Strain Name:

DW/J Mlphln Pou1f1dw/J

Stock Number:

000643

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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 DW/J Mlphln Pit1dw/J    (Changed: 21-SEP-06 )
DW/J ln Pit1dw/+    (Changed: 15-DEC-04 )
Type Mutant Strain;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
H2 Haplotypeb

Appearance
agouti leaden, small body size
Related Genotype: A/A Mlphln/Mlphln Pit1dw/Pit1dw

agouti leaden, normal size
Related Genotype: A/A Mlphln/Mlphln +/?

Description
Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1dw) are characterized by severe dwarfing, sterility, and hypothyroidism. Adult dwarf mice are about one-fourth to one-third the size of wildtype mice. There is a lack of growth hormone, prolactin and thyroid stimulating hormone producing cells in the anterior pituitary leading to severe endocrine deficiency of these hormones. Homozygous mutant mice show a transient loss in cortical thymocytes associated with the primary defect in anterior pituitary.

Development
The mutation dwarf (Pou1f1dw) arose in a stock of black silver mice obtained from an English fancier (William Turton of Ilkeson) in 1920. Dr. G. D. Snell found dwarf among the mouse stocks he had when at the Bussey Institute at Harvard University in 1921. He later received it at The Jackson Laboratory from Dr. MacDowell in 1948 after the 1947 Bar Harbor fire. A female carrier of dwarf that was brown (Tyrp1b) and chinchilla (Tyrc-ch) was mated to a jerker (Espnje) male that was also ruby (Hps5ru). A male offspring of this cross, carrying dwarf, ruby, jerker, brown and chinchilla, was mated to an ABY.B10 female. The ABY.B10 was a hybrid that was H2b. A.BY is congenic from a non-inbred, BY, which carried brachyury (T), bred onto A/Lilly and AWySn then this congenic was crossed to C57BL/10 to make the H2b strain hybrid for vigor. Mouse BY was A/a at the agouti locus. After crossing the male carrying dwarf, ruby, jerker, brown and chinchilla to the ABY.B10 female, the stock was then non-sibling mated for several generations and outcrossed once to piebald (Ednrbs) females that were segregating for other loci including leaden (Mlphln) and albino (Tyrc). In 1954 inbreeding and selection was started and at F13 in 1960 the stock was primarily agouti (A), leaden (Mlphln) and segregating dwarf (Pou1f1dw). In 1966 the stock was at F35 and called DW/J and was sent to The Jackson Laboratory Animal Resources Mutant Stocks Department. A line of compatible mice of the wild type genotype was then constructed to provide hosts for ovarian transplantation. This line used for transplantation was DW.C3-Mlph+ Pou1f1+/J (Stock No. 000681). DW/J was maintained by ovarian transplantation for many generations. DW/J was cryopreserved in 1997 at generation F104 by mating heterozygous females to homozygous males that had a pituitary transplant from heterozygous littermates and a T4 pellet implanted subcutaneously allowing them to breed.

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Mlphln allele
000112   B6.Cg-Sgk3fz H54 Mlphln/+ H54 +/J
000668   C57L/J
002902   STOCK Pax3Sp Mlphln/J
000275   V/LeJ
View Strains carrying   Mlphln     (4 strains)

Strains carrying   Pou1f1dw allele
000772   B6.DW-Pou1f1dw/J
View Strains carrying   Pou1f1dw     (1 strain)

Strains carrying other alleles of Mlph
000681   DW.C3-Mlph+ Pou1f1+/J
001640   STOCK Mlphln-l1Rk3/J
View Strains carrying other alleles of Mlph     (2 strains)

Strains carrying other alleles of Pou1f1
000510   C3H/HeJ-Pou1f1dw-J/J
000681   DW.C3-Mlph+ Pou1f1+/J
View Strains carrying other alleles of Pou1f1     (2 strains)

Additional Web Information

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

Phenotype

Phenotype Information

View Phenotypic Data

Phenotypic Data
Mouse Phenome Database
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.
Griscelli Syndrome, Type 3; GS3   (MLPH)
Pituitary Hormone Deficiency, Combined, 1; CPHD1   (POU1F1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Pou1f1dw/Pou1f1dw

