Strain Name:

B6(Cg)-Tubtub/J

Stock Number:

000562

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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

Former Names B6.Cg-Tubtub/J    (Changed: 02-FEB-07 )
B6.Cg-Hbbp +/Hbbs Tubtub/J    (Changed: 31-MAR-05 )
C57BL/6J-Hbbp +/Hbbs tub    (Changed: 15-DEC-04 )
C57BL/6J-tub/+    (Changed: 15-DEC-04 )
Type Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
H2 Haplotypeb

Appearance
black, lean, normal vision
Related Genotype: a/a Tubtub/+

black, fat, retinal degeneration
Related Genotype: a/a Tubtub/Tubtub

Important Note
This strain may be segregating for the Oca2p and s alleles of Hbb.

Description
Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tubtub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). Tubby homozygotes additionally exhibit progressive hearing loss. The hearing loss is due to apoptotic degeneration of the organ of Corti and loss of afferent neurons. Quantitative trait locus (QTL) analysis identified a region on Chromosome 2 (designated modifier of tubby hearing 1, moth1) whose wild-type allele protects tubby mice from hearing loss (Ikeda et al., 1999); the gene has been identified as Mtap1a, encoding a microtubule-associated protein (Ikeda et al., 2002). A locus suggestively associated with protection from retinal degeneration maps to the same region of Chromosome 2 (Ikeda et al., 2002). Mice homozygous for a targeted null mutation in the tubby gene (not currently available from The Jackson Laboratory) exhibit a phenotype identical to that conferred by the spontaneous tubby mutation (Stubdal, et al., 2000).

Development
The Tubtub mutation arose spontaneously in 1977 in The Jackson Laboratory Animal Resources colony of C57BL/6J which was then at F125. After initial maintenance on the C57BL/6J background, a C57BL/6J-Tubtub homozygous male was bred with a female congenic B6.AU-Hbbp and the Hbbp +/Hbbs Tubtub offspring were sibling mated. The colony was maintained by breeding siblings Hbbp +/Hbbs Tubtub x Hbbp +/Hbbs Tubtub or vice versa for many years and in 2002 reached F87. In 2004 isozyme testing for Hbb alleles was replace with PCR testing for the Tubtub allele and the colony reached F90. (Coleman et al., 1978; Coleman and Eicher, 1990.)

Control Information

  Control
   Heterozygote from the colony
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Tubtub allele
004176   BKS.B6-Tubtub/Jng
003711   CAST.B6-Tubtub/Jng
View Strains carrying   Tubtub     (2 strains)

Strains carrying other alleles of Tub
003712   B6.CAST-Tub+/J
View Strains carrying other alleles of Tub     (1 strain)

Additional Web Information

JAX® NOTES, Fall 1999; 479. moth1 Gene Protects Tubby Mice From Hearing Loss.

Phenotype

Phenotype Information

View Phenotypic Data

Phenotypic Data
Mouse Phenome Database
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).
Obesity
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Tubtub/Tubtub

