Strain Name:

B6C3Fe a/a-Relnrl/J

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Mice homozygous for the reeler (Relnrl) mutation exhibit an ataxic gait, dystonic posture and. Neuronal layer formation fails in laminated brain regions during development, and there are reduced numbers of granule and Purkinje cells. T-cell and macrophage function are suppressed in homozygous mutants. Mutant reeler mice may serve as a murine model for general lissencephalic disorders that affect humans. Additionally, mice heterozygous for the Relnrl mutation may be useful in studies of dopamine-related pathophysiological disorders such as schizophrenia.


Strain Information

Former Names B6C3Fe-a/a-Relnrl/+    (Changed: 15-DEC-04 )
Type Mutant Strain; Spontaneous Mutation;
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Mating SystemBackcross-Intercross         (Female x Male)   01-MAR-06
TJL Breeding Summary: homozygote x B6C3FeF1 a/a then heterozygote x heterozygote
Specieslaboratory mouse
GenerationN71F1 (06-AUG-14)
Generation Definitions

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

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

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).

The reeler mutation was reported by Falconer in 1951 as a spontaneous mutation in a mildly inbred stock. It is currently maintained on a B6C3FeF1 background by a backcross-Intercross mating system.

Control Information

   Untyped from the colony
  Considerations for Choosing Controls

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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
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
014608   B6;129S1-a Kitlsl-24J/GrsrJ
000231   B6;C3Fe a/a-Csf1op/J
000785   B6;D2-a Ces1ce/EiJ
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
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
000296   B6C3Fe-a/a Hoxa13Hd Mcoln3Va-J/J
000019   B6C3Fe-a/a-Itpr1opt/J
001022   B6C3FeF1/J a/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
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
000670   DBA/1J
000671   DBA/2J
001057   HPT/LeJ
000260   JGBF/LeJ
000265   MY/HuLeJ
000308   SSL/LeJ
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   a     (101 strains)

Strains carrying other alleles of Reln
005250   B6.Cg-Relnrl-4J/GrsrJ
005744   C57BL/6J-Relnrl-6J/J
View Strains carrying other alleles of Reln     (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
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
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
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
000628   B6.CE-A Amy1b Amy2a5b/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
004200   B6;CBACa Aw-J/A-Npr2cn-2J/GrsrJ
000505   B6C3 Aw-J/A-Bloc1s5mu/J
000604   B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J
000065   B6C3Fe a/a-we Pax1un at/J
003301   B6C3FeF1 a/A-Eya1bor/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
006450   B6EiC3 a/A-Vss/GrsrJ
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 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
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
001145   WSB/EiJ
View Strains carrying other alleles of a     (82 strains)


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.
Lissencephaly 2; LIS2   (RELN)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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


        involves: BALB/c
  • nervous system phenotype
  • *normal* nervous system phenotype
    • cerebellum is normally foliated and qualitatively indistinguishable from that of wild-type controls   (MGI Ref ID J:42417)
    • Purkinje cell degeneration
      • 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 extent of the cerebellum   (MGI Ref ID J:42417)
    • decreased Purkinje cell number   (MGI Ref ID J:42417)
    • small cerebellum
      • males, but not females, have reduction in overall cross-sectional area of the cerebella at 3 and 16 months of age   (MGI Ref ID J:42417)


        involves: 129S4/SvJaeSor * C57BL/6J
  • nervous system phenotype
  • abnormal cortical marginal zone morphology
    • the neocortical marginal zone is crowded with polymorphic cells unlike in wild-type mice   (MGI Ref ID J:74239)
  • abnormal dentate gyrus morphology
    • the dentate gyrus is disrupted   (MGI Ref ID J:74239)
  • abnormal hippocampus pyramidal cell layer
    • the pyramidal cells are scattered over a broad region unlike in wild-type mice   (MGI Ref ID J:74239)


        Background Not Specified
  • mortality/aging
  • complete lethality at weaning
    • many die at around 3 weeks of age, although delaying weaning and providing moist food prolongs life   (MGI Ref ID J:13038)
  • growth/size/body phenotype
  • decreased body size
    • often smaller at around 15 days of age   (MGI Ref ID J:13038)
  • postnatal growth retardation   (MGI Ref ID J:13038)
  • behavior/neurological phenotype
  • abnormal gait
    • 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   (MGI Ref ID J:13038)
    • exhibit some improvement with age as some adults are able to run without falling over, however legs are kept further apart   (MGI Ref ID J:13038)
  • hypoactivity
    • reduction in activity is identifiable at 15 days of age   (MGI Ref ID J:13038)
  • impaired balance
    • unable to keep hindquaters upright and when walking or running, frequently fall over on their sides   (MGI Ref ID J:13038)
  • tremors
    • 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   (MGI Ref ID J:13038)
  • reproductive system phenotype
  • male infertility   (MGI Ref ID J:13038)
  • reduced female fertility
    • majority of females are sterile   (MGI Ref ID J:13038)
  • integument phenotype
  • disheveled coat
    • fur of adults exhibits an unkempt appearance   (MGI Ref ID J:13038)


