Strain Name:

V/LeJ

Stock Number:

000275

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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 Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Type Inbred Strain;
Additional information on Inbred Strains.
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Specieslaboratory mouse
GenerationCPF42p
Generation Definitions

Appearance
grey with white spots, thin wavy coat, circling
Related Genotype: a/a fz Mlphln/fz Mlphln Ednrbs/Ednrbs Cdh23v/Cdh23v

grey with white spots, thin wavy coat
Related Genotype: a/a fz Mlphln/fz Mlphln Ednrbs/Ednrbs Cdh23v/+

Important Note
This strain is homozygous for fz, Mlphln, and Ednrbs, and is segregating for Cdh23v.

Description
This strain was originally used as a linkage stock for gene mapping. It is homozygous for several visible recessive mutations all located on different chromosomes including nonagouti (a), fuzzy (fz), leaden (Mlphln), and piebald (Ednrbs) and is segregating for the neurological mutation, waltzer (Cdh23v). Homozygous waltzer mice show the circling, head-tossing, deafness, and hyperactivity typical of the circling mutants. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Homozygous piebald mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. Homozygous piebald mice have dark eyes. The white areas of the coat are completely lacking in melanocytes and there is a reduction in the number of melanocytes in the choroid layer of the eye.

Development
The waltzing mutation came from the Japanese mouse fanciers and was received by George Snell at The Jackson Laboratory from Ludwin in 1947 when the stock was homozygous for nonagouti, leaden, waved 1, and piebald. This stock was crossed once to C57BL/10 and non-sibling mated for approximately 22 generations after which it was crossed to a C57BL/10 stock bearing fuzzy and jittery. The fuzzy and waved 1 mutations were selectively bred out of the stock. Sibling inbreeding of this stock began in approximately 1960. In 1983 this stock was at generation F47 and waltzer heterozygous females were bred with homozygous males to generate embryos for cryopreservation.

Control Information

  Control
   None Available
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Ednrbs allele
000577   B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J
000674   I/LnJ
003720   JF1/Ms
000676   LP/J
000308   SSL/LeJ
View Strains carrying   Ednrbs     (5 strains)

Strains carrying   Mlphln allele
000112   B6.Cg-Sgk3fz H54 Mlphln/+ H54 +/J
000668   C57L/J
000643   DW/J Mlphln Pou1f1dw/J
002902   STOCK Pax3Sp Mlphln/J
View Strains carrying   Mlphln     (4 strains)

Strains carrying   Sgk3fz allele
000112   B6.Cg-Sgk3fz H54 Mlphln/+ H54 +/J
View Strains carrying   Sgk3fz     (1 strain)

Strains carrying other alleles of Cdh23
001137   129P1/ReJ
000690   129P3/J
000691   129X1/SvJ
000646   A/J
000647   A/WySnJ
003070   ALR/LtJ
003072   ALS/LtJ
002552   B6(V)-Cdh23v-2J/J
002756   B6.CAST-Cdh23Ahl+/Kjn
010615   B6.CBACa-Cdh23CBA/CaJ/Kjn
004502   B6;AKR-Lxl2/GrsrJ
002432   B6J x B6.C-H2-Kbm1/ByJ-Cdh23v-J/J
001026   BALB/cByJ
000653   BUB/BnJ
005494   C3.129S1(B6)-Grm1rcw/J
000664   C57BL/6J
004764   C57BL/6J-Cdh23v-8J/J
004819   C57BL/6J-Cdh23v-9J/J
003129   C57BL/6J-Epha4rb-2J/GrsrJ
004820   C57BL/6J-Kcne12J/J
004703   C57BL/6J-Kcnq2Nmf134/J
004811   C57BL/6J-nmf110/J
004812   C57BL/6J-nmf111/J
004747   C57BL/6J-nmf118/J
004656   C57BL/6J-nmf88/J
004391   C57BL/6J-Chr 13A/J/NaJ
004385   C57BL/6J-Chr 7A/J/NaJ
000662   C57BLKS/J
000667   C57BR/cdJ
000668   C57L/J
000669   C58/J
010614   CBACa.B6-Cdh23ahl/Kjn
005016   CByJ;B6-Cdh23v-10J/J
000657   CE/J
000670   DBA/1J
001140   DBA/1LacJ
000671   DBA/2J
007048   DBA/2J-Gpnmb+/SjJ
002106   KK/HlJ
000675   LG/J
000676   LP/J
000677   MA/MyJ
001976   NOD/ShiLtJ
002050   NOR/LtJ
000679   P/J
002747   SENCARB/PtJ
002335   SKH2/J
003392   STOCK Crb1rd8/J
View Strains carrying other alleles of Cdh23     (48 strains)

Strains carrying other alleles of Ednrb
011080   B6;129-Ednrbtm1.1Nat/J
003295   B6;129-Ednrbtm1Ywa/J
000308   SSL/LeJ
004711   STOCK Ednrbs-52Pub
009063   STOCK Ednrbtm1Nrd/J
View Strains carrying other alleles of Ednrb     (5 strains)

Strains carrying other alleles of Mlph
000681   DW.C3-Mlph+ Pou1f1+/J
001640   STOCK Mlphln-l1Rk3/J
View Strains carrying other alleles of Mlph     (2 strains)

