Strain Name:

B6.129S2-Slc34a1tm1Hten/J

Stock Number:

004802

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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 Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
 
Donating Investigator Harriet S Tenenhouse,   McGill University

Description
Mice that are homozygous for the targeted mutation are viable and fertile, and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected by Northern blot analysis of bone, kidney, liver or lung, or by Western blot analysis of kidney. Homozygotes are smaller in size and have reduced weight compared to wildtype littermates. Secondary ossification defects revealed at weaning are followed by compensatory bone development. Mutant mice exhibit increased urinary excretion of inorganic phosphate and calcium, diet dependent hypercalciuria and hypercalcemia, as well as decreased serum parathyroid hormone levels, increased serum alkaline phosphatase activity, and elevated serum 1,25-dihyudroxyvitamin D. Homozygous mice do not respond to dietary challenges of low inorganic phosphate or parathyroid hormone content. Calcium and inorganic phosphate containing renal stones, nephrocalcinosis, are found in homozygotes at all ages. This mutant mouse strain may be useful in studies of hereditary hypophosphatemic rickets with hypercalciuria, HHRH, and familial hypercalciuria.

Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exons 6 to 10, encoding amino acids 178-389. The construct was electroporated into 129S2/SvPas derived D3 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts.

Control Information

  Control
   See control note: C57BL/6J mice (Stock 000664) may be used as controls.
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Hypophosphatemic Rickets with Hypercalciuria, Hereditary; HHRH
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Fanconi Renotubular Syndrome 2; FRTS2   (SLC34A1)
Nephrolithiasis/Osteoporosis, Hypophosphatemic, 1; NPHLOP1   (SLC34A1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Slc34a1tm1Hten/Slc34a1tm1Hten

        B6.129S2-Slc34a1tm1Hten/J
  • growth/size/body phenotype
  • decreased birth weight
    • significantly reduced body weight at birth   (MGI Ref ID J:152195)
  • decreased body weight
    • significantly reduced body weight at 12 weeks of age   (MGI Ref ID J:152195)
  • homeostasis/metabolism phenotype
  • abnormal urine homeostasis
    • renal inorganic phosphate wasting   (MGI Ref ID J:152195)
    • improves with age   (MGI Ref ID J:152195)
    • increased urine phosphate level   (MGI Ref ID J:152195)
  • abnormal vitamin D level
    • reduced plasma levels of 1,25(OH)2 vitamin D3   (MGI Ref ID J:152195)
    • improves with age   (MGI Ref ID J:152195)
  • decreased circulating phosphate level
    • improves with age   (MGI Ref ID J:152195)
  • increased circulating calcium level
  • renal/urinary system phenotype
  • abnormal urine homeostasis
    • renal inorganic phosphate wasting   (MGI Ref ID J:152195)
    • improves with age   (MGI Ref ID J:152195)
    • increased urine phosphate level   (MGI Ref ID J:152195)
  • nephrocalcinosis
    • mineral deposition in kidneys at 12 weeks of age   (MGI Ref ID J:152195)

