Strain Name:

B6.Cg-Rorasg + +/+ Myo5ad Bmp5se/J

Stock Number:

000285

Availability:

Cryopreserved - Ready for recovery

Description

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

Strain Information

Type Congenic; Mutant Strain;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain C57BL/6J
Donor Strain Bmpse , Commercial breeder; Myo5ad NB strain ; Rorasg NB strain

Appearance
black
Related Genotype: + ? ?/? + +

black , small, wasted in appearance
Related Genotype: Rora sg ? ?/Rorasg + +

slate grey, short ears
Related Genotype: + Myo5ad Bmp5 se/? Myo5ad Bmp5se

Description
Mice homozygous for the staggerer spontaneous mutation (Rorasg) show a staggering gait, mild tremor, hypotonia, and small size. The cerebellar cortex of homozygous mutant mice is grossly underdeveloped with a deficiency of granule cells and Purkinje cells. The remaining granule cells migrate inward from the external layer prematurely and then degenerate. Purkinje cells are much delayed in postnatal differentiation and lack the dendritic spines on which synapses with the parallel fibers from the granule cells normally occur. Staggerer mutant mice have been used as a source of an agranulate cerebellum in a number of investigations of the composition and function of granule cells. Kopmels et al. have reported a hyperproduction of IL1 biological activity and mRNA from LPS stimulated spleen cells of Rorasg/Rorasg mice on the C57BL/6J background relative to wild type siblings.

In this congenic strain the staggerer mutation is maintained in repulsionwith both the dilute (Myo5ad) and short ear (Bmp5se) mutations.

Control Information

  Control
   Untyped from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Bmp5se allele
000004   ABP/LeJ
000578   B6 x STOCK Tyrc-ch Bmp5se +/+ Myo6sv/J
000056   B6.Cg-Bmp5se/J
000253   DLS/LeJ
000644   SEA/GnJ
000270   SEC/1GnLeJ
View Strains carrying   Bmp5se     (6 strains)

Strains carrying   Myo5ad allele
001005   AKXD1/TyJ
001003   AKXD11/TyJ
000765   AKXD13/TyJ
000779   AKXD14/TyJ
000954   AKXD15/TyJ
001093   AKXD18/TyJ
000776   AKXD2/TyJ
001062   AKXD21/TyJ
000947   AKXD22/TyJ
000949   AKXD25/TyJ
000764   AKXD27/TyJ
000959   AKXD3/TyJ
000652   BDP/J
000036   BXD1/TyJ
000013   BXD16/TyJ
000015   BXD18/TyJ
000010   BXD19/TyJ
000077   BXD21/TyJ
000043   BXD22/TyJ
000081   BXD25/TyJ
006255   BXD25/TyJRwwJ
000029   BXD29-Tlr4lps-2J/J
010981   BXD29/Ty
000037   BXD5/TyJ
000007   BXD6/TyJ
000084   BXD8/TyJ
000105   BXD9/TyJ
000284   CWD/LeJ
000670   DBA/1J
000671   DBA/2J
000963   DBA/2J-Myo5ad+17J/Myo5ad/J
000964   DBA/2J-Myo5ad+18J/Myo5ad/J
000067   DBA/2J-Myo5ad+2J/Myo5ad/J
000673   HRS/J
000674   I/LnJ
001850   MEV-Q/TyJ
001855   MEV-V/TyJ
003345   MEV/2Ty-Emv64/J
000679   P/J
000644   SEA/GnJ
000390   STOCK Myo5ad Ds/J
000994   STOCK a Myo5ad Mregdsu/J
000286   STOCK a/a Myo5ad fd/+ +/J
View Strains carrying   Myo5ad     (43 strains)

Strains carrying   Rorasg allele
002651   B6.C3(Cg)-Rorasg/J
000237   B6C3Fe a/a-Rorasg/J
View Strains carrying   Rorasg     (2 strains)

Strains carrying other alleles of Bmp5
001496   B6(Cg)-Bmp5se-4J/J
005348   BALB/cByJ Agtpbp1pcd-3J-Bmp5cfe-se6J/GrsrJ
005420   C;129S7 Gt(ROSA)26Sor-Bmp5cfe-se7J/J
005421   CBy;B6-Bmp5cfe-se8J/J
View Strains carrying other alleles of Bmp5     (4 strains)