Strains carrying other alleles of Sgk3
006135   STOCK Sgk3fz-ica/McirJ
View Strains carrying other alleles of Sgk3     (1 strain)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Usher Syndrome, Type ID; USH1D
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Abcd Syndrome; ABCDS   (EDNRB)
Deafness, Autosomal Recessive 12; DFNB12   (CDH23)
Griscelli Syndrome, Type 3; GS3   (MLPH)
Hirschsprung Disease, Susceptibility to, 2; HSCR2   (EDNRB)
Waardenburg Syndrome, Type 4A; WS4A   (EDNRB)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Cdh23v/Cdh23v

        V/LeJ
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • no aberrant bleeding time after tail vein nick   (MGI Ref ID J:29151)

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

Cdh23v/Cdh23+

        mixed
  • hearing/vestibular/ear phenotype
  • increased susceptibility to age-related hearing loss
    • percentage of animal showing no Preyer reflex in response to the sound stimulus increase from 0% at 1 to 3 months to approximately 35% at 7 to 9 month   (MGI Ref ID J:108877)
  • behavior/neurological phenotype
  • absent pinna reflex
    • percentage of animal showing no Preyer reflex in response to the sound stimulus increase from 0% at 1 to 3 months to approximately 35% at 7 to 9 month   (MGI Ref ID J:108877)

Cdh23v/Cdh23+

        Background Not Specified
  • adipose tissue phenotype
  • increased total body fat amount   (MGI Ref ID J:175295)
  • behavior/neurological phenotype
  • increased vertical activity   (MGI Ref ID J:175295)
  • homeostasis/metabolism phenotype
  • decreased circulating amylase level   (MGI Ref ID J:175295)
  • decreased circulating cholesterol level   (MGI Ref ID J:175295)
    • decreased circulating HDL cholesterol level   (MGI Ref ID J:175295)
  • decreased circulating free fatty acid level   (MGI Ref ID J:175295)
  • increased circulating glucose level   (MGI Ref ID J:175295)
  • vision/eye phenotype
  • abnormal lens morphology   (MGI Ref ID J:175295)
  • growth/size/body phenotype
  • increased total body fat amount   (MGI Ref ID J:175295)

Cdh23v/Cdh23v

        involves: CBA/Ca
  • vision/eye phenotype
  • *normal* vision/eye phenotype
    • no histological abnormalities are seen and no evidence of photoreceptor cell loss is detected   (MGI Ref ID J:109546)
    • abnormal eye electrophysiology
      • at 100-130 days of age, electroretinography analysis showed that a-waves have reduced amplitudes and faster implicit times; the b-wave is attenuated, but the implicit time is not significantly faster   (MGI Ref ID J:109546)
  • hearing/vestibular/ear phenotype
  • abnormal inner hair cell stereociliary bundle morphology
    • disorganized in all homozygotes at all stages analyzed (E18.5, P4, and P20)   (MGI Ref ID J:108877)
  • abnormal outer hair cell stereociliary bundle morphology
    • homozygotes projected fewer recognizable stereocilia at E18.5   (MGI Ref ID J:108877)
    • arranged in irregular clumps rather than in normal "V"-shape at P4   (MGI Ref ID J:108877)
    • stereocilia remain disorganized at P20   (MGI Ref ID J:108877)
  • nervous system phenotype
  • abnormal inner hair cell stereociliary bundle morphology
    • disorganized in all homozygotes at all stages analyzed (E18.5, P4, and P20)   (MGI Ref ID J:108877)
  • abnormal outer hair cell stereociliary bundle morphology
    • homozygotes projected fewer recognizable stereocilia at E18.5   (MGI Ref ID J:108877)
    • arranged in irregular clumps rather than in normal "V"-shape at P4   (MGI Ref ID J:108877)
    • stereocilia remain disorganized at P20   (MGI Ref ID J:108877)

Cdh23v/Cdh23v

        mixed
  • behavior/neurological phenotype
  • impaired swimming
    • adults are unable to swim   (MGI Ref ID J:13130)
  • hearing/vestibular/ear phenotype
  • cochlear hair cell degeneration
    • at 2 weeks of age   (MGI Ref ID J:13130)
  • vestibular saccular macula degeneration
    • at 13 days   (MGI Ref ID J:13130)
  • nervous system phenotype
  • cochlear ganglion degeneration
    • at 4 weeks   (MGI Ref ID J:13130)
  • cochlear hair cell degeneration
    • at 2 weeks of age   (MGI Ref ID J:13130)