        B6(Cg)-Tubtub/J
  • growth/size/body phenotype
  • obese
    • slowly develop obesity   (MGI Ref ID J:32415)
  • behavior/neurological phenotype
  • increased food intake
    • gradually increase food intake   (MGI Ref ID J:32415)
  • homeostasis/metabolism phenotype
  • increased circulating cholesterol level
    • males, but not females, show a moderate increase in cholesterol levels   (MGI Ref ID J:18161)
  • increased circulating insulin level
    • gradually increase plasma insulin levels over time   (MGI Ref ID J:32415)
  • increased circulating triglyceride level
    • elevated in both males and females, although levels are higher in males than females   (MGI Ref ID J:18161)
  • vision/eye phenotype
  • abnormal electroretinogram waveform feature
    • the electroretinogram in homozygous mutant is never normal   (MGI Ref ID J:121993)
    • the waves are poorly developed and have reduced amplitudes compared to normal controls in the higher intensity waveforms   (MGI Ref ID J:121993)
    • with lower intensity flashes, the electroretinography exhibited lower amplitudes   (MGI Ref ID J:121993)
    • the amplitude loss was progressive and the electroretinogram was extinguished by 6 months   (MGI Ref ID J:121993)
  • abnormal retinal neuronal layer morphology
    • reduced and disorganized nuclear layer by 3 weeks   (MGI Ref ID J:121993)
    • abnormal retinal photoreceptor layer morphology
      • contains at most one-third of thickness of cell in this layer compared to normal mice   (MGI Ref ID J:26067)
      • abnormal photoreceptor inner segment morphology
        • are attenuated   (MGI Ref ID J:26067)
      • abnormal photoreceptor outer segment morphology
        • normal organized photoreceptor cell outer segments are not observed at any time   (MGI Ref ID J:121993)
        • composed of membranous whirls arranged in an irregular configuration   (MGI Ref ID J:121993)
        • photoreceptor outer segment degeneration
          • largely degenerated   (MGI Ref ID J:26067)
      • decreased retinal photoreceptor cell number
        • no photoreceptors were present by 8 months   (MGI Ref ID J:121993)
      • retinal photoreceptor degeneration
        • a progressive loss of the photoreceptors   (MGI Ref ID J:121993)
    • retinal outer nuclear layer degeneration
      • a progressive loss of outer nuclear layers   (MGI Ref ID J:121993)
  • abnormal retinal pigment epithelium morphology
    • granular appearance by 6 weeks   (MGI Ref ID J:121993)
    • focal and diffuse loss of pigment epithelium by 5 months   (MGI Ref ID J:121993)
  • abnormal retinal vasculature morphology
    • arteriolar attenuation, venous dilation by 6 weeks   (MGI Ref ID J:121993)
    • severe retinal vessel attenuation and sheathing by 5 months   (MGI Ref ID J:121993)
  • retinal degeneration
    • pyknotic photoreceptor cell nuclei are observed throughout the first 15 weeks   (MGI Ref ID J:121993)
    • rate of photoreceptor loss was constant and both cone and rod photoreceptor cells are degenerated at equal pace   (MGI Ref ID J:121993)
    • the rate of degeneration was similar in both the peripheral and central region   (MGI Ref ID J:121993)
    • only one to two layers of photoreceptor cell nuclei remained at 15-16 postnatal weeks   (MGI Ref ID J:121993)
    • degenerative changes within the inner retina were not observed during first 15 postnatal weeks   (MGI Ref ID J:121993)
    • develop progressive retinal degeneration   (MGI Ref ID J:32415)
  • retinal deposits
    • patches of pigment deposits by 5 months   (MGI Ref ID J:121993)
  • hearing/vestibular/ear phenotype
  • abnormal ear morphology   (MGI Ref ID J:32415)
    • abnormal bony labyrinth
      • at the basal end of the cochlea the osseous spiral lamina is partly empty, indicating loss of the afferent processes of the spiral ganglion cells   (MGI Ref ID J:26067)
    • absent tunnel of Corti   (MGI Ref ID J:26067)
    • cochlear hair cell degeneration
      • a severely degenerated organ of Corti; no hair cells or supporting cells are identifiable   (MGI Ref ID J:26067)
      • cochlear inner hair cell degeneration
        • apparent by 6 postnatal months   (MGI Ref ID J:121993)
      • cochlear outer hair cell degeneration