Strains carrying other alleles of Myo5a
005012   A.B6 Tyr+-Myo5ad-l31J/J
001013   B10.D2/nSnJ-Myo5ad-n/J
000502   B6 x B6CBCa Aw-J/A-Myo5aflr Gnb5flr/J
000963   DBA/2J-Myo5ad+17J/Myo5ad/J
000964   DBA/2J-Myo5ad+18J/Myo5ad/J
000067   DBA/2J-Myo5ad+2J/Myo5ad/J
000253   DLS/LeJ
View Strains carrying other alleles of Myo5a     (7 strains)

Strains carrying other alleles of Rora
005047   C57BL/6J-Rorasg-3J/J
View Strains carrying other alleles of Rora     (1 strain)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms
      assigned by genotype

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

Rorasg/Rorasg

        involves: C57BL/6
  • homeostasis/metabolism phenotype
  • abnormal lipid homeostasis (MGI Ref ID J:52105)
    • plasma APOA1 and APOA2 concentrations are approximately 2 fold lower than in wild-type controls on a normal diet, and the Apoa1 mRNA level in intestine is diminished relative to wild-type, although liver expression of Apoa1 is comparable with wild-type
    • the production rate of APOA1 is diminished, but the fractional catabolic rate is comparable to wild-type
    • decreased circulating cholesterol level (MGI Ref ID J:52105)
      • plasma total cholesterol levels are significantly lower in both male and female homozygotes than in wild-type controls
      • although cholesterol levels increase on an atherosclerotic diet, homozygotes still have lower plasma cholesterol than wild-type controls also fed this diet
      • decreased circulating HDL cholesterol level (MGI Ref ID J:52105)
        • plasma HDL cholesterol level is significantly lower in both male and female homozygotes than in wild-type controls, and females have significantly lower plasma HDL level than males both for the homozygous and wild-type data sets. This is true even on an atherogenic diet.
  • cardiovascular system phenotype
  • atherosclerotic lesions (MGI Ref ID J:52105)
    • the atherosclerotic lesions induced in homozygotes by 9 weeks of an atherosclerotic diet have a 6 fold greater area in female homozygotes and a 7.5 fold greater area in male homozygotes than those in wild-type controls on the same diet
    • increased susceptibility to atherosclerosis (MGI Ref ID J:52105)
      • Although homozygotes fed a normal diet do not display abnormal atherosclerotic lesions, 9 weeks of an atherosclerotic diet induces exaggerated altherosclerotic lesions compared with wild-type controls on the atherosclerotic diet
  • immune system phenotype
  • *normal* immune system phenotype (MGI Ref ID J:52105)
    • white blood cell, lymphocyte, and neutrophil counts are not significantly different between homozygotes and wild-type controls
View Research Applications

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

Bmp5se related

Developmental Biology Research
Growth Defects
Skeletal Defects

Myo5ad related

Dermatology Research
Color and White Spotting Defects

Mouse/Human Gene Homologs
Griscelli Syndrome

Rorasg related

Neurobiology Research
Ataxia (Movement) Defects
Cerebellar Defects
      Purkinje cell defect
Receptor Defects
Tremor Defects

Genes & Alleles

Gene & Allele Information

 
Allele Symbol Bmp5se
Allele Name short ear
Allele Type Spontaneous
Common Name(s) seGnJ;
Strain of Originmice from Abbie Lathrop mouse farm
Gene Symbol and Name Bmp5, bone morphogenetic protein 5
Chromosome 9
Gene Common Name(s) AU023399; MGC34244; expressed sequence AU023399; se; short ear;
Molecular Note The C to T transition creates a stop codon at amino acid 208. The resulting truncated protein does not include the carboxy terminal signaling portion of the molecule. [MGI Ref ID J:21484]
 
Allele Symbol Myo5ad
Allele Name dilute
Allele Type Spontaneous
Common Name(s) d; dv; maltese dilution;
Strain of Originold mutant of the mouse fancy
Gene Symbol and Name Myo5a, myosin VA
Chromosome 9
Gene Common Name(s) 9630007J19Rik; AI413174; AI661011; D; Dbv; Dop; GS1; MVa; MYH12; MYO5; MYR12; Myo5; MyoVA; RIKEN cDNA 9630007J19 gene; d; dilute; expressed sequence AI413174; expressed sequence AI661011; flail; flailer; flr; myosin V; nmf244;
General Note Mutations at the Myo5a locus lighten coat color through an abnormal morphology of melanocytes that causes uneven pigmentation of the hair shaft (J:11005). Most of these mutations also cause severe neurological defects; in some mutant forms, these defectslead to early death (J:12978), while in others life span is normal, but convulsions and loss of equilibrium occur after about four months of age (J:16915).

