JAX
Mouse Strain Datasheet - 000772
B6.DW-Pou1f1dw/J
Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1dw) are characterized by severe proportional 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.
Genetic overview
| Genetic Background | Generation |
|---|---|
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Pou1f1dw
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Spontaneous | Pou1f1 | POU domain, class 1, transcription factor 1 |
Research Applications
- Cell Biology Research
- Developmental Biology Research
- Endocrine Deficiency Research
- Immunology, Inflammation and Autoimmunity Research
- Reproductive Biology Research
Detailed Description
Mice homozygous mice for the dwarf spontaneous mutation (Pou1f1dw) are characterized by severe proportional 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
A heterozygous dwarf (Pou1f1dw/+) male from strain DW/J at generation F45 was crossed to a C57BL/6J female in 1969 to start the B6.DW line. Each generation thereafter a tested male carrier was backcrossed to a C57BL/6J female to N11. At N11 the strain was maintained by mating tested heterozygous siblings to F9. The strain was cryopreserved in 1981 by mating N11F9 tested heterozygous dwarf males to C57BL/6J females.
Selected References
- 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: 15379852MGI: 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: 15888324MGI: J:98300
Pou1f1dw
Allele Symbol: Pou1f1dw
| Allele Name | dwarf |
|---|---|
| Allele Type | Spontaneous |
| Allele Synonym(s) | Pit1dw; Pit1dwSn; Snell's dwarf; Snell-Bagg pituitary dwarf; dw; dwarf |
| Gene Symbol and Name | Pou1f1, POU domain, class 1, transcription factor 1 |
| Gene Synonym(s) | CPHD1; GHF-1; GHF1; GHF1A; Hmp1; PIT1; PIT1Z; POU1F1a; Pit-1; Pit-1; Pit1; Pit1; Pit1-rs1; Pit1-rs1; Snell dwarf; dw; dwarf; pituitary specific transcription factor 1; pituitary specific transcription factor 1, related sequence 1 |
| Strain of Origin | STOCK Pmelsi |
| Chromosome | 16 |
| General Note | Phenotypic Similarity to Human Syndrome: Secondary Hypothyroidism J:144823 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. |
Disease Terms
Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Research Areas By Genotype
This mouse can be used to support research in many areas including:
Genotype: 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
Mammalian Phenotype Terms by Genotype
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain
Genotype: Pou1f1dw/Pou1f1dw
Not Specified
growth/size/body region phenotype
- abnormal molar morphology
- mutants have normal molar crowns but reduced roots (MGI Ref ID J:13120)
- proportional dwarf
cellular phenotype
- abnormal cell cytoskeleton morphology
- organization of the cytoskeleton is abnormal in pillar cells at P25 which persists through P42 (MGI Ref ID J:144823)
skeleton phenotype
- abnormal molar morphology
- mutants have normal molar crowns but reduced roots (MGI Ref ID J:13120)
hearing/vestibular/ear phenotype
- abnormal Hensen stripe morphology
- the tectorial membrane has a more prominent Hensen's stripe that persists through P42 (MGI Ref ID J:144823)
- abnormal cochlear outer hair cell morphology
- abnormal hair cell physiology
- mutant outer hair cells have varying mixtures of low- and high-voltage activated conductances compared to wild-type cells which have a dominant low-voltage activated KCNQ4 current and a reduction in KCNQ4 currents (MGI Ref ID J:144823)
- abnormal orientation of outer hair cell stereociliary bundles
- the orientation of the outer hair cell bundles in P14 and P25 mutants is disrupted (MGI Ref ID J:144823)
- abnormal pillar cell morphology
- organization of the cytoskeleton is abnormal in pillar cells at P25 which persists through P42 (MGI Ref ID J:144823)
- abnormal stria vascularis morphology
- abnormalities in the stria vascularis are more obvious at P42 than at P12 or P21 (MGI Ref ID J:144823)
- accumulation of dark lipofuscin-like deposits in the stria vacularis of P42 old mutants (MGI Ref ID J:144823)
- stria is smaller in width at P21 and P42, due to reduced contribution of intermediate cells (MGI Ref ID J:144823)
- stria vascularis shows less interdigitation of the intermediate cells with the basal aspect of the marginal cells and less infolding of the basolateral membrane (MGI Ref ID J:144823)
- abnormal strial intermediate cell morphology
- deterioration of the intermediate cells (MGI Ref ID J:144823)
- abnormal tectorial membrane morphology
- the tectorial membrane contains an abnormal protrusion at P21 which appears to be a more prominent Hensens stripe that persists through P42 (MGI Ref ID J:144823)
- abnormal tectorial membrane striated-sheet matrix morphology
- abnormalities in the structure of the striated-sheet matrix in the tectorial membrane (MGI Ref ID J:144823)
- abnormal tunnel of Corti morphology
- delay in the opening of the tunnel of Corti at P12, but by P21, the opening is indistinguishable from wild-type mice (MGI Ref ID J:144823)
- absent cochlear microphonics
- absent distortion product otoacoustic emissions
- adult mutants lack DPOAE, indicating compromised outer hair cell function (MGI Ref ID J:144823)
- cochlear outer hair cell degeneration
- deafness
- (MGI Ref ID J:144823)
- decreased endocochlear potential
- 50% and 45% reduction in endocochlear potential in 3 and 6 week old mice, respectively (MGI Ref ID J:144823)
- short cochlear outer hair cells
- outer hair cells are about 24% shorter than in wild-type mice (MGI Ref ID J:144823)
pigmentation phenotype
- abnormal strial intermediate cell morphology
- deterioration of the intermediate cells (MGI Ref ID J:144823)
reproductive system phenotype
- infertility
- both males and females are entirely sterile (MGI Ref ID J:13120)
homeostasis/metabolism phenotype
- decreased circulating prolactin level
- minimal concentrations of PRL were detected in the plasma (MGI Ref ID J:6754)
- 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)