Cdh23v/Cdh23v

        involves: fancier's stocks
  • behavior/neurological phenotype
  • abnormal locomotor behavior
    • no wire mesh climbing is seen in males   (MGI Ref ID J:133042)
    • abnormal gait
      • waddling gait   (MGI Ref ID J:133042)
    • decreased vertical activity
      • no rearing behavior is seen in males   (MGI Ref ID J:133042)
  • abnormal response to novelty
    • decrease in the frequency of digging, wall gnawing, forepaw vibrations, wall leans, hair fluffing, and sniffing at wire mesh in males   (MGI Ref ID J:133042)
    • increase in the frequency of sniffing at the peat dust in males   (MGI Ref ID J:133042)
    • no food carrying is seen in males   (MGI Ref ID J:133042)
  • abnormal stationary movement
    • decrease in the frequency of single forepaw lifts in males   (MGI Ref ID J:133042)
  • circling   (MGI Ref ID J:133042)
  • decreased grooming behavior
    • reduced frequency of grooming in males   (MGI Ref ID J:133042)
  • tremors   (MGI Ref ID J:133042)
  • digestive/alimentary phenotype
  • abnormal defecation
    • reduced frequency   (MGI Ref ID J:133042)
  • hearing/vestibular/ear phenotype
  • deafness   (MGI Ref ID J:133042)

Cdh23v/Cdh23v

        Background Not Specified
  • adipose tissue phenotype
  • decreased percent body fat   (MGI Ref ID J:175295)
  • decreased total body fat amount   (MGI Ref ID J:175295)
  • behavior/neurological phenotype
  • abnormal behavior   (MGI Ref ID J:175295)
    • abnormal eating behavior   (MGI Ref ID J:175295)
    • absent pinna reflex   (MGI Ref ID J:175295)
    • decreased grip strength   (MGI Ref ID J:175295)
    • hyperactivity   (MGI Ref ID J:175295)
    • impaired coordination   (MGI Ref ID J:175295)
    • impaired righting response   (MGI Ref ID J:175295)
    • limb grasping   (MGI Ref ID J:175295)
    • stereotypic behavior   (MGI Ref ID J:175295)
    • tail dragging   (MGI Ref ID J:175295)
    • trunk curl   (MGI Ref ID J:175295)
    • unresponsive to tactile stimuli   (MGI Ref ID J:175295)
  • cardiovascular system phenotype
  • decreased heart rate   (MGI Ref ID J:175295)
  • homeostasis/metabolism phenotype
  • abnormal respiratory quotient   (MGI Ref ID J:175295)
    • increased respiratory quotient   (MGI Ref ID J:175295)
  • decreased circulating amylase level   (MGI Ref ID J:175295)
  • decreased circulating cholesterol level   (MGI Ref ID J:175295)
    • decreased circulating HDL cholesterol level   (MGI Ref ID J:175295)
    • decreased circulating LDL cholesterol level   (MGI Ref ID J:175295)
  • decreased circulating free fatty acid level   (MGI Ref ID J:175295)
  • decreased circulating glycerol level   (MGI Ref ID J:175295)
  • improved glucose tolerance   (MGI Ref ID J:175295)
  • increased carbon dioxide production   (MGI Ref ID J:175295)
  • increased energy expenditure   (MGI Ref ID J:175295)
  • increased oxygen consumption   (MGI Ref ID J:175295)
  • integument phenotype
  • unresponsive to tactile stimuli   (MGI Ref ID J:175295)
  • vision/eye phenotype
  • abnormal lens morphology   (MGI Ref ID J:175295)
  • growth/size/body phenotype
  • decreased percent body fat   (MGI Ref ID J:175295)
  • decreased total body fat amount   (MGI Ref ID J:175295)

Cdh23v/?

        Background Not Specified
  • hearing/vestibular/ear phenotype
  • abnormal auditory brainstem response   (MGI Ref ID J:175295)
View Research Applications

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

Cdh23v related

Developmental Biology Research
Defects in Cell Adhesion Molecules

Neurobiology Research
Hearing Defects
      deafness, nonsyndromic autosomal recessive 12 (DFNB12)
Vestibular Defects

Sensorineural Research
Hearing Defects
      deafness, nonsyndromic autosomal recessive 12 (DFNB12)
Vestibular Defects

Ednrbs related

Dermatology Research
Color and White Spotting Defects

Developmental Biology Research
Neural Crest Defects
Neurodevelopmental Defects

Neurobiology Research
Hearing Defects
Neurodevelopmental Defects
Receptor Defects

Sensorineural Research
Hearing Defects

Mlphln related

Dermatology Research
Color and White Spotting Defects

Sgk3fz related
Skin and Hair Texture Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Cdh23v
Allele Name waltzer
Allele Type Spontaneous
Common Name(s) v;
Strain of Originold mutant of the mouse fancy
Gene Symbol and Name Cdh23, cadherin 23 (otocadherin)
Chromosome 10
Gene Common Name(s) 4930542A03Rik; CDHR23; RIKEN cDNA 4930542A03 gene; USH1D; W; age related hearing loss 1; ahl; bob; bobby; bus; bustling; mdfw; modifier of deaf waddler; neuroscience mutagenesis facility, 112; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; nmf112; nmf181; nmf252; sals; salsa; v; waltzer;
General Note Viability and breeding ability are somewhat less than normal. Homozygotes show the typical circling, head-tossing, deafness, and hyperactivity of the circling mutants. Most of them are deaf from the beginning. Abnormalities of the inner ear include degeneration of the organ of Corti, spiral ganglion, stria vascularis, and saccular macula. Double heterozygotes with shaker-1 (Cdh23v/+ Myo7ash1/+) are deaf beginning at 3 to 6 months. They have changes similar to those of the homozygotes in the organ of Corti, stria vascularis, and spiral ganglion, but less severe and with much later onset (J:13130)(J:15164).
Molecular Note A single G nucleotide insertion at position 889 is predicted to cause a frameshift and premature termination of the encoded protein. [MGI Ref ID J:69985] [MGI Ref ID J:73941]
 
