JAX Mouse Strain Datasheet - 000454

WB.C3-Spta1^sph/BrkJ

Stock No:: 000454 |; WB-spherocytosis

Cryo Recovery

Overview

Also Known As: WB-spherocytosis

These mice carry a spontaneous mutation at the Spta1 locus characterized by spherocytic hemolytic anemia and neonatal jaundice.

Genetic overview

Genetic Background	Generation

Spta1^sph

Allele Type	Gene Symbol	Gene Name
Spontaneous	Spta1	spectrin alpha, erythrocytic 1

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Research Applications

Cardiovascular Research
Hematological Research
Internal/Organ Research

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Base Price

Starting at:

$2,595.00 Domestic price Cryo Recovery

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Details

Detailed Description

Homozygotes have spherocytic hemolytic anemia and neonatal jaundice. Erythrocytes have diminished biconcavity, a smaller than normal diameter, increased density, an appearance of exovesiculation, and a short lifespan. At birth homozygotes are very pale then become yellow during the first few hours of life and die generally within a day of being born. Although it is rare for a spherocytosis homozygote to survive beyond one day of birth on the WB/Re or C57BL/6J (stock #000450) congenic background, homozygotes on the (C57BL/6J x WB/Re)F1 background are much more robust and the majority survive to adulthood. Those that make it to wean age are expected to have a reasonable lifespan, sometimes living as long as a year. Thus, most studies of this mutation in the adult have been done on the (C57BL/6J x WB/Re)F1 background. These homozygotes display diminished hematocrit, decreased red blood cell count, very elevated red blood cell protoporphyrin levels, increased erythropoiesis, reticulocytosis, hyperbilirubinaemia, cardiomegaly, hepatomegaly, and severe splenomegaly predominantly due to increased red pulp. Large areas of splenic necrosis and fibrosis develop. Thrombi can be found in the atrioventricular valves or within the atria of adults and infarcts have been observed in the myocardium and in the cerebrum, hippocampus, and cerebellum. Iron accumulates in the liver and kidneys, blood urea nitrogen levels become high, and hydronephrosis and membranoproliferative glomerulonephritis are found. By 2 to 3 months of age the urine becomes green due to hemosiderin and ferritin laden renal tubular cells and the urine later becomes red. Kaysser et al. posited that the likely cause of death in adult homozygotes is renal failure.

Development

The spherocytosis mutation arose spontaneously in 1959 at the University of British Columbia Central Animal Depot in the progeny of an unpedigreed stock from Rockland Farms, reported to be C3H. This mutation was imported into The Jackson Laboratory before 1970 and backcrossed onto the C57BL/6J and WB/Re backgrounds by Dr. Elizabeth Russell and Dr. Seldon Bernstein. In 1970 this congenic was at backcross generation N2, in 1976 it reached N9, in 1986 it reached N21 and was subsequently passed into the care of Dr. Jane Barker. In 2010 sperm were cryopreserved from heterozygous males at generation N66.

Selected References

Bernstein SE. 1980. Inherited hemolytic disease in mice: a review and update. Lab Anim Sci 30(2 Pt 1):197-205. PubMed: 6763106 MGI: J:162532
JOE M; TEASDALE JM; MILLER JR. 1962. A new mutation (sph) causing neonatal jaundice in the house mouse. Can J Genet Cytol 4:219-25. PubMed: 14451913 MGI: J:12276
Kaysser TM; Wandersee NJ; Bronson RT; Barker JE. 1997. Thrombosis and secondary hemochromatosis play major roles in the pathogenesis of jaundiced and spherocytic mice, murine models for hereditary spherocytosis. Blood 90(11):4610-9. PubMed: 9373273 MGI: J:44313

View All References

Genetics

Spta1^sph

Allele Symbol: Spta1^sph

Allele Name	spherocytosis
Allele Type	Spontaneous
Allele Synonym(s)	sph
Gene Symbol and Name	Spta1, spectrin alpha, erythrocytic 1
Gene Synonym(s)	AF093576; AI451697; EL2; HPP; HS3; SPH3; SPTA; Spna-1; Spna-1; Spna1; Spna1; erythroid; expressed sequence AF093576; expressed sequence AI451697; ha; hemolytic anemia; iasi hereditary jaundice; ihj; ihj; spectrin alpha 1; sph; spherocytosis
Strain of Origin	C3H
Chromosome	1
General Note	This original spherocytosis mutation arose in an unpedigreed C3H stock.
Molecular Note	The mutation in the sph mouse was identified as a single base pair deletion in exon 11 that causes a frame shift and premature stop codon.

