This inbred mutant strain is homozygous for both the satin (Foxq1sa) and beige (Lystbg) mutations, and is characterized by its immunological phenotype due to the beige mutation; homozygous mutant beige mice exhibit a condition that closely resembles Chediak-Higashi disease in man.Read More +
This strain is homozygous for Lystbg, Foxq1sa and the retinal degeneration allele Pde6brd1. See article "Genetic Background Effects: Can Your Mice See?", JAX® NOTES Spring 2002, No. 485.
The SB/Le inbred strain is homozygous for both the satin (Foxq1sa) and beige (Lystbg) mutations. Most of the immunological phenotype is due to the beige mutation. Homozygous mutant beige mice 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 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. They have a severe deficiency of natural killer (NK) cells. 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 (Prkdcscid), in tissue graft and disease studies. SB/Le mice are also homozygous for white-bellied agouti (Aw) and the retinal degeneration 1 mutation (Pde6brd1). The retinal degeneration 1 mutation leads to early blindness (by weaning). Quantitative RT-PCR comparing Lyst mRNA from mice with the Lystbg, Lystbg-J, or Lystbg-2J alleles has shown that mice with the Lystbg-2J allele have the greatest reduction in mRNA, and mice with the Lystbg-J allele have the least reduction (Barbosa et al. Nature 1996 382:262-265). The precise function of the Lyst protein remains undetermined. Homology searches and defective Concanabalin A induced capping have lead to the postulate that Lyst is involved in microtubule function.
Both the satin (Foxq1sa) and the original beige (Lystbg) recessive mutations arose at Oak Ridge National Laboratory in backcross test matings from T stock female x irradiated (101/Rl x C3H/Rl)F1 male. T stock was a multiple-recessive tester strain that contained several backgrounds including C57BL10/Rl. The two separate mutations, Foxq1sa and bg, were bred together and homozygous Aw/Aw Foxq1sa bg/Foxq1sa bg mice on a mixed background were received at The Jackson Laboratory in 1961 and sibling mated thereafter. In 1963 this breeding was at F7, in 1967 it reached F20, and in 1971 the strain was re-named SB/LeJ, an inbred strain (Lane et al., 1972 Genetics 71:451-460). The Lystbg allele was found to have arisen from the retrotransposition of a LINE1 element resulting in a cDNA sequence which predicts a truncated Lyst protein product (Perou et al., Genomics 1997; 42:366-368). This insertion occurred in the C3H derived chromosome rather than the 101/R1 derived chromosome in the irradiated founder (101/Rl x C3H/Rl)F1 male (Perou et al., Nature Genetics 1996; 13:303-308). Subsequent sponta neous mutations of Lyst have been identified. It is worthwhile to note that Stock No. 000204, the C57BL/6J congenic of Lystbg named B6.Cg-Lystbg/J, and Stock No. 000629, the spontaneous mutation on C57BL/6J named C57BL/6J-Lystbg-J/J are both offered by The Jackson Laboratory and should not be confused.
|Allele Type||Radiation induced|
|Allele Synonym(s)||30B/22B; bg; CHS mice|
|Gene Symbol and Name||Lyst, lysosomal trafficking regulator|
|Strain of Origin||C3H/Rl|
|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.|
|Allele Type||Radiation induced|
|Allele Synonym(s)||sa; satin|
|Gene Symbol and Name||Foxq1, forkhead box Q1|
|Strain of Origin||(101/Rl x C3H/Rl)F1|
|Molecular Note||This allele occurred in descendants of a gamma irradiation experiment. The underlying mutation was identified as a 67 bp intragenic deletion. The deletion causes a frame shift resulting in a truncated 376 amino acid protein but does not affect the first 228 residues, including the characteristic WH DNA-binding domain. The mutant protein is predicted to bind to its DNA targets but fails at transcriptional activation or repression because the specific C-terminal domains are missing.|
|Allele Name||retinal degeneration 1|
|Allele Synonym(s)||Pdebrd1; rd; rd1; rd-1; rodless retina|
|Gene Symbol and Name||Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide|
|Strain of Origin||various|
|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 been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested.|
When using the satin beige mouse strain in a publication, please include JAX stock #000269 in your Materials and Methods section.
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