Strain Name:

ROP/GnLeJ

Stock Number:

000267

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Availability:

Cryopreserved - Ready for recovery

Description

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

Strain Information

Type Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Type Inbred Strain;
Additional information on Inbred Strains.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
GenerationF82p
Generation Definitions

Important Note
This strain is segregating for Sox18ra, Os, Pt, Es1a and Es1b.

Description
The Sox18Ra and Sox18Ra-J alleles cause a less severe phenotype than the Sox18Ra-Op allele. The Sox18Ra and Sox18Ra-J alleles are similar mutations and give a very similar phenotype. The Sox18Ra allele has been more broadly described in the literature and will be covered here. Heterozygotes are viable and fertile. Heterozygotes have developmentally retarded sinus hair growth apparent at embryonic day 16.5 and retarded development of pelage follicles apparent by embryonic day 17.5. Thus, heterozygotes have slightly shorter vibrissae evident at birth, and can be distinguished at three days of age by their pink skin which, due to the abnormally sparse development of the coat, fails to darken like that of wildtype siblings. A paucity of fur is apparent by nine days of age and persists throughout life. Compared with the wild type pelage, Sox18Ra/+ coats have longer guard hairs, shorter awls and zigzags, an increased number of guard hairs and awls, fewer zigzags, and no auchenes. There are mild morphological abnormalities in the hairs. There is no decrease in the number of hair follicles, but many of the follicles fail to grow hair. There is decreased yellow pigment in the hair causing the thin coat that develops to be darker than normal particularly in the dorsal midline. Subsequent to the first wave, hair growth is asynchronous and the normal cyclic fluctuations in skin thickness are not found. The adipose layer of the skin is thinner than normal. Despite this asynchrony of adjacent hair follicles, hair cycles do occur across the pelage, but are more diffuse than normal. The hair follicles have an aberrant shape and orientation. This aberrancy is more pronounced in homozygotes. The impact of the Sox18Ra mutation on hair is more pronounced in the anterior regions than in the posterior regions. Approximately one in ten heterozygous pups displays chylous ascites, and the most severely affected do not survive. This trait is seen in males more than in females and is modified by genetic background. (Carter and Phillips, 1954; Slee, 1956 and 1957; Mann, 1963; Herbertson and Wallace, 1964; Wallace, 1979.)

Homozygotes are nearly bald, lack vibrissae, and usually die before weaning. They have generalized edema and weigh more at birth than wildtype littermates. It has been estimated that 40% of homozygotes die as embryos. The homozygotes that survive are often 5-10% shorter in body length. There are fewer hair follicles than normal and the few hairs that do grow have abnormal morphology. There is pigment in the tail and ear pinnae, and theear pinnae are thinner than normal and are often wrinkled. (Carter and Phillips, 1954; Slee, 1956 and 1957; Mann 1963.)

Development
Ragged (Sox18Ra) arose spontaneously in a cross bred stock at Edinburgh and was imported to the Jackson Laboratory about 1957. Oligosyndactyly (Os) arose in an irradiation experiment, probably X ray induced at Oak Ridge, in offspring of an F1 male from a 101 x C3H cross mated to a multiple recessive stock female. It was imported to the Jackson Laboratory from University College London in 1957. Pintail (Pt) arose at Yale Medical School at the 21st generation of inbreeding in a strain &#-30;¿¿pBr&#-30;¿¿ (homozygous for a, Tyrpb, and p) after treatment with methylcholanthrene, and was imported to The Jackson Laboratory in the 1950&#-30;¿¿s. The linkage testing stock ROP/GnLe was established by Dr. M.C. Green by mating an Ra/+ female on a C57BL/6J congenic background to an Os/+ male in 1957. An Ra/+ Os/+ male was then mated to a B6.Cg-Pt heterozygous N11 female and the stock was within-stock bred for 8 generations. In 1959 inbreeding was started. It was then maintained by sibling matings only and cryopreserved in 1991 by mating Ra/+ Os/+ Pt/+ males to a normal non-mutant females at F80-82.