Allele Symbol Ednrbs
Allele Name piebald
Allele Type Spontaneous
Common Name(s) pied spotting; s;
Strain of Originold mutant of the mouse fancy
Gene Symbol and Name Ednrb, endothelin receptor type B
Chromosome 14
Gene Common Name(s) ABCDS; AU022549; ET-B; ET-BR; ETB; ETBR; ETR-b; ETRB; Ednra; HSCR; HSCR2; Sox10m1; WS4A; expressed sequence AU022549; piebald; s;
General Note Also called piebald spotting. This is a very old mutation of the mouse fancy, and was described in the scientific literature as early as 1920 (J23183). Some piebalds in existing stocks may be of independent origin. The white areas of the coat are completely lacking in melanocytes, and there is a reduction in the number of melanocytes in the choroid layer of the eye (J:15014, J:12970). There may also be defects in the structure of the iris, suggesting that pigment cells make some structural or inductive contribution to normal development (J:13123).
Molecular Note This mutation is allelic to a targeted mutation for this gene. Homozygous mice produce approximately 25% of the normal levels of transcript from this allele. RT-PCR analysis demonstrated that no alterations in the coding sequence would result in any alteration of the amino acid sequence. A 5.5 kb retrotransposon-like element is found in intron 1. About 75% of the mRNA produced is an aberrant 6.5 kb form lacking exons 2-6 but containing exon 1. The remaining 25% of the mRNA formed is of normal, 4.4 kb, size. [MGI Ref ID J:110573] [MGI Ref ID J:22206] [MGI Ref ID J:56133]
 
Allele Symbol Mlphln
Allele Name leaden
Allele Type Spontaneous
Common Name(s) ln;
Strain of OriginC57BR
Gene Symbol and Name Mlph, melanophilin
Chromosome 1
Gene Common Name(s) 2210418F23Rik; 5031433I09Rik; AW228792; D1Wsu84e; DNA segment, Chr 1, Wayne State University 84, expressed; SLAC2-A; Slac-2a; expressed sequence AW228792; l(1)-3Rk; l1Rk3; leaden; lethal, Chr 1, Roderick 3; ln;
Molecular Note This allele has a C to T transition at mRNA nucleotide position 266. This introduces a stop codon in the sequence of the normally spliced transcript and it also creates a new splice donor site in exon 2. Use of this alternative splice site yields a transcript with an in-frame 21 base pair deletion that deletes 7 amino acids from the translated protein. Northern blots failed to detect this size difference and did not find any change from normal in transcript expression level. [MGI Ref ID J:71302]
 
Allele Symbol Sgk3fz
Allele Name fuzzy
Allele Type Spontaneous
Strain of OriginCFW stock
Gene Symbol and Name Sgk3, serum/glucocorticoid regulated kinase 3
Chromosome 1
Gene Common Name(s) 2510015P22Rik; A330005P07Rik; CISK; RIKEN cDNA 2510015P22 gene; RIKEN cDNA A330005P07 gene; SGK2; SGKL; cytokine-independent survival kinase; frowzy; fuzzy; fy; fz;
Molecular Note This mutation comprises insertion of a single adenine following nucleotide 579 of the cDNA sequence, in a region encoded by exon 10 of the gene, that causes a shift in the amino acid reading frame and premature termination of protein translation following leucine 192 (Leu192Ter), which resides in the serine/threonine kinase domain. [MGI Ref ID J:125551]

Genotyping

Genotyping Information


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Baynash AG; Hosoda K; Giaid A; Richardson JA; Emoto N; Hammer RE; Yanagisawa M. 1994. Interaction of endothelin-3 with endothelin-B receptor is essential for development of epidermal melanocytes and enteric neurons. Cell 79(7):1277-85. [PubMed: 8001160]  [MGI Ref ID J:22207]

Bolz H; von Brederlow B; Ramirez A; Bryda EC; Kutsche K; Nothwang HG; Seeliger M; Cabrera Md; Vila MC; Molina OP; Kubisch C; Gal A. 2001. Mutation of CDH23, encoding a new member of the cadherin gene family, causes usher syndrome type 1D Nat Genet 27(1):108-12. [PubMed: 11138009]  [MGI Ref ID J:66740]

Hosoda K; Hammer RE; Richardson JA; Baynash AG; Cheung JC; Giaid A; Yanagisawa M. 1994. Targeted and natural (piebald-lethal) mutations of endothelin-B receptor gene produce megacolon associated with spotted coat color in mice. Cell 79(7):1267-76. [PubMed: 8001159]  [MGI Ref ID J:22206]

Cdh23v related

DEOL MS. 1956. The anatomy and development of the mutants pirouette, shaker-1 and waltzer in the mouse. Proc R Soc Lond B Biol Sci 145(919):206-13. [PubMed: 13336002]  [MGI Ref ID J:13130]

