Strain Name:

C57BL/6J-Ghrhrlit/J

Stock Number:

000533

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Availability:

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Mice homozygous for the little spontaneous mutation (Ghrhrlit) are characterized by a deficiency in pituitary growth hormone along with prolactin and growth retardation.

Description

Strain Information

Type Coisogenic; Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHomozygote x Heterozygote         (Female x Male)   01-MAR-06
Specieslaboratory mouse
GenerationN5F81 (11-DEC-13)
Generation Definitions

Appearance
black, small body size
Related Genotype: a/a Ghrhrlit/Ghrhrlit

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

Description
Mice homozygous for the little spontaneous mutation (Ghrhrlit) are characterized by a deficiency in pituitary growth hormone (GH) along with prolactin and growth retardation. Because GH in the circulation regulates IGF-1, homozygotes have about one-tenth the normal level of IGF-1. Male mice have reduced fertility and female mice show a delay in lactation.

Development
The little (Ghrhrlit) mutation arose spontaneously in C57BL/6J at The Jackson Laboratory in 1970. It has been maintained on this background through sibling matings with occasional backcrosses to C57BL/6J. In 1983 C57BL/6J females were bred to heterozygous males to generate embryos for cryopreservation.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, 2 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice may have been crossed to C57BL/6N or C57BL/10J in the past.

Control Information

  Control
   Heterozygote from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Ghrhrlit allele
010816   B6;C-Ghrhrlit Prkdcscid/BmJ
005764   C3.B6-Ghrhrlit/J
View Strains carrying   Ghrhrlit     (2 strains)

Strains carrying other alleles of Ghrhr
019459   B6N(Cg)-Ghrhrtm1.1(KOMP)Vlcg/2J
View Strains carrying other alleles of Ghrhr     (1 strain)

Additional Web Information

JAX® NOTES, Fall 2001; 483. Extended Life Span in Mice with Dwarfing Mutations.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Isolated Growth Hormone Deficiency, Type IB; IGHD1B   (GHRHR)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Ghrhrlit/Ghrhrlit