  • mortality/aging
  • premature death
    • 80% die by 40 days of age, the rest survive and are in normal health, indicating increased vitality than on a C57BL/6J background   (MGI Ref ID J:5312)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • 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   (MGI Ref ID J:5312)
    • ataxia
      • at around 4 weeks of age, develop a more moderate ataxia during ambulation than on a C57BL/6J background   (MGI Ref ID J:5312)
  • growth/size/body phenotype
  • postnatal growth retardation
    • growth retardation is much less severe than on a C57BL/6J background   (MGI Ref ID J:5312)
    • slow postnatal weight gain
      • 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   (MGI Ref ID J:5312)
  • digestive/alimentary phenotype
  • diarrhea
    • more than half of the mutants lost during the 20- to 30-day interval die as a consequence of diarrhea   (MGI Ref ID J:5312)
  • nervous system phenotype
  • abnormal cerebral cortex morphology
    • 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)   (MGI Ref ID J:12728)
    • 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   (MGI Ref ID J:12728)
    • 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   (MGI Ref ID J:12728)
    • abnormal stratification in cerebral cortex   (MGI Ref ID J:12728)
  • abnormal entorhinal cortex morphology
    • the entorhinal cortex exhibits an outer zone of tangentially oriented polymorphic cells in the superficial plane normally given to an external plexiform layer   (MGI Ref ID J:5312)
    • a wide inner zone of larger cells in the entorhinal cortex is cytologically similar to the outer large cell layers of the normal   (MGI Ref ID J:5312)
  • abnormal hippocampus morphology   (MGI Ref ID J:5312)
    • abnormal dentate gyrus morphology
      • many granule cells of the dentate gyrus are scattered through the hilus and are intermixed with large cells of CA4   (MGI Ref ID J:5312)
    • abnormal hippocampus CA1 region morphology
      • CA1 has two separate cellular laminae   (MGI Ref ID J:5312)
    • abnormal hippocampus CA2 region morphology
      • CA2 is subluxed away from its junction with CA1   (MGI Ref ID J:5312)
  • abnormal neuronal migration
    • 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   (MGI Ref ID J:12728)
    • 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   (MGI Ref ID J:12728)
  • abnormal olfactory cortex morphology
    • 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   (MGI Ref ID J:5312)
    • immediately subjacent to the lateral olfactory tract, the outer polymorphic zone is attenuated   (MGI Ref ID J:5312)
  • abnormal sensory neuron innervation pattern
    • 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   (MGI Ref ID J:5312)
  • cellular phenotype
  • abnormal neuronal migration
    • 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   (MGI Ref ID J:12728)
    • 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   (MGI Ref ID J:12728)


  • mortality/aging
  • premature death
    • all die by 30 days of age, earlier than on a C3H/HeJ background   (MGI Ref ID J:5312)
  • behavior/neurological phenotype
  • abnormal gait
    • legs tend to splay on smooth hard surfaces   (MGI Ref ID J:5312)
  • ataxia
    • show ataxic gait beginning at P13 that is more severe than on a C3H/HeJ background   (MGI Ref ID J:5312)
  • hypoactivity
    • general level of activity begins to decrease during the third week of life unlike on a C3H/HeJ background in which activity is normal   (MGI Ref ID J:5312)
  • impaired righting response
    • 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   (MGI Ref ID J:5312)
  • tremors
    • show rapid unsustained low amplitude tremor of the body when walking starting at P13 that is not readily observed on a C3H/HeJ background   (MGI Ref ID J:5312)
  • growth/size/body phenotype
  • decreased body weight
    • attain maximum weight by the end of the second week of life, then growth ceases during the third week and mutants remain smaller thereafter   (MGI Ref ID J:5312)
  • postnatal growth retardation
    • growth retardation is more severe than on a C3H/HeJ background   (MGI Ref ID J:5312)
  • reproductive system phenotype
  • infertility
    • mutants on a C57BL/6J background do not breed while those on a C3H/HeJ background are fertile   (MGI Ref ID J:5312)
  • nervous system phenotype
  • abnormal entorhinal cortex morphology
    • the entorhinal cortex exhibits an outer zone of tangentially oriented polymorphic cells in the superficial plane normally given to an external plexiform layer   (MGI Ref ID J:5312)
    • a wide inner zone of larger cells in the entorhinal cortex is cytologically similar to the outer large cell layers of the normal   (MGI Ref ID J:5312)
  • abnormal hippocampus morphology   (MGI Ref ID J:5312)
    • abnormal dentate gyrus morphology
      • many granule cells of the dentate gyrus are scattered through the hilus and are intermixed with large cells of CA4   (MGI Ref ID J:5312)
    • abnormal hippocampus CA1 region morphology
      • CA1 has two separate cellular laminae   (MGI Ref ID J:5312)
    • abnormal hippocampus CA2 region morphology
      • CA2 is subluxed away from its junction with CA1   (MGI Ref ID J:5312)
  • abnormal olfactory cortex morphology
    • 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   (MGI Ref ID J:5312)
    • immediately subjacent to the lateral olfactory tract, the outer polymorphic zone is attenuated   (MGI Ref ID J:5312)
  • abnormal sensory neuron innervation pattern
    • 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   (MGI Ref ID J:5312)


        involves: BALB/c
  • reproductive system phenotype
  • abnormal female reproductive system physiology
    • vestibular stimulation improves the ability of females to mate with experienced males   (MGI Ref ID J:14535)
  • abnormal male reproductive system physiology
    • vestibular stimulation improves the ability of males to mate with experienced females   (MGI Ref ID J:14535)
View Research Applications

