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- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
- Terms of Use
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 Flexed tail 1 (Changed: 15-DEC-04 ) Type Mutant Strain; Spontaneous Mutation; Additional information on Genetically Engineered and Mutant Mice. Type Inbred Strain; Additional information on Inbred Strains. Visit our online Nomenclature tutorial. Species laboratory mouse H2 Haplotype k Generation F78
Generation DefinitionsAppearance
black
Related Genotype: a/aImportant Note
See article "Genetic Background Effects: Can Your Mice See?", JAX® NOTES Spring 2002, No. 485.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.Development
The FL/1Re inbred strain, homozygous for f and wildtype for Kit, was generated in the laboratory of Elizabeth Russell from a female WB/Re heterozygous for KitW bred to a male heterozygous for f from a partially inbred stock derived from crosses between C3H/J and Snell?s WA linkage-testing stock (Russell and McFarland, 1966). This strain reached generation F60 in 1974, and in 1979 embryos were generated for cryopreservation from homozygous (f/f) females and males at generation F78. This bankstock was thawed and replenished with F82p embryos in 1996.
Related Strains
Strains carrying Pde6brd1 allele
View Strains carrying Pde6brd1 (75 strains)
000092 FL/1Re-KitW/J 000259 JE/LeJ 000791 WB.Cg-f/J
000092 FL/1Re-KitW/J 000259 JE/LeJ 000791 WB.Cg-f/J
Additional Web Information
JAX® NOTES, Spring 2002; 485. Genetic Background Effects: Can Your Mice See?
Phenotype
Phenotype Information
Festing Inbred Strain Characteristics: FL/1
assigned by genotype
f/f
FL/1ReJ
- hematopoietic system phenotype
- decreased erythrocyte cell number
- although red cell counts are significantly reduced at birth they achieve near normal levels by 7 days of age (MGI Ref ID J:24610)
- decreased hematocrit
- at birth the hematocrit is significantly lower (31.5 versus 43.4 in controls) but hematocrit reaches normal levles by 7 days of age (MGI Ref ID J:24610)
- decreased mean corpuscular volume
- significantly smaller volumes at birth but normal by 7 days of age (MGI Ref ID J:24610)
- impaired hematopoiesis
- peak numbers of embryonic erythroid colony forming units only about 50% normal numbers in the liver (MGI Ref ID J:5654)
- homeostasis/metabolism phenotype
- abnormal enzyme/coenzyme activity
- delta aminolaevulinate synthetase activity in embryonic day 16 reticulocytes on a per cell basis is reduced to 53% of that of wild-type controls, and the activity in liver at embryonic day 13-14 is also reduced but to a lesser degree (MGI Ref ID J:5591)
- delta aminolaevulinate dehydratase activity in embryonic day 17-18 reticulocytes on a per cell basis is appriximately half of that in wild-type controls (MGI Ref ID J:5591)
- growth/size phenotype
- decreased body weight
- slight reduction in body weight from birth through 60 days of age in both males and females (MGI Ref ID J:24610)
- pigmentation phenotype
- white spotting
- white pigment covers an average of 22.9% and 23.6% of the ventrum in females and males respectively (MGI Ref ID J:24610)
- integument phenotype
- white spotting
- white pigment covers an average of 22.9% and 23.6% of the ventrum in females and males respectively (MGI Ref ID J:24610)
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
f/f
Background Not Specified
- mortality/aging
- partial postnatal lethality
- death rate in the first 3 to 4 weeks after birth is about 4 times normal (MGI Ref ID J:12951)
- limbs/digits/tail phenotype
- caudal vertebral fusion
- kinked tail
- skeleton phenotype
- abnormal vertebrae morphology (MGI Ref ID J:13090)
- abnormal intervertebral disk development
- vertebral fusion
- fusions seen in caudal vertebrae also seen throughout the vertebral column (MGI Ref ID J:13090)
- hematopoietic system phenotype
- abnormal hematopoiesis
- homeostasis/metabolism phenotype
- abnormal iron homeostasis
- defective heme synthesis (MGI Ref ID J:13598)
- growth/size phenotype
- decreased body size
- smaller size at birth and through adulthood (MGI Ref ID J:13090)
- vision/eye phenotype
- eyelids fail to open
- one or both eyes sometimes remain closed (MGI Ref ID J:12951)
- craniofacial phenotype
- abnormal head morphology
- sometimes there is a dorsal enlargement of the head in front of the ears (MGI Ref ID J:12951)
- pigmentation phenotype
- belly spot (MGI Ref ID J:13598)
- embryogenesis phenotype
- abnormal neural tube morphology/development
- 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 (MGI Ref ID J:13090)
- 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 (MGI Ref ID J:13090)
- nervous system phenotype
- abnormal neural tube morphology/development
- 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 (MGI Ref ID J:13090)
- integument phenotype
- belly spot (MGI Ref ID J:13598)
This mouse can be used to support research in many areas including:
Pde6brd1 relatedSensorineural Research
Retinal Degeneration
Homozygous for Pde6brd1
f relatedMouse/Human Gene Homologs
retinitis pigmentosa, autosomal recessive
Sensorineural Research
Retinal Degeneration
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
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Pde6brd1 | ||
|---|---|---|---|
| Allele Name | retinal degeneration 1 | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | Pdebrd1; rd; rd-1; rd1; rodless retina; | ||
| Strain of Origin | various | ||
| Gene Symbol and Name | Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide | ||
| Chromosome | 5 | ||
| Gene Common Name(s) | CSNB3; CSNBAD2; PDEB; Pdeb; RP40; nmf137; phosphodiesterase, cGMP, rod receptor, beta polypeptide; r; rd; rd-1; rd1; rd10; retinal degeneration; retinal degeneration 1; retinal degeneration 10; | ||
| General Note |
The following inbred strains are known to be homozygous for Pde6b | ||
| Molecular Note | Two mutations have been identified in rd1 mice. A murine leukimia virus (Xmv-28) insertion in reverse orientation in intron 1 is found in all mouse strains with the rd1 phenotype. Further, a nonsense mutation (C to A transversion) in codon 347 that results in a truncation eliminating more than half of the predicted encoded protein, including the catalytic domain has also been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested. [MGI Ref ID J:11513] [MGI Ref ID J:4366] [MGI Ref ID J:51361] | ||
| Allele Symbol | f | ||
| Allele Name | flexed tail | ||
| Allele Type | Spontaneous | ||
| Gene Symbol and Name | f, flexed-tail | ||
| 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 ofdelta-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. [MGI Ref ID J:128616] [MGI Ref ID J:68377] [MGI Ref ID J:98445] | ||
References
References provided by MGI
Selected Reference(s)
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]
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]
Additional References
Pde6brd1 relatedf relatedAcosta ML; Fletcher EL; Azizoglu S; Foster LE; Farber DB; Kalloniatis M. 2005. Early markers of retinal degeneration in rd/rd mice. Mol Vis 11:717-28. [PubMed: 16163270] [MGI Ref ID J:103970]
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Ahuja S; Ahuja-Jensen P; Johnson LE; Caffe AR; Abrahamson M; Ekstrom PA; van Veen T. 2008. rd1 Mouse retina shows an imbalance in the activity of cysteine protease cathepsins and their endogenous inhibitor cystatin C. Invest Ophthalmol Vis Sci 49(3):1089-96. [PubMed: 18326735] [MGI Ref ID J:133024]
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We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 13 and 16 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).
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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.