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- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
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Description
Strain Information
Former Names WCB6F1/J-KitlSl/KitlSl-d (Changed: 23-FEB-06 ) Type Mutant Stock; Spontaneous Mutation; Additional information on Genetically Engineered and Mutant Mice. Type *F1 Hybrid; Additional information on Hybrid Strains. Visit our online Nomenclature tutorial. Species laboratory mouse Generation F0 (wean) (21-DEC-11)
Generation DefinitionsAppearance
black eyed, white coat, affected
Related Genotype: a/a KitlSl/KitlSl-d
grey with light belly, infrequent belly spot, affected (reversed phenotype on F1 hybrid background)
Related Genotype: a/a KitlSl/+
dark grey with white head blaze, affected (reversed phenotype on F1 hybrid background)
Related Genotype: a/a KitlSl-d/+
black, unaffected
Related Genotype: a/a +/+Important Note
This strain is heterozygous for the retinal degeneration allele Pde6brd1.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). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., KitlSl/KitlSl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have 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.
Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying KitlSl-d allele
000160 B6.D2-KitlSl-d/J 000161 WB.D2-KitlSl-d/J View Strains carrying KitlSl-d (2 strains)
000124 B6.Cg-KitlSl Krt71Ca/J 000291 C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J 000693 WC/ReJ KitlSl/J
000090 129S1/Sv-Oca2+ Tyr+ KitlSl-J/J 002993 B6.Cg-KitlSl-18H/EiJ 008656 B6.Cg-KitlSl-gb/MbeJ 000124 B6.Cg-KitlSl Krt71Ca/J 009687 B6.Cg-Tg(KRT14-Kitl*)4XTG2Bjl/J 000160 B6.D2-KitlSl-d/J 000291 C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J 001380 C3Sn.Cg-KitlSl-con/J 003252 C57BL/6J-KitlSl-20J/J 000979 STOCK KitlSl-16J/J 000161 WB.D2-KitlSl-d/J 000693 WC/ReJ KitlSl/J
Additional Web Information
JAX® NOTES, February 2001; 481. Mgf Gene Name Changes to Kitl.
JAX® NOTES, Winter 1991; 444. Coat Colors of Anemic Mice.
Phenotype
Phenotype Information
assigned by genotype
KitlSl/KitlSl-d
involves: C57BL/6 * WC
- mortality/aging
- premature death
- growth/size phenotype
- weight loss
- dermatitis is accompanied by weight loss (MGI Ref ID J:5758)
- hematopoietic system phenotype
- abnormal reticulocyte morphology
- reticulocyte percentages are higher (8-12%) than in KitlW/KitlW-v mice (MGI Ref ID J:27511)
- anemia
- decreased hematocrit
- hematocrit is lower than normal (~29%) and have lower than normal numbers of macrocytic erythrocytes (MGI Ref ID J:27511)
- thymus atrophy
- at autopsy, thymic atrophy was observed in mice that developed ulcerative dermatitis (MGI Ref ID J:5758)
- reproductive system phenotype
- *normal* reproductive system phenotype
- although mutants show a severe deficiency of primordial germ cells (PGCs), migration remaining PGCs from gut endoderm to gonadal ridges appears normal (MGI Ref ID J:5547)
- decreased primordial germ cell number
- mean of total PGC counts in embryos on E9 do not differ from mutant counts on E10 and E11; however, means of counts from normal embryos on E10 and E11 are 3 and 8-fold higher than day 9 mean PGC count, indicating a paucity of PGCs in mutants (MGI Ref ID J:5547)
- infertility
- mice carrying two mutant alleles at the Kitl locus are sterile (MGI Ref ID J:5547)
- tumorigenesis
- abnormal tumor incidence
- no mice develop reticulum cell neoplasms compared to 30% of controls at 889 days of age (MGI Ref ID J:5758)
- immune system phenotype
- dermatitis
- progressive ulcerative dermatitis develops at average age of 441 days (56% incidence), predominantly on the head and neck and in the axilla vs 20% of controls at 772 days of age; only 5 mice displayed lymphocytic leukemia as well (MGI Ref ID J:5758)
