Description

Strain Information

Former Names WB/Re-f/J    (Changed: 13-MAR-08 ) WB/Re-ff/J    (Changed: 20-JUN-05 ) WB/Re-Sfxn1f/J    (Changed: 09-JUN-05 ) Type Congenic; Mutant Strain; Spontaneous Mutation; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse Generation N23F2p

Related Strains

Strains carrying   f allele

000023	FL/1ReJ
000025	FL/4ReJ
000259	JE/LeJ

View Strains carrying   f     (3 strains)

Additional Web Information

Congenic Nomenclature

Phenotype

Phenotype Information

View Research Applications

Research Applications

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

f related

Dermatology Research
Color and White Spotting Defects

Developmental Biology Research
Skeletal Defects

Hematological Research
Anemia, Iron Deficiency and Transport Defects (microcytic) (iron deficiency)

Currently there is no phenotype information for this strain.

Genes & Alleles

Gene & Allele Information

Allele Symbol		f
Allele Name		flexed tail
Allele Type		Spontaneous
General Note		Note that two conflicting reports (J:68377 and J:98445) state that the underlying genetic defect in the flexed tail mouse is in the Sfxn1 or the Smad5 gene. 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 arenot 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 earlieruncommitted 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 abnormalitiesin 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). 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 thesestrains; in most cases it was not specified.
Molecular Note		Note that two conflicting reports (J:68377 and J:98445) state that the underlying genetic defect in the flexed tail mouse is in the Sfxn1 or the Smad5 gene. [MGI Ref ID J:128616] [MGI Ref ID J:68377] [MGI Ref ID J:98445]

Genotyping

Genotyping Information

This strain will not have a genotyping protocol or one is not currently available.

Helpful Links

Optimizing PCR Protocols

References

References

Additional References

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 Ref ID J:5439]

Bernstein SE. 1969. Hereditary disorders of the rodent erythron. In: Genetics in Laboratory Animal Medicine. Natl Acad Sci Publ, Washington, DC.  [MGI Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID J:5654]

Fleming MD; Campagna DR; Haslett JN; Trenor CC rd; 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 Ref ID 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 Ref ID J:5582]

Gruneberg H. 1942. The anaemia of flexed-tailed mice (Mus musculus L.). II. Siderocytes J Genet 44:246-71.  [MGI Ref ID 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 Ref ID J:128616]

Hunt HR; Mixter R; Permar D. 1933. Flexed Tail in the Mouse, Mus Musculus. Genetics 18(4):335-66. [PubMed: 17246696]  [MGI Ref ID J:12951]

Kamenoff RJ. 1935. Effects of the flexed-tailed gene on the development of the house mouse. J Morphol 58:117-155.  [MGI Ref ID 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 Ref ID 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 Ref ID J:98445]

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 Ref ID J:136155]

Russell ES. 1970. Abnormalities of erythropoiesis associated with mutant genes in mice. In: Regulation of Hematopoiesis. Appleton-Century-Crofts, New York.  [MGI Ref ID J:27511]

Russell ES. 1979. Hereditary anemias of the mouse: a review for geneticists. Adv Genet 20:357-459. [PubMed: 390999]  [MGI Ref ID J:25355]

Russell ES; Bernstein SE. 1966. Blood and Blood Formation. In: Biology of the Laboratory Mouse. McGraw Hill, New York.  [MGI Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID J:13598]

Health & husbandry

Health & Colony Maintenance Information

Currently there no information available for this strain. This may be due to the supply level of this strain.

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Supply Details

Standard Supply

Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information.

Supply Notes

Cryorecovery - Standard. At least two mice that carry the mutation (if it is a mutant strain) will be provided. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotypes and genders are needed. IMPORTANT NOTE: The genotypes of the 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 for possible genotypes for this specific strain. Animals typically ship within 13 to 16 weeks from your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will typically ship within 25 weeks. Cryorecovery to establish a Dedicated Supply for greater quantities of mice. One to two pairs will be recovered to establish a Dedicated Supply of mice. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 or 1-207-288-5845. Genomic DNA is available for this strain from the Mouse DNA Resource.

General Terms and Conditions

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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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