JAX Mouse Strain Datasheet - 000791

WB.Cg-f/J

Stock No:: 000791 |; flexed tail

Cryo Recovery

Overview

Also Known As: flexed tail

These mice carry the spontaneous mutation f characterized by a pale appearance, small size, defective heme synthesis in fetal reticulocytes, and vertebral fusions giving rise to tail flexures.

Genetic overview

Genetic Background	Generation

f

Allele Type	Gene Symbol	Gene Name
Spontaneous	f	flexed-tail

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Research Applications

Dermatology Research
Developmental Biology Research
Hematological Research
Neurobiology Research

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$2,595.00 Domestic price Cryo Recovery

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Details

Detailed Description

Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been found to have embryonic neural tube defects or a dorsal enlargement of the head.

Genetics

f

Allele Symbol: f

Allele Name	flexed tail
Allele Type	Spontaneous
Allele Synonym(s)
Gene Symbol and Name	f, flexed-tail
Gene Synonym(s)
Strain of Origin	Not Specified
Chromosome	13
General Note	The flexed-tail mutation appeared in a stock maintained by Dr. H.R. Hunt at Michigan State College (J:12951). Homozygotes are small at birth and have a transitory hypochromic, microcytic anemia characterized by a large number of siderocytes containing non-heme iron granules. Most homozygotes also have flexed tail and a belly spot, but these are not constant manifestations of the mutant. Because of the anemia there is probably greater postnatal mortality among f/f than among normal mice (J:14979). The anemia begins on the 12th day of embryonic life when the liver first starts to produce blood cells (J:14979). It is most intense at 15 days of gestation and still severe at birth, but by 2 weeks of age has disappeared. Although adults have normal blood values, their response to hemopoietic stress is defective (J:5439, J:27511). The results of numerous studies have led to the conclusion that the prenatal deficiency in number of erythrocytes and the defective response of adult erythropoietic cells are due to a delay in maturation of already committed erythroid stem cells, and that earlier uncommitted precursors are unaffected by f (J:5439, J:5654, J:5582). An additional effect of f in homozygotes is defective heme synthesis, which occurs in fetal reticulocytes but not in adult reticulocytes nor in erythroblasts at earlier stages of maturation. In fetal reticulocytes there is normal uptake of iron but poor incorporation into hemoglobin (J:5439), probably as a result of reduced activity of delta-aminolevulinate synthetase and dehydratase (J:5591). Fetal erythrocytes of f/f mice have more alpha than beta globin chains. In both f/f and wild-type fetal erythrocytes there is more alpha- than beta-chain mRNA; probably some regulatory mechanism bringing about equal alpha- and beta-chain synthesis exists in wild-type mice but is defective in f/f (J:5827, J:30711). The tail abnormalities are first noticeable on the 14th day of gestation as abnormal differentiation of the intervertebral discs (J:13090). The possibility that abnormal heme synthesis could cause the tail and pigment defects in f/f mice has been discussed (J:5591). It was suggested that flexed-tail might be a mutation in the mouse homolog Fancc of the gene defective in human Fanconi anemia, complementation group C, but no mutation in the Fancc gene or abnormalities in Fancc mRNA have been detected in f/f mutants (J:13598). Also, flexed-tail mice are not susceptible to increases in chromosomal aberrations induced by mitomycin C, a characteristic of Fancc mutant mice (J:35839). This allele arose on a genetically undefined stock in 1927 and was subsequently transferred onto several genetic backgrounds to create the congenic and recombinant inbred lines Je/Le-f/f, FL1/ReJ, WB/ReJ-f/f and C57BL/6J-f/f. The phenotypes listed above might be associated with any of these strains; in most cases it was not specified.
Molecular Note	Note that two conflicting reports (J:68377 and J:98445/J:128616) state that the underlying genetic defect in the flexed tail mouse is either in the Sfxn1 or the Smad5 gene.
Mutations Made By	Mark Fleming, Children's Hospital Boston

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Genotype: f related

Dermatology Research
- Color and White Spotting Defects
Developmental Biology Research
- Neural Tube Defects
- Skeletal Defects
Hematological Research
- Anemia, Iron Deficiency and Transport Defects
  - microcytic
- Hematopoietic Defects
Neurobiology Research
- Neural Tube Defects

