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Description
Strain Information
Former Names B6C3Fe-a/a-Relnrl/+ (Changed: 15-DEC-04 ) Type Mutant Strain; Spontaneous Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Mating System Backcross-Intercross (Female x Male) 01-MAR-06 TJL Breeding Summary: homozygote x B6C3FeF1 a/a then heterozygote x heterozygote Species laboratory mouse Generation N64 (19-NOV-09) Appearance
black, ataxic
Related Genotype: a/a Relnrl/Relnrl
black, unaffected
Related Genotype: a/a +/? or a/a Relnrl/+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).
Control Information
| Control | ||
|---|---|---|
| Untyped from the colony | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying a allele
View Strains carrying a (104 strains)
005250 B6.Cg-Relnrl-4J/GrsrJ 005744 C57BL/6J-Relnrl-6J/J 007892 C57BL/6J-Relnrl-7J/GrsrJ
Phenotype
Phenotype Information
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 (MGI Ref ID J:42417)
- cerebellum is normally foliated and qualitatively indistinguishable from that of wild-type controls
- Purkinje cell degeneration (MGI Ref ID 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 extent of the cerebellum
- decreased Purkinje cell number (MGI Ref ID J:42417)
- small cerebellum (MGI Ref ID 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
involves: 129S4/SvJaeSor * C57BL/6J
- nervous system phenotype
- abnormal cortical marginal zone morphology (MGI Ref ID J:74239)
- the neocortical marginal zone is crowded with polymorphic cells unlike in wild-type mice
- abnormal dentate gyrus morphology (MGI Ref ID J:74239)
- the dentate gyrus is disrupted
- abnormal hippocampus pyramidal cell layer (MGI Ref ID J:74239)
- the pyramidal cells are scattered over a broad region unlike in wild-type mice
Relnrl/Relnrl
Background Not Specified
- lethality-postnatal
- lethality at weaning (MGI Ref ID 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 (MGI Ref ID J:13038)
- often smaller at around 15 days of age
- postnatal growth retardation (MGI Ref ID J:13038)
- behavior/neurological phenotype
- abnormal gait (MGI Ref ID 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 (MGI Ref ID J:13038)
- reduction in activity is identifiable at 15 days of age
- impaired balance (MGI Ref ID J:13038)
- unable to keep hindquaters upright and when walking or running, frequently fall over on their sides
- tremors (MGI Ref ID 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 (MGI Ref ID J:13038)
- reduced female fertility (MGI Ref ID J:13038)
- majority of females are sterile
- skin/coat/nails phenotype
- disheveled coat (MGI Ref ID J:13038)
- fur of adults exhibits an unkempt appearance
Relnrl/Relnrl
C3.Cg-Relnrl
- behavior/neurological phenotype
- *normal* behavior/neurological phenotype (MGI Ref ID 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 (MGI Ref ID 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 (MGI Ref ID 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 (MGI Ref ID J:5312)
- growth retardation is much less severe than on a C57BL/6J background
- postnatal slow weight gain (MGI Ref ID 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 (MGI Ref ID 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 (MGI Ref ID 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 (MGI Ref ID J:12728)
- abnormal entorhinal cortex morphology (MGI Ref ID 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 (MGI Ref ID J:5312)
- abnormal dentate gyrus morphology (MGI Ref ID 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 (MGI Ref ID J:5312)
- CA1 has two separate cellular laminae
- abnormal hippocampus CA2 region morphology (MGI Ref ID J:5312)
- CA2 is subluxed away from its junction with CA1
- abnormal neuronal migration (MGI Ref ID 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 (MGI Ref ID 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 (MGI Ref ID 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 (MGI Ref ID J:5312)
- legs tend to splay on smooth hard surfaces
- ataxia (MGI Ref ID J:5312)
- show ataxic gait beginning at P13 that is more severe than on a C3H/HeJ background
- hypoactivity (MGI Ref ID 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 (MGI Ref ID 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 (MGI Ref ID 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 (MGI Ref ID J:5312)
- all die by 30 days of age, earlier than on a C3H/HeJ background
- growth/size phenotype
- decreased body weight (MGI Ref ID 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 (MGI Ref ID J:5312)
- growth retardation is more severe than on a C3H/HeJ background
- reproductive system phenotype
- infertility (MGI Ref ID 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 (MGI Ref ID 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 (MGI Ref ID J:5312)
- abnormal dentate gyrus morphology (MGI Ref ID 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 (MGI Ref ID J:5312)
- CA1 has two separate cellular laminae
- abnormal hippocampus CA2 region morphology (MGI Ref ID J:5312)
- CA2 is subluxed away from its junction with CA1
- abnormal olfactory cortex morphology (MGI Ref ID 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 (MGI Ref ID 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
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
Genes & Alleles
Gene & Allele Information
| Allele Symbol | Relnrl | ||
|---|---|---|---|
| Allele Name | reeler | ||
| Allele Type | Spontaneous | ||
| 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 kb deletion between D5Mit61 and D5Mit72. [MGI Ref ID J:24458] | ||
| Allele Symbol | a | ||
| Allele Name | nonagouti | ||
| Allele Type | Spontaneous | ||
Genotyping
Genotyping Information
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
