Strain Name:

SI/Col Tyrp1b Dnah11iv/J

Stock Number:

001045

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Availability:

Cryopreserved - Ready for recovery

Common Names: situs inversus;    

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

Former Names SI/Col Tyrp1b Dnahc11iv/J    (Changed: 28-MAY-13 )
Type Mutant Strain;
Additional information on Genetically Engineered and Mutant Mice.
Type Inbred Strain;
Additional information on Inbred Strains.
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Specieslaboratory mouse
H2 Haplotyped
GenerationF94p
Generation Definitions

Appearance
brown agouti
Related Genotype: A/A Tyrp1b/Tyrp1b

Description
DNAHC11 is important for developmental control of organ positioning in the left-right axis such that homozygosity for the situs inversus viscerum (iv) mutant allele can result not only in inverse placement of the visceral and thoracic organs, but also in anomalous positioning and interactions of blood vessels (including the hepatic portal, inferior vena cava, and azygos vein) and modified shape of organs and blood vessels, including abnormal lobation of lungs or liver. Approximately 50% of mice homozygous for Dnah11iv have situs inversus, and the likelihood of situs inversus is not impacted by whether the homozygous parent has situs inversus. This indicates that wild type Dnah11 instructs left-right asymmetry, and in the absence of functional Dnah11 the direction of this asymmetry is random. Heterotaxia is found in less than half of homozygotes and occurs equally in those that do and do not have situs inversus. While heterotaxia may be impacted by genetic background, the incidence of situs inversus has not shown this variation. Situs inversus can be identified shortly after birth, until the skin thickens at approximately day 5, by viewing the location of the milk-filled stomach through the skin. Homozygotes are generally viable and do breed, although poorreproductive performance with a high rate of resorption has been reported by Brown et al. (Development 1989). Some premature death has been reported and may be caused by deformities of the cardiac loop. (Hummel and Chapman, 1959; Layton 1976; Brown et al., 1989; Icardo and Colvee, 2001.)

Development
In 1956 Katherine Hummel reported finding situs inversus viscerum (iv) in 6 out of 42 mice in the F3 generation from a cross of a C3H/e female with an my/my male. This my/my male was likely from the line that was then being inbred to become My/Hu (see stock#000265). The my mutation was bred out of this new mutant stock and in 1972 the iv-bearing stock was transferred from Katherine Hummel to Robert Collins, both at The Jackson Laboratory. Collins began inbreeding from the outbred stock in 1975 and this generated the strain SI/Col which is homozygous for Dnah11iv, a, and Tyrp1b. SI/Col reached F62 in 1994 and F88 in 2004. Embryos were generated for cyropreservation from homozygous parents in 1997, when the strain was at generation F73, and again in 2007, when the strain was at generation F94.

Control Information

  Control
   None Available
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Dnah11iv allele
000773   B6;129T-Dnah11iv/J
View Strains carrying   Dnah11iv     (1 strain)

Strains carrying   Tyrp1b allele
000004   ABP/LeJ
000571   B6.Cg-Whrnwi Tyrp1b/+ +/J
000027   B6.D-Tyrp1b Dock7m/J
000670   DBA/1J
000265   MY/HuLeJ
000064   STOCK a Tyrp1b Pmelsi/J
002238   STOCK a Tyrp1b shmy/J
001432   STOCK a/a Tyrp1b Ndc1sks/Tyrp1b +/J
000594   STOCK T(2;8)26H a/T(2;8)26H a Tyrp1+/Tyrp1b/J
001101   STOCK T(3;4)5Rk Tyrp1b/J
View Strains carrying   Tyrp1b     (10 strains)

View Strains carrying other alleles of Dnah11     (6 strains)