Di Palma F; Pellegrino R; Noben-Trauth K. 2001. Genomic structure, alternative splice forms and normal and mutant alleles of cadherin 23 (Cdh23). Gene 281(1-2):31-41. [PubMed: 11750125]  [MGI Ref ID J:73941]

El-Amraoui A; Petit C. 2005. Usher I syndrome: unravelling the mechanisms that underlie the cohesion of the growing hair bundle in inner ear sensory cells. J Cell Sci 118(Pt 20):4593-603. [PubMed: 16219682]  [MGI Ref ID J:102194]

Holme RH; Steel KP. 2004. Progressive hearing loss and increased susceptibility to noise-induced hearing loss in mice carrying a Cdh23 but not a Myo7a mutation. J Assoc Res Otolaryngol 5(1):66-79. [PubMed: 14648237]  [MGI Ref ID J:134369]

Holme RH; Steel KP. 2002. Stereocilia defects in waltzer (Cdh23), shaker1 (Myo7a) and double waltzer/shaker1 mutant mice. Hear Res 169(1-2):13-23. [PubMed: 12121736]  [MGI Ref ID J:108877]

Johnson KR; Zheng QY; Noben-Trauth K. 2006. Strain background effects and genetic modifiers of hearing in mice. Brain Res 1091(1):79-88. [PubMed: 16579977]  [MGI Ref ID J:110459]

KOCHER W. 1960. [Studies on the genetics and pathology of the development of 8 labyrinth mutants (deaf-waltzer-shaker mutants) in the mouse (Mus musculus).] Z Vererbungsl 91:114-40. [PubMed: 13853422]  [MGI Ref ID J:15164]

Keeler CE. 1931. . In: The Laboratory Mouse. Its Origin, Heredity, and Culture. Harvard Univ. Press, Cambridge, MA.  [MGI Ref ID J:30784]

Libby RT; Kitamoto J; Holme RH; Williams DS; Steel KP. 2003. Cdh23 mutations in the mouse are associated with retinal dysfunction but not retinal degeneration. Exp Eye Res 77(6):731-9. [PubMed: 14609561]  [MGI Ref ID J:109546]

Manji SS; Miller KA; Williams LH; Andreasen L; Siboe M; Rose E; Bahlo M; Kuiper M; Dahl HH. 2011. An ENU-Induced Mutation of Cdh23 Causes Congenital Hearing Loss, but No Vestibular Dysfunction, in Mice. Am J Pathol 179(2):903-14. [PubMed: 21689626]  [MGI Ref ID J:174130]

Mouse Genome Informatics and the Wellcome Trust Sanger Institute Mouse Genetics Project (MGP). 2011. Obtaining and Loading Phenotype Annotations from the Wellcome Trust Sanger Institute (WTSI) Mouse Resources Portal Database Release :.  [MGI Ref ID J:175295]

Reiners J; Nagel-Wolfrum K; Jurgens K; Marker T; Wolfrum U. 2006. Molecular basis of human Usher syndrome: deciphering the meshes of the Usher protein network provides insights into the pathomechanisms of the Usher disease. Exp Eye Res 83(1):97-119. [PubMed: 16545802]  [MGI Ref ID J:116295]

Rzadzinska AK; Steel KP. 2009. Presence of interstereocilial links in waltzer mutants suggests Cdh23 is not essential for tip link formation. Neuroscience 158(2):365-8. [PubMed: 18996172]  [MGI Ref ID J:145900]

Swank RT; Reddington M; Howlett O; Novak EK. 1991. Platelet storage pool deficiency associated with inherited abnormalities of the inner ear in the mouse pigment mutants muted and mocha. Blood 78(8):2036-44. [PubMed: 1912584]  [MGI Ref ID J:29151]

Wilson SM; Householder DB; Coppola V; Tessarollo L; Fritzsch B; Lee EC; Goss D; Carlson GA; Copeland NG; Jenkins NA. 2001. Mutations in Cdh23 Cause Nonsyndromic Hearing Loss in waltzer Mice. Genomics 74(2):228-33. [PubMed: 11386759]  [MGI Ref ID J:69985]

van Abeelen JH. 1966. Behavioural profiles of neurological mutant mice. Genetica 37(2):149-58. [PubMed: 5955164]  [MGI Ref ID J:133042]

Ednrbs related

Asher JH Jr; Friedman TB. 1990. Mouse and hamster mutants as models for Waardenburg syndromes in humans. J Med Genet 27(10):618-26. [PubMed: 2246770]  [MGI Ref ID J:200892]

BIELSCHOWSKY M; SCHOFIELD GC. 1962. Studies on megacolon in piebald mice. Aust J Exp Biol Med Sci 40:395-403. [PubMed: 13968171]  [MGI Ref ID J:12312]

BILLINGHAM RE; SILVERS WK. 1960. The melanocytes of mammals. Q Rev Biol 35:1-40. [PubMed: 13800713]  [MGI Ref ID J:15014]

Cantrell VA; Owens SE; Chandler RL; Airey DC; Bradley KM; Smith JR; Southard-Smith EM. 2004. Interactions between Sox10 and EdnrB modulate penetrance and severity of aganglionosis in the Sox10Dom mouse model of Hirschsprung disease. Hum Mol Genet 13(19):2289-301. [PubMed: 15294878]  [MGI Ref ID J:93622]