        DW/J Pou1f1dw
  • mortality/aging
  • extended life span
    • lifespan of female mice housed with normal-sized control females (caretakers) is increased by 50% (872 days) over median life span (579 days) of controls   (MGI Ref ID J:73731)
    • lifespan of male mice housed with control males is reduced by 6%, however, when transferred to female caretakers the two oldest males lived 24% longer than controls   (MGI Ref ID J:73731)
  • hematopoietic system phenotype
  • decreased B cell number
    • the frequency of B lineage cells is significantly reduced   (MGI Ref ID J:110683)
    • treatment with T4 restores B lineage deficiency   (MGI Ref ID J:110683)
    • myelopoiesis and thymopoiesis were normal   (MGI Ref ID J:110683)
  • immune system phenotype
  • decreased B cell number
    • the frequency of B lineage cells is significantly reduced   (MGI Ref ID J:110683)
    • treatment with T4 restores B lineage deficiency   (MGI Ref ID J:110683)
    • myelopoiesis and thymopoiesis were normal   (MGI Ref ID J:110683)
  • endocrine/exocrine gland phenotype
  • abnormal adenohypophysis morphology
    • at 8 days of age there are fewer actively dividing cells in the pituitary but no abnormal increase in apoptosis   (MGI Ref ID J:108961)
    • at 1 day of age a slight increase in apoptosis in the pituitary is found   (MGI Ref ID J:108961)
    • absent lactotrophs   (MGI Ref ID J:7211)
    • absent somatotrophs   (MGI Ref ID J:7211)
    • adenohypophysis hypoplasia
      • although normal size and morphology at 1 day of age, the pituitary is smaller than normal by 11 days of age due to reduced growth of the anterior lobes   (MGI Ref ID J:108961)
  • nervous system phenotype
  • abnormal adenohypophysis morphology
    • at 8 days of age there are fewer actively dividing cells in the pituitary but no abnormal increase in apoptosis   (MGI Ref ID J:108961)
    • at 1 day of age a slight increase in apoptosis in the pituitary is found   (MGI Ref ID J:108961)
    • absent lactotrophs   (MGI Ref ID J:7211)
    • absent somatotrophs   (MGI Ref ID J:7211)
    • adenohypophysis hypoplasia
      • although normal size and morphology at 1 day of age, the pituitary is smaller than normal by 11 days of age due to reduced growth of the anterior lobes   (MGI Ref ID J:108961)
  • growth/size/body phenotype
  • decreased body size
    • although homozygotes are the same size as control littermates at birth, they begin to be smaller at 2 weeks of age, are noticably smaller by 3 weeks of age, and are only one third to one quarter the size of normal littermates as adults   (MGI Ref ID J:108961)

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

Pou1f1dw/Pou1f1dw

        Background Not Specified
  • growth/size/body phenotype
  • abnormal molar morphology
    • mutants have normal molar crowns but reduced roots   (MGI Ref ID J:13120)
  • proportional dwarf
    • mature individuals are only one fourth the weight of their normal sibs   (MGI Ref ID J:13120)
    • reduced size begins after 14th day   (MGI Ref ID J:13120)
  • reproductive system phenotype
  • infertility
    • both males and females are entirely sterile   (MGI Ref ID J:13120)
  • homeostasis/metabolism phenotype
  • decreased growth hormone level
    • GH was undetectable from birth to 6 weeks of age   (MGI Ref ID J:6589)
  • decreased prolactin level
    • PRL was undetectable from birth to 6 weeks of age   (MGI Ref ID J:6589)
    • decreased circulating prolactin level
      • minimal concentrations of PRL were detected in the plasma   (MGI Ref ID J:6754)
  • endocrine/exocrine gland phenotype
  • absent lactotrophs
    • PRL-producing mammotropes were absent   (MGI Ref ID J:6754)
  • absent somatotrophs
    • GH-producing somatotropes were absent   (MGI Ref ID J:7211)
  • decreased thyrotroph cell number
    • almost complete absence of TSH-producing thyrotroph   (MGI Ref ID J:12161)
  • nervous system phenotype
  • absent lactotrophs
    • PRL-producing mammotropes were absent   (MGI Ref ID J:6754)
  • absent somatotrophs
    • GH-producing somatotropes were absent   (MGI Ref ID J:7211)
  • decreased thyrotroph cell number
    • almost complete absence of TSH-producing thyrotroph   (MGI Ref ID J:12161)
  • craniofacial phenotype
  • abnormal molar morphology
    • mutants have normal molar crowns but reduced roots   (MGI Ref ID J:13120)
View Research Applications

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

Mlphln related

Dermatology Research
Color and White Spotting Defects

Pou1f1dw related

Cell Biology Research
Signal Transduction
Transcriptional Regulation

Developmental Biology Research
Extended Life Span
Growth Defects

Endocrine Deficiency Research
Hypothalamus/Pituitary Defects

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency Associated with Other Defects