Strains carrying other alleles of Tyrp1
000957   AKXD28/TyJ
000093   B6.B10(D1)-Tyrp1b-c/J
008684   B6.Cg-Rag1tm1Mom Tyrp1B-w Tg(Tcra,Tcrb)9Rest/J
017764   B6Ei.LT-Y(IsXPAR;Y)Ei Tyrp1B-lt/EiJ
000068   C57BL/6J-Tyrp1b-J/J
000671   DBA/2J
006252   LT/SvEiJ
002142   STOCK 11R30m/J
000594   STOCK T(2;8)26H a/T(2;8)26H a Tyrp1+/Tyrp1b/J
View Strains carrying other alleles of Tyrp1     (9 strains)

Phenotype

Phenotype Information

View Phenotypic Data

Phenotypic Data
Mouse Phenome Database
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).
Ciliary Dyskinesia, Primary, 7; CILD7
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Albinism, Oculocutaneous, Type III; OCA3   (TYRP1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Dnah11iv/Dnah11iv

        SI/Col Tyrp1b Dnah11iv/J
  • cardiovascular system phenotype
  • abnormal cardiovascular system morphology
    • homozygotes exhibit various cardiovascular, spleen and liver defects that may or may not co-occur in the same mouse   (MGI Ref ID J:4058)
    • 7.6% display cardiac lesions, which are more common in females (11.5%) than in males (3.1%) and in fetuses (16%) than in adults (3.6%)   (MGI Ref ID J:4058)
    • abnormal heart atrium morphology   (MGI Ref ID J:4058)
      • abnormal heart atrium auricular region morphology
        • 50.2% exhibit mirror-image arrangement of the atrial appendages   (MGI Ref ID J:4058)
        • incidence of isomerism of the atrial appendages is significantly higher in females (7.4%) than in males (1.6%) and in fetuses (12%) than in adults (1.4%)   (MGI Ref ID J:4058)
      • left atrial isomerism
        • 3.3% have left atrial isomerism   (MGI Ref ID J:4058)
      • right atrial isomerism
        • 1.5% have right atrial isomerism   (MGI Ref ID J:4058)
    • abnormal hepatic portal vein morphology
      • 26.6% exhibit a ventral portal vein, with the incidence of the ventral location significantly higher in females (33.1%) than in males (18.9%)   (MGI Ref ID J:4058)
    • abnormal inferior vena cava morphology
      • 17.8% show an abnormal connection of the inferior caval vein, with the abnormal arrangement more common in fetuses (29.3%) than in adults (15%)   (MGI Ref ID J:4058)
  • growth/size/body phenotype
  • left atrial isomerism
    • 3.3% have left atrial isomerism   (MGI Ref ID J:4058)
  • left pulmonary isomerism
    • a minority of both situs inversus and situs solitus mice have three lung lobes on the right, three lung lobes on the left, and one or two caudate lobes, instead of the normal three lobes on the right, one lobe on the left and one caudate lobe   (MGI Ref ID J:148465)
  • right atrial isomerism
    • 1.5% have right atrial isomerism   (MGI Ref ID J:4058)
  • right pulmonary isomerism
    • a minority of both situs inversus and situs solitus mice have only one lung lobe on the right, one on the left and either one or no caudate lobe, instead of the normal three lobes on the right, one lobe on the left and one caudate lobe   (MGI Ref ID J:148465)
  • situs inversus   (MGI Ref ID J:148465)
    • seen in about 50% of homozygotes   (MGI Ref ID J:4058)
  • hematopoietic system phenotype
  • abnormal spleen morphology
    • 36.4% exhibit an abnormal spleen, which is seen more often in females (44.6%) than in males (26.8%)   (MGI Ref ID J:4058)
    • spleen abnormalities include fissured, bilobed, elongated or absent spleen   (MGI Ref ID J:4058)
  • immune system phenotype
  • abnormal spleen morphology
    • 36.4% exhibit an abnormal spleen, which is seen more often in females (44.6%) than in males (26.8%)   (MGI Ref ID J:4058)
    • spleen abnormalities include fissured, bilobed, elongated or absent spleen   (MGI Ref ID J:4058)
  • liver/biliary system phenotype
  • abnormal liver morphology
    • abnormal arrangement of the liver, which is more common in females (42.6%) than in males (26.8%)   (MGI Ref ID J:4058)
    • a missing liver lobe and associated abnormal path of the inferior vena cava is found in a minority of both situs solitus and situs inversus mice, with the missing lobe usually on the right side in situs solitus and the left side in situs inversus   (MGI Ref ID J:148465)
  • reproductive system phenotype
  • abnormal embryo implantation
    • females with bilobed or fissured spleens or with abnormal livers have fewer implantation sites than those with normal spleens and livers   (MGI Ref ID J:4058)
  • reduced fertility
    • only 58% of dams with copulatory plugs are pregnant 19 days post-copulation   (MGI Ref ID J:148465)
  • homeostasis/metabolism phenotype
  • increased physiological sensitivity to xenobiotic
    • treatment with acetazolamide on day 10 of pregnancy results in an increased rate of resorption, decreased fetal weight, and increased limb defects at embryonic day 19 compared with MF1 outbred mice   (MGI Ref ID J:148465)
  • limbs/digits/tail phenotype
  • abnormal autopod morphology
    • treatment of the pregnant dam with acetazolamide results in forelimb abnormalities, most commonly (66% of defects) the absence of the fifth digit, in more severe cases (11% of defects) the absence of the third, forth, and fifth digits, and in rare cases the loss of the ulna of the affected forearm   (MGI Ref ID J:148465)
    • culturing day 9 fetuses in misonidazole for 48 hours results in limb-bud abnormalities   (MGI Ref ID J:148465)
    • these forelimb birth defects induced by acetazolamide or misonidazole follow the situs of the developing embryo such that those with situs inversus have defects in the left forelimb and those with situs solitus have defects in the right forelimb, which is where most defects are found in normal fetuses exposed to these drugs   (MGI Ref ID J:148465)
  • respiratory system phenotype
  • left pulmonary isomerism
    • a minority of both situs inversus and situs solitus mice have three lung lobes on the right, three lung lobes on the left, and one or two caudate lobes, instead of the normal three lobes on the right, one lobe on the left and one caudate lobe   (MGI Ref ID J:148465)
  • right pulmonary isomerism
    • a minority of both situs inversus and situs solitus mice have only one lung lobe on the right, one on the left and either one or no caudate lobe, instead of the normal three lobes on the right, one lobe on the left and one caudate lobe   (MGI Ref ID J:148465)

