Description

Strain Information

Type Congenic; Mutant Strain; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse Background Strain C57BL/6J Donor Strain Oak Ridge irr. Generation N14p

Description
Mice homozygous for the beige spontaneous mutation (Lyst^bg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in littermate controls, an effect thought to be due to the deficiency of NK cells. Beige mice have platelet storage pool deficiency, leading to a prolonged bleeding time. The immunodeficiency of beige mutant mice has been used, especially in combination with the scid mutation (Prkdc^scid), in tissue graft and disease studies.

Related Strains

Strains carrying   Lyst^bg allele

000494	J.Cg-Oca2+ Tyr+ Lystbg/J
000269	SB/LeJ

View Strains carrying   Lyst^bg     (2 strains)

Strains carrying other alleles of Lyst

000604	B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J
000509	C3H/HeJ-Lystbg-2J/J
000629	C57BL/6J-Lystbg-J/J

View Strains carrying other alleles of Lyst     (3 strains)

Additional Web Information

Congenic Nomenclature
JAX^® NOTES, Spring 1991; 445. Why C57BL/6J-bg^J (beige) Mice are not Beige.
JAX^® NOTES, Winter 1992; 448. The Beige (Bg^J) Mutation.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms

Chediak-Higashi Syndrome; CHS - Models with phenotypic similarity to human disease where etiologies involve orthologs.1

1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

View Mammalian Phenotype Terms

Mammalian Phenotype Terms

      assigned by genotype

Lyst^bg/Lyst^bg

        C57BL/6J-Lyst^bg

• tumorigenesis
• increased incidence of induced tumors (MGI Ref ID J:6302)
• pigmentation phenotype
• abnormal melanosome morphology (MGI Ref ID J:5346)
• enlarged melanin granules in hair follicle (MGI Ref ID J:5078)
• cellular phenotype
• abnormal lysosome morphology (MGI Ref ID J:29294)
• accumulation of giant lysosomes in kidney/renal tubule cells (MGI Ref ID J:5590)
• lysosomal protein accumulation (MGI Ref ID J:5338)
• hematopoietic system phenotype
• abnormal eosinophil morphology (MGI Ref ID J:5078)
  • presence of giant granules in cells
• abnormal lymphocyte morphology (MGI Ref ID J:5078)
  • presence of giant granules in cells
• abnormal neutrophil morphology (MGI Ref ID J:5078)
  • presence of giant granules in cells
• homeostasis/metabolism phenotype
• altered response to alphaxalone (MGI Ref ID J:29294)
• altered response to pentobarbital (MGI Ref ID J:29294)
• altered response to tribromoethanol (MGI Ref ID J:29294)
• immune system phenotype
• abnormal eosinophil morphology (MGI Ref ID J:5078)
  • presence of giant granules in cells
• abnormal lymphocyte morphology (MGI Ref ID J:5078)
  • presence of giant granules in cells
• abnormal neutrophil morphology (MGI Ref ID J:5078)
  • presence of giant granules in cells
• defective cytotoxic T cell cytolysis (MGI Ref ID J:6692)
• impaired NK cell cytolysis (MGI Ref ID J:6213)
• increased susceptibility to parasitic infection (MGI Ref ID J:6946)
• renal/urinary system phenotype
• accumulation of giant lysosomes in kidney/renal tubule cells (MGI Ref ID J:5590)
• skin/coat/nails phenotype
• enlarged melanin granules in hair follicle (MGI Ref ID J:5078)
• nervous system phenotype
• abnormal hippocampal mossy fiber morphology (MGI Ref ID J:4978)
• ectopic Bergmann glia cells (MGI Ref ID J:4978)
• ectopic Purkinje cell (MGI Ref ID J:4978)
• ectopic granule cells (MGI Ref ID J:4978)
• ectopic pyramidal neurons (MGI Ref ID J:4978)

Lyst^bg/Lyst^bg

        B6.Cg-Lyst^bg/J

• cellular phenotype
• abnormal lysosome physiology (MGI Ref ID J:6801)
  • significant increase in lysosomal enzyme activity of beta-galactosidase and beta-glucuronidase, and to a lesser extent N-acetyl-beta-hexoseaminidase, in kidney extracts
• immune system phenotype
• abnormal NK cell physiology (MGI Ref ID J:6801)
  • lower natural killer cell activity

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Lyst^bg/Lyst^bg

        C3H/Rl

• pigmentation phenotype
• abnormal eye pigmentation (MGI Ref ID J:29744)
• diluted coat color (MGI Ref ID J:29744)
• irregular coat pigmentation (MGI Ref ID J:29744)
• skin/coat/nails phenotype
• diluted coat color (MGI Ref ID J:29744)
• irregular coat pigmentation (MGI Ref ID J:29744)
• vision/eye phenotype
• abnormal eye pigmentation (MGI Ref ID J:29744)