Reproductive Biology Research
Fertility Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Mlphln
Allele Name leaden
Allele Type Spontaneous
Common Name(s) ln;
Strain of OriginC57BR
Gene Symbol and Name Mlph, melanophilin
Chromosome 1
Gene Common Name(s) 2210418F23Rik; 5031433I09Rik; AW228792; D1Wsu84e; DNA segment, Chr 1, Wayne State University 84, expressed; SLAC2-A; Slac-2a; expressed sequence AW228792; l(1)-3Rk; l1Rk3; leaden; lethal, Chr 1, Roderick 3; ln;
Molecular Note This allele has a C to T transition at mRNA nucleotide position 266. This introduces a stop codon in the sequence of the normally spliced transcript and it also creates a new splice donor site in exon 2. Use of this alternative splice site yields a transcript with an in-frame 21 base pair deletion that deletes 7 amino acids from the translated protein. Northern blots failed to detect this size difference and did not find any change from normal in transcript expression level. [MGI Ref ID J:71302]
 
Allele Symbol Pou1f1dw
Allele Name dwarf
Allele Type Spontaneous
Common Name(s) Pit1dw; Pit1dwSn; Snell's dwarf; Snell-Bagg pituitary dwarf; dw; dwarf;
Strain of OriginSTOCK Pmelsi
Gene Symbol and Name Pou1f1, POU domain, class 1, transcription factor 1
Chromosome 16
Gene Common Name(s) CPHD1; GHF-1; GHF1; GHF1A; Hmp1; PIT1; PIT1Z; POU1F1a; Pit-1; Pit1; Pit1-rs1; Snell dwarf; dw; dwarf; pituitary specific transcription factor 1; pituitary specific transcription factor 1, related sequence 1;
General Note This mutation arose in a stock of silver mice obtained from an English fancier (J:13120). Homozygous mutant mice are about one-fourth to one-third normal size and are sterile. The small size is due to a defective anterior pituitary in which there is a great deficiency of GH-producing, PRL-producing, and TSH-producing cells (J:6754, J:7211, J:12161). The anterior pituitary of the Pit1dw homozygote is already abnormal at birth with no identifiable GH or PRL cells (J:6684). GH and PRL synthesis is not detectable at any stages from birth to 6 weeks of age (J:6589), and there is probably also a deficiency of TSH and corticotropin (J:19241). Adult dwarf mouse pituitaries retain an embryonic, incompletely differentiated form of corticotrophs (J:13323). The defects in growth and fertility may be corrected by pituitary implants (J:13139) or by administration of pituitary hormones (J:30695, J:5085).

Two populations of cells give rise to thyrotrophs in the anterior pituitary in developing mouse embryos. The first population arises at day 12 in the rostral tip of the gland. This population is independent of Pit1, as it appears in Pit1dw mice, but it disappears by birth. The second population, which arises in the caudomedial portion of the gland at embryonic day 15.5, is Pit1-dependent, and is absent in Snell dwarf mice(J:17223).

Pit1dw mice have been reported to have a defective immune response that primarily affects the T cell system (J:19990), but other authors (J:6241, J:5638) have been unable to confirm these findings and attribute the previous results to secondary effects of dwarfing on overall vigor and nutritional status. Cross (J:2020) has shown that Pit1dw homozygous mice do develop normal immunocompetence, but that this development is delayed relative to that in normal littermates. Dwarf homozygotes have a severe deficiency of dopamine in the median eminence (J:6652).

Molecular Note A G-to-T transversion mutation in codon 261 is predicted to convert a tryptophan residue in the homeodomain to a cysteine in the encoded protein. [MGI Ref ID J:10774] [MGI Ref ID J:10998]

Genotyping

Genotyping Information

Genotyping Protocols

Pou1f1dw, Pyrosequencing
Pou1f1dw, End Point Analysis


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Boylston WH; Gerstner A; DeFord JH; Madsen M; Flurkey K; Harrison DE; Papaconstantinou J. 2004. Altered cholesterologenic and lipogenic transcriptional profile in livers of aging Snell dwarf (Pit1dw/dwJ) mice. Aging Cell 3(5):283-96. [PubMed: 15379852]  [MGI Ref ID J:109839]

Papaconstantinou J; Deford JH; Gerstner A; Hsieh CC; Boylston WH; Guigneaux MM; Flurkey K; Harrison DE. 2005. Hepatic gene and protein expression of primary components of the IGF-I axis in long lived Snell dwarf mice. Mech Ageing Dev 126(6-7):692-704. [PubMed: 15888324]  [MGI Ref ID J:98300]

Additional References

Camper SA; Saunders TL; Katz RW; Reeves RH. 1990. The Pit-1 transcription factor gene is a candidate for the murine Snell dwarf mutation. Genomics 8(3):586-90. [PubMed: 1981057]  [MGI Ref ID J:10998]

Chen J; Flurkey K; Harrison DE. 2002. A reduced peripheral blood CD4(+) lymphocyte proportion is a consistent ageing phenotype. Mech Ageing Dev 123(2-3):145-53. [PubMed: 11718808]  [MGI Ref ID J:73732]

Flurkey K; Papaconstantinou J; Harrison DE. 2002. The Snell dwarf mutation Pit1(dw) can increase life span in mice. Mech Ageing Dev 123(2-3):121-30. [PubMed: 11718806]  [MGI Ref ID J:73731]