Mammalian Phenotype Terms by Genotype

Genotype: f/f
Not Specified

mortality/aging

postnatal lethality, incomplete penetrance
- death rate in the first 3 to 4 weeks after birth is about 4 times normal

nervous system phenotype

abnormal neural tube morphology
- a minority of homozygotes assessed during embryonic development are found to have irregular lumen shape, longitudinal waves or angles of the tube, or locally doubled neural tube

integument phenotype

belly spot

limbs/digits/tail phenotype

caudal vertebral fusion
- first appears around E14
- flexure due to unilateral fusions of successive vertebrae

kinked tail
- 1-5 permanent angles in tail
- sometimes curves and spirals instead of sharp angles
- tails can occasionally be nearly normal

skeleton phenotype

abnormal intervertebral disk development
- abnormal development
- fibrous pad sometimes fails to develop or does not develop on one side

abnormal vertebrae morphology

caudal vertebral fusion
- first appears around E14
- flexure due to unilateral fusions of successive vertebrae

vertebral fusion
- fusions seen in caudal vertebrae also seen throughout the vertebral column

hematopoietic system phenotype

abnormal definitive hematopoiesis
- adults with a poor response to hemopoietic stress
- delayed maturation of committed erythroid stem cells

anemia
- anemia at E14 through birth
- anemia becomes less severe after E16 when hematopoetic function of bone marrow begins
- hematopoesis problem in the liver
- recovery from anemia in the first 2 weeks of life

decreased erythrocyte cell number
- adult RBC counts are normal
- reduced RBC counts from E14 through birth

hypochromic microcytic anemia
- transitory hypochromic and microcytic anemia

homeostasis/metabolism phenotype

abnormal iron homeostasis
- defective heme synthesis

growth/size/body region phenotype

abnormal head morphology
- sometimes there is a dorsal enlargement of the head in front of the ears

decreased body size
- smaller size at birth and through adulthood

vision/eye phenotype

eyelids fail to open
- one or both eyes sometimes remain closed

pigmentation phenotype

belly spot

embryo phenotype

abnormal neural tube morphology
- a minority of homozygotes assessed during embryonic development are found to have irregular lumen shape, longitudinal waves or angles of the tube, or locally doubled neural tube

abnormal notochord morphology
- a minority of homozygotes assessed during embryonic development are found to have ventral swelling of the notochord, dorsal projections, bifurcate notochord, or other morphological abnormalities in the notochord

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

Genotype: f/f
involves: CBA/St

mortality/aging

postnatal lethality, incomplete penetrance
- early postnatal depletion of homozygous animals

hematopoietic system phenotype

anemia
- first evident at embryonic day 12

decreased mean corpuscular hemoglobin

hypochromic anemia
- although the mean red blood cell size is normal, the hemoglobin concentration is reduced, there are fewer red blood cells and this transitory anemia is most significant embryonically and at birth then wanes during the first few weeks of life

increased siderocyte number
- the majority of red blood cells in newborns are siderocytes, which are incompletely haemoglobinized as evidenced by faint color and weak stain uptake
- the percentage of siderocytes decreases from 80% at birth to approximately 40% at 1 week of age and stabilizes at approximately 3% by 3 weeks of age persisting at this higher than normal level in the adult

reticulocytosis
- striking reticulocytosis at birth and reticulocyte count remains high at 13 days of age but decreases by 3 weeks of age as the anemia resolves

integument phenotype

pallor
- homozygotes are recognizably paler than normal from embryonic day 16 onward and most can be identified this way as early as embryonic day 15

