Strain Name:

WC/ReJ KitlSl/J

Stock Number:

000693

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Availability:

Cryopreserved - Ready for recovery

The spontaneous kit ligand; steel (KitlSl) mutation behaves in a semidominant fashion causing deficiencies in pigment cells, germ cells, and blood cells.

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 WC/ReJ-KitlSl/J    (Changed: 30-OCT-06 )
Type Mutant Strain;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
GenerationF26p
Generation Definitions

Appearance
dark grey with white head blaze, affected
Related Genotype: a/a KitlSl/+

black, unaffected
Related Genotype: a/a +/+

Important Note
This strain is homozygous for the retinal degeneration allele Pde6brd1. See article "Genetic Background Effects: Can Your Mice See?", JAX® NOTES Spring 2002, No. 485.

Description
The multiple steel mutations (KitlSl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. KitlSl/KitlSl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age.

Development
Inbreeding started in 1948 from a heterozygous KitlW / + stock (same origin as the WB/ReJ strain). Kitlsl (steel) mutation backcrossed to strain WB-+/+. Now maintained as a congenic strain for Kitlsl.

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Ahrd allele
000690   129P3/J
000648   AKR/J
008599   B6.Cg-Del(9Cyp1a2-Cyp1a1)1Dwn Ahrd Tg(CYP1A1,CYP1A2)1Dwn/DwnJ
002921   B6.D2N-Ahrd/J
000652   BDP/J
000928   CAST/EiJ
000671   DBA/2J
000674   I/LnJ
000675   LG/J
000676   LP/J
000684   NZB/BlNJ
000726   RBF/DnJ
000682   RF/J
000686   SJL/J
000688   ST/bJ
000689   SWR/J
000933   YBR/EiJ
View Strains carrying   Ahrd     (17 strains)

Strains carrying   KitlSl allele
000124   B6.Cg-KitlSl Krt71Ca/J
000291   C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J
View Strains carrying   KitlSl     (2 strains)

Strains carrying   Pde6brd1 allele
004202   B6.C3 Pde6brd1 Hps4le/+ +-Lmx1adr-8J/J
000002   B6.C3-Pde6brd1 Hps4le/J
001022   B6C3FeF1/J a/a
000652   BDP/J
000653   BUB/BnJ
002439   C3.129P2(B6)-B2mtm1Unc/J
005494   C3.129S1(B6)-Grm1rcw/J
000509   C3.Cg-Lystbg-2J/J
000480   C3.MRL-Faslpr/J
001957   C3A Pde6brd1.O20/A-Prph2Rd2/J
004326   C3Bir.129P2(B6)-Il10tm1Cgn/Lt
003968   C3Bir.129P2(B6)-Il10tm1Cgn/LtJ
006435   C3Fe.SW-Soaa/MonJ
001904   C3H-Atcayji-hes/J
000659   C3H/HeJ
000511   C3H/HeJ-Ap3d1mh-2J/J
000784   C3H/HeJ-Faslgld/J
002433   C3H/HeJ-Sptbn4qv-lnd2J/J
005972   C3H/HeJBirLtJ
001824   C3H/HeJSxJ
000635   C3H/HeOuJ
000474   C3H/HeSn
001431   C3H/HeSn-ocd/J
000661   C3H/HeSnJ
002333   C3H/HeSnJ-gri/J
001576   C3He-Atp7btx-J/J
000658   C3HeB/FeJ
002588   C3HeB/FeJ-Eya1bor/J
001533   C3HeB/FeJ-Mc1rE-so Gli3Xt-J/J
001908   C3HfB/BiJ
001502   C3Sn.B6-Epha4rb/EiGrsrJ
002235   C3Sn.C3-Ctnna2cdf/J
001547   C3Sn.Cg-Cm/J
001906   C3fBAnl.Cg-Catb/AnlJ
000656   CBA/J
000813   CBA/J-Atp7aMo-pew/J
000660   DA/HuSnJ
000023   FL/1ReJ
000025   FL/4ReJ
003024   FVB.129P2(B6)-Fmr1tm1Cgr/J
002539   FVB.129P2-Abcb4tm1Bor/J
002935   FVB.129S2(B6)-Ccnd1tm1Wbg/J
002953   FVB.Cg-Tg(MMTVTGFA)254Rjc/J
003170   FVB.Cg-Tg(Myh6-tTA)6Smbf/J
003078   FVB.Cg-Tg(WapIgf1)39Dlr/J
003487   FVB.Cg-Tg(XGFAP-lacZ)3Mes/J
003257   FVB/N-Tg(GFAPGFP)14Mes/J
002856   FVB/N-Tg(TIE2-lacZ)182Sato/J
002384   FVB/N-Tg(UcpDta)1Kz/J
001800   FVB/NJ
001491   FVB/NMob
000804   HPG/BmJ
000734   MOLD/RkJ
000550   MOLF/EiJ
002423   NON/ShiLtJ
000679   P/J
000680   PL/J
000268   RSV/LeJ
000269   SB/LeJ
010968   SB;C3Sn-Lrp4mdig-2J/GrsrJ
005651   SJL.AK-Thy1a/TseJ
000686   SJL/J
000688   ST/bJ
004808   STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
002648   STOCK a/a Cln6nclf/J
000279   STOCK gr +/+ Ap3d1mh/J
005965   STOCK Tg(Pomc1-cre)16Lowl/J
004770   SW.B6-Soab/J
002023   SWR.M-Emv21 Emv22/J
000689   SWR/J
000939   SWR/J-Clcn1adr-mto/J
000692   WB/ReJ KitW/J
100410   WBB6F1/J-KitW/KitW-v/J
View Strains carrying   Pde6brd1     (73 strains)