- stomach inflammation
- mixed inflammatory infiltrates are seen in lamina propria and submucosa of stomach (MGI Ref ID J:2777)
- thymus atrophy
- at autopsy, thymic atrophy was observed in mice that developed ulcerative dermatitis (MGI Ref ID J:5758)
- digestive/alimentary phenotype
- abnormal forestomach morphology
- abnormal stomach epithelium morphology
- forestomach is significantly thicker (187 um) than controls (40 um) (MGI Ref ID J:2777)
- abnormal stomach squamous epithelium morphology
- nonglandular portion of forestomach is consists of stratified squamous epithelium that is significantly thicker than controls and appears as short folds extending into lamina propria in endophytic pattern (MGI Ref ID J:2777)
- gastric ulcer
- one mutant had an ulcer in glandular portion of stomach (MGI Ref ID J:2777)
- stomach inflammation
- mixed inflammatory infiltrates are seen in lamina propria and submucosa of stomach (MGI Ref ID J:2777)
- integument phenotype
- dermatitis
- progressive ulcerative dermatitis develops at average age of 441 days (56% incidence), predominantly on the head and neck and in the axilla vs 20% of controls at 772 days of age; only 5 mice displayed lymphocytic leukemia as well (MGI Ref ID J:5758)
KitlSl/KitlSl-d
(WC/ReJ KitlSl x B6.D2-KitlSl-d/J)F1-KitlSl/KitlSl-d/J
- growth/size phenotype
- decreased body weight
- male mutants weigh 29, 27, and 13% less than than wild-type littermates at 5, 7, and 12 weeks of age (MGI Ref ID J:111273)
- postnatal growth retardation
- at 5 weeks, tibial length in males is less than controls, but by 12 weeks there has been catch-up growth and no significant difference is detected (MGI Ref ID J:111273)
- skeleton phenotype
- abnormal osteoblast physiology
- in culture, primary osteoblasts display decreased mineralization compared to wild-type when both are treated with BMP-2 (MGI Ref ID J:111273)
- abnormal osteoclast morphology
- osteoclast surface per bone surface is increased from 59% at 5 weeks to 441% at 12 weeks compared to wild-type males (MGI Ref ID J:111273)
- abnormal skeleton development
- bone formation rate is decreased in 5 week old mice and to a lesser extent at 7 weeks, but no difference is seen at 12 weeks (MGI Ref ID J:111273)
- decreased bone mineral content
- decreased bone mineral density
- bone mineral density (BMD) in males is significantly reduced at all age groups compared to controls; whole body as well as long bone and lumbar vertebral BMD are reduced (MGI Ref ID J:111273)
- in females, BMD at 5 weeks is reduced compared to controls with exception of the femur (MGI Ref ID J:111273)
- magnitude of change for each bone is larger in male mutants (9-41%) than female mutants (5-25%) (MGI Ref ID J:111273)
- decreased compact bone thickness
- cortical and marrow area of tibias is reduced in males vs controls (MGI Ref ID J:111273)
- decreased trabecular bone volume
- cancellous bone volume/tissue volume is significantly reduced compared to wild-type (MGI Ref ID J:111273)
- hematopoietic system phenotype
- abnormal osteoclast morphology
- osteoclast surface per bone surface is increased from 59% at 5 weeks to 441% at 12 weeks compared to wild-type males (MGI Ref ID J:111273)
- increased erythrocyte protoporphyrin level
- moderate but significant increase in protoporphrin levels in red blood cells compared to controls (MGI Ref ID J:5985)
- immune system phenotype
- abnormal osteoclast morphology
- osteoclast surface per bone surface is increased from 59% at 5 weeks to 441% at 12 weeks compared to wild-type males (MGI Ref ID J:111273)
- homeostasis/metabolism phenotype
- increased erythrocyte protoporphyrin level
- moderate but significant increase in protoporphrin levels in red blood cells compared to controls (MGI Ref ID J:5985)
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