        C57BL/6J-Ghrhrlit
  • adipose tissue phenotype
  • increased total body fat amount
    • greater amounts than wild-type controls   (MGI Ref ID J:3735)
  • endocrine/exocrine gland phenotype
  • abnormal lactation
    • failed milk production with first, but not subsequent, litters   (MGI Ref ID J:5647)
  • abnormal somatotroph morphology   (MGI Ref ID J:7211)
    • decreased somatotroph cell number   (MGI Ref ID J:7211)
    • decreased somatotroph cell size   (MGI Ref ID J:7211)
    • decreased somatotroph secretory granule number
      • some cells are devoid of secretory granules   (MGI Ref ID J:7211)
      • absent somatotroph secretory granules
        • some cells have reduced numbers of secretory granules   (MGI Ref ID J:7211)
  • small pituitary gland   (MGI Ref ID J:5647)
  • growth/size/body phenotype
  • abnormal postnatal growth
    • homozygous males display a linear increase of weight from 4 to 16 weeks of age; they do not have a peak growth rate at 5 weeks of age, which heterozygous males do, and out to 16 weeks of age homozygotes do not show a plateau in their body weight, which heterozygotes do by approximately 12 to 15 weeks of age   (MGI Ref ID J:81023)
    • female homozygotes mated to intact or vasectomized males gain weight as a result of pregnancy or pseudopregnancy and have increased bone length in the tibia and femur, and increased length and width in the scapula and skull   (MGI Ref ID J:5710)
    • both males and females have increased weight and bone growth as a result of pituitary grafts or a course of i.p. injections of ovine growth hormone   (MGI Ref ID J:5710)
    • postnatal growth retardation
      • reduced weight, beginning at 2 weeks of age   (MGI Ref ID J:5647)
  • increased susceptibility to age related obesity   (MGI Ref ID J:5647)
  • increased total body fat amount
    • greater amounts than wild-type controls   (MGI Ref ID J:3735)
  • obese
    • at 40 weeks of age the body fat of homozygous males is considerably higher than that of heterozygous males   (MGI Ref ID J:81023)
  • proportional dwarf
    • proportionate skeletal size reduction   (MGI Ref ID J:5710)
  • homeostasis/metabolism phenotype
  • abnormal metabolism
    • from 4 to 15 weeks of age homozygous males exhibit constant food conversion efficiency rather than the normal decay of food conversion efficiency seen in heterozygous controls   (MGI Ref ID J:81023)
    • homozygous males have a higher energy consumption per gram of body weight than do heterozygous controls   (MGI Ref ID J:81023)
  • decreased growth hormone level
    • in the pituitary   (MGI Ref ID J:5647)
    • decreased circulating growth hormone level   (MGI Ref ID J:3735)
  • decreased prolactin level
    • in the pituitary   (MGI Ref ID J:5647)
  • reproductive system phenotype
  • reduced male fertility
    • only 50% sired first litters, only 50% of these sired second litters, third litters rare   (MGI Ref ID J:5647)
  • nervous system phenotype
  • abnormal somatotroph morphology   (MGI Ref ID J:7211)
    • decreased somatotroph cell number   (MGI Ref ID J:7211)
    • decreased somatotroph cell size   (MGI Ref ID J:7211)
    • decreased somatotroph secretory granule number
      • some cells are devoid of secretory granules   (MGI Ref ID J:7211)
      • absent somatotroph secretory granules
        • some cells have reduced numbers of secretory granules   (MGI Ref ID J:7211)
  • small pituitary gland   (MGI Ref ID J:5647)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • although mature food intake is less than that of heterozygotes, it is commensurate with body weight with heterozygous males taking in an average 1.0 +/- .12 g/g body weight and homozygous males taking in an average of 1.2 +/- .23 g/g body weight   (MGI Ref ID J:81023)
    • abnormal sleep pattern
      • homozygotes have shorter non-rapid eye movement sleep episodes during the light period and have them slightly more frequently than do heterozygotes, homozygotes also have significantly decreased rapid eye movement sleep episode frequency during the light period although the duration of rapid eye movement sleep episodes is normal   (MGI Ref ID J:82887)
      • subcutaneous infusion of growth hormone increases the frequency of rapid eye movement sleep episodes during the light cycle to levels similar to those of heterozygous controls, although infusion of growth hormone does not correct the non-rapid eye movement sleep episodes   (MGI Ref ID J:82887)
      • abnormal frequency of paradoxical sleep   (MGI Ref ID J:82887)
  • skeleton phenotype
  • abnormal skeleton development
    • female homozygotes mated to intact or vasectomized males gain weight as a result of pregnancy or pseudopregnancy and have increased bone length in the tibia and femur, and increased length and width in the scapula and skull   (MGI Ref ID J:5710)
    • both males and females have increased weight and bone growth as a result of pituitary grafts or a course of i.p. injections of ovine growth hormone   (MGI Ref ID J:5710)
  • decreased bone mass
    • homozygous males have a lower bone mass than heterozygous males although the bone mass of both attains maturity at 12 to 15 weeks of age and has a maximum growth rate at 5 weeks   (MGI Ref ID J:81023)
  • integument phenotype
  • abnormal lactation
    • failed milk production with first, but not subsequent, litters   (MGI Ref ID J:5647)
  • immune system phenotype
  • decreased susceptibility to experimental autoimmune encephalomyelitis   (MGI Ref ID J:85381)