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Genotype: Spta1^sph related

Cardiovascular Research
- Vascular Defects
  - Thrombosis
Hematological Research
- Anemia, Iron Deficiency and Transport Defects
  - hemolytic
- Hematopoietic Defects
- Jaundice
Internal/Organ Research
- Kidney Defects
- Spleen Defects

Mammalian Phenotype Terms by Genotype

Genotype: Spta1^sph/Spta1^sph
WB.C3-Spta1^sph/BrkJ

mortality/aging

neonatal lethality, incomplete penetrance

postnatal lethality, complete penetrance
- on the inbred WB/Re or C57BL/6J backgrounds homozygotes rarely live to weaning, although a few may, so this mutation is best studied on the F1 hybrid background on which the majority of homozygotes survive to adulthood and some can live to a year or more

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

Genotype: Spta1^sph/Spta1⁺
either: (B6.C3-Spta1^sph x WB.C3-Spta1^sph)F1 or (WB.C3-Spta1^sph x B6.C3-Spta1^sph)F1

hematopoietic system phenotype

increased erythrocyte protoporphyrin level
- red blood cells show a higher concentration of protoporphyrin than wild-type

homeostasis/metabolism phenotype

increased erythrocyte protoporphyrin level
- red blood cells show a higher concentration of protoporphyrin than wild-type

Genotype: Spta1^sph/Spta1^sph
either: (B6.C3-Spta1^sph x WB.C3-Spta1^sph)F1 or (WB.C3-Spta1^sph x B6.C3-Spta1^sph)F1

hematopoietic system phenotype

abnormal bone marrow cell number
- CFU-E concentrations in bone marrow are significantly increased over those in wild-type, while BFU-E concentrations are halved
- granuloid:erythroid ratio is 1:3 compared to 3:1 in controls or 1:1 in bled controls

abnormal erythrocyte physiology
- erythrocyte intracellular sodium levels are three times higher than normal, erythrocyte intracellular potassium levels are lower than normal, and ouabain induced cation flux rates in erythrocytes are approximately three times higher than normal

abnormal erythropoiesis
- accelerated erythropoiesis that is associated with distinctive, dark branched cells that make up large portions of the spleen and bone marrow stroma

abnormal spleen morphology
- the spleen is extremely erythropoietic and eryhtroclastic, with sheets of erythroblasts associated with dark branching cells alternating with areas filled with macrophages and red cell debris

decreased hematocrit
- hematocrit average of 15% compared to 45% in controls

enlarged spleen

hemolytic anemia

increased bone marrow cell number
- bone marrow is hypercellular with very high erythrocyte numbers

increased erythrocyte protoporphyrin level
- Percoll-stractan gradients show a considerable increase in erythrocyte density
- red blood cell protoporphyrin levels are about 10 times higher than in controls
- scanning electron microscopy of erythrocytes shows that they have an abnormal shape with disappearance of biconcavity, smaller diameter, and the appearance of exovesiculation

increased erythroid progenitor cell number
- bone marrow contains higher numbers of erythroblasts, proerythroblasts and basophilic erythroblasts

macrocytosis

microcytosis

reticulocytosis

spherocytosis

immune system phenotype

abnormal spleen morphology
- the spleen is extremely erythropoietic and eryhtroclastic, with sheets of erythroblasts associated with dark branching cells alternating with areas filled with macrophages and red cell debris

decreased susceptibility to parasitic infection
- homozygotes are resistant to the malarial parasites, Plasmodium chabaudi adami and Plasmodium berghei

enlarged spleen

homeostasis/metabolism phenotype

increased erythrocyte protoporphyrin level
- Percoll-stractan gradients show a considerable increase in erythrocyte density
- red blood cell protoporphyrin levels are about 10 times higher than in controls
- scanning electron microscopy of erythrocytes shows that they have an abnormal shape with disappearance of biconcavity, smaller diameter, and the appearance of exovesiculation