KitlSl-d/Kitl+
either: DBA/2J or (C57BL/6 x DBA/2)F1
- pigmentation phenotype
- diluted coat color
- heterozygotes have a slightly diluted coat color (MGI Ref ID J:13392)
- integument phenotype
- diluted coat color
- heterozygotes have a slightly diluted coat color (MGI Ref ID J:13392)
KitlSl-d/Kitl+
either: (involves: C57BL/6 * DBA/2J) 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-d/Kitl+
C3.D2-KitlSl-d
- hematopoietic system phenotype
- increased mean corpuscular hemoglobin
- significantly increased compared to wild-type at P24-25 (MGI Ref ID J:79293)
- increased mean corpuscular volume
- significantly increased compared to wild-type at P24-25 (MGI Ref ID J:79293)
- low mean erythrocyte cell number
- at P1, mean red blood cell (RBC) counts are not different from KitlSl-d / KitlSl-gb compound heterozygotes (2.9 x 109 cells/ml; 4.1 x 109 cells/ml in wild-type mice) (MGI Ref ID J:79293)
- macrocytic anemia
- mild at birth (MGI Ref ID J:79293)
- pigmentation phenotype
- abnormal ventral coat pigmentation
- diluted ventrum (MGI Ref ID J:79293)
- head spot (MGI Ref ID J:79293)
- integument phenotype
- abnormal ventral coat pigmentation
- diluted ventrum (MGI Ref ID J:79293)
- head spot (MGI Ref ID J:79293)
KitlSl-d/Kitl+
involves: DBA/2J
- hematopoietic system phenotype
- macrocytic anemia
- mild macrocytic anemia (MGI Ref ID J:125080)
- pigmentation phenotype
- diluted coat color
- slightly diluted coat color is more noticeable on the belly (MGI Ref ID J:125080)
- integument phenotype
- diluted coat color
- slightly diluted coat color is more noticeable on the belly (MGI Ref ID J:125080)
KitlSl-d/KitlSl-d
C3.D2-KitlSl-d
- mortality/aging
- *normal* mortality/aging
- homozygotes are viable with expected number of homozygotes observed at P1; 83% of mice survive to P18, similar to wild-type (MGI Ref ID J:79293)
- hematopoietic system phenotype
- decreased hematocrit
- significantly lower than wild-type at P24-25 (MGI Ref ID J:79293)
- increased mean corpuscular hemoglobin concentration
- significantly increased compared to wild-type at P24-25 (MGI Ref ID J:79293)
- increased mean corpuscular volume
- significantly increased compared to wild-type at P24-25 (MGI Ref ID J:79293)
- low mean erythrocyte cell number
- significantly lower than wild-type at birth (32% of wild-type value) (MGI Ref ID J:79293)
- macrocytic anemia
- severe at birth (MGI Ref ID J:79293)
- reproductive system phenotype
- abnormal primordial germ cell migration
- at E10.5, only 45% of total PGCs have migrated from hindgut, compared to 93% in wild-type (MGI Ref ID J:115437)
- abnormal primordial germ cell morphology
- between E9.5 and 10.5, most PGCs are found with in the hindgut and these have abnormal morphology, while in wild-type embryos most PGCs are found in dorsal portions of mesentery (MGI Ref ID J:115437)
- decreased primordial germ cell number
- moderate numbers of primordial germ cells (PGCs) are seen in genital ridges relative to wild-type and KitlSl-gb homozygotes at E11.5 (MGI Ref ID J:115437)
- at E9.5, PGCs are located primarily in the ventral axis of the hindgut while in wild-type PGCs are found primarily associated with the hindgut epithelium or in the dorsal axis of the hindgut; total PGC number in mutant embryos is 22% of wild-type (MGI Ref ID J:115437)
- abnormal primordial germ cell proliferation
- proliferation indices of migratory (in mesentery and genital ridges) and postmigratory PGCs (in genital ridges) at 10.5 and 11.5 are significantly reduced compared to wild-type values (54-66% of wild-type values) (MGI Ref ID J:115437)
- cellular phenotype
- abnormal primordial germ cell migration
- at E10.5, only 45% of total PGCs have migrated from hindgut, compared to 93% in wild-type (MGI Ref ID J:115437)