Hsieh CC; DeFord JH; Flurkey K; Harrison DE; Papaconstantinou J. 2002. Implications for the insulin signaling pathway in Snell dwarf mouse longevity: a similarity with the C. elegans longevity paradigm. Mech Ageing Dev 123(9):1229-44. [PubMed: 12020945]  [MGI Ref ID J:77095]

Li S; Crenshaw EB 3rd; Rawson EJ; Simmons DM; Swanson LW; Rosenfeld MG. 1990. Dwarf locus mutants lacking three pituitary cell types result from mutations in the POU-domain gene pit-1. Nature 347(6293):528-33. [PubMed: 1977085]  [MGI Ref ID J:10774]

Madsen MA; Hsieh CC; Boylston WH; Flurkey K; Harrison D; Papaconstantinou J. 2004. Altered oxidative stress response of the long-lived Snell dwarf mouse. Biochem Biophys Res Commun 318(4):998-1005. [PubMed: 15147972]  [MGI Ref ID J:90070]

Mlphln related

Anderson MG; Hawes NL; Trantow CM; Chang B; John SW. 2008. Iris phenotypes and pigment dispersion caused by genes influencing pigmentation. Pigment Cell Melanoma Res 21(5):565-78. [PubMed: 18715234]  [MGI Ref ID J:141035]

Fisher RA. 1953. The linkage of polydactyly with leaden in the house mouse. Heredity 7:91-95.  [MGI Ref ID J:12979]

Hauschka TS; Jacobs BB; Holdridge BA. 1968. Recessive yellow and its interaction with belted in the mouse. J Hered 59(6):339-41. [PubMed: 5713933]  [MGI Ref ID J:5110]

Hearing VJ; Phillips P; Lutzner MA. 1973. The fine structure of melanogenesis in coat color mutants of the mouse. J Ultrastruct Res 43(1):88-106. [PubMed: 4634048]  [MGI Ref ID J:5346]

Hume AN; Collinson LM; Hopkins CR; Strom M; Barral DC; Bossi G; Griffiths GM; Seabra MC. 2002. The leaden gene product is required with Rab27a to recruit myosin Va to melanosomes in melanocytes. Traffic 3(3):193-202. [PubMed: 11886590]  [MGI Ref ID J:105323]

Hume AN; Tarafder AK; Ramalho JS; Sviderskaya EV; Seabra MC. 2006. A coiled-coil domain of melanophilin is essential for Myosin Va recruitment and melanosome transport in melanocytes. Mol Biol Cell 17(11):4720-35. [PubMed: 16914517]  [MGI Ref ID J:117973]

Karolyi IJ; Dootz GA; Halsey K; Beyer L; Probst FJ; Johnson KR; Parlow AF; Raphael Y; Dolan DF; Camper SA. 2007. Dietary thyroid hormone replacement ameliorates hearing deficits in hypothyroid mice. Mamm Genome 18(8):596-608. [PubMed: 17899304]  [MGI Ref ID J:125708]

Markert CL; Silvers WK. 1956. The Effects of Genotype and Cell Environment on Melanoblast Differentiation in the House Mouse. Genetics 41(3):429-50. [PubMed: 17247639]  [MGI Ref ID J:12970]

Matesic LE; Yip R; Reuss AE; Swing DA; O'Sullivan TN; Fletcher CF; Copeland NG; Jenkins NA. 2001. Mutations in Mlph, encoding a member of the Rab effector family, cause the melanosome transport defects observed in leaden mice. Proc Natl Acad Sci U S A 98(18):10238-43. [PubMed: 11504925]  [MGI Ref ID J:71302]

Moore KJ; Swing DA; Copeland NG; Jenkins NA. 1990. Interaction of the murine dilute suppressor gene (dsu) with fourteen coat color mutations [published erratum appears in Genetics 1990 Sep;126(1):285] Genetics 125(2):421-30. [PubMed: 2379821]  [MGI Ref ID J:29467]

Moore KJ; Swing DA; Rinchik EM; Mucenski ML; Buchberg AM; Copeland NG; Jenkins NA. 1988. The murine dilute suppressor gene dsu suppresses the coat-color phenotype of three pigment mutations that alter melanocyte morphology, d, ash and ln. Genetics 119(4):933-41. [PubMed: 3410303]  [MGI Ref ID J:9309]

Murray JM. 1933. "Leaden", a recent color mutation in the house mouse. Am Naturalist 67:278-283.  [MGI Ref ID J:17162]

Nadeau JH. 2001. Modifier genes in mice and humans. Nat Rev Genet 2(3):165-74. [PubMed: 11256068]  [MGI Ref ID J:88013]