Strains carrying other alleles of Ahr
000645   A/HeJ
000646   A/J
002920   B6(D2N).Spretus-Ahrb-3/J
002831   B6.129-Ahrtm1Bra/J
000130   B6.C-H17c/(HW14)ByJ
000136   B6.C-H34c/(HW22)ByJ
000370   B6.C-H38c/(HW119)ByJ
002727   B6;129-Ahrtm1Bra/J
001026   BALB/cByJ
000653   BUB/BnJ
000659   C3H/HeJ
000663   C57BL/6By
001139   C57BL/6ByJ
000664   C57BL/6J
000662   C57BLKS/J
000667   C57BR/cdJ
000668   C57L/J
000669   C58/J
000926   CAROLI/EiJ
000656   CBA/J
000657   CE/J
000351   CXB1/ByJ
000352   CXB2/ByJ
000353   CXB3/ByJ
000354   CXB4/ByJ
000355   CXB5/ByJ
000356   CXB6/ByJ
000357   CXB7/ByJ
002937   D2.B6-Ahrb-1/J
000673   HRS/J
000677   MA/MyJ
000550   MOLF/EiJ
000679   P/J
000930   PERA/EiJ
000644   SEA/GnJ
000280   SF/CamEiJ
001146   SPRET/EiJ
006203   STOCK Ahrtm3.1Bra/J
View Strains carrying other alleles of Ahr     (38 strains)

Strains carrying other alleles of Kitl
000090   129S1/Sv-Oca2+ Tyr+ KitlSl-J/J
002993   B6.Cg-KitlSl-18H/EiJ
008656   B6.Cg-KitlSl-gb/MbeJ
009687   B6.Cg-Tg(KRT14-Kitl*)4XTG2Bjl/J
000160   B6.D2-KitlSl-d/J
014608   B6;129S1-a Kitlsl-24J/GrsrJ
001380   C3Sn.Cg-KitlSl-con/J
003252   C57BL/6J-KitlSl-20J/J
000979   STOCK KitlSl-16J/J
017860   STOCK Kitltm1.1Sjm/J
017861   STOCK Kitltm2.1Sjm/J
000161   WB.D2-KitlSl-d/J
001145   WSB/EiJ
View Strains carrying other alleles of Kitl     (13 strains)

View Strains carrying other alleles of Pde6b     (13 strains)

Additional Web Information

JAX® NOTES, April 1988; 433. H-2 Haplotypes of Mice from Jackson Laboratory Production Colonies.
JAX® NOTES, February 2001; 481. Mgf Gene Name Changes to Kitl.
JAX® NOTES, Spring 2002; 485. Genetic Background Effects: Can Your Mice See?