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

Relnrl related

Neurobiology Research
Ataxia (Movement) Defects
Cerebellar Defects
Cortical Defects

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol Relnrl
Allele Name reeler
Allele Type Spontaneous
Common Name(s) rl; rl-; rlJ; rlnrl;
Strain of Origin"snowy-bellied" stock or unspecified inbred strain
Gene Symbol and Name Reln, reelin
Chromosome 5
Gene Common Name(s) LIS2; PRO1598; RL; Reelen; reeler; rl;
General Note Relnrl, reeler, recessive. The reeler mutation was identified by Falconer as a spontaneous mutation in a mildly inbred stock. The at least partially inbred "snowy-bellied" stock was outcrossed to an unspecified inbred strain and the progeny backcrossed to the "snowy-bellied" stock for two generations, then sib intercrossed. The reeler mice occurred in the first litter of the latter cross (J:13038). 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). Healthy reeler 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 byGoffinet (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 factors extrinsic to the abnormally positioned Purkinje cells were defective in reeler (J:15345).
Molecular Note This allele comprises, minimally, a 150 kb deletion between D5Mit61 and D5Mit72. [MGI Ref ID J:24458]
Allele Symbol a
Allele Name nonagouti
Allele Type Spontaneous
Strain of Originold mutant of the mouse fancy
Gene Symbol and Name a, nonagouti
Chromosome 2
Gene Common Name(s) ASP; As; agouti; agouti signal protein; agouti suppressor;
General Note Phenotypic Similarity to Human Syndrome: Metabolic Syndrome in mice homozygous for Apoetm1Unc and heterozygous for Ay and a (J:177084)
Molecular Note Characterization of this allele shows an insertion of DNA comprised of a 5.5kb virus-like element, VL30, into the first intron of the agouti gene. The VL30 element itself contains an additional 5.5 kb sequence, flanked by 526 bp of direct repeats. The host integration site is the same as for at-2Gso and Aw-38J and includes a duplication of four nucleotides of host DNA and a deletion of 2 bp from the end of each repeat. Northern analysis of mRNA from skin of homozygotes shows a smaller agouti message and levels 8 fold lower than found in wild-type. [MGI Ref ID J:16984] [MGI Ref ID J:24934]


Genotyping Information

Genotyping Protocols

Generic Pde6b, High Resolution Melting

At The Jackson Laboratory, we use the combination of breeding scheme and phenotype to maintain our B6C3Fe a/a Relnrl/J colony.

1) Relnrl/Relnrl x B6C3FeF1/J a/a to generate obligate heterozygotes (Relnrl/+).

2) Relnrl/+ x Relnrl/+ to generate homozygotes, which are identified based on their phenotype: ataxic gait, dystonic posture and tremors.

Helpful Links

Genotyping resources and troubleshooting


References provided by MGI

Additional References

Relnrl related

Adachi K; Izumi M; Takahashi M; Mitsuma T; Oda SI. 1996. Levels of thyroid hormones in the brain of ataxic mutant mice. Med Sci Res 24(10):675-7.  [MGI Ref ID J:37975]

Aguilo A; Schwartz TH; Kumar VS; Peterlin ZA; Tsiola A; Soriano E; Yuste R. 1999. Involvement of cajal-retzius neurons in spontaneous correlated activity of embryonic and postnatal layer 1 from wild-type and reeler mice. J Neurosci 19(24):10856-68. [PubMed: 10594067]  [MGI Ref ID J:58814]

Akopians AL; Babayan AH; Beffert U; Herz J; Basbaum AI; Phelps PE. 2008. Contribution of the Reelin signaling pathways to nociceptive processing. Eur J Neurosci 27(3):523-37. [PubMed: 18279306]  [MGI Ref ID J:132269]

Ammassari-Teule M; Sgobio C; Biamonte F; Marrone C; Mercuri NB; Keller F. 2009. Reelin haploinsufficiency reduces the density of PV+ neurons in circumscribed regions of the striatum and selectively alters striatal-based behaviors. Psychopharmacology (Berl) 204(3):511-21. [PubMed: 19277610]  [MGI Ref ID J:166111]

Aoki T; Setsu T; Okado H; Mikoshiba K; Watanabe Y; Terashima T. 2001. Callosal commissural neurons of Dab1 deficient mutant mouse, yotari. Neurosci Res 41(1):13-23. [PubMed: 11535289]  [MGI Ref ID J:102565]