View Research Applications

Research Applications

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

Lyst^bg related

Cardiovascular Research
Atherosclerosis

Dermatology Research
Color and White Spotting Defects

Hematological Research
Immunological Defects
Platelet Defects (platelet storage pool deficiency)

Immunology and Inflammation Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Immunodeficiency
Intracellular Signaling Molecules

Internal/Organ Research
Kidney Defects (lysosomal enzyme abnormalities)

Metabolism Research

Mouse/Human Gene Homologs
Chediak-Higashi syndrome

Research Tools
Immunology and Inflammation Research (NK Cell Deficiency)

Genes & Alleles

Gene & Allele Information

Allele Symbol		Lystbg
Allele Name		beige
Allele Type		Radiation induced
Common Name(s)		30B/22B; CHS mice; bg;
Strain of Origin		C3H/Rl
Gene Symbol and Name		Lyst, lysosomal trafficking regulator
Chromosome		13
Gene Common Name(s)		Beige; CHS; CHS1; D13Sfk13; DNA segment, Chr 13, Stephen F. Kingsmore 13; beige; bg;
General Note		The original beige mutation was probably radiation-induced at Oak Ridge National Laboratory (J:29744). The Lystbg mutation contains an insertion causing abnormal splicing of mRNA products (J:33734).In Lystbg homozygotes, eye color is light at birth and varies from ruby to almost black in adults. Ear and tail pigmentation are reduced, and coat color is lighter (J:29744).The condition in homozygotes closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle (J:5078). In fact, mouse, mink, and human Chediak-Higashi fibroblasts fail to complement one another in cell fusion studies, indicating that the same gene is defective in all three species (J:16651). Pigment granules of both optic cup and neural crest derivatives, reduced in number, are much enlarged but have normal fine structure (J:5346). Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands (J:5538, J:5514); in type II pneumocytes (J:5992); in mast cells (J:5935); and in retinal pigment epithelium (J:5656). The giant lysosomes are formed by fusion of normal-sized ones (J:6629).Granulocytes of peritoneal exudate from Lystbg/Lystbg mice show defective chemotaxis and reduced bactericidal activity (J:5405). Beige mice are more susceptible than controls to pneumonitis (J:5311) and to various viral (J:6646), bacterial (J:5471), and parasitic (J:6946) infections. They have a severe deficiency of natural killer (NK) cells (J:6213), in common with several other pigment mutations that also affect lysosomal function (Hps1, Pldn, and Bloc1s3) (J:6801). Beige mice also havea defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells (J:6213, J:6692). Syngeneic tumor cells grow better in beige mice than in littermate controls, an effect thought to be due to the deficiency of NK cells (J:6302, J:6301). The lysosomal serine proteases, elastase and cathepsin G, are profoundly decreased in peritoneal neutrophils of beige mice (J:8207), and the amount of plasminogen activator secreted by beige macrophages in culture is increased (J:7851). In the SB/Le-Lystbg strain, development of an autoimmune lupus-like syndrome in males is greatly retarded in beige homozygotes compared to rapid onset of autoimmunity in heterozygous +/Lystbg controls (J:30716). This may be a result of the immune defects cited above.The immunodeficiency of beige mutant mice has been used, especially in combination with the severe combined immunodeficiency (SCID) mutation (Prkdcscid), in tissue graft and disease studies. However, SCID-beige double mutant mice are highly susceptible to infection, even with organisms not usually regarded as mouse pathogens, and special care must be taken in maintaining these mice (J:4752).Beige mice have platelet storage pool deficiency (J:7327) similar to that observed in Hps1 and other pigment reduction mutations. The prolonged bleeding time and low dense granule content can be cured by transplantation of bone marrow from normal mice, and transferred to normal mice by transplantation of beige bone marrow (J:8056). Ithas been shown by use of concanavalin A cap formation that granulocytes of beige mice have defective membrane-related microtubular function, and that this as well as the granule abnormality can be corrected by promoters of cyclic GMP generation (J:5728).The abnormal lysosomes of kidney proximal tubules of beige mice show a striking accumulation of three lysosomal enzymes after androgen treatment, and the level of these enzymes in urine is lower than normal. Release of lysosomal contents into the tubulelumen appears to be defective (J:5590, J:6027). This also is paralleled by similar enzyme accumulation in other pigment mutants (see Hps1).Some of the pigment mutants that share the above lysosomal and platelet storage pool defects of the Lyst mutant have the capacity to resist atherogenesis when fed a diet causing development of atherosclerosis in normal mice. Beige, however, does not have this resistance; beige mice on this diet develop atherosclerosis (J:29748).Lung alveolar maturation is impaired in homozygous beige mice, so that the alveoli are left abnormally large. A soluble ß-galactoside specific lectin that is elevated during alveolar maturation in other rodent species is, however, also elevated in both normal and beige mutant mice (J:2387).Beige mice that survive to 17 months of age show a progressive neurological disorder accompanied by a complete or nearly complete loss of cerebellar Purkinje cells (J:15166). Cerebellar and hippocampal cytoarchitectonic abnormalities are found in beige mutants (J:4978). Beige and another pigment reduction mutant with lysosomal enzyme effects, Bloc1s3 (reduced pigmentation), show increased susceptibility to various anesthetics (J:29294). µ-opioid receptor function appears to be reduced in antinociceptive regions of the beige mutant brain (J:29746). Like pearl (Ap3b1) and other pigment mutant mice (see Hps1), beige mutants show greatly reduced retinal projections to the ipsilateral anterior nucleus (J:29747).
Molecular Note		This allele is an insertion of a partial LINE 1 repetitive element into an intron of the gene. The insertion included only the most 3' 1097 bp of the element producing a frameshift mutation resulting in a truncated protein predicted to be missing the last 1442 amino acids. [MGI Ref ID J:33734] [MGI Ref ID J:41243]