Novak EK; Hui SW; Swank RT. 1984. Platelet storage pool deficiency in mouse pigment mutations associated with seven distinct genetic loci. Blood 63(3):536-44. [PubMed: 6696991]  [MGI Ref ID J:7327]

Silvers WK. 1979. The Coat Colors of Mice; A Model for Mammalian Gene Action and Interaction. In: The Coat Colors of Mice. Springer-Verlag, New York.  [MGI Ref ID J:78801]

Stephenson DA; Glenister PH; Hornby JE. 1985. Site of beige (bg) and leaden (ln) pigment gene expression determined by recombinant embryonic skin grafts and aggregation mouse chimaeras employing sash (Wsh) homozygotes. Genet Res 46(2):193-205. [PubMed: 3910518]  [MGI Ref ID J:8167]

Sweet SE; Quevedo WC Jr. 1968. Role of melanocyte morphology in pigmentation of mouse hair. Anat Rec 162(2):243-54. [PubMed: 5726144]  [MGI Ref ID J:5095]

Ward RD; Stone BM; Raetzman LT; Camper SA. 2006. Cell proliferation and vascularization in mouse models of pituitary hormone deficiency. Mol Endocrinol 20(6):1378-90. [PubMed: 16556738]  [MGI Ref ID J:108961]

Pou1f1dw related

Alderman JM; Flurkey K; Brooks NL; Naik SB; Gutierrez JM; Srinivas U; Ziara KB; Jing L; Boysen G; Bronson R; Klebanov S; Chen X; Swenberg JA; Stridsberg M; Parker CE; Harrison DE; Combs TP. 2009. Neuroendocrine inhibition of glucose production and resistance to cancer in dwarf mice. Exp Gerontol 44(1-2):26-33. [PubMed: 18582556]  [MGI Ref ID J:146699]

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]

Barkley MS; Bartke A; Gross DS; Sinha YN. 1982. Prolactin status of hereditary dwarf mice. Endocrinology 110(6):2088-96. [PubMed: 7075549]  [MGI Ref ID J:6754]

Bartke A. 1967. Prolactin deficiency in genetically sterile dwarf mice. In: Endocrine Genetics. Cambridge Univ. Press, Cambridge.  [MGI Ref ID J:30695]

Bartke A. 1968. The response of dwarf mice to murine thyroid-stimulating hormone. Gen Comp Endocrinol 11(1):246-7. [PubMed: 5674697]  [MGI Ref ID J:5085]

Bartke A; Brown-Borg H; Mattison J; Kinney B; Hauck S; Wright C. 2001. Prolonged longevity of hypopituitary dwarf mice. Exp Gerontol 36(1):21-8. [PubMed: 11162909]  [MGI Ref ID J:66980]

Brooks NL; Trent CM; Raetzsch CF; Flurkey K; Boysen G; Perfetti MT; Jeong YC; Klebanov S; Patel KB; Khodush VR; Kupper LL; Carling D; Swenberg JA; Harrison DE; Combs TP. 2007. Low utilization of circulating glucose after food withdrawal in snell dwarf mice. J Biol Chem 282(48):35069-77. [PubMed: 17905742]  [MGI Ref ID J:127162]

CARSNER RL; RENNELS EG. 1960. Primary site of gene action in anterior pituitary dwarf mice. Science 131:829. [PubMed: 13807990]  [MGI Ref ID J:13139]

Camper SA; Saunders TL; Katz RW; Reeves RH. 1990. The Pit-1 transcription factor gene is a candidate for the murine Snell dwarf mutation. Genomics 8(3):586-90. [PubMed: 1981057]  [MGI Ref ID J:10998]

Chen HW; Meier H; Heiniger HJ; Huebner RJ. 1972. Tumorigenesis in strain DW-J mice and induction by prolactin of the group-specific antigen of endogenous C-type RNA tumor virus. J Natl Cancer Inst 49(4):1145-54. [PubMed: 4117317]  [MGI Ref ID J:46465]

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]

Cross RJ; Bryson JS; Roszman TL. 1992. Immunologic disparity in the hypopituitary dwarf mouse. J Immunol 148(5):1347-52. [PubMed: 1531667]  [MGI Ref ID J:2020]

DiMattia GE; Rhodes SJ; Krones A; Carriere C; O'Connell S; Kalla K; Arias C; Sawchenko P; Rosenfeld MG. 1997. The Pit-1 gene is regulated by distinct early and late pituitary-specific enhancers. Dev Biol 182(1):180-90. [PubMed: 9073460]  [MGI Ref ID J:39064]

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]

Dozmorov I; Galecki A; Chang Y; Krzesicki R; Vergara M; Miller RA. 2002. Gene expression profile of long-lived snell dwarf mice. J Gerontol A Biol Sci Med Sci 57(3):B99-108. [PubMed: 11867646]  [MGI Ref ID J:75145]