Maltese dilution, as this mutation was originally called, is an old mutation of the mouse fancy. The blue-gray color of the hair produced by this mutation in nonagouti (a/a) mice is caused by clumping of the melanin pigment into a few large masses (J:12958). The melanocytes are misshapen, with fewer and thinner dendritic processes than wild-type melanocytes, and melanin granules are largely clumped around the nucleus (J:12970). Incorporation of tyrosine into melanin proceeds at a normal rate (J:12173), and the fine structure of the melanin granules is normal (J:5346). Cultured primary melanocytesfrom dilute homozygotes are normal in morphology but display clustering of melanosomes (J:37976).

Griscelli disease (Chediak-Higashi-like syndrome, OMIM 214450) is a human autosomal recessive disorder whose symptoms include pigment dilution, immunodeficiency, and acute lethal lymphocyte and macrophage activation. Melanocyte malformation is characteristic of the pigment abnormality. The immunological abnormality includes absence of cutaneous hypersensitivity and impaired function of natural-killer cells. Griscelli disease resembles the dilute-lethal mouse mutant, except for the neurological disorder in the mouse. The locus for Griscelli disease colocalizes with the locus for myosin Va, which is mutated in at least some Griscelli patients. Griscelli disease is thus the homolog of mouse Maltese dilution (J:41253).

The original Myo5ad mutation which identified the locuswas caused by insertion of an ecotropic murine leukemia virus (see Emv3) (J:6844, J:6587). All other mutations examined lack the virus. Reversions of Myo5ad to wild-type, which have been reported frequently, are caused by excision of the virusleaving exactly one long terminal repeat in place (J:7092). The virus is integrated into a noncoding region of the DNA (J:7751).

Molecular Note This mutation is the result of the integration of the ecotropic murine leukemia virus Emv-3 into the normal Myo5ad gene. [MGI Ref ID J:6587]
 