- abnormal primordial germ cell proliferation
- proliferation indices of migratory (in mesentery and genital ridges) and postmigratory PGCs (in genital ridges) at 10.5 and 11.5 are significantly reduced compared to wild-type values (54-66% of wild-type values) (MGI Ref ID J:115437)
- increased apoptosis
- at E10.5, many PGCs in hindgut appear to be disintegrating; abnormal PGCs in hindgut tend to be nonmotile and apoptotic (MGI Ref ID J:115437)
KitlSl/KitlSl-d
involves: C3H * C57BL/6 * DBA/2J * WC
- hematopoietic system phenotype
- decreased mast cell number
- in early postnatal mice, mast cell number in skin is ~4% of wild-type number (MGI Ref ID J:6084)
- adult mice have <1% of numbers in wild-type mice (MGI Ref ID J:6084)
- no mast cells are detected in stomachs and mesenteries of adult mutants; none are found in cecum, bone marrow, spleen, thymus, heart, lung, kidney, liver or brain in mutants of various ages (MGI Ref ID J:6084)
- immune system phenotype
- abnormal response to transplant
- after receiving skin grafts from Kit
/Kit donors, a significant increase in mast cell number in skin is seen, compared no increase observed in reciprocal transplant (MGI Ref ID J:6084) - decreased mast cell number
- in early postnatal mice, mast cell number in skin is ~4% of wild-type number (MGI Ref ID J:6084)
- adult mice have <1% of numbers in wild-type mice (MGI Ref ID J:6084)
- no mast cells are detected in stomachs and mesenteries of adult mutants; none are found in cecum, bone marrow, spleen, thymus, heart, lung, kidney, liver or brain in mutants of various ages (MGI Ref ID J:6084)
This mouse can be used to support research in many areas including:
KitlSl-d relatedCancer Research
Increased Tumor Incidence
Gonadal Tumors
Gonadal Tumors: testicular teratomas
Hematological Research
Anemia, Iron Deficiency and Transport Defects
Mast Cell Deficiency
Mouse/Human Gene Homologs
synpolydactyly
KitlSl relatedCancer 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 Tube Defects
Endocrine Deficiency Research
Bone/Bone Marrow Defects
Gonad Defects
Hypothalamus/Pituitary Defects
Skin Defects
Immunology and Inflammation 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 and Inflammation Research
Mast Cell Deficiency
Sensorineural Research
Hearing Defects
Pde6brd1 relatedCancer 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 and Inflammation 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 and Inflammation Research
Mast Cell Deficiency
Sensorineural Research
Hearing Defects
Mouse/Human Gene Homologs
retinitis pigmentosa, autosomal recessive
Sensorineural Research
Retinal Degeneration
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | KitlSl-d | ||
|---|---|---|---|
| Allele Name | steel Dickie | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | KL; MGF; MgfSl-d; Sld; Sld; W/Wv; | ||
| Strain of Origin | DBA/2J | ||
| 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; cloud gray; contrasted; grizzle-belly; kit-ligand; mast cell growth factor; steel; stem cell factor; | ||
| General Note |
Genbank ID for this allele: M64262 | ||
| Molecular Note | A 4kb deletion in genomic DNA results in the absence of 241bp in the mRNA and the addition of 67bp of novel sequence, a 174bp net loss. The region that is deleted corresponds to 5 amino acids N-terminal to the transmembrane domain of the encoded protein, and results in termination of the open reading frame after an additional 3 amino acids. The resulting protein is a soluble truncated one, lacking both transmembrane and cytoplasmic domains. Northern analysis indicates that mRNA is transcribed at nearly wild-type levels in adult tissues. [MGI Ref ID J:10750] [MGI Ref ID J:20286] [MGI Ref ID J:40339] | ||
| Allele Symbol | KitlSl | ||
| Allele Name | steel | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | MgfSl; Sl; | ||