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Hyperpigmentation, Familial Progressive, 2; FPH2   (KITLG)
Night Blindness, Congenital Stationary, Autosomal Dominant 2; CSNBAD2   (PDE6B)
Retinitis Pigmentosa 40; RP40   (PDE6B)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

KitlSl/Kitl+

        involves: C3H
  • pigmentation phenotype
  • abnormal skin pigmentation
    • mice have light ears   (MGI Ref ID J:3399)
    • abnormal ear pigmentation
      • mice have light feet   (MGI Ref ID J:3399)
  • belly spot   (MGI Ref ID J:157170)
    • most mice have a white spot on the belly   (MGI Ref ID J:3399)
  • diluted coat color
    • affected mice have overall dilution of coat color, more extreme on the belly than back   (MGI Ref ID J:3399)
    • reduced coat color   (MGI Ref ID J:157170)
  • head blaze
    • very occasionally mice have a white blaze between their eyes   (MGI Ref ID J:3399)
  • head spot
    • most mice have a white spot on the belly   (MGI Ref ID J:3399)
  • hematopoietic system phenotype
  • anemia
    • mice display less severe anemia than homozygotes   (MGI Ref ID J:3399)
  • decreased erythrocyte cell number
    • at 7-13 days of age, red blood cell counts are 20-30% lower than wild-type   (MGI Ref ID J:3399)
  • hearing/vestibular/ear phenotype
  • abnormal ear pigmentation
    • mice have light feet   (MGI Ref ID J:3399)
  • reproductive system phenotype
  • *normal* reproductive system phenotype
    • heterozygotes are viable and fertile   (MGI Ref ID J:3399)
  • craniofacial phenotype
  • abnormal ear pigmentation
    • mice have light feet   (MGI Ref ID J:3399)
  • integument phenotype
  • abnormal skin pigmentation
    • mice have light ears   (MGI Ref ID J:3399)
    • abnormal ear pigmentation
      • mice have light feet   (MGI Ref ID J:3399)
  • abnormal vibrissa morphology
    • mice have light whiskers   (MGI Ref ID J:3399)
  • belly spot   (MGI Ref ID J:157170)
    • most mice have a white spot on the belly   (MGI Ref ID J:3399)
  • diluted coat color
    • affected mice have overall dilution of coat color, more extreme on the belly than back   (MGI Ref ID J:3399)
    • reduced coat color   (MGI Ref ID J:157170)
  • head blaze
    • very occasionally mice have a white blaze between their eyes   (MGI Ref ID J:3399)
  • head spot
    • most mice have a white spot on the belly   (MGI Ref ID J:3399)
  • pallor
    • some pups after birth are pale compared to littermates   (MGI Ref ID J:3399)
  • growth/size/body phenotype
  • abnormal ear pigmentation
    • mice have light feet   (MGI Ref ID J:3399)

KitlSl/Kitl+

        either: (involves: C3H * WC) or (involves: C3H * C57BL/6 * DBA/2J * WC)
  • hematopoietic system phenotype
  • anemia
    • mice are slightly anemic   (MGI Ref ID J:6084)
  • decreased mast cell number
    • heterozygotes have decreased mast cell numbers in dorsal skin compared to wild-type   (MGI Ref ID J:6084)
  • immune system phenotype
  • decreased mast cell number
    • heterozygotes have decreased mast cell numbers in dorsal skin compared to wild-type   (MGI Ref ID J:6084)