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

Dnah11iv/Dnah11iv

        Background Not Specified
  • embryogenesis phenotype
  • abnormal embryonic cilium morphology
    • the nodal cilia are rigid and appear frozen   (MGI Ref ID J:109561)
  • absent nodal flow
    • nodal cilia seldom move and beads added to the extraembryonic fluid fail to display any net directional movement indicating a lack of nodal flow   (MGI Ref ID J:109561)
  • growth/size/body phenotype
  • heterotaxia
    • situs inversus with incomplete penetrance and variable expressivity can yield complete situs inversus of thoracic and abdominal viscera and associated blood vessels, incomplete situs inversus, anomalous relationship of the postcaval and azygous veins, anomalous positioning of the hepatic portal vein, flatter more elongated spleen, and diminished or altered lobulation of the liver or lung   (MGI Ref ID J:212)
    • situs inversus   (MGI Ref ID J:212)
  • cellular phenotype
  • abnormal embryonic cilium morphology
    • the nodal cilia are rigid and appear frozen   (MGI Ref ID J:109561)
  • absent nodal flow
    • nodal cilia seldom move and beads added to the extraembryonic fluid fail to display any net directional movement indicating a lack of nodal flow   (MGI Ref ID J:109561)
View Research Applications

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

Dnah11iv related

Developmental Biology Research
Internal/Organ Defects
      heart
      heart: vasculature
      situs inversus