Arnaud L; Ballif BA; Forster E; Cooper JA. 2003. Fyn tyrosine kinase is a critical regulator of disabled-1 during brain development. Curr Biol 13(1):9-17. [PubMed: 12526739]  [MGI Ref ID J:109820]

Assadi AH; Zhang G; McNeil R; Clark GD; D'Arcangelo G. 2008. Pafah1b2 mutations suppress the development of hydrocephalus in compound Pafah1b1; Reln and Pafah1b1; Dab1 mutant mice. Neurosci Lett 439(1):100-5. [PubMed: 18514414]  [MGI Ref ID J:137048]

Baba K; Dekimoto H; Muraoka D; Agata K; Terashima T; Katsuyama Y. 2006. A mouse homologue of Strawberry Notch is transcriptionally regulated by Reelin signal. Biochem Biophys Res Commun 350(4):842-9. [PubMed: 17045962]  [MGI Ref ID J:114610]

Baba K; Sakakibara S; Setsu T; Terashima T. 2007. The superficial layers of the superior colliculus are cytoarchitectually and myeloarchitectually disorganized in the reelin-deficient mouse, reeler. Brain Res 1140:205-15. [PubMed: 17173877]  [MGI Ref ID J:120267]

Badea A; Nicholls PJ; Johnson GA; Wetsel WC. 2007. Neuroanatomical phenotypes in the reeler mouse. Neuroimage 34(4):1363-74. [PubMed: 17185001]  [MGI Ref ID J:129615]

Bakalian A; Kopmels B; Messer A; Fradelizi D; Delhaye-Bouchaud N; Wollman E; Mariani J. 1992. Peripheral macrophage abnormalities in mutant mice with spinocerebellar degeneration. Res Immunol 143(1):129-39. [PubMed: 1565842]  [MGI Ref ID J:2228]

Ballmaier M; Zoli M; Leo G; Agnati LF; Spano P. 2002. Preferential alterations in the mesolimbic dopamine pathway of heterozygous reeler mice: an emerging animal-based model of schizophrenia. Eur J Neurosci 15(7):1197-205. [PubMed: 11982630]  [MGI Ref ID J:107996]

Bar I; Lambert De Rouvroit C; Royaux I; Krizman DB; Dernoncourt C; Ruelle D; Beckers MC; Goffinet AM. 1995. A YAC contig containing the reeler locus with preliminary characterization of candidate gene fragments. Genomics 26(3):543-9. [PubMed: 7607678]  [MGI Ref ID J:24458]

Barr AM; Fish KN; Markou A; Honer WG. 2008. Heterozygous reeler mice exhibit alterations in sensorimotor gating but not presynaptic proteins. Eur J Neurosci 27(10):2568-74. [PubMed: 18547243]  [MGI Ref ID J:137142]

Bjerregaard A; Jorgensen OS. 1994. Ontogeny of the cell adhesion molecule L1 in the cerebellum of weaver and reeler mutant mice. Neurochem Res 19(7):789-93. [PubMed: 7969746]  [MGI Ref ID J:19752]

Bodea GO; Spille JH; Abe P; Andersson AS; Acker-Palmer A; Stumm R; Kubitscheck U; Blaess S. 2014. Reelin and CXCL12 regulate distinct migratory behaviors during the development of the dopaminergic system. Development 141(3):661-73. [PubMed: 24449842]  [MGI Ref ID J:208337]

Borrell V; Del Rio JA; Alcantara S; Derer M; Martinez A; D'Arcangelo G; Nakajima K; Mikoshiba K; Derer P; Curran T; Soriano E. 1999. Reelin regulates the development and synaptogenesis of the layer-specific entorhino-hippocampal connections. J Neurosci 19(4):1345-58. [PubMed: 9952412]  [MGI Ref ID J:53751]

Borrell V; Pujadas L; Simo S; Dura D; Sole M; Cooper JA; Del Rio JA; Soriano E. 2007. Reelin and mDab1 regulate the development of hippocampal connections. Mol Cell Neurosci 36(2):158-73. [PubMed: 17720534]  [MGI Ref ID J:126745]

Borrell V; Ruiz M; Del Rio JA; Soriano E. 1999. Development of commissural connections in the hippocampus of reeler mice: evidence of an inhibitory influence of Cajal-Retzius cells. Exp Neurol 156(2):268-82. [PubMed: 10328935]  [MGI Ref ID J:54646]

Boyle MP; Bernard A; Thompson CL; Ng L; Boe A; Mortrud M; Hawrylycz MJ; Jones AR; Hevner RF; Lein ES. 2011. Cell-type-specific consequences of Reelin deficiency in the mouse neocortex, hippocampus, and amygdala. J Comp Neurol 519(11):2061-89. [PubMed: 21491433]  [MGI Ref ID J:174459]

Britanova O; Alifragis P; Junek S; Jones K; Gruss P; Tarabykin V. 2006. A novel mode of tangential migration of cortical projection neurons. Dev Biol 298(1):299-311. [PubMed: 16901480]  [MGI Ref ID J:119267]

