ALS/LtJ and ALR/LtJ (Stock No. 003070) inbred strains are useful for a wide range od studies including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. Alloxan-untreated ALS/Lt males exhibit impaired glucose tolerance when tested by intraperitoneal administration of glucose, and become hyperinsulinemic . ALS/LtJ mice contain genes predisposing to both experimentally-induced type 1 and spontaneously-developing type 2 diabetes mellitus. ALS/Lt mice exhibit significantly lower antioxidant defenses than do ALR/Lt. ALS/Lt is a useful control strain for comparing inbred strain susceptibility to free radical-mediated damage.Read More +
This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss with onset prior to three months of age and for Gnat2cpfl3, cone photoreceptor function loss 3, which affects bright light (photopic) vision.
ALS/LtJ and ALR/LtJ (Stock No. 003070) inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. By 34 weeks of age, both untreated ALS/Lt and ALR/Lt males fed a 6% fat-containing chow diet attain a mean body weight of around 50 grams. Genome wide scan comparison shows that ALS/LtJ mice are more closely related to NON/ShiLtJ mice (they share the H2nb1 haplotype) than to NOD/ShiLtJ. Like two other ICR-derived inbred strains selected in Japan (NON and NSY), alloxan-untreated ALS/Lt males exhibit impaired glucose tolerance when tested by intraperitoneal administration of glucose. However, unlike NON/ShiLt males, which exhibit impaired glucose tolerance in the presence of low plasma insulin concentrations, alloxan-untreated ALS/LtJ males become hyperinsulinemic by 10 weeks of age and maintain hyperinsulinemia as they age. Four untreated males and three females in a research colony have spontaneously developed type 2 diabetes between nine to 32 weeks of age (EH Leiter, unpublished observations). ALS/LtJ mice thus contain genes predisposing to both experimentally-inducedtype 1 and spontaneously-developing type 2 diabetes mellitus. Since ALS/Lt mice exhibit significantly lower antioxidant defenses than do ALR/Lt, yet the two strains are closely related, ALS/Lt is a useful control strain for comparing inbred strain susceptibility to free radical-mediated damage.
Alloxan is a pancreatic beta cell-selective toxin that induces diabetes in rodents by generating cytotoxic free radicals. The ALS (alloxan-induced diabetes-susceptible) inbred strain was created in Japan by selective inbreeding of Crj:CD-1 (ICR) mice with selection for susceptibility to diabetes development after administration of alloxan at doses representing the ED50 for the original Crj:CD-1 strain (45 mg/kg in males, 47 mg/kg in females). These dosages are lower than what is necessary to elicit a strong diabetogenic response in most inbred strains, typically 60mg/kg. After a litter was born and weaned, the parents and some of the progeny were alloxan-treated to select for high versus low [ALR (alloxan-induced diabetes-resistant)] incidence lines based on blood glucose levels at 7 days post treatment. ALS and ALR inbred strains were obtained from Japan by Dr. EH Leiter (Lt) at The Jackson Laboratory in 1996. ALS/Lt and ALR/Lt mice were transferred to the production colony in 1998.
|Allele Name||age related hearing loss 1|
|Allele Synonym(s)||Cdh23753A; mdfw|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|Strain of Origin||multiple strains|
|Molecular Note||Genetic complementation tests have shown allelism between the mdfw (modifier of deaf waddler) locus and the ahl locus. Further analysis has shown this is caused by a G to A transition at coding nucleotide position 753 of Cdh23 (SNP rs257098870). This hypomorphic allele changes splice donor site G-GT to A-GT, causing frame skipping of exon 7. This is predicted to delete part of the 2nd and 3rd ectodomains and cause reduced message stability. Twenty-seven strains classified with ahl and carrying the 753A allele include: CD-1, RBF/DnJ, PL/J, AKR/J, RF/J, BALB/cBy, A/WySnJ, P/J, SENCARA/PtJ, DBA/1J, ALS/LtJ, C58/J, C57BLKS/J, 129P1/ReJ, C57BR/cd, SKH2/J, BUB/Bn, MA/MyJ, LP/J, 129X1/SvJ, NOR/LtJ, A/J, C57BL/6, NOD/LtJ, DBA/2J, ALR/LtJ, C57L/J. Strains classified with ahl that DO NOT carry this mutation include: 129S1/SvImJ, C3H/HeSnJ, I/LnJ, YBR/Ei, MRL/MpJ.|
|Allele Name||cone photoreceptor function loss 3|
|Allele Synonym(s)||no cones|
|Gene Symbol and Name||Gnat2, guanine nucleotide binding protein, alpha transducing 2|
|Strain of Origin||various|
|General Note||This allele has been detected in the following strains either by genotyping or complementation testing: ALS/LtJ, SENCARA/PtJ, SENCARB/PtJ, SENCARC/PtJ, PN/nBSwUmabJ. (J:122428) The allele has also been reported in NMRI and CD1 (Lluis Montoliu, J:212307)|
|Molecular Note||A single nucleotide substitution of G to A at coding nucleotide 598 in exon 6. This mutation converts codon 200 from aspartic acid to asparagine (p.D200N).|
|Allele Name||mutation 1|
|Gene Symbol and Name||mt-Tr, mitochondrially encoded tRNA arginine|
|Strain of Origin||various|
|General Note||This polymorphism is present in A/J, NZB/B1NJ, ALS/Lt and NOD/ShiLtJ. A variant with 9 adenines is found in NOD/ShiLtDvs, ALR/Lt and SKH2/J.|
|Molecular Note||The adenine repeat in the D stem is polymorphic with 10 adenines in this allele.|
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