Tyrp1b related

Dermatology Research
Color and White Spotting Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Dnah11iv
Allele Name situs inversus viscerum
Allele Type Spontaneous
Common Name(s) iv;
Strain of Origin(C3HeB/Fe x STOCK Frem2)F3
Gene Symbol and Name Dnah11, dynein, axonemal, heavy chain 11
Chromosome 12
Gene Common Name(s) CILD7; DNAHBL; DNAHC11; DNHBL; DPL11; Dnahc11; Mutant line 1203; Mutant line 1279; Mutant line 1289; Mutant line 1727; Mutant line 598; b2b1203Clo; b2b1279Clo; b2b1289Clo; b2b1727Clo; b2b598Clo; iv; lrd; situs inversus viscerum;
General Note About 50 per cent of homozygotes showed left-right transposition of stomach and abdominal viscera. About half of all the homozygotes showed discordance in asymmetry between the stomach and the major abdominal and thoracic veins, the discordance occurringwith similar frequency in mice with normal and reversed viscera. In the stock examined by Hummel and Chapman (J:212) penetrance was found to be 71 per cent when mice were classified by both these criteria. Layton (J:5788) has postulated that the wild-type allele of the Dnahc11 locus is necessary for development of the normal asymmetrical configuration of the viscera. In iv/iv mice, this control is absent, allowing random direction of the asymmetry and thus accounting for the fact that only 50 per cent ofthe homozygotes show reversed asymmetry.
Molecular Note A G-to-A transition mutation led to a substitution of a glutamate to a lysine in the encoded protein. This residue is located between the second and third P-loop motifs, a highly conserved region that constitutes the motor domain. [MGI Ref ID J:44093]
 
Allele Symbol Tyrp1b
Allele Name brown
Allele Type Spontaneous
Common Name(s) b;
Strain of Originold mutant of the mouse fancy
Gene Symbol and Name Tyrp1, tyrosinase-related protein 1
Chromosome 4
Gene Common Name(s) B; CAS2; CATB; GP75; OCA3; TRP; TRP-1; TRP1; TYRP; Tyrp; b; b-PROTEIN; brown; iris stromal atrophy; isa; tyrosinase-related protein;
Molecular Note A G-to-A transition point mutation at position 329 was shown by revertant analysis to be responsible for the mutant phenotype seen in the brown mutant. This mutation is predicted to change a cysteine residue to a tyrosine in the encoded protein. Three other point mutations in the brown sequence were identified, but do not contribute to the mutant phenotype. [MGI Ref ID J:44435]

Genotyping

Genotyping Information


Helpful Links

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References

References provided by MGI

Selected Reference(s)

Brown NA; Hoyle CI; McCarthy A; Wolpert L. 1989. The development of asymmetry: the sidedness of drug-induced limb abnormalities is reversed in situs inversus mice. Development 107(3):637-42. [PubMed: 2612382]  [MGI Ref ID J:148465]

Hummel KP; Chapman D. 1956. Situs Viscerum Inversus Mouse News Lett 14:21.  [MGI Ref ID J:24771]

Hummel KP; Chapman DB. 1959. Visceral inversion and associated anomalies in the mouse J Hered 50:9-13.  [MGI Ref ID J:212]

Lowe LA; Supp DM; Sampath K; Yokoyama T; Wright CV; Potter SS; Overbeek P; Kuehn MR. 1996. Conserved left-right asymmetry of nodal expression and alterations in murine situs inversus [see comments] Nature 381(6578):158-61. [PubMed: 8610013]  [MGI Ref ID J:32936]

Additional References

Brueckner M; D'Eustachio P; Horwich AL. 1989. Linkage mapping of a mouse gene, iv, that controls left-right asymmetry of the heart and viscera. Proc Natl Acad Sci U S A 86(13):5035-8. [PubMed: 2740340]  [MGI Ref ID J:9863]

Icardo JM; Colvee E. 2001. Origin and course of the coronary arteries in normal mice and in iv/iv mice. J Anat 199(Pt 4):473-82. [PubMed: 11693308]  [MGI Ref ID J:73207]