Genotype: Spta1^sph/Spta1^sph
involves: C3H

mortality/aging

neonatal lethality, complete penetrance
- none survive for more than 24 hours

hematopoietic system phenotype

abnormal reticulocyte morphology
- reticulocytes do not accumulate alpha spectrin in their membranes and do not synthesize detectable amounts of alpha spectrin

decreased hematocrit

decreased hemoglobin content

hemolytic anemia

poikilocytosis

spherocytosis

cardiovascular system phenotype

enlarged liver sinusoidal spaces

liver vascular congestion
- livers show considerable congestion

homeostasis/metabolism phenotype

increased circulating bilirubin level

liver/biliary system phenotype

abnormal liver morphology
- livers are much darker than in control littermates

enlarged liver

enlarged liver sinusoidal spaces

jaundice
- gradually acquire a yellow color during the first few hours of life

liver vascular congestion
- livers show considerable congestion

integument phenotype

pallor
- extremely pale at birth

Genotype: Spta1^sph/Spta1^sph
(WB.C3-Spta1^sph x B6.C3-Spta1^sph)F1

muscle phenotype

myocardial necrosis
- infarcts are found in the myocardium, ventricular or ventricular septal regions, and atrial walls of surviving adult homozygotes

mortality/aging

postnatal lethality, incomplete penetrance
- 28% die before weaning
- approximately 25% of homozygotes die postnatally

premature death
- Background Sensitivity - while approximately 75% of homozygotes on this mixed background survive to adulthood, the average lifespan is 5.75 months
- while approximately 75% of homozygotes survive to adulthood, the average lifespan is 5.75 months

reproductive system phenotype

infertility

hematopoietic system phenotype

abnormal erythrocyte morphology
- cell surface expression of phosphatidylserine is higher than in wild-type controls, with 13.1% of erythrocytes straining positive for phosphatidylserine versus 1.6% in wild-type controls

abnormal erythrocyte osmotic lysis
- the osmotic fragility curve for erythrocytes shows broader sensitivity to osmotic lysis, with a subpopulation more sensitive and a suppopulation less sensitive

abnormal erythrocyte physiology
- sodium content of erythrocytes is elevated to 64.2 mEq/l from 12.4 mEq/l in wild-type controls, and the membrane cholesterol and phospholipid content is reduced

anisopoikilocytosis

decreased cellular hemoglobin content
- decreased to 16.9% compared to 29.8% in controls

decreased erythrocyte cell number
- adults have very low red blood cell count, 3,740,000/ul instead of 9,150,000/ul

decreased hematocrit
- hematocrit of adults is much lower than normal, 22.5% instead of 45% in controls
- mean hematocrit is reduced to 24.9% from 50.4% in wild-type controls

decreased hemoglobin content
- greatly reduced hemoglobin of 3.7 g/dL compared to 13.5 g/dL in controls
- mean hemoglobin content is reduced to 5.35 g/dl from 15.64 g/dl in wild-type controls

enlarged spleen
- severe splenomegaly with areas of necrosis and fibrosis develops in adults with most of the splenic mass made of red pulp

extramedullary hematopoiesis

hemolysis

hemolytic anemia

increased erythrocyte clearance
- average erythrocyte lifespan of approximately 1 day

increased mean corpuscular volume
- mean MCV raised from 48.1 in wild-type controls to 59.7

increased nucleated erythrocyte cell number
- more than 4 times normal levels

low mean erythrocyte cell number
- less than half of normal numbers

microcytosis
- the percentage of erythroid cells that are microcytes is much larger than in wild-type controls

poikilocytosis

reticulocytosis
- mean percent of reticulocytes is substantially increased from 3.16% in wild-type controls to 91.2%

schistocytosis

immune system phenotype

enlarged spleen
- severe splenomegaly with areas of necrosis and fibrosis develops in adults with most of the splenic mass made of red pulp

glomerulonephritis

tubular nephritis

homeostasis/metabolism phenotype

abnormal cardiac thrombosis
- 100% of homozygous adults display cardiac thrombi
- in surviving adults large thrombi are found within the heart mainly in the mitral or left atrioventricular valve

increased circulating bilirubin level

increased kidney iron level
- extraordinary amounts of iron accumulate in the adult kidney, particularly within the proximal convoluted tubules, leading to green colored urine by 2 to 3 months of age and progressing to hydronephrosis and possible renal failure

increased liver iron level
- significant iron stores are found in hepatic cells of the adult, but not in the hematopoietic regions of the liver or in the Kupffer cells

renal/urinary system phenotype

glomerulonephritis

increased kidney iron level
- extraordinary amounts of iron accumulate in the adult kidney, particularly within the proximal convoluted tubules, leading to green colored urine by 2 to 3 months of age and progressing to hydronephrosis and possible renal failure

renal tubular necrosis

tubular nephritis

liver/biliary system phenotype

enlarged liver

focal hepatic necrosis

increased liver iron level
- significant iron stores are found in hepatic cells of the adult, but not in the hematopoietic regions of the liver or in the Kupffer cells