Britto JM; Tait KJ; Johnston LA; Hammond VE; Kalloniatis M; Tan SS. 2011. Altered speeds and trajectories of neurons migrating in the ventricular and subventricular zones of the reeler neocortex. Cereb Cortex 21(5):1018-27. [PubMed: 20847150]  [MGI Ref ID J:183824]

Brunne B; Franco S; Bouche E; Herz J; Howell BW; Pahle J; Muller U; May P; Frotscher M; Bock HH. 2013. Role of the postnatal radial glial scaffold for the development of the dentate gyrus as revealed by reelin signaling mutant mice. Glia 61(8):1347-63. [PubMed: 23828756]  [MGI Ref ID J:199451]

Cariboni A; Rakic S; Liapi A; Maggi R; Goffinet A; Parnavelas JG. 2005. Reelin provides an inhibitory signal in the migration of gonadotropin-releasing hormone neurons. Development 132(21):4709-18. [PubMed: 16207762]  [MGI Ref ID J:102848]

Caviness VS Jr; So DK; Sidman RL. 1972. The hybrid reeler mouse. J Hered 63(5):241-6. [PubMed: 4644329]  [MGI Ref ID J:5312]

Chu HC; Lee HY; Huang YS; Tseng WL; Yen CJ; Cheng JC; Tseng CP. 2014. Erythroid differentiation is augmented in Reelin-deficient K562 cells and homozygous reeler mice. FEBS Lett 588(1):58-64. [PubMed: 24239537]  [MGI Ref ID J:206162]

Coulin C; Drakew A; Frotscher M; Deller T. 2001. Stereological estimates of total neuron numbers in the hippocampus of adult reeler mutant mice: Evidence for an increased survival of Cajal-Retzius cells. J Comp Neurol 439(1):19-31. [PubMed: 11579379]  [MGI Ref ID J:118006]

D'Arcangelo G; Miao GG; Chen SC; Soares HD; Morgan JI; Curran T. 1995. A protein related to extracellular matrix proteins deleted in the mouse mutant reeler [see comments] Nature 374(6524):719-23. [PubMed: 7715726]  [MGI Ref ID J:24459]

D'Arcangelo G; Miao GG; Curran T. 1996. Detection of the reelin breakpoint in reeler mice. Brain Res Mol Brain Res 39(1-2):234-6. [PubMed: 8804731]  [MGI Ref ID J:33769]

Dalezios Y; Matsokis N; Valcana T. 1995. Interaction between [3H]flunitrazepam and [3H]GABA binding in the cerebellum of reeler mice. Neurochem Int 26(1):41-6. [PubMed: 7787761]  [MGI Ref ID J:23726]

Del Rio JA; Heimrich B; Borrell V; Forster E; Drakew A; Alcantara S; Nakajima K; Miyata T; Ogawa M; Mikoshiba K; Derer P; Frotscher M; Soriano E. 1997. A role for Cajal-Retzius cells and reelin in the development of hippocampal connections [see comments] Nature 385(6611):70-4. [PubMed: 8985248]  [MGI Ref ID J:37527]

Deller T; Drakew A; Frotscher M. 1999. Different primary target cells are important for fiber lamination in the fascia dentata: a lesson from reeler mutant mice. Exp Neurol 156(2):239-53. [PubMed: 10328933]  [MGI Ref ID J:54648]

Deller T; Drakew A; Heimrich B; Forster E; Tielsch A; Frotscher M. 1999. The hippocampus of the reeler mutant mouse: fiber segregation in area CA1 depends on the position of the postsynaptic target cells. Exp Neurol 156(2):254-67. [PubMed: 10328934]  [MGI Ref ID J:54647]

Deller T; Haas CA; Deissenrieder K; Del Turco D; Coulin C; Gebhardt C; Drakew A; Schwarz K; Mundel P; Frotscher M. 2002. Laminar distribution of synaptopodin in normal and reeler mouse brain depends on the position of spine-bearing neurons. J Comp Neurol 453(1):33-44. [PubMed: 12357430]  [MGI Ref ID J:126830]

Dulabon L; Olson EC; Taglienti MG; Eisenhuth S; McGrath B; Walsh CA; Kreidberg JA; Anton ES. 2000. Reelin binds alpha3beta1 integrin and inhibits neuronal migration. Neuron 27(1):33-44. [PubMed: 10939329]  [MGI Ref ID J:107720]

Dwyer ND; Manning DK; Moran JL; Mudbhary R; Fleming MS; Favero CB; Vock VM; O'Leary DD; Walsh CA; Beier DR. 2011. A forward genetic screen with a thalamocortical axon reporter mouse yields novel neurodevelopment mutants and a distinct emx2 mutant phenotype. Neural Dev 6:3. [PubMed: 21214893]  [MGI Ref ID J:168258]

Edelman GM; Chuong CM. 1982. Embryonic to adult conversion of neural cell adhesion molecules in normal and staggerer mice. Proc Natl Acad Sci U S A 79(22):7036-40. [PubMed: 6960362]  [MGI Ref ID J:6930]

