Description

Strain Information

Type Congenic; Mutant Strain; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse

Appearance
black, fused digits
Related Genotype: a/a Os/+

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

Development
The Os mutation was transferred from mice of strain ROP/Le onto the C57BL/6J background by repeated backcrossing reaching N27 in 2005.

Control Information

	Control
	000664 C57BL/6J
Considerations for Choosing Controls

Related Strains

Strains carrying   Os allele

000566	B6.Cg-Os +/+ Cacna1atg-la/J
000125	B6By.Cg-Sox18Ra Pt Os/J
000300	MYD/Le-Os +/+ Largemyd/J
000267	ROP/GnLeJ
002503	ROP/Le-Os Es1a/+ Es1a/J

View Strains carrying   Os     (5 strains)

Additional Web Information

Congenic Nomenclature
Genetic Quality Control Annual Report

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.

Os/Os⁺

        involves: 101 * C3H

• embryogenesis phenotype
• abnormal limb bud morphology (MGI Ref ID J:5107)
  • retardation of the mesodermal growth in the preaxial area of the footplate of the forelimb buds is found at embryonic day 10 hour 16 and in the hindlimb buds at embryonic day 10 hour 21
  • although normal at early embryonic day 11, by embryonic day 11 to 12 there are cytolytic changes, cellular degeneration, in the preaxial part of the footplate mesoderm, leading to coalescence of the second and third digital rudiments
• limbs/digits/tail phenotype
• abnormal limb bud morphology (MGI Ref ID J:5107)
  • retardation of the mesodermal growth in the preaxial area of the footplate of the forelimb buds is found at embryonic day 10 hour 16 and in the hindlimb buds at embryonic day 10 hour 21
  • although normal at early embryonic day 11, by embryonic day 11 to 12 there are cytolytic changes, cellular degeneration, in the preaxial part of the footplate mesoderm, leading to coalescence of the second and third digital rudiments

Os/Os⁺

        involves: 101 * C3H * CBA/Gr

• lethality-prenatal/perinatal
• prenatal lethality (MGI Ref ID J:13049)
• limbs/digits/tail phenotype
• abnormal carpal bone morphology (MGI Ref ID J:13049)
  • ulnar end of the hamatum articulates with metacarpal 4, but does not reach metacarpal 5
  • metacarpal 5 is in a fixed state of abduction
• fused carpal bones (MGI Ref ID J:13049)
  • extensive fusions in carpus
• abnormal foot plate morphology (MGI Ref ID J:12942)
  • beginning at E11 the preaxial border of the foot plate is flattened, displaying an ovoid rather than circular outline
  • blastemata are crowded and small
  • interdigital area between digits 2 and 3 is reduced by E13
  • in most cases, digit 2 is formed closer to and may fuse to digit 3
• abnormal tarsus morphology (MGI Ref ID J:13049)
  • extensive and varied fusions in tarsus, which includes a solid fusion between talus and calcaneus
  • calcaneus frequently lacks process trochlearis
  • fusion occurs between the naviculare and a composite of cuneiforme 3 and cuboideum in all animals
  • naviculare is narrow as compared to wildtype
  • long axis of calcaneus and metararsalia are not parallel, as a result hindfeet point outward
• oligodactyly (MGI Ref ID J:13049)
  • digits 2 and 3 are typically involved
  • different digits in the same foot can be both polydactylous and oligodactylous
  • digit loss arises by fusion of digits 2 and 3, however, digit 2 is often thinner than normal and may vanish without fusion to digit 3
• polydactyly (MGI Ref ID J:13049)
  • exhibited in the hindfeet of some animals
  • different digits in the same foot can be both polydactylous and oligodactylous
• polysyndactyly (MGI Ref ID J:13049)
  • exhibited in some animals
• syndactyly (MGI Ref ID J:13049)
  • all four feet are affected, although the forefeet are less severely affected than the hindfeet
  • syndactylism primarily involves digits 2 and 3
  • nearly all animals exhibit osseous fusions of the bases of metacarpalia or metatarsalia 4 and 5
  • some animals exhibit fusion of metatarsalia 1 and 2
  • most fusions are secondary, only a few of the fusions are primary hard tissue in both embryo and adult
  • in the tarsus, only the cuneiforme 3 and cuboideum fusion is primary
  • hard tissue fusions start at the basal phalanges and spread distally
  • all fusions between metacarpal and metatarsals are secondary
• polysyndactyly (MGI Ref ID J:13049)
  • exhibited in some animals
• skeleton phenotype
• abnormal carpal bone morphology (MGI Ref ID J:13049)
  • ulnar end of the hamatum articulates with metacarpal 4, but does not reach metacarpal 5
  • metacarpal 5 is in a fixed state of abduction
• fused carpal bones (MGI Ref ID J:13049)
  • extensive fusions in carpus
• abnormal tarsus morphology (MGI Ref ID J:13049)
  • extensive and varied fusions in tarsus, which includes a solid fusion between talus and calcaneus
  • calcaneus frequently lacks process trochlearis
  • fusion occurs between the naviculare and a composite of cuneiforme 3 and cuboideum in all animals
  • naviculare is narrow as compared to wildtype
  • long axis of calcaneus and metararsalia are not parallel, as a result hindfeet point outward
• embryogenesis phenotype
• abnormal embryonic tissue morphology (MGI Ref ID J:13049)
  • at E14 projections of digits 2 and 3 at the edge of the foot plate are closer together than wildtype and there is only a single basal phalanx common to both digits
  • at E14-5 cuneiforme 3 and cuboideum have fused to a single element and are elongated in a diagonal direction rather than circular
  • at E16 metacarpalia 4 and 5 are fused
• abnormal mesenchyme morphology (MGI Ref ID J:12942)
  • a reduction in the amount of mesenchyme in the preaxial area of the foot plate is observed by E13