jaundice
- although not jaundiced at birth, homozygotes develop severe jaundice within hours of being born

cardiovascular system phenotype

cardiac hypertrophy

enlarged heart
- cardiac chambers of surviving adults are dilated

myocardial necrosis
- infarcts are found in the myocardium, ventricular or ventricular septal regions, and atrial walls of surviving adult homozygotes

nervous system phenotype

abnormal brain morphology
- infarctions are found in adult cerebrum, hippocampus, and cerebellum, are generally unilateral, and microthrombi are sometimes found close to the infarction

growth/size/body region phenotype

decreased body size

References

Bernstein SE. 1980. Inherited hemolytic disease in mice: a review and update. Lab Anim Sci 30(2 Pt 1):197-205. PubMed: 6763106 MGI: J:162532
JOE M; TEASDALE JM; MILLER JR. 1962. A new mutation (sph) causing neonatal jaundice in the house mouse. Can J Genet Cytol 4:219-25. PubMed: 14451913 MGI: J:12276
Kaysser TM; Wandersee NJ; Bronson RT; Barker JE. 1997. Thrombosis and secondary hemochromatosis play major roles in the pathogenesis of jaundiced and spherocytic mice, murine models for hereditary spherocytosis. Blood 90(11):4610-9. PubMed: 9373273 MGI: J:44313

Additional - Spta1^sph related

Bernstein SE. 1969. Hereditary disorders of the rodent erythron. In: Genetics in Laboratory Animal Medicine. Natl Acad Sci Publ, Washington, DC. MGI: J:30699
Birkenmeier C. 2010. Genetic background effects on spherocytosis Personal Communication :. MGI: J:162758
Birkenmeier CS; McFarland-Starr EC; Barker JE. 1988. Chromosomal location of three spectrin genes: relationship to the inherited hemolytic anemias of mouse and man. Proc Natl Acad Sci U S A 85(21):8121-5. PubMed: 3186715 MGI: J:9457
Bodine DM 4th; Birkenmeier CS; Barker JE. 1984. Spectrin deficient inherited hemolytic anemias in the mouse: characterization by spectrin synthesis and mRNA activity in reticulocytes. Cell 37(3):721-9. PubMed: 6234993 MGI: J:7501
Brookoff D; Maggio-Price L; Bernstein S; Weiss L. 1982. Erythropoiesis in ha/ha and sph/sph mice, mutants which produce spectrin-deficient erythrocytes. Blood 59(3):646-51. PubMed: 7059672 MGI: J:6695
Campanella ME; Chu H; Wandersee NJ; Peters LL; Mohandas N; Gilligan DM; Low PS. 2008. Characterization of glycolytic enzyme interactions with murine erythrocyte membranes in wild-type and membrane protein knockout mice. Blood 112(9):3900-6. PubMed: 18698006 MGI: J:142120
Dahl SC; Geib RW; Fox MT; Edidin M; Branton D. 1994. Rapid capping in alpha-spectrin-deficient MEL cells from mice afflicted with hereditary hemolytic anemia. J Cell Biol 125(5):1057-65. PubMed: 8195289 MGI: J:19025
Frei AC; Guo Y; Jones DW; Pritchard KA Jr; Fagan KA; Hogg N; Wandersee NJ. 2008. Vascular dysfunction in a murine model of severe hemolysis. Blood 112(2):398-405. PubMed: 18477769 MGI: J:138597
Hanson MS; Xu H; Flewelen TC; Holzhauer SL; Retherford D; Jones DW; Frei AC; Pritchard KA Jr; Hillery CA; Hogg N; Wandersee NJ. 2013. A novel hemoglobin-binding peptide reduces cell-free hemoglobin in murine hemolytic anemia. Am J Physiol Heart Circ Physiol 304(2):H328-36. PubMed: 23125208 MGI: J:192837
Joiner CH; Franco RS; Jiang M; Franco MS; Barker JE; Lux SE. 1995. Increased cation permeability in mutant mouse red blood cells with defective membrane skeletons. Blood 86(11):4307-14. PubMed: 7492791 MGI: J:30033
Peters LL; Barker JE. 2001. Spontaneous and targeted mutations in erthrocyte membrane skeleton genes: mouse models of heredity spherocytosis. In: Hematopoiesis A Developmental Approach. Oxford University Press. MGI: J:88022
Robledo RF; Lambert AJ; Birkenmeier CS; Cirlan MV; Cirlan AF; Campagna DR; Lux SE; Peters LL. 2010. Analysis of novel sph (spherocytosis) alleles in mice reveals allele-specific loss of band 3 and adducin in {alpha}-spectrin-deficient red cells. Blood 115(9):1804-14. PubMed: 20056793 MGI: J:157766
Russell ES; Bernstein SE. 1966. Blood and Blood Formation. In: Biology of the Laboratory Mouse. McGraw Hill, New York. MGI: J:24829
Sassa S; Bernstein SE. 1978. Studies of erythrocyte protoporphyrin in anemic mutant mice: use of a modified hematofluorometer for the detection of heterozygotes for hemolytic disease. Exp Hematol 6(5):479-87. PubMed: 658175 MGI: J:5985
Shear HL; Roth EF Jr; Ng C; Nagel RL. 1991. Resistance to malaria in ankyrin and spectrin deficient mice. Br J Haematol 78(4):555-60. PubMed: 1832936 MGI: J:111131
Unger AE; Harris MJ; Bernstein SE; Falcone JC; Lux SE. 1983. Hemolytic anemia in the mouse. Report of a new mutation and clarification of its genetics. J Hered 74(2):88-92. PubMed: 6841965 MGI: J:7048
Wandersee NJ; Birkenmeier CS; Gifford EJ; Mohandas N; Barker JE. 2000. Murine recessive hereditary spherocytosis, sph/sph, is caused by a mutation in the erythroid alpha-spectrin gene. Hematol J 1(4):235-42. PubMed: 11920196 MGI: J:80999
Wandersee NJ; Tait JF; Barker JE. 2000. Erythroid phosphatidyl serine exposure is not predictive of thrombotic risk in mice with hemolytic anemia Blood Cells Mol Dis 26(1):75-83. PubMed: 10772878 MGI: J:62355

