSnJ-Ahvy/J
000099   C3HeB/FeJ-Avy/J
000338   C57BL/6J Aw-J-EdaTa-6J/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
002468   KK.Cg-Ay/J
000262   LS/LeJ
000283   LT.CAST-A/J
001759   STOCK A Tyrc Sha/J
001427   STOCK Aw us/J
View Strains carrying other alleles of a     (67 strains)

Animal Health Reports

Room Number           FGB29

Research Applications

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

Relnrl related

Mouse/Human Gene Homologs
autosomal recessive lissencephaly

Neurobiology Research
Ataxia (Movement) Defects
Cerebellar Defects
Cortical Defects

References

Additional References

Price and Supply Information

Strain Name: B6C3Fe a/a-Relnrl/J
Stock Number: 000235

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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.
This strain is included in the Mouse Mutant Resource collection.
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.

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The Jackson Laboratory's Genotype Promise

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

      Purchasing Information
      JAX® Mice Orders
      Surgical Services

Contact Information
Orders & Technical Support
Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
Technical Support Email Form

Go to JAX® Mice Query Form

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