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

Slc34a1tm1Hten/Slc34a1tm1Hten

        involves: 129S2/SvPas * C57BL/6J
  • mortality/aging
  • postnatal lethality
    • 44% of homozygotes die before or at weaning   (MGI Ref ID J:47637)
    • death is attributed to poor nutritional status   (MGI Ref ID J:47637)
    • homozygotes that survive weaning appear normal thereafter, despite smaller size and lower body weight   (MGI Ref ID J:47637)
  • behavior/neurological phenotype
  • abnormal eating behavior
    • homozygotes frequently have difficulties in feeding during the first 2 weeks of life   (MGI Ref ID J:47637)
  • lethargy
    • homozygotes display some lethargy during the first 2 weeks of life   (MGI Ref ID J:47637)
  • growth/size/body phenotype
  • decreased birth body size
    • at birth, homozygotes are noticeably smaller than wild-type littermates   (MGI Ref ID J:47637)
    • decreased birth weight
      • at birth, homozygotes exhibit a significantly reduced body weight relative to wild-type controls (1.49 0.08 g vs 1.89 0.12 g)   (MGI Ref ID J:47637)
  • decreased body size
    • homozygotes remain significantly smaller than wild-type littermates for at least 4 months after birth   (MGI Ref ID J:47637)
    • decreased body weight
      • homozygotes maintain a significantly lower body weight for at least 4 months after birth   (MGI Ref ID J:47637)
  • homeostasis/metabolism phenotype
  • abnormal vitamin D level
    • at 1-3 months of age, homozygotes exhibit an appropriate adaptive increase in serum 1,25(OH)2D levels in response to hypophosphatemia   (MGI Ref ID J:47637)
  • decreased circulating parathyroid hormone level
    • at 2-3 months of age, serum PTH levels are appropriately decreased in response to hypercalciuria   (MGI Ref ID J:47637)
  • decreased circulating phosphate level
    • at 1-7 months of age, serum inorganic phosphate (Pi) levels are significantly reduced   (MGI Ref ID J:47637)
  • increased circulating alkaline phosphatase level
    • young homozygotes display significantly higher serum ALPase activity relative to age-matched wild-type and heterozygous mice   (MGI Ref ID J:47637)
    • however, by 4 months of age, serum ALPase activity is comparable in all three genotypes   (MGI Ref ID J:47637)
  • increased circulating calcium level
    • serum calcium levels are slightly but significantly increased at all ages examined, in an age-independent manner   (MGI Ref ID J:47637)
  • increased urine calcium level
    • at 1 month of age, the urine calcium/creatinine ratio and the fractional excretion index for calcium (FEICa) are significantly increased   (MGI Ref ID J:47637)
  • increased urine phosphate level
    • at 1 month of age, the urine Pi/creatinine ratio and the fractional excretion index for Pi (FEIPi) are strikingly increased   (MGI Ref ID J:47637)
  • renal/urinary system phenotype
  • *normal* renal/urinary system phenotype
    • homozygotes show no evidence for amino aciduria, glycosuria, or proteinuria, indicating that the renal inorganic phosphate leak is not due to a generalized tubulopathy   (MGI Ref ID J:47637)
    • increased urine calcium level
      • at 1 month of age, the urine calcium/creatinine ratio and the fractional excretion index for calcium (FEICa) are significantly increased   (MGI Ref ID J:47637)
    • increased urine phosphate level
      • at 1 month of age, the urine Pi/creatinine ratio and the fractional excretion index for Pi (FEIPi) are strikingly increased   (MGI Ref ID J:47637)
  • skeleton phenotype
  • *normal* skeleton phenotype
    • homozygotes do not exhibit rickets or osteomalacia   (MGI Ref ID J:47637)
    • abnormal skeleton development
      • initial impairment of secondary ossification in the epiphysis observed at 21 days of age   (MGI Ref ID J:47637)
      • by 45 days of age, the skeletal phenotype had reversed and overcompensated   (MGI Ref ID J:47637)
    • abnormal trabecular bone morphology
      • poor initial development of cancellous bone   (MGI Ref ID J:47637)
      • by 45 days of age, the number metaphyseal trabeculae exceeded that in wild-type   (MGI Ref ID J:47637)
    • delayed bone ossification   (MGI Ref ID J:47637)
  • muscle phenotype
  • muscle weakness
    • homozygotes display apparent muscle weakness during the first 2 weeks of life   (MGI Ref ID J:47637)
  • reproductive system phenotype
  • reduced fertility
    • homozygotes display reduced reproductive ability relative to wild-type and heterozygous controls   (MGI Ref ID J:47637)
View Research Applications

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

Slc34a1tm1Hten related

Cell Biology Research
Channel and Transporter Defects

Endocrine Deficiency Research
Kidney Defects

Internal/Organ Research
Kidney Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Slc34a1tm1Hten
Allele Name targeted mutation 1, Harriet S Tenenhouse
Allele Type Targeted (Null/Knockout)
Common Name(s) NaPi2a-; Npt2-; Npt2a KO;
Mutation Made By Harriet Tenenhouse,   McGill University
Strain of Origin129S2/SvPas
ES Cell Line NameD3
ES Cell Line Strain129S2/SvPas
Gene Symbol and Name Slc34a1, solute carrier family 34 (sodium phosphate), member 1
Chromosome 13
Gene Common Name(s) FRTS2; NAPI-3; NPHLOP1; NPT2; NPTIIa; Na/Pi cotransporter; NaPi-2; NaPi-IIa; NaPi2A; Npt2; SLC11; SLC17A2; Slc17a2; renal Na+/Pi transporter; sodium phosphate transport 2; solute carrier family 17 (sodium/hydrogen exchanger), member 2;
Molecular Note Exons 6 through 10 were replaced by a neomycin selection cassette inserted by homologous recombination. The deleted region encoded amino acids 178 through 389. Northern blot and RT-PCR analyses showed reduced levels of transcript in heterozygous mice andand an absence of transcript in homozygous mutant mice. While protein was undetected in homozygous mutant mice by Western blot analysis of renal tissue, normal levels of protein were detected in heterozygotes. [MGI Ref ID J:47637]