KitlSl/Kitl+

        involves: 129/Sv * C3H
  • tumorigenesis
  • increased tumor incidence
    • male mice develop ~2-fold more tumors than controls   (MGI Ref ID J:50508)
    • increased testicular teratoma incidence
      • incidence is 6.92% compared to ~2.6% in controls   (MGI Ref ID J:50508)
      • tumors are predominantly in left testis (71%) vs right (27%) or bilateral (2%)   (MGI Ref ID J:50508)
      • percentage is greater in second and subsequent litters compared to first litter or in first litter of older females compared to young mothers   (MGI Ref ID J:50508)

KitlSl/KitlSl

        involves: C3H
  • mortality/aging
  • complete lethality throughout fetal growth and development
    • no presumed homozygotes are born; homozygotes begin to die at ~E15-15.5 from anemia   (MGI Ref ID J:3399)
    • an occasional mutant survives until birth   (MGI Ref ID J:3399)
  • nervous system phenotype
  • abnormal brain development
    • at E10.5-12.5, small number of embryos, presumably homozygous, have brain abnormalities, including a collapsed brain, pseudoencephaly or a narrowed brain region   (MGI Ref ID J:3399)
    • from E14.5-17.5, some embryos show abnormal brain development (3/330) as described in younger embryos   (MGI Ref ID J:3399)
    • myelencephalic blebs
      • one E17.5 embryo displayed a bleb near the midline in the cervical region   (MGI Ref ID J:3399)
  • spina bifida
    • 4/330 embryos aged E14.5-17.5 displayed spina bifida   (MGI Ref ID J:3399)
  • hematopoietic system phenotype
  • anemia
    • starting around E13.5 and peaking at E14.5, presumed homozygotes display anemia recognized by overall paleness of the embryos   (MGI Ref ID J:3399)
  • cardiovascular system phenotype
  • abnormal blood circulation
    • in affected (anemic) animals, individual clumps or red blood cells can be seen in umbilical vessels; in controls, vessels are uniformly red with normal blood flow   (MGI Ref ID J:3399)
  • reproductive system phenotype
  • infertility
    • mice carrying two mutant alleles are sterile   (MGI Ref ID J:5547)
  • pigmentation phenotype
  • absent skin pigmentation
    • transplantation of skin grafts from E14, E15 and newborn mutants to normal siblings produced unpigmented hair   (MGI Ref ID J:28098)
  • embryogenesis phenotype
  • spina bifida
    • 4/330 embryos aged E14.5-17.5 displayed spina bifida   (MGI Ref ID J:3399)
  • integument phenotype
  • absent skin pigmentation
    • transplantation of skin grafts from E14, E15 and newborn mutants to normal siblings produced unpigmented hair   (MGI Ref ID J:28098)
  • pallor
    • characteristic of anemic embryos   (MGI Ref ID J:3399)
View Research Applications

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

Ahrd related

Metabolism Research

Research Tools
Toxicology Research

KitlSl related

Cancer Research
Growth Factors/Receptors/Cytokines
Increased Tumor Incidence
      Gonadal Tumors
      Gonadal Tumors: ovarian and testicular

Dermatology Research
Color and White Spotting Defects

Developmental Biology Research
Neural Crest Defects

Endocrine Deficiency Research
Bone/Bone Marrow Defects
Gonad Defects
Hypothalamus/Pituitary Defects
Skin Defects

Immunology, Inflammation and Autoimmunity Research
Growth Factors/Receptors/Cytokines
Immunodeficiency
      Mast Cell Deficiency

Neurobiology Research
Hearing Defects

Reproductive Biology Research
Developmental Defects Affecting Gonads
      germ cell deficient
Fertility Defects
Gonadal Tumors
      ovarian and testicular

Research Tools
Immunology, Inflammation and Autoimmunity Research
      Mast Cell Deficiency