Edwards MA; Leclerc N; Crandall JE; Yamamoto M. 1994. Purkinje cell compartments in the reeler mutant mouse as revealed by Zebrin II and 90-acetylated glycolipid antigen expression. Anat Embryol (Berl) 190(5):417-28. [PubMed: 7887492]  [MGI Ref ID J:22136]

Efthimiopoulos S; Giompres P; Valcana T. 1991. Kinetics of dopamine and noradrenaline transport in synaptosomes from cerebellum, striatum and frontal cortex of normal and reeler mice. J Neurosci Res 29(4):510-9. [PubMed: 1838778]  [MGI Ref ID J:456]

Englund C; Kowalczyk T; Daza RA; Dagan A; Lau C; Rose MF; Hevner RF. 2006. Unipolar brush cells of the cerebellum are produced in the rhombic lip and migrate through developing white matter. J Neurosci 26(36):9184-95. [PubMed: 16957075]  [MGI Ref ID J:112207]

Falconer DS. 1952. Location of "reeler" in linkage group III in the mouse Heredity 6:255-7.  [MGI Ref ID J:248]

Falconer DS. 1951. Two new mutants, "trembler" and "reeler," with neurological actions in the house mouse. J Genet 50:192-201.  [MGI Ref ID J:13038]

Fink AJ; Englund C; Daza RA; Pham D; Lau C; Nivison M; Kowalczyk T; Hevner RF. 2006. Development of the deep cerebellar nuclei: transcription factors and cell migration from the rhombic lip. J Neurosci 26(11):3066-76. [PubMed: 16540585]  [MGI Ref ID J:106708]

Fish KN; Krucker T. 2008. Functional consequences of hippocampal neuronal ectopia in the apolipoprotein E receptor-2 knockout mouse. Neurobiol Dis 32(3):391-401. [PubMed: 18778775]  [MGI Ref ID J:142541]

Frostholm A; Zdilar D; Chang A; Rotter A. 1991. Stability of GABAA/benzodiazepine receptor alpha 1 subunit mRNA expression in reeler mouse cerebellar Purkinje cells during postnatal development. Brain Res Dev Brain Res 64(1-2):121-8. [PubMed: 1664786]  [MGI Ref ID J:1666]

Fujimoto Y; Setsu T; Ikeda Y; Miwa A; Okado H; Terashima T. 1998. Ambiguus nucleus neurons innervating the abdominal esophagus are malpositioned in the reeler mouse. Brain Res 811(1-2):156-60. [PubMed: 9804938]  [MGI Ref ID J:51051]

Fukaya M; Yamada K; Nagashima M; Tanaka K; Watanabe M. 1999. Down-regulated expression of glutamate transporter GLAST in Purkinje cell-associated astrocytes of reeler and weaver mutant cerebella. Neurosci Res 34(3):165-75. [PubMed: 10515259]  [MGI Ref ID J:59731]

Gebhardt C; Del Turco D; Drakew A; Tielsch A; Herz J; Frotscher M; Deller T. 2002. Abnormal positioning of granule cells alters afferent fiber distribution in the mouse fascia dentata: Morphologic evidence from reeler, apolipoprotein E receptor 2-, and very low density lipoprotein receptor knockout mice. J Comp Neurol 445(3):278-92. [PubMed: 11920707]  [MGI Ref ID J:75080]

Gil-Sanz C; Franco SJ; Martinez-Garay I; Espinosa A; Harkins-Perry S; Muller U. 2013. Cajal-Retzius cells instruct neuronal migration by coincidence signaling between secreted and contact-dependent guidance cues. Neuron 79(3):461-77. [PubMed: 23931996]  [MGI Ref ID J:201651]

Goffinet AM. 1984. Events governing organization of postmigratory neurons: studies on brain development in normal and reeler mice. Brain Res 319(3):261-96. [PubMed: 6383524]  [MGI Ref ID J:12281]

Goffinet AM. 1992. The reeler gene: a clue to brain development and evolution. Int J Dev Biol 36(1):101-7. [PubMed: 1627461]  [MGI Ref ID J:1525]

Green-Johnson JM; Zalcman S; Vriend CY; Nance DM; Greenberg AH. 1995. Suppressed T cell and macrophage function in the reeler (rl/rl) mutant, a murine strain with elevated cerebellar norepinephrine concentration. Brain Behav Immun 9(1):47-60. [PubMed: 7620210]  [MGI Ref ID J:24987]

Guastavino JM; Larsson K; Allain C; Jaisson P. 1993. Neonatal vestibular stimulation and mating in cerebellar mutants. Behav Genet 23(3):265-9. [PubMed: 8352721]  [MGI Ref ID J:14535]

Guo H; Sekiguchi M; Tanaka O; Inoue T; Shima H; Nagao M; Tamura S; Abe H. 1995. Protein phosphatase mRNA expression in Purkinje cells of staggerer and reeler mutant mice. Brain Res Mol Brain Res 33(1):121-6. [PubMed: 8774953]  [MGI Ref ID J:28842]