Service	Genotype	Price
	Heterozygous or wildtype for Spna1<sph>

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Also Known As: WB-spherocytosis

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Selected References

Spta1sph

Allele Symbol: Spta1sph

Disease Terms

Research Areas By Genotype

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

Genotype: Spta1sph related

Mammalian Phenotype Terms by Genotype

Genotype: Spta1sph/Spta1sphWB.C3-Spta1sph/BrkJ

mortality/aging

Genotype: Spta1sph/Spta1+either: (B6.C3-Spta1sph x WB.C3-Spta1sph)F1 or (WB.C3-Spta1sph x B6.C3-Spta1sph)F1

hematopoietic system phenotype

homeostasis/metabolism phenotype

Genotype: Spta1sph/Spta1spheither: (B6.C3-Spta1sph x WB.C3-Spta1sph)F1 or (WB.C3-Spta1sph x B6.C3-Spta1sph)F1

hematopoietic system phenotype

immune system phenotype

homeostasis/metabolism phenotype

Genotype: Spta1sph/Spta1sphinvolves: C3H

mortality/aging

hematopoietic system phenotype

cardiovascular system phenotype

homeostasis/metabolism phenotype

liver/biliary system phenotype

integument phenotype

Genotype: Spta1sph/Spta1sph(WB.C3-Spta1sph x B6.C3-Spta1sph)F1

muscle phenotype

mortality/aging

reproductive system phenotype

hematopoietic system phenotype

immune system phenotype

homeostasis/metabolism phenotype

renal/urinary system phenotype

liver/biliary system phenotype

cardiovascular system phenotype

nervous system phenotype

growth/size/body region phenotype

References

Additional - Spta1sph 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

Payment Terms and Conditions

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

Spta1^sph

Allele Symbol: Spta1^sph

Genotype: Spta1^sph related

Genotype: Spta1^sph/Spta1^sph
WB.C3-Spta1^sph/BrkJ

Genotype: Spta1^sph/Spta1⁺
either: (B6.C3-Spta1^sph x WB.C3-Spta1^sph)F1 or (WB.C3-Spta1^sph x B6.C3-Spta1^sph)F1

Genotype: Spta1^sph/Spta1^sph
either: (B6.C3-Spta1^sph x WB.C3-Spta1^sph)F1 or (WB.C3-Spta1^sph x B6.C3-Spta1^sph)F1

Genotype: Spta1^sph/Spta1^sph
involves: C3H

Genotype: Spta1^sph/Spta1^sph
(WB.C3-Spta1^sph x B6.C3-Spta1^sph)F1

Additional - Spta1^sph related