        • only the innermost row of outer hair cells is seen, suggesting a partial loss of outer hair cells   (MGI Ref ID J:26067)
        • any reduction in the number of outer hair cells in the apical half of mutant cochlea at 5-6 months of age is modest   (MGI Ref ID J:26067)
        • apparent by 6 postnatal months   (MGI Ref ID J:121993)
    • degeneration of organ of Corti supporting cells
      • a severely degenerated organ of Corti; no hair cells or supporting cells are identifiable   (MGI Ref ID J:26067)
      • degeneration of phalangeal and other support cells was also observed   (MGI Ref ID J:121993)
    • organ of Corti degeneration
      • a degeneration of organ of Corti in the basal end of the cochlea   (MGI Ref ID J:26067)
      • the transition from a well organized organ of Corti with at least a partial complement of inner and outer hair cells, to a mass of undifferentiated cells occurred in the lower basal turn   (MGI Ref ID J:26067)
      • apical half of the cochlea are normal with preservation of hair cells, supporting cells, and afferent dendrites   (MGI Ref ID J:26067)
      • the features of Reissner's membrane, stria vascularis, and the density of nerve fibers within the modiolus are normal   (MGI Ref ID J:26067)
      • Rosenthal's canal, is similar in appearance in all turns   (MGI Ref ID J:26067)
      • neither behavioral nor structural evidence of vestibular abnormalities   (MGI Ref ID J:26067)
  • abnormal hearing physiology   (MGI Ref ID J:32415)
    • impaired hearing   (MGI Ref ID J:32415)
      • progressive hearing loss, so that by 5-6 months of age, virtually deaf at 90-100 dB   (MGI Ref ID J:121993)
    • increased or absent threshold for auditory brainstem response
      • some homozygous mutants showed elevated ABR thresholds to clicks and 32-kHz pips at 3 weeks of age   (MGI Ref ID J:121993)
      • at 7, 9, and 12 weeks of age, homozygous mutant mice exhibited 20- to 30-dB higher ABR thresholds across all stimuli at click, 8 kHz, 16 kHz, and 32 kHz   (MGI Ref ID J:121993)
  • nervous system phenotype
  • abnormal photoreceptor inner segment morphology
    • are attenuated   (MGI Ref ID J:26067)
  • abnormal photoreceptor outer segment morphology
    • normal organized photoreceptor cell outer segments are not observed at any time   (MGI Ref ID J:121993)
    • composed of membranous whirls arranged in an irregular configuration   (MGI Ref ID J:121993)
    • photoreceptor outer segment degeneration
      • largely degenerated   (MGI Ref ID J:26067)
  • cochlear ganglion degeneration
    • at the basal end of the cochlea the osseous spiral lamina is partly empty, indicating loss of the afferent processes of the spiral ganglion cells   (MGI Ref ID J:26067)
    • spiral ganglion cell bodies in Rosenthal's canal in the most basal half turn were lost in some cochlea   (MGI Ref ID J:26067)
  • cochlear hair cell degeneration
    • a severely degenerated organ of Corti; no hair cells or supporting cells are identifiable   (MGI Ref ID J:26067)
    • cochlear inner hair cell degeneration
      • apparent by 6 postnatal months   (MGI Ref ID J:121993)
    • cochlear outer hair cell degeneration
      • only the innermost row of outer hair cells is seen, suggesting a partial loss of outer hair cells   (MGI Ref ID J:26067)
      • any reduction in the number of outer hair cells in the apical half of mutant cochlea at 5-6 months of age is modest   (MGI Ref ID J:26067)
      • apparent by 6 postnatal months   (MGI Ref ID J:121993)
  • decreased retinal photoreceptor cell number
    • no photoreceptors were present by 8 months   (MGI Ref ID J:121993)
  • retinal photoreceptor degeneration
    • a progressive loss of the photoreceptors   (MGI Ref ID J:121993)
  • pigmentation phenotype
  • abnormal retinal pigment epithelium morphology
    • granular appearance by 6 weeks   (MGI Ref ID J:121993)
    • focal and diffuse loss of pigment epithelium by 5 months   (MGI Ref ID J:121993)
  • cardiovascular system phenotype
  • abnormal retinal vasculature morphology
    • arteriolar attenuation, venous dilation by 6 weeks   (MGI Ref ID J:121993)
    • severe retinal vessel attenuation and sheathing by 5 months   (MGI Ref ID J:121993)