Hadj-Sahraoui N; Frederic F; DelhayeBouchaud N; Mariani J. 1996. Gender effect on Purkinje cell loss in the cerebellum of the heterozygous reeler mouse. J Neurogenet 11(1-2):45-58. [PubMed: 10876649]  [MGI Ref ID J:42417]

Hammond V; So E; Gunnersen J; Valcanis H; Kalloniatis M; Tan SS. 2006. Layer positioning of late-born cortical interneurons is dependent on Reelin but not p35 signaling. J Neurosci 26(5):1646-55. [PubMed: 16452688]  [MGI Ref ID J:105191]

Harsan LA; David C; Reisert M; Schnell S; Hennig J; von Elverfeldt D; Staiger JF. 2013. Mapping remodeling of thalamocortical projections in the living reeler mouse brain by diffusion tractography. Proc Natl Acad Sci U S A 110(19):E1797-806. [PubMed: 23610438]  [MGI Ref ID J:197343]

Hartfuss E; Forster E; Bock HH; Hack MA; Leprince P; Luque JM; Herz J; Frotscher M; Gotz M. 2003. Reelin signaling directly affects radial glia morphology and biochemical maturation. Development 130(19):4597-609. [PubMed: 12925587]  [MGI Ref ID J:84752]

Hashimoto-Torii K; Torii M; Sarkisian MR; Bartley CM; Shen J; Radtke F; Gridley T; Sestan N; Rakic P. 2008. Interaction between Reelin and Notch signaling regulates neuronal migration in the cerebral cortex. Neuron 60(2):273-84. [PubMed: 18957219]  [MGI Ref ID J:144065]

Hellwig S; Hack I; Kowalski J; Brunne B; Jarowyj J; Unger A; Bock HH; Junghans D; Frotscher M. 2011. Role for reelin in neurotransmitter release. J Neurosci 31(7):2352-60. [PubMed: 21325502]  [MGI Ref ID J:169445]

Herrick TM; Cooper JA. 2002. A hypomorphic allele of dab1 reveals regional differences in reelin-Dab1 signaling during brain development. Development 129(3):787-96. [PubMed: 11830577]  [MGI Ref ID J:74239]

Herrick TM; Cooper JA. 2004. High affinity binding of Dab1 to Reelin receptors promotes normal positioning of upper layer cortical plate neurons. Brain Res Mol Brain Res 126(2):121-8. [PubMed: 15249135]  [MGI Ref ID J:91679]

Hertel N; Redies C. 2011. Absence of layer-specific cadherin expression profiles in the neocortex of the reeler mutant mouse. Cereb Cortex 21(5):1105-17. [PubMed: 20847152]  [MGI Ref ID J:183823]

Hevner RF; Daza RA; Englund C; Kohtz J; Fink A. 2004. Postnatal shifts of interneuron position in the neocortex of normal and reeler mice: evidence for inward radial migration. Neuroscience 124(3):605-18. [PubMed: 14980731]  [MGI Ref ID J:89993]

Hiesberger T; Trommsdorff M; Howell BW; Goffinet A; Mumby MC; Cooper JA; Herz J. 1999. Direct binding of Reelin to VLDL receptor and ApoE receptor 2 induces tyrosine phosphorylation of disabled-1 and modulates tau phosphorylation. Neuron 24(2):481-9. [PubMed: 10571241]  [MGI Ref ID J:212819]

Hill RA; Wu YW; Gogos A; van den Buuse M. 2013. Sex-dependent alterations in BDNF-TrkB signaling in the hippocampus of reelin heterozygous mice: a role for sex steroid hormones. J Neurochem 126(3):389-99. [PubMed: 23414458]  [MGI Ref ID J:199629]

Hirotsune S; Takahara T; Sasaki N; Hirose K; Yoshiki A; Ohashi T; Kusakabe M; Murakami Y; Muramatsu M; Watanabe S; Nakao K; Katsuki M; Hayashizaki. 1995. The reeler gene encodes a protein with an EGF-like motif expressed by pioneer neurons [see comments] Nat Genet 10(1):77-83. [PubMed: 7647795]  [MGI Ref ID J:24460]

Hoe HS; Lee KJ; Carney RS; Lee J; Markova A; Lee JY; Howell BW; Hyman BT; Pak DT; Bu G; Rebeck GW. 2009. Interaction of reelin with amyloid precursor protein promotes neurite outgrowth. J Neurosci 29(23):7459-73. [PubMed: 19515914]  [MGI Ref ID J:149815]

Hoffarth RM; Johnston JG; Krushel LA; van der Kooy D. 1995. The mouse mutation reeler causes increased adhesion within a subpopulation of early postmitotic cortical neurons. J Neurosci 15(7 Pt 1):4838-50. [PubMed: 7623115]  [MGI Ref ID J:26896]

Howell BW; Herrick TM; Cooper JA. 1999. Reelin-induced tryosine phosphorylation of disabled 1 during neuronal positioning. Genes Dev 13(6):643-8. [PubMed: 10090720]  [MGI Ref ID J:54100]