Ghrhrlit/Ghrhrlit

        C57BL/6J-Ghrhrlit/J
  • homeostasis/metabolism phenotype
  • abnormal glucose homeostasis
    • at P7, the ratio of glucose to insulin is increased compared to in wild-type mice or either single homozygote   (MGI Ref ID J:95779)
    • decreased circulating glucose level
      • at 3 and 12 months, mice exhibit decreased serum glucose level compared with wild-type mice   (MGI Ref ID J:95779)
    • increased circulating insulin level
      • at P7 and in adult mice   (MGI Ref ID J:95779)
  • abnormal insulin-like growth factor I level
    • average IGF-1 levels in homozygous females (37 ng/ml) is much lower than in heterozygous females (171 ng/ml) and in homozygous males (31.2 ng/ml) is much lower than in heterozygous males (171.4 ng/ml)   (MGI Ref ID J:209717)
    • decreased circulating insulin-like growth factor I level
  • growth/size/body phenotype
  • decreased body weight
    • through 500 days, female mice exhibit decreased body weight compared with wild-type mice   (MGI Ref ID J:95779)
    • at 4 months of age homozygous females weigh an average of 16.5g compared with heterozygous females 21.9g, and homozygous males weigh an average of 20.1g compared with heterozgyous males 30.2g   (MGI Ref ID J:209717)
    • slow postnatal weight gain
      • male and female mice exhibit reduced body weight gain compared with wild-type mice   (MGI Ref ID J:95779)
      • however, male mice exhibit catch-up weight-gain at 120 to 180 days of life   (MGI Ref ID J:95779)
  • decreased lean body mass
    • relative to body weight in male mice   (MGI Ref ID J:95779)
  • increased total body fat amount
    • body fat relative to femur length in male mice is increased compared to in wild-type mice   (MGI Ref ID J:95779)
  • skeleton phenotype
  • abnormal bone structure
    • At 4 months of age, the average periosteal circumference in homozygous females (3.8 mm) is significantly less than in heterozygotes (4.76 mm), and in homozygous males (3.66 mm) is also significantly less than in heterozygotes (4.9 mm)   (MGI Ref ID J:209717)
    • decreased bone mineral density
      • the whole body bone mineral density measured between 4 and 16 weeks of age is significantly lower in homozygotes on the C57BL/6J background than on the C3H/HeJ background and is lower in homozygotes than heterozygotes   (MGI Ref ID J:209717)
      • at 4 months of age homozygous females have a femoral bone mineral density of 0.451 mg/mm3 where heterozygote have 0.482 mg/mm3   (MGI Ref ID J:209717)
      • at 4 months of age homozygous males have a femoral bone mineral density of 0..453 mg/mm3 where heterozygote have 0.502 mg/mm3   (MGI Ref ID J:209717)
    • increased bone mineral density   (MGI Ref ID J:95779)
  • short femur   (MGI Ref ID J:95779)
    • at 4 months of age the average femur length in homozygous females on the C57BL/6J background is 12mm versus 15.4mm in heterozygotes, and in homozygous males is 12mm versus 15.6mm in heterozygotes   (MGI Ref ID J:209717)
  • adipose tissue phenotype
  • increased total body fat amount
    • body fat relative to femur length in male mice is increased compared to in wild-type mice   (MGI Ref ID J:95779)
  • limbs/digits/tail phenotype
  • short femur   (MGI Ref ID J:95779)
    • at 4 months of age the average femur length in homozygous females on the C57BL/6J background is 12mm versus 15.4mm in heterozygotes, and in homozygous males is 12mm versus 15.6mm in heterozygotes   (MGI Ref ID J:209717)

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

Ghrhrlit/Ghrhrlit

        C3.B6-Ghrhrlit/J
  • skeleton phenotype
  • abnormal bone structure
    • The average periosteal circumference in homozygous females (3.43 mm) is significantly less than in heterozygotes (4.36 mm) and similar results are found on the C57BL/6J background so there is not a strong impact of genetic background on body size and bone geometry as there is on bone mineral density   (MGI Ref ID J:209717)
    • The average periosteal circumference in homozygous males (3.85 mm) is significantly less than in heterozygotes (4.88 mm) and similar results are found on the C57BL/6J background so there is not a strong impact of genetic background on body size and bone geometry as there is on bone mineral density   (MGI Ref ID J:209717)
    • abnormal bone mineral density
      • on a C3H/HeJ congenic background homozygous females at 4 months of age have a femoral bone mineral density of 0.582 mg/mm3 compared with 0.451 mg/mm3 on the C57BL/6J background   (MGI Ref ID J:209717)
      • on a C3H/HeJ congenic background homozygous males at 4 months of age have a femoral bone mineral density of 0.61 mg/mm3 compared with 0.453 mg/mm3 on the C57BL/6J background   (MGI Ref ID J:209717)
      • the whole body bone mineral density measured between 4 and 16 weeks of age is significantly lower in homozygotes on the C57BL/6J background than on the C3H/HeJ background and is lower in homozygotes than heterozygotes   (MGI Ref ID J:209717)
      • decreased bone mineral density
        • at 4 months of age homozygous females have a femoral bone mineral density of 0.582 mg/mm3 where heterozygote have 0.698 mg/mm3   (MGI Ref ID J:209717)
        • at 4 months of age homozygous males have a femoral bone mineral density of 0.61 mg/mm3 where heterozygote have 0.691 mg/mm3   (MGI Ref ID J:209717)
        • decreased bone mineral density of femur   (MGI Ref ID J:209717)
  • short femur
    • at 4 months of age the average femur length in homozygous females on the C3H/HeJ background is 12.3mm versus 15.2mm in heterozygotes   (MGI Ref ID J:209717)
    • at 4 months of age the average femur length in homozygous males on the C3H/HeJ background is 12.4mm versus 15.7mm in heterozygotes   (MGI Ref ID J:209717)
  • growth/size/body phenotype
  • decreased body weight
    • homozygous females at 4 months of age weigh on average 15.8g whereas heterozygotes weigh 27.5g   (MGI Ref ID J:209717)
    • homozygous males at 4 months of age weigh on average 25.8g whereas heterozygotes weigh 35.8g   (MGI Ref ID J:209717)
  • limbs/digits/tail phenotype
  • short femur
    • at 4 months of age the average femur length in homozygous females on the C3H/HeJ background is 12.3mm versus 15.2mm in heterozygotes   (MGI Ref ID J:209717)
    • at 4 months of age the average femur length in homozygous males on the C3H/HeJ background is 12.4mm versus 15.7mm in heterozygotes   (MGI Ref ID J:209717)
  • homeostasis/metabolism phenotype
  • abnormal insulin-like growth factor I level
    • average IGF-1 levels in homozygous males (46.5 ng/ml) is much lower than in heterozygous males (208.8 ng/ml) but simlar to homozygous females on a C57BL/6J background (37.0 ng/ml)   (MGI Ref ID J:209717)
    • average IGF-1 levels in homozygous males (34.2 ng/ml) is much lower than in heterozygous males (186.3 ng/ml) but simlar to homozygous males on a C57BL/6J background (31.2 ng/ml)   (MGI Ref ID J:209717)
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Research Applications
This mouse can be used to support research in many areas including:

Ghrhrlit related

Developmental Biology Research
Growth Defects

Endocrine Deficiency Research
Hypothalamus/Pituitary Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Ghrhrlit
Allele Name little
Allele Type Spontaneous
Common Name(s) lit; litm;
Strain of OriginC57BL/6J
Gene Symbol and Name Ghrhr, growth hormone releasing hormone receptor
Chromosome 6
Gene Common Name(s) GHRFR; GHRHREC; GRFR; Ghrfr; IGHD1B; growth hormone releasing factor receptor; lit; little;
Molecular Note The mutation in little mice is a A-to-G transition in codon 60 that is predicted to alter this residue from a aspartate to a glycine in the encoded protein. Reduced levels of mRNA were noted in total RNA derived from pituitary of homozygous mice, and invitro assays demonstrated that no functional protein is made from this allele. [MGI Ref ID J:12846] [MGI Ref ID J:13404]

Genotyping

Genotyping Information

Genotyping Protocols

Ghrhrlit, End Point Analysis


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Bugni JM; Poole TM; Drinkwater NR. 2001. The little mutation suppresses DEN-induced hepatocarcinogenesis in mice and abrogates genetic and hormonal modulation of susceptibility. Carcinogenesis 22(11):1853-62. [PubMed: 11698349]  [MGI Ref ID J:72758]

Godfrey P; Rahal JO; Beamer WG; Copeland NG; Jenkins NA; Mayo KE. 1993. GHRH receptor of little mice contains a missense mutation in the extracellular domain that disrupts receptor function. Nat Genet 4(3):227-32. [PubMed: 8395283]  [MGI Ref ID J:12846]

Lin SC; Lin CR; Gukovsky I; Lusis AJ; Sawchenko PE; Rosenfeld MG. 1993. Molecular basis of the little mouse phenotype and implications for cell type-specific growth [see comments] Nature 364(6434):208-13. [PubMed: 8391647]  [MGI Ref ID J:13404]

Obal F Jr; Alt J; Taishi P; Gardi J; Krueger JM. 2003. Sleep in mice with nonfunctional growth hormone-releasing hormone receptors. Am J Physiol Regul Integr Comp Physiol 284(1):R131-9. [PubMed: 12388430]  [MGI Ref ID J:82887]

Ghrhrlit related

Barger JL; Walford RL; Weindruch R. 2003. The retardation of aging by caloric restriction: its significance in the transgenic era. Exp Gerontol 38(11-12):1343-51. [PubMed: 14698815]  [MGI Ref ID J:87701]

Beamer WG; Shultz KL; Tennent BJ; Shultz LD. 1993. Granulosa cell tumorigenesis in genetically hypogonadal-immunodeficient mice grafted with ovaries from tumor-susceptible donors. Cancer Res 53(16):3741-6. [PubMed: 8339285]  [MGI Ref ID J:14443]

Beamer WH; Eicher EM. 1976. Stimulation of growth in the little mouse. J Endocrinol 71(1):37-45. [PubMed: 978118]  [MGI Ref ID J:5710]