Carrasquillo MM; McCallion AS; Puffenberger EG; Kashuk CS; Nouri N; Chakravarti A. 2002. Genome-wide association study and mouse model identify interaction between RET and EDNRB pathways in Hirschsprung disease. Nat Genet 32(2):237-44. [PubMed: 12355085]  [MGI Ref ID J:112429]

Cattanach BM. 1961. A chemically-induced variegated-type position effect in the mouse. Z Vererbungsl 92:165-82. [PubMed: 13877379]  [MGI Ref ID J:160128]

Dang R; Sasaki N; Torigoe D; Agui T. 2012. Anatomic modifications in the enteric nervous system of JF1 mice with the classic piebald mutation. J Vet Med Sci 74(3):391-4. [PubMed: 22067082]  [MGI Ref ID J:193523]

Deol MS. 1971. Spotting genes and internal pigmentation patterns in the mouse. J Embryol Exp Morphol 26(1):123-33. [PubMed: 5565074]  [MGI Ref ID J:5220]

Dunn LC. 1920. Types of white spotting in mice Am Naturalist 54:465-95.  [MGI Ref ID J:23183]

Dunn LC; Charles DR. 1937. Studies on Spotting Patterns I. Analysis of Quantitative Variations in the Pied Spotting of the House Mouse. Genetics 22(1):14-42. [PubMed: 17246828]  [MGI Ref ID J:12952]

Dunn LC; Macdowell EC; Lebedeff GA. 1937. Studies on Spotting Patterns III. Interaction between Genes Affecting White Spotting and Those Affecting Color in the House Mouse. Genetics 22(2):307-18. [PubMed: 17246842]  [MGI Ref ID J:12954]

Dunn LC; Mohr J. 1952. An Association of Hereditary Eye Defects with White Spotting. Proc Natl Acad Sci U S A 38(10):872-5. [PubMed: 16589191]  [MGI Ref ID J:13123]

Eicher EM; Green MC. 1972. The T6 translocation in the mouse: its use in trisomy mapping, centromere localization, and cytological identification of linkage group 3. Genetics 71(4):621-32. [PubMed: 5055128]  [MGI Ref ID J:5291]

Gruneberg H. 1952. . In: The Genetics of the Mouse. Martinus Nijhoff, The Hague.  [MGI Ref ID J:30758]

Hauschka TS; Jacobs BB; Holdridge BA. 1968. Recessive yellow and its interaction with belted in the mouse. J Hered 59(6):339-41. [PubMed: 5713933]  [MGI Ref ID J:5110]

Hosoda K; Hammer RE; Richardson JA; Baynash AG; Cheung JC; Giaid A; Yanagisawa M. 1994. Targeted and natural (piebald-lethal) mutations of endothelin-B receptor gene produce megacolon associated with spotted coat color in mice. Cell 79(7):1267-76. [PubMed: 8001159]  [MGI Ref ID J:22206]

Keeler CE. 1931. The Independence of Dominant Spotting and Recessive Spotting ('Piebald') in the House Mouse. Proc Natl Acad Sci U S A 17(2):101-2. [PubMed: 16587618]  [MGI Ref ID J:153352]

Koide T; Moriwaki K; Uchida K; Mita A; Sagai T; Yonekawa H; Katoh H; Miyashita N; Tsuchiya K; Nielsen TJ; Shiroishi T. 1998. A new inbred strain JF1 established from Japanese fancy mouse carrying the classic piebald allele [published erratum appears in Mamm Genome 1998 Apr;9(4):344] Mamm Genome 9(1):15-9. [PubMed: 9434939]  [MGI Ref ID J:42684]

Kumagai T; Wada A; Tsudzuki M; Nishimura M; Kunieda T. 1998. Nucleotide sequence of endothelin-B receptor gene reveals origin of piebald mutation in laboratory mouse. Exp Anim 47(4):265-9. [PubMed: 10067171]  [MGI Ref ID J:56133]

Kuwaki T; Ling GY; Onodera M; Ishii T; Nakamura A; Ju KH; Cao WH; Kumada M; Kurihara H; Kurihara Y; Yazaki Y; Ohuchi T; Yanagisawa M; Fukuda Y. 1999. Endothelin in the central control of cardiovascular and respiratory functions. Clin Exp Pharmacol Physiol 26(12):989-94. [PubMed: 10626068]  [MGI Ref ID J:60070]

Lamoreux ML. 1999. Strain-specific white-spotting patterns in laboratory mice Pigment Cell Res 12(6):383-90. [PubMed: 10614578]  [MGI Ref ID J:106083]

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]

Matsushima Y; Shinkai Y; Kobayashi Y; Sakamoto M; Kunieda T; Tachibana M. 2002. A mouse model of Waardenburg syndrome type 4 with a new spontaneous mutation of the endothelin-B receptor gene. Mamm Genome 13(1):30-5. [PubMed: 11773966]  [MGI Ref ID J:76584]

Mayer TC. 1977. Enhancement of melanocyte development from piebald neural crest by a favorable tissue environment. Dev Biol 56(2):255-62. [PubMed: 849800]  [MGI Ref ID J:5782]