References

Additional - f related

Bannerman RM; Edwards JA; Pinkerton PH. 1973. Hereditary disorders of the red cell in animals. Prog Hematol 8:131-79. PubMed: 4596202 MGI: J:5439
Bernstein SE. 1969. Hereditary disorders of the rodent erythron. In: Genetics in Laboratory Animal Medicine. Natl Acad Sci Publ, Washington, DC. MGI: J:30699
Chui DH; Patterson M; Bayley ST. 1977. Unequal alpha and beta globin mRNA in reticulocytes of normal and mutant (f/f) fetal mice Blood 50(Suppl 1):104 (Abstr.). MGI: J:30711
Chui DH; Sweeney GD; Patterson M; Russell ES. 1977. Hemoglobin synthesis in siderocytes of flexed-tailed mutant (f/f) fetal mice. Blood 50(1):165-77. PubMed: 559515 MGI: J:5827
Cole RJ; Garlick J; Cheek EM. 1975. Activities of haem synthetic enzymes in blood cells of pre-natal flexed-tailed (f/f) anaemic mice. J Embryol Exp Morphol 34(2):373-86. PubMed: 1194836 MGI: J:5591
Cole RJ; Regan T. 1976. Haemopoietic progenitor cells in prenatal congenitally anaemic 'flexed-tailed' (f/f) mice. Br J Haematol 33(3):387-94. PubMed: 1276083 MGI: J:5654
Coleman DL; Russell ES; Levin EY. 1969. Enzymatic studies of the hemopoietic defect in flexed mice. Genetics 61(3):631-42. PubMed: 5393940 MGI: J:152369
Fleming MD; Campagna DR; Haslett JN; Trenor CC 3rd; Andrews NC. 2001. A mutation in a mitochondrial transmembrane protein is responsible for the pleiotropic hematological and skeletal phenotype of flexed-tail (f/f) mice. Genes Dev 15(6):652-7. PubMed: 11274051 MGI: J:68377
Gregory CJ; McCulloch EA; Till JE. 1975. The cellular basis for the defect in haemopoiesis in flexed-tailed mice. III. Restriction of the defect to erythropoietic progenitors capable of transient colony formation in vivo. Br J Haematol 30(4):401-10. PubMed: 1201223 MGI: J:5582
Gruneberg H. 1942. The anaemia of flexed-tailed mice (mus musculus L) J Genet 43:45-68. MGI: J:164714
Gruneberg H. 1942. The anaemia of flexed-tailed mice (Mus musculus L.). II. Siderocytes J Genet 44:246-71. MGI: J:14979
Hegde S; Lenox LE; Lariviere A; Porayette P; Perry JM; Yon M; Paulson RF. 2007. An intronic sequence mutated in flexed-tail mice regulates splicing of Smad5. Mamm Genome 18(12):852-60. PubMed: 18060457 MGI: J:128616
Hunt HR; Mixter R; Permar D. 1933. Flexed Tail in the Mouse, Mus Musculus. Genetics 18(4):335-66. PubMed: 17246696 MGI: J:12951
Kamenoff RJ. 1935. Effects of the flexed-tailed gene on the development of the house mouse. J Morphol 58:117-155. MGI: J:13090
Kreimer-Birnbaum M; Bannerman RM; Russell ES; Bernstein SE. 1972. Pyrrole pigments in normal and congenitally anaemic mice (+:+, W-W v , ha-ha, nb-nb, mk-mk, f-f and sla-Y). Comp Biochem Physiol A 43(1):21-30. PubMed: 4404581 MGI: J:31039
Lenox LE; Perry JM; Paulson RF. 2005. BMP4 and Madh5 regulate the erythroid response to acute anemia. Blood 105(7):2741-8. PubMed: 15591122 MGI: J:98445
Lenox LE; Shi L; Hegde S; Paulson RF. 2009. Extramedullary erythropoiesis in the adult liver requires BMP-4/Smad5-dependent signaling. Exp Hematol 37(5):549-58. PubMed: 19375646 MGI: J:151008
Oberhauser AF; Fernandez JM. 1996. A fusion pore phenotype in mast cells of the ruby-eye mouse. Proc Natl Acad Sci U S A 93(25):14349-54. PubMed: 8962054 MGI: J:37255
Porayette P; Paulson RF. 2008. BMP4/Smad5 dependent stress erythropoiesis is required for the expansion of erythroid progenitors during fetal development. Dev Biol 317(1):24-35. PubMed: 18374325 MGI: J:136155
Russell ES. 1979. Hereditary anemias of the mouse: a review for geneticists. Adv Genet 20:357-459. PubMed: 390999 MGI: J:25355
Russell ES; Bernstein SE. 1966. Blood and Blood Formation. In: Biology of the Laboratory Mouse. McGraw Hill, New York. MGI: J:24829
Russell ES; McFarland EC. 1966. Analysis of pleiotropic effects of W and f genic substitutions in the mouse. Genetics 53(5):949-59. PubMed: 5929249 MGI: J:24610
Sotelo C. 1990. Axonal abnormalities in cerebellar Purkinje cells of the 'hyperspiny Purkinje cell' mutant mouse. J Neurocytol 19(5):737-55. PubMed: 2077114 MGI: J:106784
Urlando C; Krasnoshtein F; Heddle JA; Buchwald M. 1996. Assessment of the flexed-tail mouse as a possible model for Fanconi anemia: analysis of mitomycin C-induced micronuclei. Mutat Res 370(2):99-106. PubMed: 8879267 MGI: J:35839
Wevrick R; Barker JE; Nadeau JH; Szpirer C; Buchwald M. 1993. Mapping of the murine and rat Facc genes and assessment of flexed-tail as a candidate mouse homolog of Fanconi anemia group C. Mamm Genome 4(8):440-4. PubMed: 7690622 MGI: J:13598

Service	Genotype	Price
	Heterozygous for f

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Also Known As: flexed tail

Genetic overview

Research Applications

Base Price

Detailed Description

f

Allele Symbol: f

Disease Terms

Research Areas By Genotype

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

Genotype: f related

Mammalian Phenotype Terms by Genotype

Genotype: f/fNot Specified

mortality/aging

nervous system phenotype

integument phenotype

limbs/digits/tail phenotype

skeleton phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

growth/size/body region phenotype

vision/eye phenotype

pigmentation phenotype

embryo phenotype

Genotype: f/finvolves: CBA/St

mortality/aging

hematopoietic system phenotype

integument phenotype

References

Additional - f related

Genotyping Protocols

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

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The Jackson Laboratory's Genotype Promise

Terms of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Genotype: f/f
Not Specified

Genotype: f/f
involves: CBA/St