Related Strains

Strains carrying   Os allele
000566   B6.Cg-Os +/+ Cacna1atg-la/J
003523   B6.ROP/Le-Os/J
000125   B6By.Cg-Sox18Ra Pt Os/J
000300   MYD/Le-Os +/+ Largemyd/J
002503   ROP/Le-Os Ces1ca/+ Ces1ca/J
View Strains carrying   Os     (5 strains)

Strains carrying   Pt allele
000125   B6By.Cg-Sox18Ra Pt Os/J
View Strains carrying   Pt     (1 strain)

Strains carrying   Sox18Ra allele
000018   B6.Cg-Sox18Ra/J
000125   B6By.Cg-Sox18Ra Pt Os/J
View Strains carrying   Sox18Ra     (2 strains)

Strains carrying other alleles of Sox18
010987   B6;129S-Sox18tm1(GFP/cre/ERT2)Pzg/J
000508   B6D2-Sox18Ra-Op/J
023020   B6N(Cg)-Sox18tm1.1(KOMP)Vlcg/J
002261   C3H/HeSnJ-Sox18Ra-J/J
View Strains carrying other alleles of Sox18     (4 strains)

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.
Hypotrichosis-Lymphedema-Telangiectasia Syndrome; HLTS   (SOX18)
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.

Os/Os

        involves: 101 * C3H
  • mortality/aging
  • complete embryonic lethality between implantation and placentation   (MGI Ref ID J:5017)
  • embryogenesis phenotype
  • decreased embryo size
    • noted as early as E4.5   (MGI Ref ID J:5768)
  • embryonic growth arrest
    • cells of the developing embryo appear abnormal between the 7th and 8th division with suggestion of mitotic dysfunction   (MGI Ref ID J:5017)
    • the most striking abnormalities are seen by the middle of the 4th day when many embryonic cells contain fragmented, pycnotic chromatin and lack nuclear membrane and nucleolus   (MGI Ref ID J:5017)
    • in culture, blastocysts show rapid degeneration of the inner cell mass compared with control embryos   (MGI Ref ID J:5768)
  • cellular phenotype
  • abnormal mitosis   (MGI Ref ID J:5768)
    • increased mitotic index
      • E4.5 embryos have an index nine times that of controls   (MGI Ref ID J:5768)
      • more than one third of cells contain mitotic figures   (MGI Ref ID J:5768)
  • growth/size/body phenotype
  • decreased embryo size
    • noted as early as E4.5   (MGI Ref ID J:5768)

Os/Os+

        B6.ROP/Le-Os/J
  • renal/urinary system phenotype
  • abnormal renal glomerulus morphology
    • glomerular volume is increased 2-fold relative to controls at 3 months of age and 3-fold at 5 months of age but the glomerulosclerosis found on the ROP background is absent with only a minimal increase in extracellular matrix at 5 months of age   (MGI Ref ID J:32764)
    • the mean cell number per glomerulus is increased 21% relative to controls and the glomerular labeling index is increased 2.6 fold at 3 and 5 months of age   (MGI Ref ID J:32764)
    • decreased renal glomerulus number
      • mean glomerular number per kidney is reduced by 50% at 3 months of age   (MGI Ref ID J:32764)
    • expanded mesangial matrix
      • only a minimal increase in extracellular matrix is noted at 5 months of age   (MGI Ref ID J:32764)
  • decreased kidney weight
    • 34% reduction in kidney weight compared with controls at 3 months of age   (MGI Ref ID J:32764)