Howell KR; Hoda MN; Pillai A. 2013. VEGF activates NR2B phosphorylation through Dab1 pathway. Neurosci Lett 552:30-4. [PubMed: 23916658]  [MGI Ref ID J:201654]

Hunter-Schaedle KE. 1997. Radial glial cell development and transformation are disturbed in reeler forebrain. J Neurobiol 33(4):459-72. [PubMed: 9322161]  [MGI Ref ID J:43544]

Ichinohe N; Knight A; Ogawa M; Ohshima T; Mikoshiba K; Yoshihara Y; Terashima T; Rockland KS. 2008. Unusual patch-matrix organization in the retrosplenial cortex of the reeler mouse and Shaking rat Kawasaki. Cereb Cortex 18(5):1125-38. [PubMed: 17728262]  [MGI Ref ID J:158489]

Ikeda Y; Terashima T. 1997. Expression of reelin, the gene responsible for the reeler mutation, in embryonic development and adulthood in the mouse. Dev Dyn 210(2):157-72. [PubMed: 9337136]  [MGI Ref ID J:43264]

Ilijic E; Guidotti A; Mugnaini E. 2005. Moving up or moving down? Malpositioned cerebellar unipolar brush cells in reeler mouse. Neuroscience 136(3):633-47. [PubMed: 16344141]  [MGI Ref ID J:104589]

Inoue K; Terashima T; Inoue Y. 1991. The intracortical position of pyramidal tract neurons in the motor cortex of the reeler changes from postnatal day 10 to adulthood. Brain Res Dev Brain Res 62(1):146-50. [PubMed: 1760869]  [MGI Ref ID J:1944]

Ishida A; Shimazaki K; Terashima T; Kawai N. 1994. An electrophysiological and immunohistochemical study of the hippocampus of the reeler mutant mouse. Brain Res 662(1-2):60-8. [PubMed: 7859091]  [MGI Ref ID J:21088]

Isosaka T; Hattori K; Yagi T. 2006. NMDA-receptor proteins are upregulated in the hippocampus of postnatal heterozygous reeler mice. Brain Res 1073-1074:11-9. [PubMed: 16438943]  [MGI Ref ID J:106956]

Jacquet BV; Muthusamy N; Sommerville LJ; Xiao G; Liang H; Zhang Y; Holtzman MJ; Ghashghaei HT. 2011. Specification of a Foxj1-Dependent Lineage in the Forebrain Is Required for Embryonic-to-Postnatal Transition of Neurogenesis in the Olfactory Bulb. J Neurosci 31(25):9368-82. [PubMed: 21697387]  [MGI Ref ID J:173598]

Jorgensen OS. 1994. Neural cell adhesion molecule and D3 protein in the cerebellum of weaver mutant mice. Int J Dev Neurosci 12(3):213-25. [PubMed: 7942094]  [MGI Ref ID J:19350]

Kambouris M; Sangameswaran L; Dlouhy SR; Hodes ME; Ghetti B; Triarhou LC. 1993. Cellular distribution of the RNA transcripts of a newly discovered gene in the brain of normal, weaver, Purkinje cell degeneration and reeler mutant mice as evidenced by in situ hybridization histochemistry. Brain Res Mol Brain Res 18(4):321-8. [PubMed: 8326827]  [MGI Ref ID J:11897]

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Suto J. 2008. Coincidence of loci for glucosuria and obesity in type 2 diabetes-prone KK-Ay mice. Med Sci Monit 14(2):CR65-74. [PubMed: 18227763]  [MGI Ref ID J:131439]

Suto J. 2009. Identification of multiple quantitative trait loci affecting the size and shape of the mandible in mice. Mamm Genome 20(1):1-13. [PubMed: 19067046]  [MGI Ref ID J:143893]

Suto J; Matsuura S; Imamura K; Yamanaka H; Sekikawa K. 1998. Genetics of obesity in KK mouse and effects of A(y) allele on quantitative regulation. Mamm Genome 9(7):506-10. [PubMed: 9657845]  [MGI Ref ID J:48704]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           FGB27

Colony Maintenance

Mating SystemBackcross-Intercross         (Female x Male)   01-MAR-06
TJL Breeding Summary: homozygote x B6C3FeF1 a/a then heterozygote x heterozygote
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

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

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $239.00Female or MaleHeterozygous for Relnrl  
$239.00Female or MaleHomozygous for Relnrl  
Price per Pair (US dollars $)Pair Genotype
$478.00Heterozygous for Relnrl x Heterozygous for Relnrl  

Standard Supply

Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $310.70Female or MaleHeterozygous for Relnrl  
$310.70Female or MaleHomozygous for Relnrl  
Price per Pair (US dollars $)Pair Genotype
$621.40Heterozygous for Relnrl x Heterozygous for Relnrl  

Standard Supply

Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

General Supply Notes

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

Control Information

   Untyped from the colony
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.

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Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

See Terms of Use tab for General Terms and Conditions

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.
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JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty


In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.