| Strain of Origin | C3H | ||
| 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; cloud gray; contrasted; grizzle-belly; kit-ligand; mast cell growth factor; steel; stem cell factor; | ||
| Associated Marker Note | Affected-Count: 24Af1-Gene: MGI:1919082Af2-Gene: MGI:89794Af3-Gene: MGI:5010055Af4-Gene: MGI:96974Af5-Gene: MGI:88800Af6-Gene: MGI:3646823Af7-Gene: MGI:3779885Af8-Gene: MGI:3647354Af9-Gene: MGI:3646142Af10-Gene: MGI:3782481Af11-Gene: MGI:3782482Af12-Gene: MGI:3782483Af13-Gene: MGI:3782485Af14-Gene: MGI:3644351Af15-Gene: MGI:3782487Af16-Gene: MGI:3782489Af17-Gene: MGI:3782491Af18-Gene: MGI:3647757Af19-Gene: MGI:3782493Af20-Gene: MGI:3643164Af21-Gene: MGI:3036255Af22-Gene: MGI:2384917Af23-Gene: MGI:1921197Af24-Gene: MGI:1913855 | ||
| 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 | Pde6brd1 | ||
| Allele Name | retinal degeneration 1 | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | Pdebrd1; rd; rd-1; rd1; rodless retina; | ||
| Strain of Origin | various | ||
| 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 | ||
| 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] | ||
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
Feldweg AM; Friend DS; Zhou JS; Kanaoka Y; Daheshia M; Li L; Austen KF; Katz HR. 2003. gp49B1 suppresses stem cell factor-induced mast cell activation-secretion and attendant inflammation in vivo. Eur J Immunol 33(8):2262-8. [PubMed: 12884301] [MGI Ref ID J:84936]
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]
KitlSl-d relatedKitlSl relatedBarker JE. 1997. Early transplantation to a normal microenvironment prevents the development of Steel hematopoietic stem cell defects. Exp Hematol 25(6):542-7. [PubMed: 9197334] [MGI Ref ID J:41120]
Beckett EA; Horiguchi K; Khoyi M; Sanders KM; Ward SM. 2002. Loss of enteric motor neurotransmission in the gastric fundus of Sl/Sl(d) mice. J Physiol 543(Pt 3):871-87. [PubMed: 12231645] [MGI Ref ID J:105989]
Bernstein S. 1960. Steel Dickie Mouse News Lett 23:33-4. [MGI Ref ID J:13392]
Brannan CI; Lyman SD; Williams DE; Eisenman J; Anderson DM; Cosman D; Bedell MA; Jenkins NA; Copeland NG. 1991. Steel-Dickie mutation encodes a c-kit ligand lacking transmembrane and cytoplasmic domains. Proc Natl Acad Sci U S A 88(11):4671-4. [PubMed: 1711207] [MGI Ref ID J:20286]
Chen R; Fairley JA; Zhao ML; Giudice GJ; Zillikens D; Diaz LA; Liu Z. 2002. Macrophages, but not T and B lymphocytes, are critical for subepidermal blister formation in experimental bullous pemphigoid: macrophage-mediated neutrophil infiltration depends on mast cell activation. J Immunol 169(7):3987-92. [PubMed: 12244200] [MGI Ref ID J:120403]
Chen R; Ning G; Zhao ML; Fleming MG; Diaz LA; Werb Z; Liu Z. 2001. Mast cells play a key role in neutrophil recruitment in experimental bullous pemphigoid. J Clin Invest 108(8):1151-8. [PubMed: 11602622] [MGI Ref ID J:72195]
Choi Y; Rajkovic A. 2006. Genetics of early mammalian folliculogenesis. Cell Mol Life Sci 63(5):579-90. [PubMed: 16416028] [MGI Ref ID J:108336]
Deol MS. 1970. The relationship between abnormalities of pigmentation and of the inner ear. Proc R Soc Lond B Biol Sci 175(39):201-17. [PubMed: 4392283] [MGI Ref ID J:125080]
Ding H; Nedrud JG; Wershil B; Redline RW; Blanchard TG; Czinn SJ. 2009. Partial protection against Helicobacter pylori in the absence of mast cells in mice. Infect Immun 77(12):5543-50. [PubMed: 19822650] [MGI Ref ID J:155471]
Flanagan JG; Chan DC; Leder P. 1991. Transmembrane form of the kit ligand growth factor is determined by alternative splicing and is missing in the Sld mutant. Cell 64(5):1025-35. [PubMed: 1705866] [MGI Ref ID J:40339]
Galli SJ; Hammel I. 1984. Unequivocal delayed hypersensitivity in mast cell-deficient and beige mice. Science 226(4675):710-3. [PubMed: 6494907] [MGI Ref ID J:127346]