Pt/Pt

        PBR
  • mortality/aging
  • decreased survivor rate
    • survivors are healthy and fertile   (MGI Ref ID J:15)
  • partial preweaning lethality
    • there is a high preweaning mortality   (MGI Ref ID J:15)
  • growth/size/body phenotype
  • decreased body size   (MGI Ref ID J:15)
  • limbs/digits/tail phenotype
  • abnormal tail tip morphology
    • tail tip is thin and threadlike   (MGI Ref ID J:15)
  • kinked tail
    • kinks are at the end of the tail   (MGI Ref ID J:15)
  • short tail
    • tails are much shorter than those of heterozygotes   (MGI Ref ID J:15)
  • skeleton phenotype
  • abnormal nucleus pulposus morphology
    • there is a progressive reduction, from head to tail, of the nucleus pulposus   (MGI Ref ID J:15)
    • reduction is more severe than found in heterozygous mice   (MGI Ref ID J:15)
  • small intervertebral disk   (MGI Ref ID J:15)

Pt/Pt

        involves: CBA/Gr * PBR
  • embryogenesis phenotype
  • abnormal notochord morphology
    • noticeable at E10 as a reduced rate of cell division in the notochord   (MGI Ref ID J:14974)
    • small notochord   (MGI Ref ID J:14974)
  • limbs/digits/tail phenotype
  • abnormal caudal vertebrae morphology
    • caused by a notochord defect   (MGI Ref ID J:14974)
    • decreased caudal vertebrae number
      • there are always fewer than ten caudal vertebrae   (MGI Ref ID J:14974)
  • skeleton phenotype
  • abnormal caudal vertebrae morphology
    • caused by a notochord defect   (MGI Ref ID J:14974)
    • decreased caudal vertebrae number
      • there are always fewer than ten caudal vertebrae   (MGI Ref ID J:14974)
  • small intervertebral disk
    • smaller intervertebral discs are the result of a small notochord   (MGI Ref ID J:14974)

Pt/Pt+

        PBR
  • limbs/digits/tail phenotype
  • abnormal tail tip morphology
    • tip of the tail is threadlike   (MGI Ref ID J:15)
  • kinked tail
    • kinks are near the end of the tail   (MGI Ref ID J:15)
  • short tail
    • tail length is variable but longer than tails of homozygotes   (MGI Ref ID J:15)
  • skeleton phenotype
  • abnormal nucleus pulposus morphology
    • there is a progressive reduction, head to tail, of the nucleus pulposus   (MGI Ref ID J:15)
    • the reduction is less severe in heterozygotes than in homozygotes   (MGI Ref ID J:15)
  • small intervertebral disk   (MGI Ref ID J:15)

Pt/Pt+

        involves: CBA/Gr * PBR
  • limbs/digits/tail phenotype
  • decreased caudal vertebrae number
    • the number of tail vertebrae is usually reduced by a third   (MGI Ref ID J:14974)
  • skeleton phenotype
  • decreased caudal vertebrae number
    • the number of tail vertebrae is usually reduced by a third   (MGI Ref ID J:14974)
  • small intervertebral disk
    • a smaller than normal notochord results in smaller than normal intervertebral disks in affected areas of the tail   (MGI Ref ID J:14974)
  • embryogenesis phenotype
  • abnormal notochord morphology
    • at E10 there is a reduced rate of cell division in the notochord   (MGI Ref ID J:14974)
    • small notochord   (MGI Ref ID J:14974)
View Research Applications