Tubtub/Tubtub

        involves: C57BL/6J
  • nervous system phenotype
  • abnormal hypothalamus morphology
    • defect in neuronal ciliary localization of SSTR3 and MCHR1 in the hippocampus CA1 region   (MGI Ref ID J:204140)
    • absence of NPY2R in arcuate nucleus cilia; however, overall NPY2R expression levels in the hypothalamus are similar to controls   (MGI Ref ID J:204140)

Tubtub/Tubtub

        C57BL/6J-Tubtub
  • growth/size/body phenotype
  • increased total body fat amount
    • the increase in weight is due to excess adipose tissue associated with all fat deposits   (MGI Ref ID J:13772)
  • obese
    • increased body weight first becomes obvious at 3-4 months of age in males and 4-6 months in females   (MGI Ref ID J:13772)
  • adipose tissue phenotype
  • increased total body fat amount
    • the increase in weight is due to excess adipose tissue associated with all fat deposits   (MGI Ref ID J:13772)
  • homeostasis/metabolism phenotype
  • increased circulating insulin level
    • plasma immunoreactive insulin is increased to 2 times the normal prior to signs of obesity   (MGI Ref ID J:13772)
    • plasma insulin concentrations increase gradually through out life   (MGI Ref ID J:13772)
    • however, blood sugar levels are normal up to 9 months of age, the oldest mice tested   (MGI Ref ID J:13772)
  • increased glycogen level
    • liver glycogen is slightly increased   (MGI Ref ID J:13772)
  • endocrine/exocrine gland phenotype
  • enlarged pancreatic islets
    • islets of Langerhans are moderately enlarged   (MGI Ref ID J:13772)
  • immune system phenotype
  • abnormal Langerhans cell physiology
    • islets of Langerhans show indication of hyperactivity in the later stages   (MGI Ref ID J:13772)
  • liver/biliary system phenotype
  • hepatic steatosis
    • total liver lipids range from 2-3 times the normal   (MGI Ref ID J:13772)
View Research Applications

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

Tubtub related

Diabetes and Obesity Research
Hyperinsulinemia
Obesity With Diabetes
      adult onset
Type 2 Diabetes (NIDDM)

Endocrine Deficiency Research
Adipose Defects
Hypothalamus/Pituitary Defects
Pancreas Defects

Internal/Organ Research
Adipose Defects

Neurobiology Research
Hearing Defects

Sensorineural Research
Hearing Defects
Retinal Degeneration

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tubtub
Allele Name tubby
Allele Type Spontaneous
Common Name(s) rd5; tub;
Strain of OriginC57BL/6J
Gene Symbol and Name Tub, tubby candidate gene
Chromosome 7
Gene Common Name(s) rd5; retinal degeneration 5; tubby;
General Note The phenotype associated with retinal degeneration in the tubby stock was referred to as a separate locus, rd5. rd5 was identified in the tubby stock but absent from the parental C57BL/6J stock. Based on the tight linkage of the two phenotypes and the molecular defect underlying the tub mutation, it seemed likely that tub and rd5 were the same gene. This was further supported by a knockout of the tub gene that recapitulated the retinal degeneration phenotype.
Molecular Note A donor splice site in the 3' region of the gene is abolished by a G to T transversion resulting in a larger transcript containing the unspliced intron. [MGI Ref ID J:32415]

Genotyping

Genotyping Information

Genotyping Protocols

Tubtub, Pyrosequencing


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Tubtub related

Backberg M; Madjid N; Ogren SO; Meister B. 2004. Down-regulated expression of agouti-related protein (AGRP) mRNA in the hypothalamic arcuate nucleus of hyperphagic and obese tub/tub mice. Brain Res Mol Brain Res 125(1-2):129-39. [PubMed: 15193430]  [MGI Ref ID J:115482]

Berk PD; Zhou S; Kiang C; Stump DD; Fan X; Bradbury MW. 1999. Selective up-regulation of fatty acid uptake by adipocytes characterizes both genetic and diet-induced obesity in rodents. J Biol Chem 274(40):28626-31. [PubMed: 10497230]  [MGI Ref ID J:57965]

Bouchard G; Johnson D; Carver T; Paigen B; Carey MC. 2002. Cholesterol gallstone formation in overweight mice establishes that obesity per se is not linked directly to cholelithiasis risk. J Lipid Res 43(7):1105-13. [PubMed: 12091495]  [MGI Ref ID J:88773]