Sensorineural Research
Hearing Defects

Pde6brd1 related
Retinal Degeneration

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol KitlSl
Allele Name steel
Allele Type Spontaneous
Common Name(s) MgfSl; Sl;
Strain of OriginC3H
Gene Symbol and Name Kitl, kit ligand
Chromosome 10
Gene Common Name(s) Clo; Con; FPH2; Gb; KL-1; MGF; Mgf; SCF; SF; SHEP7; SLF; Sl; Steel; Steel factor; blaze; blz; cloud gray; contrasted; grizzle-belly; mast cell growth factor; steel; stem cell factor;
Molecular Note By Southern blotting, it was concluded that this allele contains a deletion encompassing most, if not all, of the coding region of the gene. A probe corresponding to nucleotides 6 to 685 of the cDNA failed to hybridize to DNA obtained from embryos homozygous for this allele. PCR analysis with primers for sequences at various distances from the Kit gene narrowed the 5' and 3' deletion endpoints to a 350 and a 380 base-pair region, respectively. Sequencing of the product of PCR using primers designed to span the deletion revealed that it extends through 973,366 base pairs on Chromosome 10 between nucleotide positions 99,177,807 and 100,151,173 (NCBI Map Viewer, Build 36.1), with a 4-base pair insertion joining the deletion endpoints, and contains 6 predicted and 3 known genes. [MGI Ref ID J:10750] [MGI Ref ID J:115283]
 
Allele Symbol Ahrd
Allele Name d variant
Allele Type Not Applicable
Common Name(s) Ahd; Ahk; AhRd; Ahhn; ah; in;
Gene Symbol and Name Ahr, aryl-hydrocarbon receptor
Chromosome 12
Gene Common Name(s) Ah; Ahh; Ahre; In; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; bHLHe76; dioxin receptor; inflammatory reactivity;
General Note Compared with Ahrd/Ahrd mice, Ahrb/Ahrb individuals have a high inflammatory response to cutaneous application of dimethylbenzanthracene; a high susceptibility to methylcholanthrene- and benzopyrene-induced subcutaneous sarcomas and methylcholanthrene-induced lung tumors; an increased resistance to zoxazolamine-induced paralysis, lindane toxicity, and benzo[a]pyrene-induced aplastic anemia and leukemia; a high susceptibility to acetaminophen-induced hepatic necrosis and cataract formation; and an increased susceptibility to polycyclic hydrocarbon-induced birth defects, stillbirths, resorptions, decreased body weight, ovarian primordial oocyte depletion, and spermatozoal aberrations (J:5822). The Ahrballele is associated with increases in numerous metabolites of chemical carcinogens binding to DNA nucleotides (J:12156). The effectiveness of several mutagens for Salmonella in vitro is enhanced by presence of a liver fraction from Ahrb/Ahrb> mice treated with polycyclic hydrocarbons, but not from similarly treated Ahrd/Ahr mice (J:5564). In contrast, oral doses of benzopyrene cause a high rate of leukemia in Ahrd/Ahrd but not in Ahrd/Ahrd mice, probably because the carcinogenic metabolites produced in responsive Ahrb/Ahrd mice are rapidly degraded in the intestine and excreted in the feces (J:6074).

Strain of origin - this allele was found in DBA/2J, AKR/J, 129, SWR, RF, NZB strains

Molecular Note This allele encodes a 104 kDa receptor that is stabilized by molybdate and has an affinity for ligand 10-100 fold lower than that of the receptor produced by the C57BL/6J allele. PCR sequencing of cDNA revealed ten nucleotide differences between the coding sequences of the DBA/2J and C57BL/6J receptors. Five of the ten differences would cause amino acid changes. One of these, an apparent T to C transition replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the DBA/2J allele. This change would extend translation of the DBA/2J mRNA by 43 amino acids, accounting for the larger size of the peptide produced by this allele (104 kDa vs 95 kDa for the C57BL/6J allele). A second T to C transition changes a leucine codon in the C57BL/6J allele to a proline codon in the DBA/2J allele, and would likely change secondary structure of the peptide and thus ligand affinity. [MGI Ref ID J:15153] [MGI Ref ID J:17460] [MGI Ref ID J:22144]
 