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

Schiller NK; Black AS; Bradshaw GP; Bonnet DJ; Curtiss LK. 2004. Participation of macrophages in atherosclerotic lesion morphology in LDLr-/- mice. J Lipid Res 45(8):1398-409. [PubMed: 15175354]  [MGI Ref ID J:91367]

Lyst^bg related

Ahmed F; Lundin LG; Shire JG. 1989. Lysosomal mutations increase susceptibility to anaesthetics. Experientia 45(11-12):1133-5. [PubMed: 2513223]  [MGI Ref ID J:29294]

Ahmed F; Shire JG. 1985. Lysosomal mutations inhibit lipofuscinosis of the spleen in C57BL mice. J Hered 76(4):311-2. [PubMed: 4031470]  [MGI Ref ID J:7980]

Andoh M; Zhang G; Russell-Lodrigue KE; Shive HR; Weeks BR; Samuel JE. 2007. T Cells Are Essential for Bacterial Clearance, and Gamma Interferon, Tumor Necrosis Factor Alpha, and B Cells Are Crucial for Disease Development in Coxiella burnetii Infection in Mice. Infect Immun 75(7):3245-55. [PubMed: 17438029]  [MGI Ref ID J:122426]

Appelberg R; Castro AG; Gomes S; Pedrosa J; Silva MT. 1995. Susceptibility of beige mice to Mycobacterium avium: role of neutrophils. Infect Immun 63(9):3381-7. [PubMed: 7642266]  [MGI Ref ID J:28292]

Barthold SW; de Souza M. 1995. Exacerbation of Lyme arthritis in beige mice. J Infect Dis 172(3):778-84. [PubMed: 7658072]  [MGI Ref ID J:28297]

Bertin A. 1992. Comparison of susceptibility of inbred and outbred infant mice to Escherichia coli heat-stable enterotoxin STa. Infect Immun 60(8):3117-21. [PubMed: 1639480]  [MGI Ref ID J:2117]

Borges R; Jaen R; Freire F; Gomez JF; Villafruela C; Yanes E. 2001. Morphological and functional characterization of beige mouse adrenomedullary secretory vesicles. Cell Tissue Res 304(1):159-64. [PubMed: 11383882]  [MGI Ref ID J:105112]

Brandt EJ; Elliott RW; Swank RT. 1975. Defective lysosomal enzyme secretion in kidneys of Chediak-Higashi (beige) mice. J Cell Biol 67(3):774-88. [PubMed: 408]  [MGI Ref ID J:5590]

Cavarra E; Martorana PA; de Santi M; Bartalesi B; Cortese S; Gambelli F; Lungarella G. 1999. Neutrophil influx into the lungs of beige mice is followed by elastolytic damage and emphysema. Am J Respir Cell Mol Biol 20(2):264-9. [PubMed: 9922217]  [MGI Ref ID J:53722]

Chi EY; Ignacio E; Lagunoff D. 1978. Mast cell granule formation in the beige mouse. J Histochem Cytochem 26(2):131-7. [PubMed: 624833]  [MGI Ref ID J:5935]

Chow LH. 1993. Studies of virus-induced myocardial injury in mice: value of the scid mutation on different genetic backgrounds and combined with other mutations. Lab Anim Sci 43(2):133-5. [PubMed: 8391609]  [MGI Ref ID J:12476]

Clark EA; Roths JB; Murphy ED; Ledbetter JA; Clagett JA. 1982. The beige (bg) gene influences the development of autoimmune disease in SB/Le male mice. In: NK Cells and Other Natural Effector Cells. Academic Press, New York.  [MGI Ref ID J:30716]

Clark EA; Shultz LD; Pollack SB. 1981. Mutations in mice that influence natural killer (NK) cell activity. Immunogenetics 12(5-6):601-13. [PubMed: 6971254]  [MGI Ref ID J:6485]