Caberoy NB; Maiguel D; Kim Y; Li W. 2010. Identification of tubby and tubby-like protein 1 as eat-me signals by phage display. Exp Cell Res 316(2):245-57. [PubMed: 19837063]  [MGI Ref ID J:159050]

Chang B; Hawes NL; Hurd RE; Davisson MT; Nusinowitz S; Heckenlively JR. 2002. Retinal degeneration mutants in the mouse. Vision Res 42(4):517-25. [PubMed: 11853768]  [MGI Ref ID J:75095]

Chang B; Hawes NL; Hurd RE; Wang J; Howell D; Davisson MT; Roderick TH; Nusinowitz S; Heckenlively JR. 2005. Mouse models of ocular diseases. Vis Neurosci 22(5):587-93. [PubMed: 16332269]  [MGI Ref ID J:156373]

Chiellini C; Costa M; Novelli SE; Amri EZ; Benzi L; Bertacca A; Cohen P; Del Prato S; Friedman JM; Maffei M. 2003. Identification of cathepsin K as a novel marker of adiposity in white adipose tissue. J Cell Physiol 195(2):309-21. [PubMed: 12652657]  [MGI Ref ID J:106181]

Chung WK; Goldberg-Berman J; Power-Kehoe L; Leibel RL. 1996. Molecular mapping of the tubby (tub) mutation on mouse chromosome 7. Genomics 32(2):210-7. [PubMed: 8833147]  [MGI Ref ID J:31841]

Coleman DL; Eicher EM. 1990. Fat (fat) and tubby (tub): two autosomal recessive mutations causing obesity syndromes in the mouse. J Hered 81(6):424-7. [PubMed: 2250094]  [MGI Ref ID J:10872]

Coleman DL; Eicher EM; Southard JL. 1978. Tubby (tub) Mouse News Lett 59:25.  [MGI Ref ID J:13772]

Collins S; Surwit RS. 1996. Pharmacologic manipulation of ob expression in a dietary model of obesity. J Biol Chem 271(16):9437-40. [PubMed: 8621612]  [MGI Ref ID J:33332]

Guan XM; Yu H; Van der Ploeg LH. 1998. Evidence of altered hypothalamic pro-opiomelanocortin/ neuropeptide Y mRNA expression in tubby mice. Brain Res Mol Brain Res 59(2):273-9. [PubMed: 9729427]  [MGI Ref ID J:50229]

Hagstrom SA; Adamian M; Scimeca M; Pawlyk BS; Yue G; Li T. 2001. A role for the Tubby-like protein 1 in rhodopsin transport. Invest Ophthalmol Vis Sci 42(9):1955-62. [PubMed: 11481257]  [MGI Ref ID J:70710]

Heckenlively JR; Chang B; Erway LC; Peng C; Hawes NL; Hageman GS; Roderick TH. 1995. Mouse model for Usher syndrome: linkage mapping suggests homology to Usher type I reported at human chromosome 11p15. Proc Natl Acad Sci U S A 92(24):11100-4. [PubMed: 7479945]  [MGI Ref ID J:121993]

Johnson KR; Zheng QY; Noben-Trauth K. 2006. Strain background effects and genetic modifiers of hearing in mice. Brain Res 1091(1):79-88. [PubMed: 16579977]  [MGI Ref ID J:110459]

Kleyn PW; Fan W; Kovats SG; Lee JJ; Pulido JC; Wu Y; Berkemeier LR; Misumi DJ; Holmgren L; Charlat O; Woolf EA; Tayber O; Brody T; Shu P; Hawkins F; Kennedy B; Baldini L; Ebeling C; Alperin GD; Deeds J; Lakey ND; Culpepper J; Chen H; Glucksmann-Kuis MA;oore KJ; et al. 1996. Identification and characterization of the mouse obesity gene tubby: a member of a novel gene family. Cell 85(2):281-90. [PubMed: 8612280]  [MGI Ref ID J:32718]