Gore BB; Wong KG; Tessier-Lavigne M. 2008. Stem cell factor functions as an outgrowth-promoting factor to enable axon exit from the midline intermediate target. Neuron 57(4):501-10. [PubMed: 18304480] [MGI Ref ID J:132880]
Gu Y; Runyan C; Shoemaker A; Surani MA; Wylie C. 2011. Membrane-bound steel factor maintains a high local concentration for mouse primordial germ cell motility, and defines the region of their migration. PLoS One 6(10):e25984. [PubMed: 21998739] [MGI Ref ID J:179622]
Gurish MF; Tao H; Abonia JP; Arya A; Friend DS; Parker CM; Austen KF. 2001. Intestinal mast cell progenitors require CD49dbeta7 (alpha4beta7 integrin) for tissue-specific homing. J Exp Med 194(9):1243-52. [PubMed: 11696590] [MGI Ref ID J:119138]
Heissig B; Rafii S; Akiyama H; Ohki Y; Sato Y; Rafael T; Zhu Z; Hicklin DJ; Okumura K; Ogawa H; Werb Z; Hattori K. 2005. Low-dose irradiation promotes tissue revascularization through VEGF release from mast cells and MMP-9-mediated progenitor cell mobilization. J Exp Med 202(6):739-50. [PubMed: 16157686] [MGI Ref ID J:107445]
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Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Room Number FGB27
Colony Maintenance
Diet Information LabDiet® 5K52/5K67
Purchasing information
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
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Live Mice
Price (US dollars $) Gender Genotypes Provided Individual Mouse $172.00 Female or Male Compound Heterozygote for allele KitlSl and allele KitlSl-d
Pairs /Price (US dollars $) Pair Genotype $263.00 WC/ReJ KitlSl/J (000693) x B6.D2-KitlSl-d/J (000160) Standard Supply
Repository-Live. The Repository Strains represent an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. We treat orders for these strains as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
| Pricing for International shipping destinations |
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Live Mice
Price (US dollars $) Gender Genotypes Provided Individual Mouse $223.60 Female or Male Compound Heterozygote for allele KitlSl and allele KitlSl-d
Pairs /Price (US dollars $) Pair Genotype $341.90 WC/ReJ KitlSl/J (000693) x B6.D2-KitlSl-d/J (000160) Standard Supply
Repository-Live. The Repository Strains represent an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. We treat orders for these strains as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
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Standard Supply
Repository-Live. The Repository Strains represent an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. We treat orders for these strains as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
General Supply Notes
- This strain is included in the Mouse Mutant Resource collection.
- Genomic DNA is available for this strain from the Mouse DNA Resource.
Control Information
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
Important Note
This strain is heterozygous for the retinal degeneration allele Pde6brd1.
Payment Terms and Conditions
Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.
See Terms of Use tab for General Terms and Conditions
The Jackson Laboratory's Genotype Promise
The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.Ordering Information
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General inquiriesContracts Administration
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
JAX® Mice, Products & Services Conditions of Use
"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.No Warranty
MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.
In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.
No Liability
In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. 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.