JAX Mouse Strain Datasheet - 000451

WB.D1-Spta1^sph-ha/BrkJ

Stock No:: 000451

Cryo Recovery

Overview

Homozygotes provide a molecular and phenotypic model of hereditary spherocytosis type 3 and a phenotypic model for hereditary spherocytosis type 1 and some aspects of sickle cell anemia. Most phenotypic assessment has been performed using F1 homozygous offspring of heterozygotes from the C57BL/6J and WB/Re congenic strains or homozygotes generated on a B6;WB segregating background. Approximately half die by 6 months of age. Homozygotes display hemolytic anemia with spherocytosis, microcytosis, reduced hematocrit, reticulocytisis, extramedullary hematopoiesis in the spleen and liver, lymphocytosis, neutrophilia, lymph node hyperlasia, and cardiac hypertrophy. Homozygotes can be identified within the first day of birth by their jaundiced color. Consequent to the underlying disorder, homozygotes are prone to developing gallstones, pneumonitis, and vaso-occulsive disease in multiple organs.

Genetic overview

Genetic Background	Generation

Spta1^sph-ha

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

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Research Applications

Developmental Biology Research
Hematological Research

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Base Price

Starting at:

$2,595.00 Domestic price Cryo Recovery

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Details

Detailed Description

Development

The hymolytic anemia mutation arose spontaneously in the DBA/1J inbred strain at The Jackson Laboratory in approximately 1960. This mutation was backcrossed onto the C57BL/6J and WB/Re inbred backgrounds by Seldon Bernstein. The WB/Re congenic reached generation N5 in 1968, N9 in 1970, N24 in 1978, N34 in 1986 and was subsequently transferred to the colony of Dr. Jane Barker. In 2010 sperm were cryopreserved from heterozygous males at generation N81.

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

View All References

Genetics

Spta1^sph-ha

Allele Symbol: Spta1^sph-ha

Allele Name	hemolytic anemia
Allele Type	Spontaneous
Allele Synonym(s)	Sph-J; ha; sph^1J
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	DBA/1J
Chromosome	1
Molecular Note	The mutation in the sph-ha mouse (also known as sph-J) was identified as a C to A transversion in exon 52 that converts a tyrosine to a stop codon. This mutation truncates the protein by 13 amino acids.

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Genotype: Spta1^sph-ha related

Developmental Biology Research
- Postnatal Lethality
  - Homozygous
Hematological Research
- Anemia, Iron Deficiency and Transport Defects
  - hemolytic
  - hypochromic anemia
  - microcytic
- Hematopoietic Defects
- Jaundice

Mammalian Phenotype Terms by Genotype

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

Genotype: Spta1^sph-ha/Spta1⁺
involves: DBA/1J

hematopoietic system phenotype

increased erythrocyte clearance
- although erythrocytes are nearly normal in size and hemoglobin concentration, the survival time of erythrocytes in heterozygotes is reduced to 16 days compared with 24 days in controls

Genotype: Spta1^sph-ha/Spta1⁺
either:(B6.D1-Spta1^sph-ha x WB.D1-Spta1^sph-ha)F1 or (WB.D1-Spta1^sph-ha x B6.D1-Spta1^sph-ha)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-ha/Spta1^sph-ha
involves: DBA/1J

mortality/aging

postnatal lethality, incomplete penetrance
- Background Sensitivity - most homozygotes die within the first week of life, but some survive to adulthood
- many animals die within a few days of birth

prenatal lethality, incomplete penetrance
- Background Sensitivity - a small percentage of homozygotes die in utero

pigmentation phenotype

abnormal skin pigmentation

hematopoietic system phenotype

abnormal erythrocyte morphology
- red blood cells are bizzare in shape and staining capacity

abnormal reticulocyte morphology
- reticulocytes synthesize 6-fold and initially bind 5-fold greater than normal amounts of newly synthesized alpha spectrin, yet accumulate very little in the membrane skeleton

decreased hematocrit
- newborns have a mean hematocrit of 26.4 compared with 38.8 in controls and adults have a mean hematocrit of 29.1 compared with 48.7 in controls

decreased hemoglobin content
- newborns and adults have less than half the normal hemoglobin concentration