Dumont F; Robert F; Bischoff P. 1979. T and B lymphocytes in pituitary dwarf Snell-Bagg mice. Immunology 38(1):23-31. [PubMed: 315916]  [MGI Ref ID J:6241]

Duquesnoy RJ; Pedersen GM. 1981. Immunologic and hematologic deficiencies of the ypopituitary dwarf mouse. In: Immunologic Defects in Laboratory Animals. Plenum Press, New York, New York.  [MGI Ref ID J:19990]

ELFTMAN H; WEGELIUS O. 1959. Anterior pituitary cytology of the dwarf mouse. Anat Rec 135:43-9. [PubMed: 13819893]  [MGI Ref ID J:12161]

Fang Q; Longo-Guess C; Gagnon LH; Mortensen AH; Dolan DF; Camper SA; Johnson KR. 2011. A modifier gene alleviates hypothyroidism-induced hearing impairment in Pou1f1dw dwarf mice. Genetics 189(2):665-73. [PubMed: 21840860]  [MGI Ref ID J:177740]

Flurkey K; Papaconstantinou J; Harrison DE. 2002. The Snell dwarf mutation Pit1(dw) can increase life span in mice. Mech Ageing Dev 123(2-3):121-30. [PubMed: 11718806]  [MGI Ref ID J:73731]

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]

Gala RR. 1995. Influence of thyroxine and thyroxine with growth hormone and prolactin on splenocyte subsets and on the expression of interleukin-2 and prolactin receptors on splenocyte subsets of Snell dwarf mice. Proc Soc Exp Biol Med 210(2):117-25. [PubMed: 7568281]  [MGI Ref ID J:29337]

Gala RR. 1995. The influence of thyroxine, growth hormone and prolactin alone and in combination on the production of prolactin-like activity by splenocytes from Snell dwarf mice. Life Sci 57(2):113-22. [PubMed: 7603293]  [MGI Ref ID J:26825]

Gala RR; Shevach EM. 1993. Influence of prolactin and growth hormone on the activation of dwarf mouse lymphocytes in vivo. Proc Soc Exp Biol Med 204(2):224-30. [PubMed: 8415780]  [MGI Ref ID J:15274]

Gruneberg H. 1965. Genes and genotypes affecting the teeth of the mouse. J Embryol Exp Morphol 14(2):137-59. [PubMed: 5893447]  [MGI Ref ID J:12999]

Hsieh CC; DeFord JH; Flurkey K; Harrison DE; Papaconstantinou J. 2002. Effects of the Pit1 mutation on the insulin signaling pathway: implications on the longevity of the long-lived Snell dwarf mouse. Mech Ageing Dev 123(9):1245-55. [PubMed: 12020946]  [MGI Ref ID J:77094]

Hsieh CC; DeFord JH; Flurkey K; Harrison DE; Papaconstantinou J. 2002. Implications for the insulin signaling pathway in Snell dwarf mouse longevity: a similarity with the C. elegans longevity paradigm. Mech Ageing Dev 123(9):1229-44. [PubMed: 12020945]  [MGI Ref ID J:77095]

Hsieh CC; Papaconstantinou J. 2006. Thioredoxin-ASK1 complex levels regulate ROS-mediated p38 MAPK pathway activity in livers of aged and long-lived Snell dwarf mice. FASEB J 20(2):259-68. [PubMed: 16449798]  [MGI Ref ID J:105801]

Hurley DL; Birch DV; Almond MC; Estrada IJ; Phelps CJ. 2003. Reduced hypothalamic neuropeptide Y expression in growth hormone- and prolactin-deficient Ames and Snell dwarf mice. Endocrinology 144(11):4783-9. [PubMed: 12960004]  [MGI Ref ID J:105617]

Karolyi IJ; Dootz GA; Halsey K; Beyer L; Probst FJ; Johnson KR; Parlow AF; Raphael Y; Dolan DF; Camper SA. 2007. Dietary thyroid hormone replacement ameliorates hearing deficits in hypothyroid mice. Mamm Genome 18(8):596-608. [PubMed: 17899304]  [MGI Ref ID J:125708]

Koedam JA; Hoogerbrugge CM; van Buul-Offers SC. 1998. Insulin-like growth factor-binding protein-3 protease activity in Snell normal and Pit-1 deficient dwarf mice. J Endocrinol 157(2):295-303. [PubMed: 9659293]  [MGI Ref ID J:47738]

Kooijman R; Malur A; Van Buul-Offers SC; Hooghe-Peters EL. 1997. Growth hormone expression in murine bone marrow cells is independent of the pituitary transcription factor Pit-1. Endocrinology 138(9):3949-55. [PubMed: 9275086]  [MGI Ref ID J:42905]