Allele Symbol Pde6brd1
Allele Name retinal degeneration 1
Allele Type Spontaneous
Common Name(s) Pdebrd1; rd; rd-1; rd1; rodless retina;
Strain of Originvarious
Gene Symbol and Name Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide
Chromosome 5
Gene Common Name(s) CSNB3; CSNBAD2; PDEB; Pdeb; RP40; nmf137; phosphodiesterase, cGMP, rod receptor, beta polypeptide; r; rd; rd-1; rd1; rd10; retinal degeneration; retinal degeneration 1; retinal degeneration 10;
General Note The following inbred strains are known to be homozygous for Pde6b: C3H sublines, CBA/J, FVB/NJ, PL/J, SB, SJL/J, and SWR/J.
Molecular Note Two mutations have been identified in rd1 mice. A murine leukimia virus (Xmv-28) insertion in reverse orientation in intron 1 is found in all mouse strains with the rd1 phenotype. Further, a nonsense mutation (C to A transversion) in codon 347 that results in a truncation eliminating more than half of the predicted encoded protein, including the catalytic domain has also been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested. [MGI Ref ID J:11513] [MGI Ref ID J:4366] [MGI Ref ID J:51361]

Genotyping

Genotyping Information


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Arguello F; Furlanetto RW; Baggs RB; Graves BT; Harwell SE; Cohen HJ; Frantz CN. 1992. Incidence and distribution of experimental metastases in mutant mice with defective organ microenvironments (genotypes Sl/Sld and W/Wv). Cancer Res 52(8):2304-9. [PubMed: 1559233]  [MGI Ref ID J:468]

Hayashi C; Sonoda T; Nakano T; Nakayama H; Kitamura Y. 1985. Mast-cell precursors in the skin of mouse embryos and their deficiency in embryos of Sl/Sld genotype. Dev Biol 109(1):234-41. [PubMed: 3987963]  [MGI Ref ID J:7810]

Huang E; Nocka K; Beier DR; Chu TY; Buck J; Lahm HW; Wellner D; Leder P; Besmer P. 1990. The hematopoietic growth factor KL is encoded by the Sl locus and is the ligand of the c-kit receptor, the gene product of the W locus. Cell 63(1):225-33. [PubMed: 1698557]  [MGI Ref ID J:10751]

Murphy ED. 1977. Effects of mutant steel alleles on leukemogenesis and life-span in the mouse. J Natl Cancer Inst 58(1):107-10. [PubMed: 319242]  [MGI Ref ID J:5758]

Shinohara T; Avarbock MR; Brinster RL. 2000. Functional analysis of spermatogonial stem cells in Steel and cryptorchid infertile mouse models. Dev Biol 220(2):401-11. [PubMed: 10753526]  [MGI Ref ID J:61712]

Zsebo KM; Williams DA; Geissler EN; Broudy VC; Martin FH; Atkins HL; Hsu RY; Birkett NC; Okino KH; Murdock DC; Jacobsen FW; Langley KE; Smith KA; Takeishi T; Cattanach BM; Galli SJ; Suggs SV. 1990. Stem cell factor is encoded at the Sl locus of the mouse and is the ligand for the c-kit tyrosine kinase receptor. Cell 63(1):213-24. [PubMed: 1698556]  [MGI Ref ID J:10750]

Additional References

Chang B; Hawes NL; Hurd RE; Davisson MT; Nusinowitz S; Heckenlively JR. 2002. Retinal degeneration mutants in the mouse. Vision Res 42(4):517-25. [PubMed: 11853768]  [MGI Ref ID J:75095]

Poland A; Glover E. 1990. Characterization and strain distribution pattern of the murine Ah receptor specified by the Ahd and Ahb-3 alleles. Mol Pharmacol 38(3):306-12. [PubMed: 2169579]  [MGI Ref ID J:34840]

Schrott A; Egg G; Spoendlin H. 1988. Intermediate filaments in the cochleas of normal and mutant (w/wv, sl/sld) mice. Arch Otorhinolaryngol 245(4):250-4. [PubMed: 2460075]  [MGI Ref ID J:9423]