decreased mean corpuscular volume
- significantly reduced in both newborn homozygotes and adults

enlarged spleen

erythroblastosis

hemolytic anemia

hypochromic microcytic anemia
- severe neonatal hypochromic microcytic anemia

microcytic anemia

microcytosis

reproductive system phenotype

infertility

cardiovascular system phenotype

cardiac hypertrophy

immune system phenotype

enlarged spleen

liver/biliary system phenotype

enlarged liver

jaundice

skeleton phenotype

abnormal bone marrow morphology
- bone marrow is hyperplastic

integument phenotype

abnormal skin pigmentation

Genotype: Spta1^sph-ha/Spta1^sph-ha
either:(B6.D1-Spta1^sph-ha x WB.D1-Spta1^sph-ha)F1 or (WB.D1-Spta1^sph-ha x B6.D1-Spta1^sph-ha)F1

mortality/aging

premature death
- 50% of homozygotes die by 6 months of age

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
- erythroid hyperplasia in the bone marrow
- granuloid:erythroid ratio is 1:2 compared to 3:1 in controls or 1:1 in bled controls
- mean percentage of sIgM+ and B220+ cells is significantly lower in the bone marrow, indicating fewer B lineage lymphocytes in the marrow
- rate of proliferation of large lymphocytes is retarded in the bone marrow

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

abnormal splenic cell ratio
- decrease in percentage of lymphocytes in spleen; while control spleens consist of 85-90% lymphocytes, mutants spleens are only about 10-15% lymphocytes

decreased hematocrit
- hematocrit average of 21% compared to 45% in controls

enlarged spleen

extramedullary hematopoiesis
- extramedullary hematopoiesis in the spleen and liver

hemolytic anemia
- chronic hemolytic anemia

increased B cell number
- increased numbers of circulating B lymphocytes

increased B cell proliferation

increased CD4-positive, alpha beta T cell number

increased CD8-positive, alpha-beta T cell number

increased IgA level
- in clinically sick mutants

increased IgG level
- in clinically sick mutants

increased T cell number
- increased numbers of circulating T cells

increased T cell proliferation

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

increased erythrocyte protoporphyrin level
- red blood cell protoporphyrin levels are about 10 times higher than in controls

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

increased leukocyte cell number

increased lymphocyte cell number
- lymphoid expansion is due to redistribution of lymphocytes from the spleen to other peripheral lymphoid tissues as well as increased proliferation of T and B lymphocytes in lymph nodes
- significant increase in CD4+, CD8+, and sIgM+ lymphocytes in peripheral blood

increased monocyte cell number

increased neutrophil cell number

macrocytosis

microcytosis

reticulocytosis

spherocytosis

immune system phenotype

abnormal lymph node cell ratio
- absolute increase in the number of proliferating lymphocytes in the lymph nodes
- mutants have a higher percentage of B cells and lower percentage of T cells in their lymph nodes

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

abnormal splenic cell ratio
- decrease in percentage of lymphocytes in spleen; while control spleens consist of 85-90% lymphocytes, mutants spleens are only about 10-15% lymphocytes

alveolitis
- alveolitis seen in clinically sick mutants

enlarged spleen

increased B cell number
- increased numbers of circulating B lymphocytes

increased B cell proliferation

increased CD4-positive, alpha beta T cell number

increased CD8-positive, alpha-beta T cell number

increased IgA level
- in clinically sick mutants

increased IgG level
- in clinically sick mutants

increased T cell number
- increased numbers of circulating T cells

increased T cell proliferation

increased leukocyte cell number

increased lymphocyte cell number
- lymphoid expansion is due to redistribution of lymphocytes from the spleen to other peripheral lymphoid tissues as well as increased proliferation of T and B lymphocytes in lymph nodes
- significant increase in CD4+, CD8+, and sIgM+ lymphocytes in peripheral blood

increased monocyte cell number

increased neutrophil cell number

increased susceptibility to bacterial infection
- 45% of clinically sick homozygotes develop bacteremia

interstitial pneumonia
- 18 of 19 clinically sick homozygotes develop actue-to-chronic pneumonitis with variable severity