Leiser SF; Miller RA. 2010. Nrf2 signaling, a mechanism for cellular stress resistance in long-lived mice. Mol Cell Biol 30(3):871-84. [PubMed: 19933842]  [MGI Ref ID J:156388]

Lewis UJ. 1967. Growth Hormone of Normal and Dwarf mice.. In: Endocrine Genetics. Cambridge Univ. Press, London, Cambridge.  [MGI Ref ID J:19241]

Li S; Crenshaw EB 3rd; Rawson EJ; Simmons DM; Swanson LW; Rosenfeld MG. 1990. Dwarf locus mutants lacking three pituitary cell types result from mutations in the POU-domain gene pit-1. Nature 347(6293):528-33. [PubMed: 1977085]  [MGI Ref ID J:10774]

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; Li S; Drolet DW; Rosenfeld MG. 1994. Pituitary ontogeny of the Snell dwarf mouse reveals Pit-1-independent and Pit-1-dependent origins of the thyrotrope. Development 120(3):515-22. [PubMed: 8162852]  [MGI Ref ID J:17223]

Madsen MA; Hsieh CC; Boylston WH; Flurkey K; Harrison D; Papaconstantinou J. 2004. Altered oxidative stress response of the long-lived Snell dwarf mouse. Biochem Biophys Res Commun 318(4):998-1005. [PubMed: 15147972]  [MGI Ref ID J:90070]

Marquis G; Montplaisir S; Pelletier M; Auger P; Lapp WS. 1988. Genetics of resistance to infection with Candida albicans in mice. Br J Exp Pathol 69(5):651-60. [PubMed: 3058198]  [MGI Ref ID J:27324]

Meseguer A; Catterall JF. 1992. Effects of pituitary hormones on the cell-specific expression of the KAP gene. Mol Cell Endocrinol 89(1-2):153-62. [PubMed: 1338721]  [MGI Ref ID J:3165]

Montecino-Rodriguez E; Clark R; Johnson A; Collins L; Dorshkind K. 1996. Defective B cell development in Snell dwarf (dw/dw) mice can be corrected by thyroxine treatment. J Immunol 157(8):3334-40. [PubMed: 8871629]  [MGI Ref ID J:38361]

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]

Morgan WW; Bartke A; Pfeil K. 1981. Deficiency of dopamine in the median eminence of Snell dwarf mice. Endocrinology 109(6):2069-75. [PubMed: 7308142]  [MGI Ref ID J:6652]

Murphy WJ; Durum SK; Anver MR; Longo DL. 1992. Immunologic and hematologic effects of neuroendocrine hormones. Studies on DW/J dwarf mice. J Immunol 148(12):3799-805. [PubMed: 1602129]  [MGI Ref ID J:1229]

Murphy WJ; Durum SK; Longo DL. 1993. Differential effects of growth hormone and prolactin on murine T cell development and function. J Exp Med 178(1):231-6. [PubMed: 8315380]  [MGI Ref ID J:13108]

Mustapha M; Fang Q; Gong TW; Dolan DF; Raphael Y; Camper SA; Duncan RK. 2009. Deafness and permanently reduced potassium channel gene expression and function in hypothyroid Pit1dw mutants. J Neurosci 29(4):1212-23. [PubMed: 19176829]  [MGI Ref ID J:144823]

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]

Noguchi T; Kurata LM; Sugisaki T. 1987. Presence of a somatomedin-C-immunoreactive substance in the central nervous system: immunohistochemical mapping studies. Neuroendocrinology 46(4):277-82. [PubMed: 3313091]  [MGI Ref ID J:30358]

O'Hara BF; Bendotti C; Reeves RH; Oster-Granite ML; Coyle JT; Gearhart JD. 1988. Genetic mapping and analysis of somatostatin expression in Snell dwarf mice. Brain Res 464(4):283-92. [PubMed: 2906811]  [MGI Ref ID J:4468]

Page MM; Salmon AB; Leiser SF; Robb EL; Brown MF; Miller RA; Stuart JA. 2009. Mechanisms of stress resistance in Snell dwarf mouse fibroblasts: enhanced antioxidant and DNA base excision repair capacity, but no differences in mitochondrial metabolism. Free Radic Biol Med 46(8):1109-18. [PubMed: 19439226]  [MGI Ref ID J:149215]

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]

Phelps CJ. 2004. Postnatal regression of hypothalamic dopaminergic neurons in prolactin-deficient Snell dwarf mice. Endocrinology 145(12):5656-64. [PubMed: 15345680]  [MGI Ref ID J:95756]

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]

Postiglione MP; Parlato R; Rodriguez-Mallon A; Rosica A; Mithbaokar P; Maresca M; Marians RC; Davies TF; Zannini MS; De Felice M; Di Lauro R. 2002. Role of the thyroid-stimulating hormone receptor signaling in development and differentiation of the thyroid gland. Proc Natl Acad Sci U S A 99(24):15462-7. [PubMed: 12432093]  [MGI Ref ID J:80538]