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

Os related

Developmental Biology Research
Skeletal Defects
      Oligodactyly

Internal/Organ Research
Kidney Defects
      diabetes insipidus

Pt related

Developmental Biology Research
Skeletal Defects

Sox18Ra related

Dermatology Research
Skin and Hair Texture Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Os
Allele Name Os
Allele Type Radiation induced
Strain of Origin(101 x C3H)F1
Gene Symbol and Name Os, oligosyndactylism
Chromosome 8
Gene Common Name(s) 94-A; 94-K; PlmTgN(Pgk1)1Ddp; PlmTgN(Pgk1)2Ddp; postimplantation lethal mutation induced by Pgk1 transgene insertion-Dimitrina D. Pravtcheva 1; postimplantation lethal mutation induced by Pgk1 transgene insertion-Dimitrina D. Pravtcheva 2;
General Note Heterozygotes are affected on all four feet. Fusion usually occurs between the second and third digits and occasionally involves the fourth (J:13049). The muscles of the forearms and lower legs as well as of the feet show anomalous arrangements not necessarily correlated with the skeletal changes (J:12944). At 11 days of gestation the preaxial border of the limbs can be seen to be reduced (J:12942), and a histological examination at this time shows that there is a small amount of cellular degeneration in the preaxial part of the footplate mesoderm, leading to coalescence of the second and third digital rudiments (J:5107). Os /+ mice have a mild diabetes insipidus present at 5 weeks and increasing with age. In combination with one or more recessive modifying genes in the selected DI stock, Os/+ mice have a severe diabetes insipidus (J:12948). The cause of the diabetes is a 45% reduction in size of the kidneys with an 80% reduction in number of glomeruli. Compensatory hypertrophy of the nephrons is not sufficient to restore normal urine-concentrating ability (J:5127)(J:5128).
Molecular Note The oligosyndactylism mutation is due to a chromosomal inversion that has breakpoints approximately 10 Mb apart. One breakpoint appears to reside in the Anapc10 gene, and an aberrant transcript consisting of part of Anapc10 and an unrelated sequence is expressed at low levels. [MGI Ref ID J:81567] [MGI Ref ID J:95333]
 
Allele Symbol Pt
Allele Name pintail
Allele Type Chemically induced (other)
Strain of OriginPBR
Gene Symbol and Name Pt, pintail
Chromosome 4
General Note This mutation rose in a strain protractedly treated with methylcholanthrene (MCA).
Molecular Note This mutation was isolated at the Yale University School of Medicine in 1951.
 
Allele Symbol Sox18Ra
Allele Name ragged
Allele Type Spontaneous
Common Name(s) Ra;
Strain of OriginTranslocation stock
Gene Symbol and Name Sox18, SRY (sex determining region Y)-box 18
Chromosome 2
Gene Common Name(s) AI385749; HLTS; Ra; Ragl; Sry-related HMG-box gene 18; expressed sequence AI385749; ragged; ragged-like;
General Note Sox18ra, ragged, semidominant. Arose spontaneously in a crossbred stock. In heterozygotes the first coat develops a little more slowly than normal. The coat contains guard hairs and awls but no auchenes and very few zigzags. This gives the coat a thin ragged appearance. The agouti pattern is modified, the entire coat being unusually dark. Heterozygotes are normally viable and fertile. Homozygotes are almost completely naked. Many are edematous at birth, and almost all die before weaning. A fewsurvive and may breed (J:86). Developmental studies have shown that in Sox18ra/+ mice, growth of the late differentiating hair follicles which produce auchenes and zigzags is very retarded or arrested (J:12991). A low percentage of Sox18ra/+ mice in some stocks were found by Herbertson and Wallace (J:13089) to have a white chylous fluid in the abdomen from shortly after birth until a week or so of age. The incidence of chylous ascites in these mice is affected by one or more genes unlinked to Sox18Ra, and also by two mutant genes linked to Sox18Ra, (fi, we) and one on a different chromosome (py, Chr 1) (J:6220).

The phenotypes of Sox18Ra and Sox18ra-J have been described as indistinguishable (J:51188).