Kong L; Li F; Soleman CE; Li S; Elias RV; Zhou X; Lewis DA; McGinnis JF; Cao W. 2006. Bright cyclic light accelerates photoreceptor cell degeneration in tubby mice. Neurobiol Dis 21(3):468-77. [PubMed: 16216520]  [MGI Ref ID J:108013]

Kong L; Tanito M; Huang Z; Li F; Zhou X; Zaharia A; Yodoi J; McGinnis JF; Cao W. 2007. Delay of photoreceptor degeneration in tubby mouse by sulforaphane. J Neurochem 101(4):1041-52. [PubMed: 17394579]  [MGI Ref ID J:121572]

Kong L; Zhou X; Li F; Yodoi J; McGinnis J; Cao W. 2010. Neuroprotective effect of overexpression of thioredoxin on photoreceptor degeneration in Tubby mice. Neurobiol Dis 38(3):446-55. [PubMed: 20298786]  [MGI Ref ID J:163048]

Loktev AV; Jackson PK. 2013. Neuropeptide Y Family Receptors Traffic via the Bardet-Biedl Syndrome Pathway to Signal in Neuronal Primary Cilia. Cell Rep 5(5):1316-29. [PubMed: 24316073]  [MGI Ref ID J:204140]

Maddatu T; Naggert JK. 1997. Allele-specific PCR assays for the tub and cpefat mutations. Mamm Genome 8(11):857-8. [PubMed: 9337402]  [MGI Ref ID J:44056]

Maddox DM; Ikeda S; Ikeda A; Zhang W; Krebs MP; Nishina PM; Naggert JK. 2012. An allele of microtubule-associated protein 1A (Mtap1a) reduces photoreceptor degeneration in Tulp1 and Tub Mutant Mice. Invest Ophthalmol Vis Sci 53(3):1663-9. [PubMed: 22323461]  [MGI Ref ID J:196742]

Mukhopadhyay S; Jackson PK. 2013. Cilia, tubby mice, and obesity. Cilia 2(1):1. [PubMed: 23351214]  [MGI Ref ID J:195052]

Nadeau JH. 2003. Modifier genes and protective alleles in humans and mice. Curr Opin Genet Dev 13(3):290-5. [PubMed: 12787792]  [MGI Ref ID J:88012]

Nakahara K; Bannai M; Maruyama K; Suzuki Y; Okame R; Murakami N. 2013. Characterization of a novel genetically obese mouse model demonstrating early onset hyperphagia and hyperleptinemia. Am J Physiol Endocrinol Metab 305(3):E451-63. [PubMed: 23736543]  [MGI Ref ID J:203210]

Nishina PM; Lowe S; Wang J; Paigen B. 1994. Characterization of plasma lipids in genetically obese mice: the mutants obese, diabetes, fat, tubby, and lethal yellow. Metabolism 43(5):549-53. [PubMed: 8177042]  [MGI Ref ID J:18161]

Nishina PM; Naggert JK; Verstuyft J; Paigen B. 1994. Atherosclerosis in genetically obese mice: the mutants obese, diabetes, fat, tubby, and lethal yellow. Metabolism 43(5):554-8. [PubMed: 8177043]  [MGI Ref ID J:19043]

Noben-Trauth K; Naggert JK; North MA; Nishina PM. 1996. A candidate gene for the mouse mutation tubby. Nature 380(6574):534-8. [PubMed: 8606774]  [MGI Ref ID J:32415]

Ohlemiller KK; Hughes RM; Lett JM; Ogilvie JM; Speck JD; Wright JS; Faddis BT. 1997. Progression of cochlear and retinal degeneration in the tubby (rd5) mouse. Audiol Neurootol 2(4):175-185. [PubMed: 9390831]  [MGI Ref ID J:41594]

Ohlemiller KK; Hughes RM; Mosinger-Ogilvie J; Speck JD; Grosof DH; Silverman MS. 1995. Cochlear and retinal degeneration in the tubby mouse. Neuroreport 6(6):845-9. [PubMed: 7612867]  [MGI Ref ID J:26067]