lymph node hyperplasia
- lymph nodes are 3 times more cellular than wild-type

cardiovascular system phenotype

vasculature congestion
- 14 of 20 clinically sick homozygotes exhibit myocardial infarction or thrombosis
- 18 of 19 clinically sick mutants develop acute vaso-occlusive disease
- 5 of 20 clinically sick homozygotes exhibit splenic infraction
- 8 of 20 clinically sick homozygotes exhibit either liver, bone marrow, pancreas or skeletal muscle infarction

homeostasis/metabolism phenotype

abnormal thrombosis
- 80% of homozygotes show evidence of thrombosis in venules and small-to-medium-sized veins, with ischemic tissue damage in one or more organs, including spleen, myocardium, pancreas, and bone marrow

hemosiderosis
- renal hemosiderosis is seen in clinically sick homozygotes

increased circulating bilirubin level
- chronic hyperbillirubinemia is seen in clinically sick mutants

increased erythrocyte protoporphyrin level
- red blood cell protoporphyrin levels are about 10 times higher than in controls

liver/biliary system phenotype

gallstones
- in clinically sick mutants

respiratory system phenotype

abnormal lung morphology
- 95% of clinically sick homozygotes exhibit lung lesions, ranging from increased cellularity, alveolar wall thickening, exudative pneumonitis and alveolitis, and pulmonary fibrosis

abnormal pulmonary alveolus wall morphology
- alveolar wall thickening seen in clinically sick mutants

alveolitis
- alveolitis seen in clinically sick mutants

interstitial pneumonia
- 18 of 19 clinically sick homozygotes develop actue-to-chronic pneumonitis with variable severity

pulmonary fibrosis
- seen in clinically sick mutants

Genotype: Spta1^sph-ha/Spta1^sph-ha
(WB.D1-Spta1^sph-ha/Brk x B6.D1-Spta1^sph-ha/Brk)F1

mortality/aging

preweaning lethality, incomplete penetrance
- approximately 35% die before weaning

hematopoietic system phenotype

abnormal erythrocyte morphology
- cell surface expression of phosphatidylserine is higher than in wild-type controls, with 11.6% of erythrocytes straining positive for phosphatidylserine versus 1.6% in wild-type controls

abnormal erythrocyte osmotic lysis
- increased sensitivity to osmotic lysis

abnormal erythrocyte physiology
- sodium content of erythrocytes is elevated to 55.1 mEq/l from 12.4 mEq/l in wild-type controls, and the membrane cholesterol and phospholipid content is reduced

abnormal red blood cell deformability
- red blood cells exhibit a profound decrease in surface area and marked increase in osmotic fragility

anisopoikilocytosis

decreased hematocrit
- mean hematocrit is reduced to 26.5% from 50.4% in wild-type controls

decreased hemoglobin content
- mean hemoglobin is decreased to 5.52 g/dL compared with 15.64 g/dL in wild-type controls

enlarged spleen

extramedullary hematopoiesis

hemolysis

hemolytic anemia

increased erythrocyte clearance
- average erythrocyte lifespan is approximately 1.1 days

increased mean corpuscular volume
- MCV raised from 48.1 in wil-type controls to 61.6

increased nucleated erythrocyte cell number
- more than 3 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 93.2%