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
- abnormal cochlear outer hair cell morphology
- abnormal hair cell physiology
- mutant outer hair cells have varying mixtures of low- and high-voltage activated conductances compared to wild-type cells which have a dominant low-voltage activated KCNQ4 current and a reduction in KCNQ4 currents (MGI Ref ID J:144823)
- abnormal orientation of outer hair cell stereociliary bundles
- the orientation of the outer hair cell bundles in P14 and P25 mutants is disrupted (MGI Ref ID J:144823)
- absent cochlear microphonics
- absent lactotrophs
- PRL-producing mammotropes were absent (MGI Ref ID J:6754)
- absent somatotrophs
- GH-producing somatotropes were absent (MGI Ref ID J:7211)
- cochlear outer hair cell degeneration
- decreased thyrotroph cell number
- almost complete absence of TSH-producing thyrotroph (MGI Ref ID J:12161)
- short cochlear outer hair cells
- outer hair cells are about 24% shorter than in wild-type mice (MGI Ref ID J:144823)
craniofacial phenotype
- abnormal molar morphology
- mutants have normal molar crowns but reduced roots (MGI Ref ID J:13120)
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
immune system phenotype
- decreased B cell number
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)
- 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)
- increased pituitary gland apoptosis
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)
- 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)
- increased pituitary gland apoptosis
growth/size/body region 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)
References
- 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: 15379852MGI: 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: 15888324MGI: 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: 1981057MGI: J:10998
- 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: 11718806MGI: J:73731
- 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: 1977085MGI: 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: 15147972MGI: J:90070
Additional - 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: 18582556MGI: 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: 14698815MGI: J:87701
- Barkley MS; Bartke A; Gross DS; Sinha YN. 1982. Prolactin status of hereditary dwarf mice. Endocrinology 110(6):2088-96. PubMed: 7075549MGI: J:6754
- Bartke A. 1968. The response of dwarf mice to murine thyroid-stimulating hormone. Gen Comp Endocrinol 11(1):246-7. PubMed: 5674697MGI: J:5085
- Bartke A. 1967. Prolactin deficiency in genetically sterile dwarf mice. In: Endocrine Genetics. Cambridge Univ. Press, Cambridge. MGI: J:30695
- 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: 11162909MGI: 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: 17905742MGI: J:127162
- Brown-Borg HM. 2015. The somatotropic axis and longevity in mice. Am J Physiol Endocrinol Metab 309(6):E503-10. PubMed: 26219867MGI: J:228355
- CARSNER RL; RENNELS EG. 1960. Primary site of gene action in anterior pituitary dwarf mice. Science 131:829. PubMed: 13807990MGI: 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: 1981057MGI: 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: 4117317MGI: J:46465
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- Cross RJ; Bryson JS; Roszman TL. 1992. Immunologic disparity in the hypopituitary dwarf mouse. J Immunol 148(5):1347-52. PubMed: 1531667MGI: J:2020
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- 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: 7595148MGI: J:29289
- Dominick G; Berryman DE; List EO; Kopchick JJ; Li X; Miller RA; Garcia GG. 2015. Regulation of mTOR activity in Snell dwarf and GH receptor gene-disrupted mice. Endocrinology 156(2):565-75. PubMed: 25456069MGI: J:220762
- Dominick G; Bowman J; Li X; Miller RA; Garcia GG. 2017. mTOR regulates the expression of DNA damage response enzymes in long-lived Snell dwarf, GHRKO, and PAPPA-KO mice. Aging Cell 16(1):52-60. PubMed: 27618784MGI: J:238760
- 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: 11867646MGI: J:75145
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- 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: 21840860MGI: 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: 11718806MGI: 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: 11371619MGI: 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: 7568281MGI: 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: 7603293MGI: J:26825
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- 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: 12020946MGI: J:77094
- 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: 16449798MGI: 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: 12960004MGI: 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: 17899304MGI: 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: 9659293MGI: 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: 9275086MGI: J:42905
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- Lewis UJ. 1967. Growth Hormone of Normal and Dwarf mice.. In: Endocrine Genetics. Cambridge Univ. Press, London, Cambridge. MGI: 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: 1977085MGI: 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: 14698816MGI: 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: 8162852MGI: 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: 15147972MGI: J:90070
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- Perez Millan MI; Brinkmeier ML; Mortensen AH; Camper SA. 2016. PROP1 triggers epithelial-mesenchymal transition-like process in pituitary stem cells. Elife 5:. PubMed: 27351100MGI: J:234328
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- Phelps CJ. 2004. Postnatal regression of hypothalamic dopaminergic neurons in prolactin-deficient Snell dwarf mice. Endocrinology 145(12):5656-64. PubMed: 15345680MGI: J:95756
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