Molecular Note A deletion of a cytosine residue introduced a frameshift mutation affecting amino acids downstream of 314. Translation was prematurely stopped at codon 435. The deleted nucleotide was reported as nucleotide 960 in J:61488 and as nucleotide 938 in J:74211and J:83731. [MGI Ref ID J:61488] [MGI Ref ID J:74211] [MGI Ref ID J:83731]

Genotyping

Genotyping Information


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

He C; Esposito C; Phillips C; Zalups RK; Henderson DA; Striker GE; Striker LJ. 1996. Dissociation of glomerular hypertrophy, cell proliferation, and glomerulosclerosis in mouse strains heterozygous for a mutation (Os) which induces a 50% reduction in nephron number. J Clin Invest 97(5):1242-9. [PubMed: 8636436]  [MGI Ref ID J:32764]

Additional References

Dunn TL; Mynett-Johnson L; Wright EM; Hosking BM; Koopman PA; Muscat GE. 1995. Sequence and expression of Sox-18 encoding a new HMG-box transcription factor. Gene 161(2):223-5. [PubMed: 7665083]  [MGI Ref ID J:28369]

Hosking BM; Wyeth JR; Pennisi DJ; Wang SC; Koopman P; Muscat GE. 2001. Cloning and functional analysis of the Sry-related HMG box gene, Sox18. Gene 262(1-2):239-47. [PubMed: 11179689]  [MGI Ref ID J:67559]

James K; Hosking B; Gardner J; Muscat GE; Koopman P. 2003. Sox18 mutations in the ragged mouse alleles ragged-like and opossum. Genesis 36(1):1-6. [PubMed: 12748961]  [MGI Ref ID J:83731]

Pennisi D; Bowles J; Nagy A; Muscat G; Koopman P. 2000. Mice null for sox18 are viable and display a mild coat defect Mol Cell Biol 20(24):9331-6. [PubMed: 11094083]  [MGI Ref ID J:66010]

Pennisi D; Gardner J; Chambers D; Hosking B; Peters J; Muscat G; Abbott C; Koopman P. 2000. Mutations in Sox18 underlie cardiovascular and hair follicle defects in ragged mice. Nat Genet 24(4):434-7. [PubMed: 10742113]  [MGI Ref ID J:61488]

Pravtcheva DD; Wise TL. 1996. A transgene-induced mitotic arrest mutation in the mouse allelic with Oligosyndactylism. Genetics 144(4):1747-56. [PubMed: 8978060]  [MGI Ref ID J:38877]

Pravtcheva DD; Wise TL. 2001. Disruption of Apc10/Doc1 in three alleles of oligosyndactylism. Genomics 72(1):78-87. [PubMed: 11247669]  [MGI Ref ID J:81567]

Wallace ME. 1979. Analysis of genetic control of chylous ascites in ragged mice. Heredity (Edinburgh) 43(1):9-18. [PubMed: 291594]  [MGI Ref ID J:6220]

Os related

Cornacchia F; Fornoni A; Plati AR; Thomas A; Wang Y; Inverardi L; Striker LJ; Striker GE. 2001. Glomerulosclerosis is transmitted by bone marrow-derived mesangial cell progenitors. J Clin Invest 108(11):1649-56. [PubMed: 11733560]  [MGI Ref ID J:166810]

Elliot SJ; Karl M; Berho M; Potier M; Zheng F; Leclercq B; Striker GE; Striker LJ. 2003. Estrogen deficiency accelerates progression of glomerulosclerosis in susceptible mice. Am J Pathol 162(5):1441-8. [PubMed: 12707027]  [MGI Ref ID J:83190]

Esposito C; He CJ; Striker GE; Zalups RK; Striker LJ. 1999. Nature and severity of the glomerular response to nephron reduction is strain-dependent in mice. Am J Pathol 154(3):891-7. [PubMed: 10079267]  [MGI Ref ID J:53353]

Falconer DS; Latyszewski M; Isaacson JH. 1964. Diabetes insipidus associated with oligosyndactylism in the mouse. Genet Res 5:473-488.  [MGI Ref ID J:12948]

Gruneberg H. 1956. Genetical studies on the skeleton of the mouse. XVIII. Three genes for syndactylism. J Genet 54:113-145.  [MGI Ref ID J:13049]