Allele Symbol Rorasg
Allele Name staggerer
Allele Type Spontaneous
Common Name(s) RORalpha-; sg;
Strain of Originobese stock
Gene Symbol and Name Rora, RAR-related orphan receptor alpha
Chromosome 9
Gene Common Name(s) 9530021D13Rik; DKFZp686M2414; MGC119326; MGC119329; NR1F1; RIKEN cDNA 9530021D13 gene; ROR1; ROR2; ROR3; RZR-ALPHA; RZRA; neuroscience mutagenesis facility, 267; nmf267; sg; staggerer;
General Note Homozygotes for the staggerer mutation show a staggering gait, mild tremor, hypotonia, and small size (J:13140). The cerebellar cortex is grossly underdeveloped with a deficiency of granule cells and Purkinje cells. The deficiency of granule cells in theexternal granular layer is already evident at birth. The remaining granule cells migrate inward from the external layer prematurely and then degenerate (J:5304). Purkinje cells are much delayed in postnatal differentiation and lack the dendritic spines on which synapses with the parallel fibers from the granule cells normally occur (J:5968). Golgi cells are not clearly distinguishable from Purkinje cells and it is possible that their number is also reduced (J:6185). Examination of the cerebellum of chimeras of Rorasg/Rorasg with wild-type using cellular markers for Purkinje cells and granule cells has shown that the Rorasg effect is intrinsic to the Purkinje cells and that granule cells are affected secondarily (J:28093, J:11945). Purkinje cells are probably defective as early as postnatal day 4 (J:6875). The granule cell deficiency may result from failure of Purkinje cells to adequately stimulate granule cell genesis (J:28092), as well as from later cell death due to failure of synapsis with Purkinje cells. Staggerer mice have been used as a source of an agranulate cerebellum in a number of investigations of the composition and function of granule cells.Other effects of Rorasg include persistence of multipleinnervation of Purkinje cells by climbing fibers (J:6260), reduction in size of deep cerebellar nuclei (J:6554) and inferior olivary complex (J:7948), and abnormal patterns of ganglioside composition and enzymatic activity (J:7910). Inferior olivary neuron numbers and definition of the olivary subnuclei are normal at birth but decline thereafter (J:20982). Death of inferior olivary neurons, like that of granule cells, is apparently an indirect effect of the Rorasg gene, caused by the lack of Purkinje cells with which to synapse (J:28468).Cerebellar cells of Rorasg/Rorasg mice at 7 days postnatal have immature cell surface components of a type which are present in +/+ cells at late prenatal and neonatal stages (J:6068, J:6088). In particular, the conversion of neural cell adhesion molecules (NCAM) from embryonic to adult form which is normally complete by 21 days does not occur in Rorasg/Rorasg mice (J:6930).Purkinje cells are the predominant siteof expression of calmodulin in the cerebellum of normal mice, but Rorasg/Rorasg mice do not produce any mRNA for the Calm1 locus in these cells (J:28469).Peripheral macrophages of staggerer mice, and those of several other cerebellar mutant mice, show greatly increased production of interleukin 1 beta (J:28095). Since Il1a and Tnf are also hyperexpressed in staggerer macrophages, the increases represent a general condition of hyperexcitability of these cells (J:1431). Il6 hyperexpression was also found in Rorasg/Rorasg mice but not in Grid2/+ animals (J:11652), although the latter did show hyperexpression of Il1a, Il1b, and Tnf (J:2228). Matsui et al. (J:28478) report elevated levels of somatostatin in brainsof several ataxic mouse mutants, including Rorasg homozygotes. The concentration of thyrotropin releasing hormone (TH) is also elevated in brains of these mutants (J:28467), and administration of a TRH analog, YM-14673, ameliorated the ataxia,suggesting that excess TRH may have an ataxic effect (J:18435).The reproductive life of Rorasg/Rorasg female mice is curtailed by late sexual maturation, irregular estrous cycling, and a shortened post-puberal period of reproduction (J:1960). Neonatal vestibular stimulation by rotation on a tilted plain improved gait and body balance in Rorasg/Rorasg mice and also led to improved mating efficiency (J:14535), suggesting that mating defects in these mice may bea secondary effect of the gait and balance difficulties. Long-term selection for ability to reproduce improved the maternal behavior of homozygous staggerer females without abolishing gait and balance difficulties, suggesting that Rorasg effects on reproduction are not entirely due to these difficulties (J:28416).Male staggerer mice are able to differentiate between pheromones secreted by estrous and anestrous females (J:15645). Some male Rorasg/Rorasg mice suffer from a penile disability, the penis in erection being directed rearward. The disability is intermittent even in those males subject to it, and is of little importance in determining male mating deficiency (J:32193).Although Rorasg/+ heterozygotes are behaviorally normal with normal cerebellar cytoarchitecture and composition, these heterozygotes suffer accelerated loss of Purkinje cells, granule cells, and inferior olivary neurons with age (J:1431).Rorasg/Rorasg homozygotesusually die during the fourth week of life. Some survive to adulthood, and one male has bred (J:13140).
Molecular Note This allele contains a 6.5kb genomic deletion of an exon encoding part of the ligand binding domain. The deletion results in an exon-skipping event that introduces a shift in the reading frame. The resulting protein is predicted to be truncated due to introduction of a premature stop codon. [MGI Ref ID J:31470]

Genotyping

Genotyping Information

Genotyping Protocols

Rorasg, Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References

Selected Reference(s)

Mamontova A; Seguret-Mace S; Esposito B; Chaniale C; Bouly M; Delhaye-Bouchaud N; Luc G; Staels B; Duverger N; Mariani J; Tedgui A. 1998. Severe atherosclerosis and hypoalphalipoproteinemia in the staggerer mouse, a mutant of the nuclear receptor RORalpha. Circulation 98(24):2738-43. [PubMed: 9851961]  [MGI Ref ID J:52105]