Ohlemiller KK; Mosinger Ogilvie J; Lett JM; Hughes RM; LaRegina MC ; Olson LM. 1998. The murine tub (rd5) mutation is not associated with a primary axonemal defect. Cell Tissue Res 291(3):489-95. [PubMed: 9477305]  [MGI Ref ID J:46471]

Petrolonis AJ; Yang Q; Tummino PJ; Fish SM; Prack AE; Jain S; Parsons TF; Li P; Dales NA; Ge L; Langston SP; Schuller AG; An WF; Tartaglia LA; Chen H; Hong SB. 2004. Enzymatic characterization of the pancreatic islet-specific glucose-6-phosphatase-related protein (IGRP). J Biol Chem 279(14):13976-83. [PubMed: 14722102]  [MGI Ref ID J:124542]

Stratigopoulos G; Padilla SL; Leduc CA; Watson E; Hattersley AT; McCarthy MI; Zeltser LM; Chung WK; Leibel RL. 2008. Regulation of Fto/Ftm gene expression in mice and humans. Am J Physiol Regul Integr Comp Physiol 294(4):R1185-96. [PubMed: 18256137]  [MGI Ref ID J:133509]

Sun X; Haley J; Bulgakov OV; Cai X; McGinnis J; Li T. 2012. Tubby is required for trafficking G protein-coupled receptors to neuronal cilia. Cilia 1(1):21. [PubMed: 23351594]  [MGI Ref ID J:196505]

Wang F; Tong Q. 2008. Transcription factor PU.1 is expressed in white adipose and inhibits adipocyte differentiation. Am J Physiol Cell Physiol 295(1):C213-20. [PubMed: 18463231]  [MGI Ref ID J:138523]

Wang Y; Seburn K; Bechtel L; Lee BY; Szatkiewicz JP; Nishina PM; Naggert JK. 2006. Defective carbohydrate metabolism in mice homozygous for the tubby mutation. Physiol Genomics 27(2):131-40. [PubMed: 16849632]  [MGI Ref ID J:113659]

Won J; Shi LY; Hicks W; Wang J; Hurd R; Naggert JK; Chang B; Nishina PM. 2011. Mouse model resources for vision research. J Ophthalmol 2011:391384. [PubMed: 21052544]  [MGI Ref ID J:166679]

Xu H; Barnes GT; Yang Q; Tan G; Yang D; Chou CJ; Sole J; Nichols A; Ross JS; Tartaglia LA; Chen H. 2003. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest 112(12):1821-30. [PubMed: 14679177]  [MGI Ref ID J:86952]

Health & husbandry

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.

Health & Colony Maintenance Information

Animal Health Reports

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

Colony Maintenance

Breeding & HusbandryThis strain was maintained for many years by breeding Hbbp +/Hbbs Tubtub + x Hbbs Tubtub/Hbbs Tubtub or vice versa. Hbb and Tub are approximately 1.5 cM apart on Chromosome 7. Tubby heterozygotes were distinguished from homozygotes by typing for the Hbb allele. This was done by cellulose acetate gel analysis of cystamine treated red blood cell lysates as described by Whitney, 1978. The Hbbs allele yields a single fast migrating band of hemoglobin while the Hbbp allele yields a slow migrating band and a second smaller, trailing band that may actually have cathodal migration on cellulose acetate (but not in starch or acrylamide gels). The mice carrying only the Hbbs allele were presumed homozygous for the Tubtub mutation by linkage; those with both the Hbbs and Hbbp alleles were presumed heterozygous for Tubtub by linkage. In 2004 genotyping of the Tubtub allele by PCR became the standard method for colony maintenance. Recombination can be expected to eventually remove the Hbbp allele from this strain. Heterozygous females are better mothers than homozygous females.

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 will fulfill 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 will fulfill 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.

General Supply Notes

  • View the complete collection of spontaneous mutants in the Mouse Mutant Resource.

Control Information

  Control
   Heterozygote from the colony
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Important Note

This strain may be segregating for the Oca2p and s alleles of Hbb.

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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