Gruneberg H. 1961. Genetical studies on the skeleton of the mouse. XXVII. The development of oligosyndactylism. Genet Res 2:33-42.  [MGI Ref ID J:12942]

He C; Zalups RK; Henderson DA; Striker GE; Striker LJ. 1995. Molecular analysis of spontaneous glomerulosclerosis in Os/+ mice, a model with reduced nephron mass. Am J Physiol 269(2 Pt 2):F266-73. [PubMed: 7544540]  [MGI Ref ID J:28323]

Jarad G; Lakhe-Reddy S; Blatnik J; Koepke M; Khan S; El-Meanawy MA; O'Connor AS; Sedor JR; Schelling JR. 2004. Renal phenotype is exacerbated in Os and lpr double mutant mice. Kidney Int 66(3):1029-35. [PubMed: 15327396]  [MGI Ref ID J:102341]

Kadam KM. 1962. Genetical studies on the skeleton of the mouse. XXXI. The muscular anatomy of syndactylism and oligosyndactylism. Genet Res 3:139-156.  [MGI Ref ID J:12944]

Liu S; Friel DD. 2008. Impact of the leaner P/Q-type Ca2+ channel mutation on excitatory synaptic transmission in cerebellar Purkinje cells. J Physiol 586(Pt 18):4501-15. [PubMed: 18669535]  [MGI Ref ID J:176384]

McLaren A. 1976. Genetics of the early mouse embryo. Annu Rev Genet 10:361-88. [PubMed: 797312]  [MGI Ref ID J:5768]

Milaire J. 1967. Histochemical observations on the developing foot of normal, oligosyndactylous (Os-plus) and syndactylous (sm-sm) mouse embryos. Arch Biol (Liege) 78(2):223-88. [PubMed: 4305644]  [MGI Ref ID J:5107]

Muhlfeld AS; Spencer MW; Hudkins KL; Kirk E; LeBoeuf RC; Alpers CE. 2004. Hyperlipidemia aggravates renal disease in B6.ROP Os/+ mice. Kidney Int 66(4):1393-402. [PubMed: 15458432]  [MGI Ref ID J:102315]

Naik DV; Valtin H. 1969. Hereditary vasopressin-resistant urinary concentrating defects in mice. Am J Physiol 217(4):1183-90. [PubMed: 5824320]  [MGI Ref ID J:5127]

Ovsepian SV; Friel DD. 2008. The leaner P/Q-type calcium channel mutation renders cerebellar Purkinje neurons hyper-excitable and eliminates Ca2+-Na+ spike bursts. Eur J Neurosci 27(1):93-103. [PubMed: 18093175]  [MGI Ref ID J:132196]

Pravtcheva DD; Wise TL. 2001. Disruption of Apc10/Doc1 in three alleles of oligosyndactylism. Genomics 72(1):78-87. [PubMed: 11247669]  [MGI Ref ID J:81567]

Sorenson CM; Rogers SA; Hammerman MR. 1996. Abnormal renal development in the Os/+ mouse is intrinsic to the kidney. Am J Physiol 271(1 Pt 2):F234-8. [PubMed: 8760267]  [MGI Ref ID J:34503]

Stewart AD; Stewart J. 1969. Studies on syndrome of diabetes insipidus associated with oligosyndactyly in mice. Am J Physiol 217(4):1191-8. [PubMed: 4309975]  [MGI Ref ID J:5128]

Van Valen P. 1966. Oligosyndactylism, an early embryonic lethal in the mouse. J Embryol Exp Morphol 15(2):119-24. [PubMed: 4289631]  [MGI Ref ID J:5017]

Wang Y; Heilig KO; Minto AW; Chen S; Xiang M; Dean DA; Geiger RC; Chang A; Pravtcheva DD; Schlimme M; Deb DK; Wang Y; Heilig CW. 2010. Nephron-deficient Fvb mice develop rapidly progressive renal failure and heavy albuminuria involving excess glomerular GLUT1 and VEGF. Lab Invest 90(1):83-97. [PubMed: 19918242]  [MGI Ref ID J:156400]