Additional References

Kopmels B; Wollman EE; Guastavino JM; Delhaye-Bouchaud N; Fradelizi D; Mariani J. 1990. Interleukin-1 hyperproduction by in vitro activated peripheral macrophages from cerebellar mutant mice. J Neurochem 55(6):1980-5. [PubMed: 2230805]  [MGI Ref ID J:28095]

Yoon CH. 1972. Developmental mechanism for changes in cerebellum of staggerer mouse, a neurological mutant of genetic origin. Neurology 22(7):743-54. [PubMed: 4673255]  [MGI Ref ID J:5304]

Bmp5se related

GREEN MC. 1958. Effects of the short ear gene in the mouse on cartilage formation in healing bone fractures. J Exp Zool 137(1):75-88. [PubMed: 13563786]  [MGI Ref ID J:13011]

Green EL; Green MC. 1946. Effect of the short ear gene on number of ribs and presacral vertebrae in the house mouse Am Naturalist 80:619-25.  [MGI Ref ID J:100198]

Green EL; Green MC. 1942. The development of three manifestations of the short ear gene in the mouse J Morphol 70:1-19.  [MGI Ref ID J:15478]

Green MC. 1951. Further morphological effects of the short ear gene in the house mouse. J Morphol 88:1-22.  [MGI Ref ID J:13091]

Green MC. 1968. Mechanism of the pleiotropic effects of the short-ear mutant gene in the mouse. J Exp Zool 167(2):129-50. [PubMed: 5692092]  [MGI Ref ID J:5086]

Johnson DR. 1976. The interfrontal bone and mutant genes in the mouse. J Anat 121(3):507-13. [PubMed: 1018005]  [MGI Ref ID J:5776]

Jones JM; Huang JD; Mermall V; Hamilton BA; Mooseker MS; Escayg A; Copeland NG; Jenkins NA; Meisler MH. 2000. The mouse neurological mutant flailer expresses a novel hybrid gene derived by exon shuffling between Gnb5 and Myo5a. Hum Mol Genet 9(5):821-8. [PubMed: 10749990]  [MGI Ref ID J:61324]

Katagiri T; Boorla S; Frendo JL; Hogan BL; Karsenty G. 1998. Skeletal abnormalities in doubly heterozygous Bmp4 and Bmp7 mice. Dev Genet 22(4):340-8. [PubMed: 9664686]  [MGI Ref ID J:48538]

King JA; Marker PC; Seung KJ; Kingsley DM. 1994. BMP5 and the molecular, skeletal, and soft-tissue alterations in short ear mice. Dev Biol 166(1):112-22. [PubMed: 7958439]  [MGI Ref ID J:21484]

Lacombe D; Toutain A; Gorlin RJ; Oley CA; Battin J. 1994. Clinical identification of a human equivalent to the short ear (se) murine phenotype. Ann Genet 37(4):184-91. [PubMed: 7710253]  [MGI Ref ID J:24474]

Lynch CJ. 1921. Short ears, an autosomal mutation in the house mouse Am Naturalist 55:421-426.  [MGI Ref ID J:14849]

Nadeau JH. 2001. Modifier genes in mice and humans. Nat Rev Genet 2(3):165-74. [PubMed: 11256068]  [MGI Ref ID J:88013]

Pfendler KC; Yoon J; Taborn GU; Kuehn MR; Iannaccone PM. 2000. Nodal and bone morphogenetic protein 5 interact in murine mesoderm formation and implantation. Genesis 28(1):1-14. [PubMed: 11020711]  [MGI Ref ID J:65690]

Sloane JA; Vartanian TK. 2007. Myosin Va controls oligodendrocyte morphogenesis and myelination. J Neurosci 27(42):11366-75. [PubMed: 17942731]  [MGI Ref ID J:126066]

Solloway MJ; Dudley AT; Bikoff EK; Lyons KM; Hogan BL; Robertson EJ. 1998. Mice lacking Bmp6 function. Dev Genet 22(4):321-39. [PubMed: 9664685]  [MGI Ref ID J:48561]

Solloway MJ; Robertson EJ. 1999. Early embryonic lethality in Bmp5;Bmp7 double mutant mice suggests functional redundancy within the 60A subgroup. Development 126(8):1753-68. [PubMed: 10079236]  [MGI Ref ID J:53294]