Boughner JC; Wat S; Diewert VM; Young NM; Browder LW; Hallgrimsson B. 2008. Short-faced mice and developmental interactions between the brain and the face. J Anat 213(6):646-62. [PubMed: 19094181]  [MGI Ref ID J:158720]

Bugni JM; Poole TM; Drinkwater NR. 2001. The little mutation suppresses DEN-induced hepatocarcinogenesis in mice and abrogates genetic and hormonal modulation of susceptibility. Carcinogenesis 22(11):1853-62. [PubMed: 11698349]  [MGI Ref ID J:72758]

Bunger L; Hill WG. 1999. Role of growth hormone in the genetic change of mice divergently selected for body weight and fatness. Genet Res 74(3):351-60. [PubMed: 10689811]  [MGI Ref ID J:60661]

Cheng TC; Beamer WG; Phillips JA 3rd; Bartke A; Mallonee RL; Dowling C. 1983. Etiology of growth hormone deficiency in little, Ames, and Snell dwarf mice. Endocrinology 113(5):1669-78. [PubMed: 6194978]  [MGI Ref ID J:7211]

Cheng X; Klaassen CD. 2012. Hormonal and chemical regulation of paraoxonases in mice. J Pharmacol Exp Ther 342(3):688-95. [PubMed: 22653878]  [MGI Ref ID J:188071]

Christensen E; Wilson DB. 1981. Fine structure of somatotrophs and mammotrophs in the pituitary pars distalis of the little (lit) mutant mouse. Virchows Arch B Cell Pathol Incl Mol Pathol 37(1):89-96. [PubMed: 6116352]  [MGI Ref ID J:15348]

Dickson SL; Doutrelant-Viltart O; Leng G. 1995. GH-deficient dw/dw rats and lit/lit mice show increased Fos expression in the hypothalamic arcuate nucleus following systemic injection of GH-releasing peptide-6. J Endocrinol 146(3):519-26. [PubMed: 7595148]  [MGI Ref ID J:29289]

Donahue LR. 2014. Characterization data for C3.B6-Ghrhr<lit>/J MGI Direct Data Submission :.  [MGI Ref ID J:209717]

Donahue LR; Beamer WG. 1993. Growth hormone deficiency in 'little' mice results in aberrant body composition, reduced insulin-like growth factor-I and insulin-like growth factor-binding protein-3 (IGFBP-3), but does not affect IGFBP-2, -1 or -4. J Endocrinol 136(1):91-104. [PubMed: 7679139]  [MGI Ref ID J:3735]

Donahue LR; Watson G; Beamer WG. 1993. Regulation of metabolic water and protein compartments by insulin-like growth factor-I and testosterone in growth hormone-deficient lit/lit mice. J Endocrinol 139(3):431-9. [PubMed: 7510770]  [MGI Ref ID J:16863]

Eicher EM. 1972. lit - little Mouse News Lett 47:36.  [MGI Ref ID J:64445]

Eicher EM; Beamer WG. 1976. Inherited ateliotic dwarfism in mice. Characteristics of the mutation, little, on chromosome 6. J Hered 67(2):87-91. [PubMed: 1270792]  [MGI Ref ID J:5647]

Eleswarapu S; Gu Z; Jiang H. 2008. Growth hormone regulation of insulin-like growth factor-I gene expression may be mediated by multiple distal signal transducer and activator of transcription 5 binding sites. Endocrinology 149(5):2230-40. [PubMed: 18276757]  [MGI Ref ID J:136020]

Fleenor D; Oden J; Kelly PA; Mohan S; Alliouachene S; Pende M; Wentz S; Kerr J; Freemark M. 2005. Roles of the lactogens and somatogens in perinatal and postnatal metabolism and growth: studies of a novel mouse model combining lactogen resistance and growth hormone deficiency. Endocrinology 146(1):103-12. [PubMed: 15388648]  [MGI Ref ID J:95779]

Flurkey K; Papaconstantinou J; Miller RA; Harrison DE. 2001. Lifespan extension and delayed immune and collagen aging in mutant mice with defects in growth hormone production. Proc Natl Acad Sci U S A 98(12):6736-41. [PubMed: 11371619]  [MGI Ref ID J:69878]

Foster MP; Jensen ER; Montecino-Rodriguez E; Leathers H; Horseman N; Dorshkind K. 2000. Humoral and cell-mediated immunity in mice with genetic deficiencies of prolactin, growth hormone, insulin-like growth factor-I, and thyroid hormone. Clin Immunol 96(2):140-9. [PubMed: 10900161]  [MGI Ref ID J:63735]