References
Additional References
Assadi AH; Zhang G; Beffert U; McNeil RS; Renfro AL; Niu S; Quattrocchi CC; Antalffy BA; Sheldon M; Armstrong DD; Wynshaw-Boris A; Herz J; D'Arcangelo G; Clark GD. 2003. Interaction of reelin signaling and Lis1 in brain development. Nat Genet 35(3):270-6. [PubMed: 14578885] [MGI Ref ID J:86398]
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]
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]
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]
Drakew A; Deller T; Heimrich B; Gebhardt C; Del Turco D; Tielsch A; Forster E; Herz J; Frotscher M. 2002. Dentate granule cells in reeler mutants and VLDLR and ApoER2 knockout mice. Exp Neurol 176(1):12-24. [PubMed: 12093079] [MGI Ref ID J:78001]
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]
Goffinet AM. 1995. Developmental neurobiology. A real gene for reeler [news; comment] Nature 374(6524):675-6. [PubMed: 7715721] [MGI Ref ID J:24507]
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]
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]
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]
Jossin Y; Ignatova N; Hiesberger T; Herz J; Lambert de Rouvroit C; Goffinet AM. 2004. The central fragment of Reelin, generated by proteolytic processing in vivo, is critical to its function during cortical plate development. J Neurosci 24(2):514-21. [PubMed: 14724251] [MGI Ref ID J:87733]
Kubasak MD; Brooks R; Chen S; Villeda SA; Phelps PE. 2004. Developmental distribution of Reelin-positive cells and their secreted product in the rodent spinal cord. J Comp Neurol 468(2):165-78. [PubMed: 14648677] [MGI Ref ID J:86850]
Nishikawa S; Goto S; Yamada K; Hamasaki T; Ushio Y. 2003. Lack of Reelin causes malpositioning of nigral dopaminergic neurons: evidence from comparison of normal and Reln(rl) mutant mice. J Comp Neurol 461(2):166-73. [PubMed: 12724835] [MGI Ref ID J:83566]
Niu S; Renfro A; Quattrocchi CC; Sheldon M; D'Arcangelo G. 2004. Reelin Promotes Hippocampal Dendrite Development through the VLDLR/ApoER2-Dab1 Pathway. Neuron 41(1):71-84. [PubMed: 14715136] [MGI Ref ID J:87427]
Podhorna J; Didriksen M. 2004. The heterozygous reeler mouse: behavioural phenotype. Behav Brain Res 153(1):43-54. [PubMed: 15219705] [MGI Ref ID J:91244]
Royaux I; Lambert de Rouvroit C; D'Arcangelo G; Demirov D; Goffinet AM. 1997. Genomic organization of the mouse reelin gene. Genomics 46(2):240-50. [PubMed: 9417911] [MGI Ref ID J:44722]
Sheppard AM; Pearlman AL. 1997. Abnormal reorganization of preplate neurons and their associated extracellular matrix: an early manifestation of altered neocortical development in the reeler mutant mouse. J Comp Neurol 378(2):173-9. [PubMed: 9120058] [MGI Ref ID J:38642]
Soriano E; Alvarado-Mallart RM; Dumesnil N; Del Rio JA; Sotelo C. 1997. Cajal-Retzius cells regulate the radial glia phenotype in the adult and developing cerebellum and alter granule cell migration. Neuron 18(4):563-77. [PubMed: 9136766] [MGI Ref ID J:39950]
Weiss KH; Johanssen C; Tielsch A; Herz J; Deller T; Frotscher M; Forster E. 2003. Malformation of the radial glial scaffold in the dentate gyrus of reeler mice, scrambler mice, and ApoER2/VLDLR-deficient mice. J Comp Neurol 460(1):56-65. [PubMed: 12687696] [MGI Ref ID J:83151]
Yamamoto T; Sakakibara S; Mikoshiba K; Terashima T. 2003. Ectopic corticospinal tract and corticothalamic tract neurons in the cerebral cortex of yotari and reeler mice. J Comp Neurol 461(1):61-75. [PubMed: 12722105] [MGI Ref ID J:83585]
Yip JW; Yip YP; Nakajima K; Capriotti C. 2000. Reelin controls position of autonomic neurons in the spinal cord Proc Natl Acad Sci U S A 97(15):8612-6. [PubMed: 10880573] [MGI Ref ID J:63408]
Yip YP; Capriotti C; Magdaleno S; Benhayon D; Curran T; Nakajima K; Yip JW. 2004. Components of the reelin signaling pathway are expressed in the spinal cord. J Comp Neurol 470(2):210-9. [PubMed: 14750162] [MGI Ref ID J:88816]
Relnrl relatedAdachi 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]
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]
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]
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]
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]
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]
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Health & husbandry
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Animal Health Reports
Room Number FGB29
Colony Maintenance
Mating System Backcross-Intercross (Female x Male) 01-MAR-06 TJL Breeding Summary: homozygote x B6C3FeF1 a/a then heterozygote x heterozygote Diet Information LabDiet® 5K52/5K67
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Pricing
| Pricing for USA, Canada and Mexico shipping destinations |
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Weeks of Age Price (US dollars $) Gender Genotypes Provided Individual Mouse $132.00 Female or Male Heterozygous for Relnrl $209.40 Female or Male Homozygous for Relnrl
Pairs /Price (US dollars $) Pair Genotype $264.00 Heterozygous for Relnrl x Heterozygous for Relnrl
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Weeks of Age Price (US dollars $) Gender Genotypes Provided Individual Mouse $171.60 Female or Male Heterozygous for Relnrl $272.30 Female or Male Homozygous for Relnrl
Pairs /Price (US dollars $) Pair Genotype $343.20 Heterozygous for Relnrl x Heterozygous for Relnrl
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Supply Details
| Standard Supply | Repository-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 approximately 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 two business days following order placement. |
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Control Information
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