Myo5ad related

Coleman DL. 1962. Effect of genic substitution on the incorporation of tyrosine into the melanin of mouse skin. Arch Biochem Biophys 96:562-8. [PubMed: 13880466]  [MGI Ref ID J:12173]

Copeland NG; Hutchison KW; Jenkins NA. 1983. Excision of the DBA ecotropic provirus in dilute coat-color revertants of mice occurs by homologous recombination involving the viral LTRs. Cell 33(2):379-87. [PubMed: 6305507]  [MGI Ref ID J:7092]

Engle LJ; Kennett RH. 1994. Cloning, analysis, and chromosomal localization of myoxin (MYH12), the human homologue to the mouse dilute gene. Genomics 19(3):407-16. [PubMed: 8188282]  [MGI Ref ID J:16915]

Grobman AB; Charles DR. 1947. Mutant white mice. A new dominant autosomal mutant affecting coat color in Mus musculus. J Hered 38:381-384.  [MGI Ref ID J:13058]

Hearing VJ; Phillips P; Lutzner MA. 1973. The fine structure of melanogenesis in coat color mutants of the mouse. J Ultrastruct Res 43(1):88-106. [PubMed: 4634048]  [MGI Ref ID J:5346]

Hutchison KW; Copeland NG; Jenkins NA. 1984. Dilute-coat-color locus of mice: nucleotide sequence analysis of the d+2J and d+Ha revertant alleles. Mol Cell Biol 4(12):2899-904. [PubMed: 6098826]  [MGI Ref ID J:7751]

Jenkins NA; Copeland NG; Taylor BA; Lee BK. 1981. Dilute (d) coat colour mutation of DBA/2J mice is associated with the site of integration of an ecotropic MuLV genome. Nature 293(5831):370-4. [PubMed: 6268990]  [MGI Ref ID J:6587]

Jenkins NA; Copeland NG; Taylor BA; Lee BK. 1982. Organization, distribution, and stability of endogenous ecotropic murine leukemia virus DNA sequences in chromosomes of Mus musculus. J Virol 43(1):26-36. [PubMed: 6287001]  [MGI Ref ID J:6844]

Libby RT; Lillo C; Kitamoto J; Williams DS; Steel KP. 2004. Myosin Va is required for normal photoreceptor synaptic activity. J Cell Sci 117(Pt 19):4509-15. [PubMed: 15316067]  [MGI Ref ID J:92181]

Markert CL; Silvers WK. 1956. The Effects of Genotype and Cell Environment on Melanoblast Differentiation in the House Mouse. Genetics 41(3):429-50. [PubMed: 17247639]  [MGI Ref ID J:12970]

Mercer JA; Seperack PK; Strobel MC; Copeland NG; Jenkins NA. 1991. Novel myosin heavy chain encoded by murine dilute coat colour locus [published erratum appears in Nature 1991 Aug 8;352(6335):547] Nature 349(6311):709-13. [PubMed: 1996138]  [MGI Ref ID J:11005]

Moore KJ; Swing DA; Copeland NG; Jenkins NA. 1990. Interaction of the murine dilute suppressor gene (dsu) with fourteen coat color mutations [published erratum appears in Genetics 1990 Sep;126(1):285] Genetics 125(2):421-30. [PubMed: 2379821]  [MGI Ref ID J:29467]

Moore KJ; Swing DA; Copeland NG; Jenkins NA. 1994. The murine dilute suppressor gene encodes a cell autonomous suppressor. Genetics 138(2):491-7. [PubMed: 7828830]  [MGI Ref ID J:20796]

Moore KJ; Swing DA; Rinchik EM; Mucenski ML; Buchberg AM; Copeland NG; Jenkins NA. 1988. The murine dilute suppressor gene dsu suppresses the coat-color phenotype of three pigment mutations that alter melanocyte morphology, d, ash and ln. Genetics 119(4):933-41. [PubMed: 3410303]  [MGI Ref ID J:9309]

Murray WS. 1934. The breeding behavior of the dilute brown stock of mice (Little dba) Am J Cancer 20:573-593.  [MGI Ref ID J:2464]