Gaylinn BD; Dealmeida VI; Lyons CE Jr; Wu KC; Mayo KE; Thorner MO. 1999. The mutant growth hormone-releasing hormone (GHRH) receptor of the little mouse does not bind GHRH. Endocrinology 140(11):5066-74. [PubMed: 10537133]  [MGI Ref ID J:58346]

Godfrey P; Rahal JO; Beamer WG; Copeland NG; Jenkins NA; Mayo KE. 1993. GHRH receptor of little mice contains a missense mutation in the extracellular domain that disrupts receptor function. Nat Genet 4(3):227-32. [PubMed: 8395283]  [MGI Ref ID J:12846]

Greenhalgh CJ; Rico-Bautista E; Lorentzon M; Thaus AL; Morgan PO; Willson TA; Zervoudakis P; Metcalf D; Street I; Nicola NA; Nash AD; Fabri LJ; Norstedt G; Ohlsson C; Flores-Morales A; Alexander WS; Hilton DJ. 2005. SOCS2 negatively regulates growth hormone action in vitro and in vivo. J Clin Invest 115(2):397-406. [PubMed: 15690087]  [MGI Ref ID J:95918]

Herington AC; Harrison D; Graystone J. 1983. Hepatic binding of human and bovine growth hormones and ovine prolactin in the dwarf little mouse. Endocrinology 112(6):2032-8. [PubMed: 6303755]  [MGI Ref ID J:7060]

Iida K; Del Rincon JP; Kim DS; Itoh E; Nass R; Coschigano KT; Kopchick JJ; Thorner MO. 2004. Tissue-specific regulation of growth hormone (GH) receptor and insulin-like growth factor-I gene expression in the pituitary and liver of GH-deficient (lit/lit) mice and transgenic mice that overexpress bovine GH (bGH) or a bGH antagonist. Endocrinology 145(4):1564-70. [PubMed: 14726438]  [MGI Ref ID J:105653]

Iida K; Itoh E; Kim DS; del Rincon JP; Coschigano KT; Kopchick JJ; Thorner MO. 2004. Muscle mechano growth factor is preferentially induced by growth hormone in growth hormone-deficient lit/lit mice. J Physiol 560(Pt 2):341-9. [PubMed: 15308683]  [MGI Ref ID J:133848]

Iida K; del Rincon JP; Kim DS; Itoh E; Coschigano KT; Kopchick JJ; Thorner MO. 2004. Regulation of full-length and truncated growth hormone (GH) receptor by GH in tissues of lit/lit or bovine GH transgenic mice. Am J Physiol Endocrinol Metab 287(3):E566-73. [PubMed: 15165994]  [MGI Ref ID J:133236]

Ikushima H; Kanaoka M; Kojima S. 2003. Cutting edge: Requirement for growth hormone-releasing hormone in the development of experimental autoimmune encephalomyelitis. J Immunol 171(6):2769-72. [PubMed: 12960295]  [MGI Ref ID J:85381]

Itoh E; Iida K; del Rincon JP; Kim DS; Thorner MO. 2004. Diurnal variation in growth hormone receptor messenger ribonucleic acid in liver and skeletal muscle of lit/+ and lit/lit mice. Endocr J 51(6):529-35. [PubMed: 15644570]  [MGI Ref ID J:103494]

Jansson JO; Downs TR; Beamer WG; Frohman LA. 1986. Receptor-associated resistance to growth hormone-releasing factor in dwarf little mice. Science 232(4749):511-2. [PubMed: 3008329]  [MGI Ref ID J:8252]

Johnson D; al-Shawi R; Bishop JO. 1995. Sexual dimorphism and growth hormone induction of murine pheromone-binding proteins. J Mol Endocrinol 14(1):21-34. [PubMed: 7772239]  [MGI Ref ID J:24099]

Kasukawa Y; Baylink DJ; Guo R; Mohan S. 2003. Evidence that sensitivity to growth hormone (GH) is growth period and tissue type dependent: studies in GH-deficient lit/lit mice. Endocrinology 144(9):3950-7. [PubMed: 12933669]  [MGI Ref ID J:85595]

Lehman DM; Hale DE; Cody JT; Harrison JM; Leach RJ. 1999. Molecular, morphometric and functional analyses demonstrate that the growth hormone deficient little mouse is not hypomyelinated. Brain Res Dev Brain Res 116(2):191-9. [PubMed: 10521563]  [MGI Ref ID J:57626]