Layton WM Jr. 1976. Random determination of a developmental process: reversal of normal visceral asymmetry in the mouse. J Hered 67(6):336-8. [PubMed: 1021593]  [MGI Ref ID J:5788]

Oh SP; Li E. 2002. Gene-dosage-sensitive genetic interactions between inversus viscerum (iv), nodal, and activin type IIB receptor (ActRIIB) genes in asymmetrical patterning of the visceral organs along the left-right axis. Dev Dyn 224(3):279-90. [PubMed: 12112458]  [MGI Ref ID J:78247]

Okada Y; Nonaka S; Tanaka Y; Saijoh Y; Hamada H; Hirokawa N. 1999. Abnormal nodal flow precedes situs inversus in iv and inv mice. Mol Cell 4(4):459-68. [PubMed: 10549278]  [MGI Ref ID J:109561]

Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11. [PubMed: 15081119]  [MGI Ref ID J:89298]

Supp DM; Witte DP; Potter SS; Brueckner M. 1997. Mutation of an axonemal dynein affects left-right asymmetry in inversus viscerum mice. Nature 389(6654):963-6. [PubMed: 9353118]  [MGI Ref ID J:44093]

Dnah11iv related

Adachi H; Saijoh Y; Mochida K; Ohishi S; Hashiguchi H; Hirao A; Hamada H. 1999. Determination of left/right asymmetric expression of nodal by a left side-specific enhancer with sequence similarity to a lefty-2 enhancer. Genes Dev 13(12):1589-600. [PubMed: 10385627]  [MGI Ref ID J:56146]

Campione M; Ros MA; Icardo JM; Piedra E; Christoffels VM; Schweickert A; Blum M; Franco D; Moorman AF. 2001. Pitx2 expression defines a left cardiac lineage of cells: evidence for atrial and ventricular molecular isomerism in the iv/iv mice. Dev Biol 231(1):252-64. [PubMed: 11180966]  [MGI Ref ID J:67751]

Franco D; Kelly R; Moorman AF; Lamers WH; Buckingham M; Brown NA. 2001. MLC3F transgene expression in iv mutant mice reveals the importance of left-right signalling pathways for the acquisition of left and right atrial but not ventricular compartment identity. Dev Dyn 221(2):206-15. [PubMed: 11376488]  [MGI Ref ID J:69780]

Golding JP; Partridge TA; Beauchamp JR; King T; Brown NA; Gassmann M; Zammit PS. 2004. Mouse myotomes pairs exhibit left-right asymmetric expression of MLC3F and alpha-skeletal actin. Dev Dyn 231(4):795-800. [PubMed: 15499557]  [MGI Ref ID J:93818]

Goto K; Kurashima R; Gokan H; Inoue N; Ito I; Watanabe S. 2010. Left-right asymmetry defect in the hippocampal circuitry impairs spatial learning and working memory in iv mice. PLoS One 5(11):e15468. [PubMed: 21103351]  [MGI Ref ID J:166986]

Icardo JM; Colvee E. 2001. Origin and course of the coronary arteries in normal mice and in iv/iv mice. J Anat 199(Pt 4):473-82. [PubMed: 11693308]  [MGI Ref ID J:73207]

Kawakami R; Dobi A; Shigemoto R; Ito I. 2008. Right isomerism of the brain in inversus viscerum mutant mice. PLoS ONE 3(4):e1945. [PubMed: 18414654]  [MGI Ref ID J:134302]

Kawasumi A; Nakamura T; Iwai N; Yashiro K; Saijoh Y; Belo JA; Shiratori H; Hamada H. 2011. Left-right asymmetry in the level of active Nodal protein produced in the node is translated into left-right asymmetry in the lateral plate of mouse embryos. Dev Biol 353(2):321-30. [PubMed: 21419113]  [MGI Ref ID J:173964]