O'Sullivan TN; Wu XS; Rachel RA; Huang JD; Swing DA; Matesic LE; Hammer JA rd; Copeland NG; Jenkins NA. 2004. dsu functions in a MYO5A-independent pathway to suppress the coat color of dilute mice. Proc Natl Acad Sci U S A 101(48):16831-6. [PubMed: 15550542]  [MGI Ref ID J:94728]

PIERRO LJ; CHASE HB. 1963. Slate--a new coat color mutant in the mouse. J Hered 54:47-50. [PubMed: 13943454]  [MGI Ref ID J:25388]

Pastural E; Barrat FJ; Dufourcq-Lagelouse R; Certain S; Sanal O ; Jabado N ; Seger R ; Griscelli C ; Fischer A ; de Saint Basile G. 1997. Griscelli disease maps to chromosome 15q21 and is associated with mutations in the myosin-Va gene. Nat Genet 16(3):289-92. [PubMed: 9207796]  [MGI Ref ID J:41253]

Provance DW Jr; Wei M; Ipe V; Mercer JA. 1996. Cultured melanocytes from dilute mutant mice exhibit dendritic morphology and altered melanosome distribution. Proc Natl Acad Sci U S A 93(25):14554-8. [PubMed: 8962090]  [MGI Ref ID J:37976]

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

RIKEN BioResource Center/RIKEN Genomic Sciences Center. 2008. A Large Scale Mutagenesis Program in RIKEN GSC PhenoSITE, World Wide Web (URL: http://www.brc.riken.jp/lab/gsc/mouse/) :.  [MGI Ref ID J:133634]

RUSSELL ES. 1949. A quantitative histological study of the pigment found in the coat-color mutants of the house mouse; interdependence among the variable granule attributes. Genetics 34(2):133-45. [PubMed: 18117146]  [MGI Ref ID J:148461]

Russell ES. 1948. A Quantitative Histological Study of the Pigment Found in the Coat Color Mutants of the House Mouse. II. Estimates of the Total Volume of Pigment. Genetics 33(3):228-36. [PubMed: 17247280]  [MGI Ref ID J:148462]

Russell ES. 1946. A Quantitative Histological Study of the Pigment Found in the Coat-Color Mutants of the House Mouse. I. Variable Attributes of the Pigment Granules. Genetics 31(3):327-46. [PubMed: 17247200]  [MGI Ref ID J:148463]

Russell ES. 1949. A Quantitative Histological Study of the Pigment Found in the Coat-Color Mutants of the House Mouse. IV. the Nature of the Effects of Genic Substitution in Five Major Allelic Series. Genetics 34(2):146-66. [PubMed: 17247308]  [MGI Ref ID J:12958]

Sweet HO. 1983. Dilute suppressor, a new suppressor gene in the house mouse. J Hered 74(4):305-6. [PubMed: 6886377]  [MGI Ref ID J:7171]

Yoshimura A; Fujii R; Watanabe Y; Okabe S; Fukui K; Takumi T. 2006. Myosin-Va facilitates the accumulation of mRNA/protein complex in dendritic spines. Curr Biol 16(23):2345-51. [PubMed: 17141617]  [MGI Ref ID J:117928]

Rorasg related

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Vernet-der Garabedian B; Lemaigre-Dubreuil Y; Delhaye-Bouchaud N ; Mariani J. 1998. Abnormal IL-1beta cytokine expression in the cerebellum of the ataxic mutant mice staggerer and lurcher. Brain Res Mol Brain Res 62(2):224-7. [PubMed: 9813341]  [MGI Ref ID J:51056]

Vogel MW; Sinclair M; Qiu D; Fan H. 2000. Purkinje cell fate in staggerer mutants: agenesis versus cell death. J Neurobiol 42(3):323-37. [PubMed: 10645972]  [MGI Ref ID J:113250]

Yamazaki T; Yang XO; Chung Y; Fukunaga A; Nurieva R; Pappu B; Martin-Orozco N; Kang HS; Ma L; Panopoulos AD; Craig S; Watowich SS; Jetten AM; Tian Q; Dong C. 2008. CCR6 regulates the migration of inflammatory and regulatory T cells. J Immunol 181(12):8391-401. [PubMed: 19050256]  [MGI Ref ID J:142071]