Liang H; Masoro EJ; Nelson JF; Strong R; McMahan CA; Richardson A. 2003. Genetic mouse models of extended lifespan. Exp Gerontol 38(11-12):1353-64. [PubMed: 14698816]  [MGI Ref ID J:87700]

Lin SC; Lin CR; Gukovsky I; Lusis AJ; Sawchenko PE; Rosenfeld MG. 1993. Molecular basis of the little mouse phenotype and implications for cell type-specific growth [see comments] Nature 364(6434):208-13. [PubMed: 8391647]  [MGI Ref ID J:13404]

Majeed N; Blouin MJ; Kaplan-Lefko PJ; Barry-Shaw J; Greenberg NM; Gaudreau P; Bismar TA; Pollak M. 2005. A germ line mutation that delays prostate cancer progression and prolongs survival in a murine prostate cancer model. Oncogene 24(29):4736-40. [PubMed: 15870705]  [MGI Ref ID J:99544]

Menagh PJ; Turner RT; Jump DB; Wong CP; Lowry MB; Yakar S; Rosen CJ; Iwaniec UT. 2010. Growth hormone regulates the balance between bone formation and bone marrow adiposity. J Bone Miner Res 25(4):757-68. [PubMed: 19821771]  [MGI Ref ID J:179868]

Mohan S; Baylink DJ; Srivastava AK. 2008. A chemical mutagenesis screen to identify modifier genes that interact with growth hormone and TGF-beta signaling pathways. Bone 42(2):388-95. [PubMed: 18063435]  [MGI Ref ID J:141536]

Montecino-Rodriguez E; Clark RG; Powell-Braxton L; Dorshkind K. 1997. Primary B cell development is impaired in mice with defects of the pituitary/thyroid axis. J Immunol 159(6):2712-9. [PubMed: 9300691]  [MGI Ref ID J:110683]

Niermann GL; Watson GL. 1999. Growth hormone and insulin-like growth factor-I enhance beta-glucuronidase gene activation by androgen in mouse kidney. Mol Cell Endocrinol 153(1-2):47-55. [PubMed: 10459853]  [MGI Ref ID J:56310]

Nissley SP; Knazek RA; Wolff GL. 1980. Somatomedin activity in sera of genetically small mice. Horm Metab Res 12(4):158-64. [PubMed: 7390396]  [MGI Ref ID J:6340]

Nordstrom SM; Holliday BA; Sos BC; Smyth JW; Levy RE; Dukes JW; Lord ST; Weiss EJ. 2010. Increased thrombosis susceptibility and altered fibrin formation in STAT5-deficient mice. Blood 116(25):5724-33. [PubMed: 20823455]  [MGI Ref ID J:167417]

Obal F Jr; Alt J; Taishi P; Gardi J; Krueger JM. 2003. Sleep in mice with nonfunctional growth hormone-releasing hormone receptors. Am J Physiol Regul Integr Comp Physiol 284(1):R131-9. [PubMed: 12388430]  [MGI Ref ID J:82887]

Pati D; Zhang N; Plon SE. 2002. Linking sister chromatid cohesion and apoptosis: role of rad21. Mol Cell Biol 22(23):8267-77. [PubMed: 12417729]  [MGI Ref ID J:80123]

Phelps CJ. 1994. Pituitary hormones as neurotrophic signals: anomalous hypophysiotrophic neuron differentiation in hypopituitary dwarf mice. Proc Soc Exp Biol Med 206(1):6-23. [PubMed: 7910409]  [MGI Ref ID J:18152]

Phillips JA 3rd; Beamer WG; Bartke A. 1982. Analysis of growth hormone genes in mice with genetic defects of growth hormone expression. J Endocrinol 92(3):405-7. [PubMed: 7069343]  [MGI Ref ID J:6741]

Puche RC; Alloatti R; Chapo G. 2002. Growth and development of male 'little' mice assessed with Parks' theory of feeding and growth. Growth Dev Aging 66(2):71-8. [PubMed: 12537301]  [MGI Ref ID J:81023]

Richards RG; Klotz DM; Walker MP; Diaugustine RP. 2004. Mammary gland branching morphogenesis is diminished in mice with a deficiency of insulin-like growth factor-I (IGF-I), but not in mice with a liver-specific deletion of IGF-I. Endocrinology 145(7):3106-10. [PubMed: 15059953]  [MGI Ref ID J:105630]