Layton WM Jr. 1976. Random determination of a developmental process: reversal of normal visceral asymmetry in the mouse. J Hered 67(6):336-8. [PubMed: 1021593]  [MGI Ref ID J:5788]

Layton WM; Layton MW; Binder M; Kurnit DM; Hanzlik AJ; Van Keuren M; Biddle FG. 1993. Expression of the IV (reversed and/or heterotaxic) phenotype in SWV mice. Teratology 47(6):595-602. [PubMed: 8367832]  [MGI Ref ID J:11908]

Matin A; Collin GB; Varnum DS; Nadeau JH. 1998. Testicular teratocarcinogenesis in mice--a review. APMIS 106(1):174-82. [PubMed: 9524576]  [MGI Ref ID J:46683]

Meno C; Ito Y; Saijoh Y; Matsuda Y; Tashiro K; Kuhara S; Hamada H. 1997. Two closely-related left-right asymmetrically expressed genes, lefty-1 and lefty-2: their distinct expression domains, chromosomal linkage and direct neuralizing activity in Xenopus embryos. Genes Cells 2(8):513-24. [PubMed: 9348041]  [MGI Ref ID J:49270]

Meno C; Saijoh Y; Fujii H; Ikeda M; Yokoyama T; Yokoyama M; Toyoda Y; Hamada H. 1996. Left-right asymmetric expression of the TGF beta-family member lefty in mouse embryos. Nature 381(6578):151-5. [PubMed: 8610011]  [MGI Ref ID J:32932]

Metzger RJ; Klein OD; Martin GR; Krasnow MA. 2008. The branching programme of mouse lung development. Nature 453(7196):745-50. [PubMed: 18463632]  [MGI Ref ID J:136198]

Meyer RA; Cohen MF; Recalde S; Zakany J; Bell SM; Scott WJ Jr; Lo CW. 1997. Developmental regulation and asymmetric expression of the gene encoding Cx43 gap junctions in the mouse limb bud. Dev Genet 21(4):290-300. [PubMed: 9438343]  [MGI Ref ID J:45219]

Nakamura T; Mine N; Nakaguchi E; Mochizuki A; Yamamoto M; Yashiro K; Meno C; Hamada H. 2006. Generation of robust left-right asymmetry in the mouse embryo requires a self-enhancement and lateral-inhibition system. Dev Cell 11(4):495-504. [PubMed: 17011489]  [MGI Ref ID J:119676]

Novobrantseva TI; Martin VM; Pelanda R; Muller W; Rajewsky K ; Ehlich A. 1999. Rearrangement and expression of immunoglobulin light chain genes can precede heavy chain expression during normal B cell development in mice. J Exp Med 189(1):75-88. [PubMed: 9874565]  [MGI Ref ID J:52061]

Oh SP; Li E. 2002. Gene-dosage-sensitive genetic interactions between inversus viscerum (iv), nodal, and activin type IIB receptor (ActRIIB) genes in asymmetrical patterning of the visceral organs along the left-right axis. Dev Dyn 224(3):279-90. [PubMed: 12112458]  [MGI Ref ID J:78247]

Okada Y; Nonaka S; Tanaka Y; Saijoh Y; Hamada H; Hirokawa N. 1999. Abnormal nodal flow precedes situs inversus in iv and inv mice. Mol Cell 4(4):459-68. [PubMed: 10549278]  [MGI Ref ID J:109561]

Okada Y; Takeda S; Tanaka Y; Belmonte JC; Hirokawa N. 2005. Mechanism of nodal flow: a conserved symmetry breaking event in left-right axis determination. Cell 121(4):633-44. [PubMed: 15907475]  [MGI Ref ID J:98946]

Piedra ME; Icardo JM; Albajar M; Rodriguez-Rey JC; Ros MA. 1998. Pitx2 participates in the late phase of the pathway controlling left-right asymmetry. Cell 94(3):319-24. [PubMed: 9708734]  [MGI Ref ID J:49089]