Mayer TC. 1967. Pigment cell migration in piebald mice. Dev Biol 15(6):521-35. [PubMed: 5340422]  [MGI Ref ID J:5036]

Mayer TC. 1967. Temporal skin factors influencing the development of melanoblasts in piebald mice. J Exp Zool 166(3):397-403. [PubMed: 4868265]  [MGI Ref ID J:5060]

Mayer TC. 1965. The development of piebald spotting in mice. Dev Biol 11:319-334. [PubMed: 5320391]  [MGI Ref ID J:12725]

McCallion AS; Stames E; Conlon RA; Chakravarti A. 2003. Phenotype variation in two-locus mouse models of Hirschsprung disease: tissue-specific interaction between Ret and Ednrb. Proc Natl Acad Sci U S A 100(4):1826-31. [PubMed: 12574515]  [MGI Ref ID J:81970]

Metallinos DL; Oppenheimer AJ; Rinchik EM; Russell LB; Dietrich W; Tilghman SM. 1994. Fine structure mapping and deletion analysis of the murine piebald locus. Genetics 136(1):217-23. [PubMed: 8138159]  [MGI Ref ID J:16291]

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]

Nadler EP; Boyle P; Murdock AD; Dilorenzo C; Barksdale EM; Ford HR. 2003. Newborn endothelin receptor type B mutant (piebald) mice have a higher resting anal sphincter pressure than newborn C57BL/6 mice. Contemp Top Lab Anim Sci 42(6):36-8. [PubMed: 14615959]  [MGI Ref ID J:86743]

Oak Ridge National Laboratory. 2005. Information obtained from the Oak Ridge National Laboratory Mutant Mouse Database (ORNL), Oak Ridge, TN Unpublished :.  [MGI Ref ID J:100221]

Ohuchi T; Kuwaki T; Ling GY; Dewit D; Ju KH; Onodera M; Cao WH; Yanagisawa M; Kumada M. 1999. Elevation of blood pressure by genetic and pharmacological disruption of the ETB receptor in mice. Am J Physiol 276(4 Pt 2):R1071-7. [PubMed: 10198387]  [MGI Ref ID J:54703]

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]

Pavan WJ; Mac S; Cheng M; Tilghman SM. 1995. Quantitative trait loci that modify the severity of spotting in piebald mice. Genome Res 5(1):29-41. [PubMed: 8717053]  [MGI Ref ID J:28905]

Ro S; Hwang SJ; Muto M; Jewett WK; Spencer NJ. 2006. Anatomic modifications in the enteric nervous system of piebald mice and physiological consequences to colonic motor activity. Am J Physiol Gastrointest Liver Physiol 290(4):G710-8. [PubMed: 16339294]  [MGI Ref ID J:109114]

Silvers WK. 1979. The Coat Colors of Mice; A Model for Mammalian Gene Action and Interaction. In: The Coat Colors of Mice. Springer-Verlag, New York.  [MGI Ref ID J:78801]

Sviderskaya EV; Easty DJ; Bennett DC. 1998. Impaired growth and differentiation of diploid but not immortal melanoblasts from endothelin receptor B mutant (piebald) mice. Dev Dyn 213(4):452-63. [PubMed: 9853966]  [MGI Ref ID J:51286]

Yamada T; Ohtani S; Sakurai T; Tsuji T; Kunieda T; Yanagisawa M. 2006. Reduced expression of the endothelin receptor type B gene in piebald mice caused by insertion of a retroposon-like element in intron 1. J Biol Chem 281(16):10799-807. [PubMed: 16500897]  [MGI Ref ID J:110573]

Mlphln related

Anderson MG; Hawes NL; Trantow CM; Chang B; John SW. 2008. Iris phenotypes and pigment dispersion caused by genes influencing pigmentation. Pigment Cell Melanoma Res 21(5):565-78. [PubMed: 18715234]  [MGI Ref ID J:141035]

Fisher RA. 1953. The linkage of polydactyly with leaden in the house mouse. Heredity 7:91-95.  [MGI Ref ID J:12979]

Hauschka TS; Jacobs BB; Holdridge BA. 1968. Recessive yellow and its interaction with belted in the mouse. J Hered 59(6):339-41. [PubMed: 5713933]  [MGI Ref ID J:5110]

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]

Hume AN; Collinson LM; Hopkins CR; Strom M; Barral DC; Bossi G; Griffiths GM; Seabra MC. 2002. The leaden gene product is required with Rab27a to recruit myosin Va to melanosomes in melanocytes. Traffic 3(3):193-202. [PubMed: 11886590]  [MGI Ref ID J:105323]

Hume AN; Tarafder AK; Ramalho JS; Sviderskaya EV; Seabra MC. 2006. A coiled-coil domain of melanophilin is essential for Myosin Va recruitment and melanosome transport in melanocytes. Mol Biol Cell 17(11):4720-35. [PubMed: 16914517]  [MGI Ref ID J:117973]