Yang XO; Nurieva R; Martinez GJ; Kang HS; Chung Y; Pappu BP; Shah B; Chang SH; Schluns KS; Watowich SS; Feng XH; Jetten AM; Dong C. 2008. Molecular antagonism and plasticity of regulatory and inflammatory T cell programs. Immunity 29(1):44-56. [PubMed: 18585065]  [MGI Ref ID J:137851]

Yang XO; Pappu BP; Nurieva R; Akimzhanov A; Kang HS; Chung Y; Ma L; Shah B; Panopoulos AD; Schluns KS; Watowich SS; Tian Q; Jetten AM; Dong C. 2008. T helper 17 lineage differentiation is programmed by orphan nuclear receptors ROR alpha and ROR gamma. Immunity 28(1):29-39. [PubMed: 18164222]  [MGI Ref ID J:131020]

Yoon CH. 1972. Developmental mechanism for changes in cerebellum of staggerer mouse, a neurological mutant of genetic origin. Neurology 22(7):743-54. [PubMed: 4673255]  [MGI Ref ID J:5304]

Zanjani HS; Herrup K; Guastavino JM; Delhaye-Bouchaud N; Mariani J. 1994. Developmental studies of the inferior olivary nucleus in staggerer mutant mice. Brain Res Dev Brain Res 82(1-2):18-28. [PubMed: 7842506]  [MGI Ref ID J:20982]

Zanjani HS; Mariani J; Delhaye-Bouchaud N; Herrup K. 1992. Neuronal cell loss in heterozygous staggerer mutant mice: a model for genetic contributions to the aging process. Brain Res Dev Brain Res 67(2):153-60. [PubMed: 1511513]  [MGI Ref ID J:1431]

Zanjani HS; Mariani J; Herrup K. 1990. Cell loss in the inferior olive of the staggerer mutant mouse is an indirect effect of the gene. J Neurogenet 6(4):229-41. [PubMed: 2231177]  [MGI Ref ID J:28468]

Health & husbandry

Health & Colony Maintenance Information

Currently there no information available for this strain. This may be due to the supply level of this strain.

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Pricing for USA, Canada and Mexico shipping destinations View International pricing
Price (US dollars $)
Cryorecovery Fee $1900.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Additional Supply Details

Pricing for International shipping destinations View USA Canada and Mexico pricing
Price (US dollars $)
Cryorecovery Fee $2470.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Additional Supply Details

Supply Details

Standard SupplyCryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
Supply Notes
  • Cryorecovery of Strains Needing Progeny Testing.
    At least two untested males and two untested females (two pairs) will be recovered (eight or more mice is typical). The total number of animals provided, their gender and genotype will vary. Untested animals typically are available to ship between 13 and 16 weeks from the date of your order. If the first recovery attempt is unsuccessful, a second recovery will be done, extending the overall recovery time to approximately 25 weeks.

    Progeny testing is required to identify the genotype of mice of this strain, as a genotyping assay is not available. This type of testing involves breeding the recovered animals and assessing the phenotype of the offspring in order to identify animals carrying the mutation of interest. We can perform the progeny testing for you as a service or we can ship all recovered animals to you for progeny testing at your facility. If you perform the progeny testing, there is NO guarantee that a carrier will be identified. If we perform progeny testing as a service, additional breeding time will be required. In this case, when a male and female (one pair) are identified that carry the mutation, they and their offspring will be shipped. Delivery time for strains requiring progeny testing often exceeds 25 weeks and may take 12 months or more due to the difficulties in breeding some strains. The progeny testing cost is in addition to the recovery cost and is based on the number of boxes used and the time taken to produce the mice identified as carrying the mutation. Please note that identified pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Please contact Customer Service for more information on the cost of progeny testing for a strain: Tel: 1-800-422-6423 (from U.S.A., Canada and Puerto Rico only) or 1-207-288-5845 (from any location). The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

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

  • Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

  Control
   Untyped from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
  International - Control Pricing Information for Genetically Engineered Mutant Strains.

Payment Terms and Conditions

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.
Ordering and Purchasing Information

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Contact Information
Orders & Technical Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries

Contracts Administration

phone:207-288-6470
fax:207-288-6655

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

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

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. 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.


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