Description

Strain Information

Former Names C57BL/6By-Sox18Ra Pt Os/J    (Changed: 13-MAR-08 ) Type Chemically Induced Mutation; Congenic; Mutant Strain; Radiation Induced Mutation; Spontaneous Mutation; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse Generation F25N1p

Description
The Sox18^Ra and Sox18^Ra-J alleles cause a less severe phenotype than the Sox18^Ra-Op allele. The Sox18^Ra and Sox18^Ra-J alleles are similar mutations and give a very similar phenotype. The Sox18^Ra 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, Sox18^Ra/+ 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 Sox18^Ra 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.)

Related Strains

Strains carrying   Os allele

000566	B6.Cg-Os +/+ Cacna1atg-la/J
003523	B6.ROP/Le-Os/J
000300	MYD/Le-Os +/+ Largemyd/J
000267	ROP/GnLeJ
002503	ROP/Le-Os Es1a/+ Es1a/J

View Strains carrying   Os     (5 strains)

Strains carrying   Pt allele

000267

ROP/GnLeJ

View Strains carrying   Pt     (1 strain)

Strains carrying   Sox18^Ra allele

000018	B6.Cg-Sox18Ra/J
000267	ROP/GnLeJ

View Strains carrying   Sox18^Ra     (2 strains)

Strains carrying other alleles of Sox18

000508	B6D2-Sox18Ra-Op/J
002261	C3H/HeSnJ-Sox18Ra-J/J

View Strains carrying other alleles of Sox18     (2 strains)

Additional Web Information

Congenic Nomenclature

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms

      assigned by genotype

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Pt/Pt

        STOCK a Tyrp1^b Oca2^p-Pt

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

Pt/Pt

        involves: CBA/Gr * PBR

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

Pt/Pt⁺

        STOCK a Tyrp1^b Oca2^p-Pt

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

Pt/Pt⁺

        involves: CBA/Gr * PBR

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

Internal/Organ Research
Kidney Defects (diabetes insipidus)

Pt related

Developmental Biology Research
Skeletal Defects

Sox18^Ra related

Dermatology Research
Skin and Hair Texture Defects

Genes & Alleles

Gene & Allele Information

Allele Symbol		Os
Allele Name		Os
Allele Type		Radiation induced
Strain of Origin		(101 x C3H)F1
General Note		This mutation arose in an irradiation experiment and was probably X-ray induced. Homozygotes die by the fifth day of embryonic life, shortly after the 64-cell stage, as a result of abnormalities occurring during the seventh and eighth divisions (J:5017).There is a very high mitotic index, more than a third of the cells containing mitotic figures. Os in homozygotes may exert its primary effect on the mitotic apparatus (J:5768). 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 thesecond 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). Itis not known how the kidney and foot defects are related, or how either is related to the early death of the homozygote.
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 Origin		STOCK a Tyrp1 Oca2
General Note		This mutation rose in a strain protractedly treated with methylcholanthrene (MCA).
Allele Symbol		Sox18Ra
Allele Name		ragged
Allele Type		Spontaneous
Common Name(s)		Ra;
Strain of Origin		Translocation stock
Gene Symbol and Name		Sox18, SRY-box containing gene 18
Chromosome		2
Gene Common Name(s)		AI385749; HLTS; Ra; Ragl; Sry-related HMG-box gene; 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]

Genotyping

Genotyping Information

This strain will not have a genotyping protocol or one is not currently available.

Helpful Links

Optimizing PCR Protocols

References

References

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

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; 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]

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]

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]

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

Sox18^Ra 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]

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. . 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

Currently there no information available for this strain. This may be due to the supply level of this strain.

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Supply Details

Standard Supply

Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information.

Supply Notes

Cryorecovery - Standard. The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two males and two females (two pairs) will be provided, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the delivery time to approximately 25 weeks. At least one member of each pair will be of known genotype and will carry the mutation if it is a mutant strain. Please note that pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Price represents a repository maintenance fee, which includes the cost of recovery of the strain from the cryopreservation resource and the periodic replacement of the frozen embryos used for recovery. Cryorecovery to establish a Dedicated Supply for greater quantities of mice. One to two pairs will be recovered to establish a Dedicated Supply of mice. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 or 1-207-288-5845.

General Terms and Conditions

See Terms of Use

The Jackson Laboratory's Genotype Promise

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

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JAX^® Mice & Services Conditions of Use

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