Wolf NS. 1978. Dissecting the hematopoietic microenvironment. II. The kinetics of the erythron of the S1/S1d mouse and the dual nature of its anemia. Cell Tissue Kinet 11(4):325-34. [PubMed: 688326]  [MGI Ref ID J:6031]

Ahrd related

Benedict WF; Considine N; Nebert DW. 1973. Genetic differences in aryl hydrocarbon hydroxylase induction and benzo(a)pyrene-produced tumorigenesis in the mouse. Mol Pharmacol 9(2):266-77. [PubMed: 4123113]  [MGI Ref ID J:84312]

Boobis AR; Nebert DW. 1976. Genetic differences in the metabolism of carcinogens and in the binding of benzo (a) pyrene metabolites to DNA. Adv Enzyme Regul 15:339-62. [PubMed: 1030186]  [MGI Ref ID J:12156]

Castro DJ; Lohr CV; Fischer KA; Pereira CB; Williams DE. 2008. Lymphoma and lung cancer in offspring born to pregnant mice dosed with dibenzo[a,l]pyrene: the importance of in utero vs. lactational exposure. Toxicol Appl Pharmacol 233(3):454-8. [PubMed: 18848954]  [MGI Ref ID J:143604]

Chang C; Smith DR; Prasad VS; Sidman CL; Nebert DW; Puga A. 1993. Ten nucleotide differences, five of which cause amino acid changes, are associated with the Ah receptor locus polymorphism of C57BL/6 and DBA/2 mice. Pharmacogenetics 3(6):312-21. [PubMed: 8148872]  [MGI Ref ID J:17460]

Curran CP; Miller KA; Dalton TP; Vorhees CV; Miller ML; Shertzer HG; Nebert DW. 2006. Genetic differences in lethality of newborn mice treated in utero with coplanar versus non-coplanar hexabromobiphenyl. Toxicol Sci 89(2):454-64. [PubMed: 16291824]  [MGI Ref ID J:113285]

Felton JS; Nebert DW. 1975. Mutagenesis of certain activated carcinogens in vitro associated with genetically mediated increases in monooxygenase activity and cytochrome P 1-450. J Biol Chem 250(17):6769-78. [PubMed: 808546]  [MGI Ref ID J:5564]

Gielen JE; Goujon FM; Nebert DW. 1972. Genetic regulation of aryl hydrocarbon hydroxylase induction. II. Simple Mendelian expression in mouse tissues in vivo. J Biol Chem 247(4):1125-37. [PubMed: 4110756]  [MGI Ref ID J:84250]

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Ruggiero L; Allen CN; Lane Brown R; Robinson DW. 2009. The development of melanopsin-containing retinal ganglion cells in mice with early retinal degeneration. Eur J Neurosci 29(2):359-67. [PubMed: 19200239]  [MGI Ref ID J:146465]

Ryu SB; Ye JH; Goo YS; Kim CH; Kim KH. 2010. Temporal response properties of retinal ganglion cells in rd1 mice evoked by amplitude-modulated electrical pulse trains. Invest Ophthalmol Vis Sci 51(12):6762-9. [PubMed: 20671284]  [MGI Ref ID J:171389]

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Samardzija M; Wenzel A; Aufenberg S; Thiersch M; Reme C; Grimm C. 2006. Differential role of Jak-STAT signaling in retinal degenerations. FASEB J 20(13):2411-3. [PubMed: 16966486]  [MGI Ref ID J:114638]

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Selby CP; Thompson C; Schmitz TM; Van Gelder RN; Sancar A. 2000. Functional redundancy of cryptochromes and classical photoreceptors for nonvisual ocular photoreception in mice Proc Natl Acad Sci U S A 97(26):14697-702. [PubMed: 11114194]  [MGI Ref ID J:66580]