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Dominique V; Francis L. 1995. Interactions of the scid or beige mutations with the viable motheaten mutation. Autoimmunity 22(4):199-207. [PubMed: 8781712]  [MGI Ref ID J:33985]

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Galli SJ; Hammel I. 1984. Unequivocal delayed hypersensitivity in mast cell-deficient and beige mice. Science 226(4675):710-3. [PubMed: 6494907]  [MGI Ref ID J:127346]

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Orn A; Hakansson EM; Gidlund M; Ramstedt U; Axberg I; Wigzell H; Lundin LG. 1982. Pigment mutations in the mouse which also affect lysosomal functions lead to suppressed natural killer cell activity. Scand J Immunol 15(3):305-10. [PubMed: 7089489]  [MGI Ref ID J:6801]

Pak MW; Giolli RA; Pinto LH; Mangini NJ; Gregory KM; Vanable JW Jr. 1987. Retinopretectal and accessory optic projections of normal mice and the OKN-defective mutant mice beige, beige-J, and pearl. J Comp Neurol 258(3):435-46. [PubMed: 3584547]  [MGI Ref ID J:29747]

Percy DH; Auger DC; Croy BA. 1994. Signs and lesions of experimental Sendai virus infection in two genetically distinct strains of SCID/beige mice. Vet Pathol 31(1):67-73. [PubMed: 8140728]  [MGI Ref ID J:17913]

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Perou CM; Kaplan J. 1993. Complementation analysis of Chediak-Higashi syndrome: the same gene may be responsible for the defect in all patients and species. Somat Cell Mol Genet 19(5):459-68. [PubMed: 8291023]  [MGI Ref ID J:16651]

Perou CM; Leslie JD; Green W; Li L; Ward DM; Kaplan J. 1997. The Beige/Chediak-Higashi syndrome gene encodes a widely expressed cytosolic protein. J Biol Chem 272(47):29790-4. [PubMed: 9368050]  [MGI Ref ID J:44170]

Perou CM; Moore KJ; Nagle DL; Misumi DJ; Woolf EA; McGrail SH; Holmgren L; Brody TH; Dussault BJ Jr; Monroe CA; Duyk GM; Pryor RJ; Li L; Justice MJ; Kaplan J. 1996. Identification of the murine beige gene by YAC complementation and positional cloning. Nat Genet 13(3):303-8. [PubMed: 8673129]  [MGI Ref ID J:33734]

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Pierce EM; Carpenter K; Jakubzick C; Kunkel SL; Flaherty KR; Martinez FJ; Hogaboam CM. 2007. Therapeutic targeting of CC ligand 21 or CC chemokine receptor 7 abrogates pulmonary fibrosis induced by the adoptive transfer of human pulmonary fibroblasts to immunodeficient mice. Am J Pathol 170(4):1152-64. [PubMed: 17392156]  [MGI Ref ID J:120124]

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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. The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two males and two females (two pairs) will be provided, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the delivery time to approximately 25 weeks. At least one member of each pair will be of known genotype and will carry the mutation if it is a mutant strain. Please note that pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Price represents a repository maintenance fee, which includes the cost of recovery of the strain from the cryopreservation resource and the periodic replacement of the frozen embryos used for recovery. 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

See Terms of Use

The Jackson Laboratory's Genotype Promise

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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Terms of Use

Terms of Use

General Terms and Conditions

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phone:	207-288-6470
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JAX^® Mice & Services Conditions of Use

“Each recipient institution, including its employees and other researchers under its control (RECIPIENT), of mice or services using mice from The Jackson Laboratory (TJL) agrees that such mice, descendants of those mice derived by inbreeding or crossbreeding, including unmodified derivatives of those mice or their descendants (“MICE”) shall not be: (i) used for any purpose other than the internal research of the RECIPIENT, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services with respect to MICE. Acceptance of MICE from TJL shall be deemed agreement by RECIPIENT to these conditions, and departure from these conditions requires The Jackson Laboratory’s prior written authorization.”

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, The Jackson Laboratory will, at its option, provide credit or replacement for the MICE or product received or the services provided.

No Liability

In no event shall The Jackson Laboratory, 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 The Jackson Laboratory, its agents or employees. In purchasing or receiving MICE, products or services from The Jackson Laboratory, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges The Jackson Laboratory from all such causes of action or damages, and further agrees to defend and indemnify The Jackson Laboratory from any costs or damages arising out of any third party claims.

MICE and biological materials 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 The Jackson Laboratory’s MICE, products and services. In addition, special terms and conditions of sale of certain MICE, products and services may be set forth separately in The Jackson Laboratory 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 The Jackson Laboratory, 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 The Jackson Laboratory, 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 services by The Jackson Laboratory.