Genotyping

Genotyping Information

Genotyping Protocols

Slc34a1tm1Hten, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Beck L; Karaplis AC; Amizuka N; Hewson AS; Ozawa H; Tenenhouse HS. 1998. Targeted inactivation of Npt2 in mice leads to severe renal phosphate wasting, hypercalciuria, and skeletal abnormalities. Proc Natl Acad Sci U S A 95(9):5372-7. [PubMed: 9560283]  [MGI Ref ID J:47637]

Additional References

Khadeer MA; Tang Z; Tenenhouse HS; Eiden MV; Murer H; Hernando N; Weinman EJ; Chellaiah MA; Gupta A. 2003. Na+-dependent phosphate transporters in the murine osteoclast: cellular distribution and protein interactions. Am J Physiol Cell Physiol 284(6):C1633-44. [PubMed: 12606316]  [MGI Ref ID J:83898]

Slc34a1tm1Hten related

Boskey AL; Lukashova L; Spevak L; Ma Y; Khan SR. 2013. The kidney sodium-phosphate co-transporter alters bone quality in an age and gender specific manner. Bone 53(2):546-53. [PubMed: 23333524]  [MGI Ref ID J:193830]

Chau H; El-Maadawy S; McKee MD; Tenenhouse HS. 2003. Renal calcification in mice homozygous for the disrupted type IIa Na/Pi cotransporter gene Npt2. J Bone Miner Res 18(4):644-57. [PubMed: 12674325]  [MGI Ref ID J:111272]

Guo J; Song L; Liu M; Segawa H; Miyamoto K; Bringhurst FR; Kronenberg HM; Juppner H. 2013. Activation of a non-cAMP/PKA signaling pathway downstream of the PTH/PTHrP receptor is essential for a sustained hypophosphatemic response to PTH infusion in male mice. Endocrinology 154(5):1680-9. [PubMed: 23515284]  [MGI Ref ID J:197919]

Gupta A; Tenenhouse HS; Hoag HM; Wang D; Khadeer MA; Namba N; Feng X; Hruska KA. 2001. Identification of the type II Na(+)-Pi cotransporter (Npt2) in the osteoclast and the skeletal phenotype of Npt2-/- mice. Bone 29(5):467-76. [PubMed: 11704500]  [MGI Ref ID J:109413]

Hoag HM; Martel J; Gauthier C; Tenenhouse HS. 1999. Effects of Npt2 gene ablation and low-phosphate diet on renal Na(+)/phosphate cotransport and cotransporter gene expression. J Clin Invest 104(6):679-86. [PubMed: 10491403]  [MGI Ref ID J:110765]

Khan SR; Glenton PA. 2008. Calcium oxalate crystal deposition in kidneys of hypercalciuric mice with disrupted type IIa sodium-phosphate cotransporter. Am J Physiol Renal Physiol 294(5):F1109-15. [PubMed: 18337544]  [MGI Ref ID J:135986]

Larsson M; Morland C; Poblete-Naredo I; Biber J; Danbolt NC; Gundersen V. 2011. The sodium-dependent inorganic phosphate transporter SLC34A1 (NaPi-IIa) is not localized in the mouse brain: a case of tissue-specific antigenic cross-reactivity. J Histochem Cytochem 59(9):807-12. [PubMed: 21606201]  [MGI Ref ID J:181077]

Ohnishi M; Razzaque MS. 2010. Dietary and genetic evidence for phosphate toxicity accelerating mammalian aging. FASEB J 24(9):3562-71. [PubMed: 20418498]  [MGI Ref ID J:163563]

Perwad F; Azam N; Zhang MY; Yamashita T; Tenenhouse HS; Portale AA. 2005. Dietary and serum phosphorus regulate fibroblast growth factor 23 expression and 1,25-dihydroxyvitamin D metabolism in mice. Endocrinology 146(12):5358-64. [PubMed: 16123154]  [MGI Ref ID J:129835]