schistocytosis

cardiovascular system phenotype

cardiac hypertrophy

growth/size/body region phenotype

decreased body size

homeostasis/metabolism phenotype

abnormal thrombosis
- 85% of homozygotes display cardiac thrombi

increased circulating bilirubin level

immune system phenotype

enlarged spleen

liver/biliary system phenotype

enlarged liver

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

reproductive system phenotype

infertility

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

Additional - Spta1^sph-ha 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 S. 1960. New mutant: Hemolytic anemia - ha Mouse News Lett 23:33. MGI: J:24729
Bernstein SE. 1963. Analysis of gene action and characterization of a new hematological abnormality, hemolytic anemia Genet Today 1:186. MGI: J:14946
Bernstein SE. 1969. Hereditary disorders of the rodent erythron. In: Genetics in Laboratory Animal Medicine. Natl Acad Sci Publ, Washington, DC. MGI: J:30699
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
Grossmann A; Maggio-Price L; Shiota FM; Liggitt DV. 1993. Pathologic features associated with decreased longevity of mutant sphha/sphha mice with chronic hemolytic anemia: similarities to sequelae of sickle cell anemia in humans. Lab Anim Sci 43(3):217-21. PubMed: 8355480 MGI: J:12830
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
Korsgren C; Lux SE. 2010. The carboxyterminal EF domain of erythroid alpha-spectrin is necessary for optimal spectrin-actin binding. Blood 116(14):2600-7. PubMed: 20585040 MGI: J:165884
Maggio-Price L; Grossmann A; Engel D; Rosse C. 1991. Altered lymphocyte populations in sphha/sphha mice with chronic hemolytic anemia. Cell Immunol 138(2):360-71. PubMed: 1934076 MGI: J:1967
Maggio-Price L; Grossmann A; Shiota F; Engel D. 1993. Increased proliferative capacity of CD4+ and CD8+ T lymphocytes from mutant sphha/sphha mice is associated with increased IL-2 receptor expression. Cell Immunol 148(2):346-56. PubMed: 7684329 MGI: J:4748
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
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; Bodine DM; Mohandas N; Barker JE. 2003. Mutations in the murine erythroid alpha -spectrin gene alter spectrin mRNA and protein levels and spectrin incorporation into the red blood cell membrane skeleton. Blood 101(1):325-30. PubMed: 12393645 MGI: J:81125
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<spa-ha>

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Genetic overview

Research Applications

Base Price

Detailed Description

Development

Selected References

Spta1sph-ha

Allele Symbol: Spta1sph-ha

Disease Terms

Research Areas By Genotype

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

Genotype: Spta1sph-ha related

Mammalian Phenotype Terms by Genotype

Genotype: Spta1sph-ha/Spta1+involves: DBA/1J

hematopoietic system phenotype

Genotype: Spta1sph-ha/Spta1+either:(B6.D1-Spta1sph-ha x WB.D1-Spta1sph-ha)F1 or (WB.D1-Spta1sph-ha x B6.D1-Spta1sph-ha)F1

hematopoietic system phenotype

homeostasis/metabolism phenotype

Genotype: Spta1sph-ha/Spta1sph-hainvolves: DBA/1J

mortality/aging

pigmentation phenotype

hematopoietic system phenotype

reproductive system phenotype

cardiovascular system phenotype

immune system phenotype

liver/biliary system phenotype

skeleton phenotype

integument phenotype

Genotype: Spta1sph-ha/Spta1sph-haeither:(B6.D1-Spta1sph-ha x WB.D1-Spta1sph-ha)F1 or (WB.D1-Spta1sph-ha x B6.D1-Spta1sph-ha)F1

mortality/aging

hematopoietic system phenotype

immune system phenotype

cardiovascular system phenotype

homeostasis/metabolism phenotype

liver/biliary system phenotype

respiratory system phenotype

Genotype: Spta1sph-ha/Spta1sph-ha(WB.D1-Spta1sph-ha/Brk x B6.D1-Spta1sph-ha/Brk)F1

mortality/aging

hematopoietic system phenotype

cardiovascular system phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

immune system phenotype

liver/biliary system phenotype

reproductive system phenotype

References

Additional - Spta1sph-ha 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

Progeny testing is not required

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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

Spta1^sph-ha

Allele Symbol: Spta1^sph-ha

Genotype: Spta1^sph-ha related

Genotype: Spta1^sph-ha/Spta1⁺
involves: DBA/1J

Genotype: Spta1^sph-ha/Spta1⁺
either:(B6.D1-Spta1^sph-ha x WB.D1-Spta1^sph-ha)F1 or (WB.D1-Spta1^sph-ha x B6.D1-Spta1^sph-ha)F1

Genotype: Spta1^sph-ha/Spta1^sph-ha
involves: DBA/1J

Genotype: Spta1^sph-ha/Spta1^sph-ha
either:(B6.D1-Spta1^sph-ha x WB.D1-Spta1^sph-ha)F1 or (WB.D1-Spta1^sph-ha x B6.D1-Spta1^sph-ha)F1

Genotype: Spta1^sph-ha/Spta1^sph-ha
(WB.D1-Spta1^sph-ha/Brk x B6.D1-Spta1^sph-ha/Brk)F1

Additional - Spta1^sph-ha related