Semo M; Gias C; Ahmado A; Sugano E; Allen AE; Lawrence JM; Tomita H; Coffey PJ; Vugler AA. 2010. Dissecting a role for melanopsin in behavioural light aversion reveals a response independent of conventional photoreception. PLoS One 5(11):e15009. [PubMed: 21124784]  [MGI Ref ID J:167120]

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Strettoi E; Pignatelli V; Rossi C; Porciatti V; Falsini B. 2003. Remodeling of second-order neurons in the retina of rd/rd mutant mice. Vision Res 43(8):867-77. [PubMed: 12668056]  [MGI Ref ID J:92316]

Strettoi E; Porciatti V; Falsini B; Pignatelli V; Rossi C. 2002. Morphological and functional abnormalities in the inner retina of the rd/rd mouse. J Neurosci 22(13):5492-504. [PubMed: 12097501]  [MGI Ref ID J:109225]

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Takahashi M; Miyoshi H; Verma IM; Gage FH. 1999. Rescue from photoreceptor degeneration in the rd mouse by human immunodeficiency virus vector-mediated gene transfer. J Virol 73(9):7812-6. [PubMed: 10438872]  [MGI Ref ID J:56759]

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Thompson CL; Selby CP; Partch CL; Plante DT; Thresher RJ; Araujo F; Sancar A. 2004. Further evidence for the role of cryptochromes in retinohypothalamic photoreception/phototransduction. Brain Res Mol Brain Res 122(2):158-66. [PubMed: 15010208]  [MGI Ref ID J:88468]

Thompson S; Foster RG; Stone EM; Sheffield VC; Mrosovsky N. 2008. Classical and melanopsin photoreception in irradiance detection: negative masking of locomotor activity by light. Eur J Neurosci 27(8):1973-9. [PubMed: 18412618]  [MGI Ref ID J:136825]

Thompson S; Lupi D; Hankins MW; Peirson SN; Foster RG. 2008. The effects of rod and cone loss on the photic regulation of locomotor activity and heart rate. Eur J Neurosci 28(4):724-9. [PubMed: 18702692]  [MGI Ref ID J:140577]

Thompson S; Mullins RF; Philp AR; Stone EM; Mrosovsky N. 2008. Divergent phenotypes of vision and accessory visual function in mice with visual cycle dysfunction (Rpe65 rd12) or retinal degeneration (rd/rd). Invest Ophthalmol Vis Sci 49(6):2737-42. [PubMed: 18515598]  [MGI Ref ID J:137044]

Thompson S; Stasheff SF; Hernandez J; Nylen E; East JS; Kardon RH; Pinto LH; Mullins RF; Stone EM. 2011. Different inner retinal pathways mediate rod-cone input in irradiance detection for the pupillary light reflex and regulation of behavioral state in mice. Invest Ophthalmol Vis Sci 52(1):618-23. [PubMed: 20847113]  [MGI Ref ID J:171559]

Thyagarajan S; van Wyk M; Lehmann K; Lowel S; Feng G; Wassle H. 2010. Visual function in mice with photoreceptor degeneration and transgenic expression of channelrhodopsin 2 in ganglion cells. J Neurosci 30(26):8745-58. [PubMed: 20592196]  [MGI Ref ID J:161847]

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Tu DC; Owens LA; Anderson L; Golczak M; Doyle SE; McCall M; Menaker M; Palczewski K; Van Gelder RN. 2006. Inner retinal photoreception independent of the visual retinoid cycle. Proc Natl Acad Sci U S A 103(27):10426-31. [PubMed: 16788071]  [MGI Ref ID J:111700]

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Vazquez-Chona FR; Clark AM; Levine EM. 2009. Rlbp1 promoter drives robust Muller glial GFP expression in transgenic mice. Invest Ophthalmol Vis Sci 50(8):3996-4003. [PubMed: 19324864]  [MGI Ref ID J:154561]

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    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).

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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.

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    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).

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

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This strain is homozygous for the retinal degeneration allele Pde6brd1. See article "Genetic Background Effects: Can Your Mice See?", JAX® NOTES Spring 2002, No. 485.

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