Wise TL; Pravtcheva DD. 2004. Oligosyndactylism mice have an inversion of chromosome 8. Genetics 168(4):2099-112. [PubMed: 15611179]  [MGI Ref ID J:95333]

Zalups RK. 1993. The Os/+ mouse: a genetic animal model of reduced renal mass. Am J Physiol 264(1 Pt 2):F53-60. [PubMed: 8430831]  [MGI Ref ID J:3842]

Pt related

Berry RJ. 1960. Genetical studies on the skeleton of the mouse. XXVI. Pintail Genet Res 1:439-51.  [MGI Ref ID J:14974]

Berry RJ. 1961. Genetically controlled degeneration of the nucleus pulposus in the mouse J Bone Joint Surg Br 43B:387-93.  [MGI Ref ID J:30698]

Dietrich S; Schubert FR; Gruss P. 1993. Altered Pax gene expression in murine notochord mutants: the notochord is required to initiate and maintain ventral identity in the somite. Mech Dev 44(2-3):189-207. [PubMed: 8155581]  [MGI Ref ID J:16484]

Dietrich S; Schubert FR; Gruss P; Lumsden A. 1999. The role of the notochord for epaxial myotome formation in the mouse. Cell Mol Biol (Noisy-le-grand) 45(5):601-16. [PubMed: 10512192]  [MGI Ref ID J:59749]

Hollander WF. 1976. Genetic spina bifida occulta in the mouse. Am J Anat 146(2):173-9. [PubMed: 782223]  [MGI Ref ID J:5675]

Hollander WF; Strong LC. 1951. Pintail, a dominant mutation linked with brown in the house mouse J Hered 42:179-182.  [MGI Ref ID J:15]

Sox18Ra related

Carter TC; Phillips RJS. 1954. Ragged, a semidominant coat texture mutant J Hered 45:151-154.  [MGI Ref ID J:86]

Downes M; Koopman P. 2001. SOX18 and the transcriptional regulation of blood vessel development. Trends Cardiovasc Med 11(8):318-24. [PubMed: 11728880]  [MGI Ref ID J:74211]

Herbertson BM; Wallace ME. 1964. Chylous ascites in newborn mice. J Med Genet 1:10-23.  [MGI Ref ID J:13089]

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

James K; Hosking B; Gardner J; Muscat GE; Koopman P. 2003. Sox18 mutations in the ragged mouse alleles ragged-like and opossum. Genesis 36(1):1-6. [PubMed: 12748961]  [MGI Ref ID J:83731]

Mann S. 1962. Prenatal formation of hair follicle types Anat Rec 144:135-142.  [MGI Ref ID J:155792]

Pennisi D; Gardner J; Chambers D; Hosking B; Peters J; Muscat G; Abbott C; Koopman P. 2000. Mutations in Sox18 underlie cardiovascular and hair follicle defects in ragged mice. Nat Genet 24(4):434-7. [PubMed: 10742113]  [MGI Ref ID J:61488]

SLEE J. 1962. Developmental morphology of the skin and hair follicles in normal and in 'ragged' mice. J Embryol Exp Morphol 10:507-29. [PubMed: 13989207]  [MGI Ref ID J:12991]

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

Wallace ME. 1979. Analysis of genetic control of chylous ascites in ragged mice. Heredity (Edinburgh) 43(1):9-18. [PubMed: 291594]  [MGI Ref ID J:6220]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

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

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3300.00
Animals Provided

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

Standard Supply

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

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

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

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

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $4290.00
Animals Provided

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

Standard Supply

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

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We willfulfill 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.

Important Note

This strain is segregating for Sox18ra, Os, Pt, Es1a and Es1b.

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
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


Contact information

General inquiries regarding Terms of Use

Contracts Administration

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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