Saijoh Y; Adachi H; Sakuma R; Yeo CY; Yashiro K; Watanabe M; Hashiguchi H; Mochida K; Ohishi S; Kawabata M; Miyazono K; Whitman M; Hamada H. 2000. Left-right asymmetric expression of lefty2 and nodal is induced by a signaling pathway that includes the transcription factor FAST2. Mol Cell 5(1):35-47. [PubMed: 10678167]  [MGI Ref ID J:60152]

Saijoh Y; Oki S; Tanaka C; Nakamura T; Adachi H; Yan YT; Shen MM; Hamada H. 2005. Two nodal-responsive enhancers control left-right asymmetric expression of Nodal. Dev Dyn 232(4):1031-6. [PubMed: 15736223]  [MGI Ref ID J:97079]

Schweickert A; Deissler K; Britsch S; Albrecht M; Ehmann H; Mauch V; Gaio U; Blum M. 2008. Left-asymmetric expression of Galanin in the linear heart tube of the mouse embryo is independent of the nodal co-receptor gene cryptic. Dev Dyn 237(12):3557-64. [PubMed: 18773496]  [MGI Ref ID J:141520]

Seo JW; Brown NA; Ho SY; Anderson RH. 1992. Abnormal laterality and congenital cardiac anomalies. Relations of visceral and cardiac morphologies in the iv/iv mouse. Circulation 86(2):642-50. [PubMed: 1638728]  [MGI Ref ID J:4058]

Stevens J; Ermakov A; Braganca J; Hilton H; Underhill P; Bhattacharya S; Brown NA; Norris DP. 2010. Analysis of the asymmetrically expressed Ablim1 locus reveals existence of a lateral plate Nodal-independent left sided signal and an early, left-right independent role for nodal flow. BMC Dev Biol 10:54. [PubMed: 20487527]  [MGI Ref ID J:161404]

Supp DM; Witte DP; Potter SS; Brueckner M. 1997. Mutation of an axonemal dynein affects left-right asymmetry in inversus viscerum mice. Nature 389(6654):963-6. [PubMed: 9353118]  [MGI Ref ID J:44093]

Takao D; Nemoto T; Abe T; Kiyonari H; Kajiura-Kobayashi H; Shiratori H; Nonaka S. 2013. Asymmetric distribution of dynamic calcium signals in the node of mouse embryo during left-right axis formation. Dev Biol 376(1):23-30. [PubMed: 23357539]  [MGI Ref ID J:195164]

Tanaka Y; Okada Y; Hirokawa N. 2005. FGF-induced vesicular release of Sonic hedgehog and retinoic acid in leftward nodal flow is critical for left-right determination. Nature 435(7039):172-7. [PubMed: 15889083]  [MGI Ref ID J:98555]

Vermot J; Pourquie O. 2005. Retinoic acid coordinates somitogenesis and left-right patterning in vertebrate embryos. Nature 435(7039):215-20. [PubMed: 15889094]  [MGI Ref ID J:98584]

Tyrp1b related

Anderson MG; Libby RT; Mao M; Cosma IM; Wilson LA; Smith RS; John SW. 2006. Genetic context determines susceptibility to intraocular pressure elevation in a mouse pigmentary glaucoma. BMC Biol 4:20. [PubMed: 16827931]  [MGI Ref ID J:128215]

Anderson MG; Nair KS; Amonoo LA; Mehalow A; Trantow CM; Masli S; John SW. 2008. GpnmbR150X allele must be present in bone marrow derived cells to mediate DBA/2J glaucoma. BMC Genet 9:30. [PubMed: 18402690]  [MGI Ref ID J:134670]

Barabas P; Huang W; Chen H; Koehler CL; Howell G; John SW; Tian N; Renteria RC; Krizaj D. 2011. Missing optomotor head-turning reflex in the DBA/2J mouse. Invest Ophthalmol Vis Sci 52(9):6766-73. [PubMed: 21757588]  [MGI Ref ID J:181395]