Santhanam M; Chia DJ. 2013. Hepatic-specific accessibility of Igf1 gene enhancers is independent of growth hormone signaling. Mol Endocrinol 27(12):2080-92. [PubMed: 24109593]  [MGI Ref ID J:211911]

Schneider P; Stauber M; Voide R; Stampanoni M; Donahue LR; Muller R. 2007. Ultrastructural properties in cortical bone vary greatly in two inbred strains of mice as assessed by synchrotron light based micro- and nano-CT. J Bone Miner Res 22(10):1557-70. [PubMed: 17605631]  [MGI Ref ID J:141352]

Sharma MC; Agrawal AK; Sharma MR; Shapiro BH. 1998. Interactions of gender, growth hormone, and phenobarbital induction on murine Cyp2b expression. Biochem Pharmacol 56(9):1251-8. [PubMed: 9802338]  [MGI Ref ID J:50483]

Sharma Y; Flurkey K; Astle CM; Harrison DE. 2005. Mice severely deficient in growth hormone have normal hematopoiesis. Exp Hematol 33(7):776-83. [PubMed: 15963853]  [MGI Ref ID J:99029]

Sos BC; Harris C; Nordstrom SM; Tran JL; Balazs M; Caplazi P; Febbraio M; Applegate MA; Wagner KU; Weiss EJ. 2011. Abrogation of growth hormone secretion rescues fatty liver in mice with hepatocyte-specific deletion of JAK2. J Clin Invest 121(4):1412-23. [PubMed: 21364286]  [MGI Ref ID J:172022]

Swindell WR. 2009. Accelerated failure time models provide a useful statistical framework for aging research. Exp Gerontol 44(3):190-200. [PubMed: 19007875]  [MGI Ref ID J:146582]

Wilson DB; Wyatt DP. 1992. Adrenocorticotropic cell distribution in adult and embryonic pituitaries of the little (lit) mutant mouse. Anat Embryol (Berl) 186(4):347-53. [PubMed: 1329576]  [MGI Ref ID J:15586]

Wilson DB; Wyatt DP. 1986. Growth hormone and prolactin immunoreactivity in the pituitary gland of postnatal little (lit) mice. Histol Histopathol 1(4):309-13. [PubMed: 2980124]  [MGI Ref ID J:802]

Wilson DB; Wyatt DP. 1992. Histopathology of the pituitary gland in neonatal little (lit) mutant mice. Histol Histopathol 7(3):451-5. [PubMed: 1504465]  [MGI Ref ID J:3198]

Wong JH; Dukes J; Levy RE; Sos B; Mason SE; Fong TS; Weiss EJ. 2008. Sex differences in thrombosis in mice are mediated by sex-specific growth hormone secretion patterns. J Clin Invest 118(8):2969-78. [PubMed: 18618017]  [MGI Ref ID J:140880]

Woodall SM; Breier BH; O'Sullivan U; Gluckman PD. 1991. The effect of the frequency of subcutaneous insulin-like growth factor-1 administration on weight gain in growth hormone deficient mice. Horm Metab Res 23(12):581-4. [PubMed: 1778592]  [MGI Ref ID J:1793]

del Rincon JP; Iida K; Gaylinn BD; McCurdy CE; Leitner JW; Barbour LA; Kopchick JJ; Friedman JE; Draznin B; Thorner MO. 2007. Growth hormone regulation of p85alpha expression and phosphoinositide 3-kinase activity in adipose tissue: mechanism for growth hormone-mediated insulin resistance. Diabetes 56(6):1638-46. [PubMed: 17363744]  [MGI Ref ID J:126470]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Mating SystemHomozygote x Heterozygote         (Female x Male)   01-MAR-06
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $199.90Female or MaleHeterozygous for Ghrhrlit  
$199.90Female or MaleHomozygous for Ghrhrlit  
Price per Pair (US dollars $)Pair Genotype
$399.80Homozygous for Ghrhrlit x Heterozygous for Ghrhrlit  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $259.90Female or MaleHeterozygous for Ghrhrlit  
$259.90Female or MaleHomozygous for Ghrhrlit  
Price per Pair (US dollars $)Pair Genotype
$519.80Homozygous for Ghrhrlit x Heterozygous for Ghrhrlit  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

General Supply Notes

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

Control Information

  Control
   Heterozygote from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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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.
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JAX® Mice
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Terms of Use


General Terms and Conditions


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General inquiries regarding Terms of Use

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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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