Segawa H; Onitsuka A; Furutani J; Kaneko I; Aranami F; Matsumoto N; Tomoe Y; Kuwahata M; Ito M; Matsumoto M; Li M; Amizuka N; Miyamoto K. 2009. Npt2a and Npt2c in mice play distinct and synergistic roles in inorganic phosphate metabolism and skeletal development. Am J Physiol Renal Physiol 297(3):F671-8. [PubMed: 19570882]  [MGI Ref ID J:152195]

Segawa H; Onitsuka A; Kuwahata M; Hanabusa E; Furutani J; Kaneko I; Tomoe Y; Aranami F; Matsumoto N; Ito M; Matsumoto M; Li M; Amizuka N; Miyamoto K. 2009. Type IIc sodium-dependent phosphate transporter regulates calcium metabolism. J Am Soc Nephrol 20(1):104-13. [PubMed: 19056871]  [MGI Ref ID J:152521]

Sitara D; Kim S; Razzaque MS; Bergwitz C; Taguchi T; Schuler C; Erben RG; Lanske B. 2008. Genetic evidence of serum phosphate-independent functions of FGF-23 on bone. PLoS Genet 4(8):e1000154. [PubMed: 18688277]  [MGI Ref ID J:161653]

Sitara D; Razzaque MS; St-Arnaud R; Huang W; Taguchi T; Erben RG; Lanske B. 2006. Genetic ablation of vitamin D activation pathway reverses biochemical and skeletal anomalies in Fgf-23-null animals. Am J Pathol 169(6):2161-70. [PubMed: 17148678]  [MGI Ref ID J:116289]

Tenenhouse HS; Gauthier C; Chau H; St-Arnaud R. 2004. 1alpha-Hydroxylase gene ablation and Pi supplementation inhibit renal calcification in mice homozygous for the disrupted Npt2a gene. Am J Physiol Renal Physiol 286(4):F675-81. [PubMed: 14656762]  [MGI Ref ID J:95432]

Tenenhouse HS; Gauthier C; Martel J; Hoenderop JG; Hartog A; Meyer MH; Meyer RA Jr; Bindels RJ. 2002. Na/P(i) cotransporter ( Npt2) gene disruption increases duodenal calcium absorption and expression of epithelial calcium channels 1 and 2. Pflugers Arch 444(5):670-6. [PubMed: 12194021]  [MGI Ref ID J:106184]

Tenenhouse HS; Martel J; Gauthier C; Segawa H; Miyamoto K. 2003. Differential effects of Npt2a gene ablation and X-linked Hyp mutation on renal expression of Npt2c. Am J Physiol Renal Physiol 285(6):F1271-8. [PubMed: 12952859]  [MGI Ref ID J:87132]

Tenenhouse HS; Martel J; Gauthier C; Zhang MY; Portale AA. 2001. Renal expression of the sodium/phosphate cotransporter gene, Npt2, is not required for regulation of renal 1 alpha-hydroxylase by phosphate. Endocrinology 142(3):1124-9. [PubMed: 11181527]  [MGI Ref ID J:68782]

Tomoe Y; Segawa H; Shiozawa K; Kaneko I; Tominaga R; Hanabusa E; Aranami F; Furutani J; Kuwahara S; Tatsumi S; Matsumoto M; Ito M; Miyamoto K. 2010. Phosphaturic action of fibroblast growth factor 23 in Npt2 null mice. Am J Physiol Renal Physiol 298(6):F1341-50. [PubMed: 20357029]  [MGI Ref ID J:159977]

Zhao N; Tenenhouse HS. 2000. Npt2 gene disruption confers resistance to the inhibitory action of parathyroid hormone on renal sodium-phosphate cotransport. Endocrinology 141(6):2159-65. [PubMed: 10830304]  [MGI Ref ID J:108816]

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* $2525.00
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.

Frozen Products

Price (US dollars $)
Frozen Embryo $1650.00

Standard Supply

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

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • 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* $3283.00
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.

Frozen Products

Price (US dollars $)
Frozen Embryo $2145.00

Standard Supply

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

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • 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.

Control Information

  Control
   See control note: C57BL/6J mice (Stock 000664) may be used as controls.
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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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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