Brooks BP; Larson DM; Chan CC; Kjellstrom S; Smith RS; Crawford MA; Lamoreux L; Huizing M; Hess R; Jiao X; Hejtmancik JF; Maminishkis A; John SW; Bush R; Pavan WJ. 2007. Analysis of ocular hypopigmentation in Rab38cht/cht mice. Invest Ophthalmol Vis Sci 48(9):3905-13. [PubMed: 17724166]  [MGI Ref ID J:124886]

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]

Center EM; Hunter RL; Dodge AH. 1967. Effects of the luxoid gene (lu) on liver esterase isozymes of the mouse. Genetics 55(2):349-58. [PubMed: 6067640]  [MGI Ref ID J:109970]

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]

Gajewska M; Krysiak E; Wirth-Dziecialowska E. 2010. New coat color mutation mapped in distal part MMU10 MGI Direct Data Submission :.  [MGI Ref ID J:162146]

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

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]

Howell GR; Libby RT; Jakobs TC; Smith RS; Phalan FC; Barter JW; Barbay JM; Marchant JK; Mahesh N; Porciatti V; Whitmore AV; Masland RH; John SW. 2007. Axons of retinal ganglion cells are insulted in the optic nerve early in DBA/2J glaucoma. J Cell Biol 179(7):1523-37. [PubMed: 18158332]  [MGI Ref ID J:131073]

Hunsicker PR. 1969. White-based brown, B<W> Mouse News Lett 40:41.  [MGI Ref ID J:13492]

Kelly EM. 1957. Beige, bg Mouse News Lett 16:36.  [MGI Ref ID J:29744]

Kobayashi T; Imokawa G; Bennett DC; Hearing VJ. 1998. Tyrosinase stabilization by Tyrp1 (the brown locus protein). J Biol Chem 273(48):31801-5. [PubMed: 9822646]  [MGI Ref ID J:51301]

Lamoreux ML; Wakamatsu K; Ito S. 2001. Interaction of major coat color gene functions in mice as studied by chemical analysis of eumelanin and pheomelanin. Pigment Cell Res 14(1):23-31. [PubMed: 11277491]  [MGI Ref ID J:103803]

Little CC. 1916. The occurrence of three recognized coat mutations in mice Am Naturalist 1:335-349.  [MGI Ref ID J:150254]

Manor U; Disanza A; Grati M; Andrade L; Lin H; Di Fiore PP; Scita G; Kachar B. 2011. Regulation of stereocilia length by myosin XVa and whirlin depends on the actin-regulatory protein Eps8. Curr Biol 21(2):167-72. [PubMed: 21236676]  [MGI Ref ID J:171832]

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]

Matheu A; Pantoja C; Efeyan A; Criado LM; Martin-Caballero J; Flores JM; Klatt P; Serrano M. 2004. Increased gene dosage of Ink4a/Arf results in cancer resistance and normal aging. Genes Dev 18(22):2736-46. [PubMed: 15520276]  [MGI Ref ID J:93879]

Medical Research Council (MRC) Harwell. 2012. Direct Data Submission 2012/03/01 MGI Direct Data Submission :.  [MGI Ref ID J:180879]

Moyer FH. 1966. Genetic variations in the fine structure and ontogeny of mouse melanin granules. Am Zool 6(1):43-66. [PubMed: 5902512]  [MGI Ref ID J:5001]

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]

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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]

Raymond S; Jackson IJ. 1994. Molecular characterization of the mouse B<w> mutation causing premature melanocyte death - melanocytes and early development Genet Res 63(2):155 (Abstr).  [MGI Ref ID J:18590]

Rittenhouse E. 1968. Genetic effect on fine structure and development of pigment granules in mouse hair bulb melanocytes. I. The b and d loci. Dev Biol 17(4):351-65. [PubMed: 5650006]  [MGI Ref ID J:5068]

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]

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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* $2525.00
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* $3283.00
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.

General Supply Notes

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

Control Information

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

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


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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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phone:207-288-6470

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. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

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

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

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


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