Karolyi IJ; Dootz GA; Halsey K; Beyer L; Probst FJ; Johnson KR; Parlow AF; Raphael Y; Dolan DF; Camper SA. 2007. Dietary thyroid hormone replacement ameliorates hearing deficits in hypothyroid mice. Mamm Genome 18(8):596-608. [PubMed: 17899304]  [MGI Ref ID J:125708]

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]

Matesic LE; Yip R; Reuss AE; Swing DA; O'Sullivan TN; Fletcher CF; Copeland NG; Jenkins NA. 2001. Mutations in Mlph, encoding a member of the Rab effector family, cause the melanosome transport defects observed in leaden mice. Proc Natl Acad Sci U S A 98(18):10238-43. [PubMed: 11504925]  [MGI Ref ID J:71302]

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; 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 JM. 1933. "Leaden", a recent color mutation in the house mouse. Am Naturalist 67:278-283.  [MGI Ref ID J:17162]

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

Novak EK; Hui SW; Swank RT. 1984. Platelet storage pool deficiency in mouse pigment mutations associated with seven distinct genetic loci. Blood 63(3):536-44. [PubMed: 6696991]  [MGI Ref ID J:7327]

Silvers WK. 1979. The Coat Colors of Mice; A Model for Mammalian Gene Action and Interaction. In: The Coat Colors of Mice. Springer-Verlag, New York.  [MGI Ref ID J:78801]

Singh RK; Mizuno K; Wasmeier C; Wavre-Shapton ST; Recchi C; Catz SD; Futter C; Tolmachova T; Hume AN; Seabra MC. 2013. Distinct and opposing roles for Rab27a/Mlph/MyoVa and Rab27b/Munc13-4 in mast cell secretion. FEBS J 280(3):892-903. [PubMed: 23281710]  [MGI Ref ID J:211540]

Stephenson DA; Glenister PH; Hornby JE. 1985. Site of beige (bg) and leaden (ln) pigment gene expression determined by recombinant embryonic skin grafts and aggregation mouse chimaeras employing sash (Wsh) homozygotes. Genet Res 46(2):193-205. [PubMed: 3910518]  [MGI Ref ID J:8167]

Sweet SE; Quevedo WC Jr. 1968. Role of melanocyte morphology in pigmentation of mouse hair. Anat Rec 162(2):243-54. [PubMed: 5726144]  [MGI Ref ID J:5095]

Ward RD; Stone BM; Raetzman LT; Camper SA. 2006. Cell proliferation and vascularization in mouse models of pituitary hormone deficiency. Mol Endocrinol 20(6):1378-90. [PubMed: 16556738]  [MGI Ref ID J:108961]

Sgk3fz related

Campagna DR; Custodio AO; Antiochos BB; Cirlan MV; Fleming MD. 2008. Mutations in the Serum/Glucocorticoid regulated kinase 3 (Sgk3) are responsible for the mouse Fuzzy (fz) hair phenotype J Invest Dermatol 128(3):730-2. [PubMed: 17914447]  [MGI Ref ID J:125551]

DICKIE MM; WOOLLEY GW. 1950. Fuzzy mice. J Hered 41(7):193-6. [PubMed: 14779004]  [MGI Ref ID J:90]

Hogan ME; King LE Jr; Sundberg JP. 1995. Defects of pelage hairs in 20 mouse mutations. J Invest Dermatol 104(5 Suppl):31S-32S. [PubMed: 7738386]  [MGI Ref ID J:25255]

Hume AN; Collinson LM; Hopkins CR; Strom M; Barral DC; Bossi G; Griffiths GM; Seabra MC. 2002. The leaden gene product is required with Rab27a to recruit myosin Va to melanosomes in melanocytes. Traffic 3(3):193-202. [PubMed: 11886590]  [MGI Ref ID J:105323]

MANN SJ. 1964. THE HAIR OF THE FUZZY MOUSE. J Hered 55:121-3. [PubMed: 14170401]  [MGI Ref ID J:13086]

Mayer TC; Mittelberger JA; Green MC. 1974. The site of action of the fuzzy locus (fz) in the mouse, as determined by dermal-epidermal recombinations. J Embryol Exp Morphol 32(3):707-13. [PubMed: 4618567]  [MGI Ref ID J:5551]

Monroe; Major MH; Hawkins MS. 1958. Hair abnormality (fz) Mouse News Lett 19:37.  [MGI Ref ID J:13377]

Novak EK; Hui SW; Swank RT. 1984. Platelet storage pool deficiency in mouse pigment mutations associated with seven distinct genetic loci. Blood 63(3):536-44. [PubMed: 6696991]  [MGI Ref ID J:7327]

Sundberg JP (ed.). 1994. Handbook of Mouse Mutations with Skin and Hair Abnormalities: Animal Models and Biomedical Tools. In: Handbook of Mouse Mutations with Skin and Hair Abnormalities: Animal Models and Biomedical Tools. CRC Press, Boca Raton.  [MGI Ref ID J:30359]

Trigg MJ. 1972. Hair growth in mouse mutants affecting coat texture. J Zool 168:165-198.  [MGI Ref ID J:15247]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3300.00
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.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. 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).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $4290.00
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.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. 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).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   None Available
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Important Note

This strain is homozygous for fz, Mlphln, and Ednrbs, and is segregating for Cdh23v.

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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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"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.

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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.

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