Salmon AB; Murakami S; Bartke A; Kopchick J; Yasumura K; Miller RA. 2005. Fibroblast cell lines from young adult mice of long-lived mutant strains are resistant to multiple forms of stress. Am J Physiol Endocrinol Metab 289(1):E23-9. [PubMed: 15701676]  [MGI Ref ID J:99517]

Schneider GB. 1976. Immunological competence in Snell-Bagg pituitary dwarf mice: response to the contact-sensitizing agent oxazolone. Am J Anat 145(3):371-93. [PubMed: 1266774]  [MGI Ref ID J:5638]

Slabaugh MB; Lieberman ME; Rutledge JJ; Gorski J. 1981. Growth hormone and prolactin synthesis in normal and homozygous Snell and Ames dwarf mice. Endocrinology 109(4):1040-6. [PubMed: 7285859]  [MGI Ref ID J:6589]

Snell GD. 1929. DWARF, A NEW MENDELIAN RECESSIVE CHARACTER OF THE HOUSE MOUSE. Proc Natl Acad Sci U S A 15(9):733-4. [PubMed: 16577229]  [MGI Ref ID J:13120]

Steinbaugh MJ; Sun LY; Bartke A; Miller RA. 2012. Activation of genes involved in xenobiotic metabolism is a shared signature of mouse models with extended lifespan. Am J Physiol Endocrinol Metab 303(4):E488-95. [PubMed: 22693205]  [MGI Ref ID J:187426]

Stickland NC; Crook AR; Sutton CM. 1994. Effects of pituitary dwarfism in the mouse on fast and slow skeletal muscles. Acta Anat (Basel) 151(4):245-9. [PubMed: 7740919]  [MGI Ref ID J:24150]

Sugisaki T; Yamada T; Saitoh S; Takamatsu K; Kubota C; Noguchi T. 1994. Hippocalcin expression in the brain of the Snell dwarf mutant mouse. Brain Res 665(1):101-6. [PubMed: 7882001]  [MGI Ref ID J:21733]

Sun LY; Steinbaugh MJ; Masternak MM; Bartke A; Miller RA. 2009. Fibroblasts from long-lived mutant mice show diminished ERK1/2 phosphorylation but exaggerated induction of immediate early genes. Free Radic Biol Med 47(12):1753-61. [PubMed: 19786089]  [MGI Ref ID J:155129]

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]

Swindell WR; Masternak MM; Bartke A. 2010. In vivo analysis of gene expression in long-lived mice lacking the pregnancy-associated plasma protein A (PappA) gene. Exp Gerontol 45(5):366-74. [PubMed: 20197085]  [MGI Ref ID J:164141]

Tomita K; Yoshida T; Morita J; Atsumi S; Totsuka T. 1995. In vivo responsiveness of thyroid glands to TSH in normal and novel 'growth-retarded' mice: transient elevation in normal mice and impairment in 'growth-retarded' mice. J Endocrinol 144(2):209-14. [PubMed: 7706974]  [MGI Ref ID J:23121]

Vergara M; Smith-Wheelock M; Harper JM; Sigler R; Miller RA. 2004. Hormone-treated snell dwarf mice regain fertility but remain long lived and disease resistant. J Gerontol A Biol Sci Med Sci 59(12):1244-50. [PubMed: 15699523]  [MGI Ref ID J:105551]

Ward RD; Stone BM; Raetzman LT; Camper SA. 2006. Cell proliferation and vascularization in mouse models of pituitary hormone deficiency. Mol Endocrinol 20(6):1378-90. [PubMed: 16556738]  [MGI Ref ID J:108961]

Wilson DB; Christensen E. 1981. Fine structure of somatotrophs and mammotrophs during development of the dwarf (dw) mutant mouse. J Anat 133(Pt 3):407-17. [PubMed: 7328047]  [MGI Ref ID J:6684]

Wilson DB; Wyatt DP. 1993. Immunocytochemical effects of thyroxine stimulation on the adenohypophysis of dwarf (dw) mutant mice. Cell Tissue Res 274(3):579-85. [PubMed: 8293449]  [MGI Ref ID J:21449]

Wilson DB; Wyatt DP. 1993. Immunocytochemistry of ambiguous cells in adult and embryonic dwarf (dw) mouse pituitaries. Anat Rec 236(4):671-8. [PubMed: 8397485]  [MGI Ref ID J:13323]

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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 & HusbandryHomozygotes require powdered food and easy access to water to survive. Homozygotes are often not weaned until 4 weeks of age.

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.

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 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.

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 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.

General Supply Notes

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

Control Information

  Control
   Wild-type from the colony
 
  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.


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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, 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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