Os/Os⁺

        ROP/GnLeJ

• renal/urinary system phenotype
• abnormal kidney morphology (MGI Ref ID J:3842)
  • renal mass is reduced by 38% in comparison to wild-type
  • in nephrectomized heterozygote males, compensatory kidney growth is reduced in comparison to control
• abnormal kidney collecting duct (MGI Ref ID J:3842)
  • the principal cell type in the collecting duct is hypertrophied, with the greatest degree of hypertrophy in the nephrectomized heterozygotes
• abnormal renal glomerulus morphology (MGI Ref ID J:3842)
  • size of glomeruli is slightly increased in left kidney following unilateral nephrectomy as compared to control
• decreased renal glomerulus number (MGI Ref ID J:3842)
  • midtranverse sections from the left kidney indicate that glomeruli density is reduced by 50% in heterozygotes
• abnormal renal tubule morphology (MGI Ref ID J:3842)
  • diameters of the proximal convoluted and straight tubules are increased in size as compared to wild-type
  • tubular epithelial cells are hypertrophied in both heterozyote and nephrectomized heterozygotes, however, the magnitude of hypertrophy is increased in unaltered mice
• abnormal proximal convoluted tubule morphology (MGI Ref ID J:3842)
  • segments of proximal tubule, especially pars recta, exhibit hypertrophy
• polyuria (MGI Ref ID J:3842)
  • rate of urine flow is increased in heterozygotes as compared to controls, however glomerular filtration rate is not affected
  • excretion of creatinine, sodium and potassium is similar to control
• homeostasis/metabolism phenotype
• increased blood urea nitrogen level (MGI Ref ID J:3842)
  • BUN levels are increased by almost 50% in both heterozyote and nephrectomized heterozygotes as compared to controls

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)

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]

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

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]

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]

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. This strain is included in the Mouse Mutant Resource collection.

Control Information

	Control
	000664 C57BL/6J
Considerations for Choosing Controls
USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
International - Control Pricing Information for Genetically Engineered Mutant Strains.

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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Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
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Terms of Use

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Contact information

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phone:	207-288-6470
fax:	207-288-6655

JAX^® Mice & Services Conditions of Use

“Each recipient institution, including its employees and other researchers under its control (RECIPIENT), of mice or services using mice from The Jackson Laboratory (TJL) agrees that such mice, descendants of those mice derived by inbreeding or crossbreeding, including unmodified derivatives of those mice or their descendants (“MICE”) shall not be: (i) used for any purpose other than the internal research of the RECIPIENT, (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 with respect to MICE. Acceptance of MICE from TJL shall be deemed agreement by RECIPIENT to these conditions, and departure from these conditions requires The Jackson Laboratory’s prior written authorization.”

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