Strain Name: |
ALS/LtJ |
|---|---|
Stock Number: |
003072 |
Availability: | Repository- Live |
Price and Supply Information | |
General Terms and Conditions |
| Strain Common Names | Alloxan Susceptibility; |
| Genes & Alleles | Cdh23; Cdh23ahl; Gnat2; Gnat2cpfl3; |
Type Inbred Strain Additional information on Inbred Strains. Mating System Sibling x Sibling (Female x Male) Species laboratory mouse H2 Haplotype nb1 Generation F?+14+19 (21-JAN-08) Appearance
albino
Related Genotype: a/a Tyrc/TyrcImportant Note
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 3 months of age and for Gnat2cpfl3, cone photoreceptor function loss 3, which affects bright light (photopic) vision.Strain Description
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 wk 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 wk 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and three females in a research colony have spontaneously developed type 2 diabetes between 9-32 wk of age (EH Leiter, unpublished observations).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.Strain Development
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 Symbol | Cdh23ahl | ||
|---|---|---|---|
| Allele Name | age related hearing loss 1 | ||
| Common Name(s) | Cdh23753A; mdfw; | ||
| Strain of Origin | C57BL/6J | ||
| Gene Symbol and Name | Cdh23, cadherin 23 (otocadherin) | ||
| Chromosome | 10 | ||
| Gene Common Name(s) | 4930542A03Rik; DFNB12; DKFZp434P2350; FLJ00233; FLJ36499; KIAA1774; KIAA1812; MGC102761; RIKEN cDNA 4930542A03 gene; USH1D; W; age related hearing loss 1; ahl; bob; bobby; bus; bustling; mdfw; modifier of deaf waddler; neuroscience mutagenesis facility, 112; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; nmf112; nmf181; nmf252; v; waltzer; | ||
| Molecular Note | Genetic complementation tests have shown allelism between the mdfw (modifier of deaf waddler) locus and the ahl locus. Further analysis has identified an association between ahl and a G to A transition at nucleotide position 753 of Cdh23. This hypomorphic allele causes in frame skipping of exon 7 and reduced message stability. Twenty-seven strains classified with ahl and carrying the 753A allele include: CD1, 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/LyJ, DBA/2J, ALR/LtJ, C57L/J. Strains classified with ahl that DO NOT carry this mutation include: C3H/HeSnJ, I/LnJ,YBR/Ei, MRL/MpJ. [J:86905] | ||
| Allele Symbol | Gnat2cpfl3 | ||
| Allele Name | cone photoreceptor function loss 3 | ||
| Common Name(s) | Gnat2; | ||
| Strain of Origin | various | ||
| Gene Symbol and Name | Gnat2, guanine nucleotide binding protein, alpha transducing 2 | ||
| Chromosome | 3 | ||
| Gene Common Name(s) | ACHM4; AW490837; GNATC; Gnat-2; Gt-2; Tcalpha; expressed sequence AW490837; | ||
| 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) Phenotypic Similarity to Human Syndrome in Orthologous Human Gene: OMIM +139340 ACHROMATOPSIA 4. | ||
| Molecular Note | A single nucleotide substitution of G to A at position 598 in exon 6. This mutation converts codon 200 from apartic acid to asparagine. [J:122428] | ||
| Diet Information | LabDiet® 5K52/5K67 |
|---|
Alloxan Resistance and Susceptibility Strains
003070 ALR/LtJ View Alloxan Resistance and Susceptibility Strains (1 strain)
Strains carrying Cdh23ahl allele
001137 129P1/ReJ 000690 129P3/J 002065 129T2/SvEmsJ 000691 129X1/SvJ 000646 A/J 000647 A/WySnJ 003070 ALR/LtJ 004502 B6;AKR-Lxl2/J 001026 BALB/cByJ 000653 BUB/BnJ 005494 C3.129S1(B6)-Grm1rcw/J 000664 C57BL/6J 004764 C57BL/6J-Cdh23v-8J/J 003129 C57BL/6J-Epha4rb-2J/J 004820 C57BL/6J-Kcne12J/J 004703 C57BL/6J-Nmf134/J 004811 C57BL/6J-nmf110/J 004812 C57BL/6J-nmf111/J 004747 C57BL/6J-nmf118/J 004656 C57BL/6J-nmf88/J 004391 C57BL/6J-Chr 13A/J/NaJ 004385 C57BL/6J-Chr 7A/J/NaJ 000662 C57BLKS/J 000667 C57BR/cdJ 000668 C57L/J 000669 C58/J 000657 CE/J 000670 DBA/1J 001140 DBA/1LacJ 000671 DBA/2J 007048 DBA/2J-Gpnmb+/SjJ 002106 KK/HlJ 000675 LG/J 000676 LP/J 000677 MA/MyJ 001976 NOD/ShiLtJ 002050 NOR/LtJ 000679 P/J 002747 SENCARB/PtJ 002335 SKH2/J 003392 STOCK Crb1rd8/J View Strains carrying Cdh23ahl (41 strains)
Strains carrying Gnat2cpfl3 allele
002448 129S1/SvImJ 006180 CD10/JlsJ 005052 PN/nBSwUmabJ 002746 SENCARA/PtJ 002747 SENCARB/PtJ 002748 SENCARC/PtJ 006135 STOCK Sgk3fz-ica/McirJ 003773 STOCK Tg(CAG-ECFP)CK6Nagy/J 005645 STOCK Tg(CAG-mRFP1)1F1Hadj/J 004623 STOCK Tg(Fos-lacZ)34Efu/J 005667 STOCK Tg(Neurog3-cre)C1Able/J 003262 STOCK Tg(Trp53A135V)L3Ber/J 005104 STOCK Tg(tetO-HIST1H2BJ/GFP)47Efu/J 005699 STOCK Tg(tetO-Ipf1,EGFP)956.6Macd/J View Strains carrying Gnat2cpfl3 (14 strains)
Strains carrying other alleles of Cdh23
008288 B6(Cg)-Cdh23v-11J/J 002756 B6.CAST-Cdh23Ahl+/Kjn 002432 B6J x B6.C-H2bm1/ByJ-Cdh23v-J/J 002552 C57BL/6J-Cdh23v-2J/J 004764 C57BL/6J-Cdh23v-8J/J 004819 C57BL/6J-Cdh23v-9J/J 005016 CByJ;B6-Cdh23v-10J/J 000275 V/LeJ View Strains carrying other alleles of Cdh23 (8 strains)
Mouse Phenome Database
JAX Notes, Fall 1999; 479. New Mouse Models for Diabetes and Free Radical Research.
JAX Notes, Spring 1999; 477. Control Strains for NOD/LtJ Mice in Diabetes Research.
Room Number FGB27
Cdh23ahl relatedDiabetes and Obesity Research
Hyperglycemia (alloxan induced)
Hyperinsulinemia (males; spontaneous, alloxan untreated)
Hypoinsulinemia (alloxan induced)
Insulin Resistance (males; spontaneous, alloxan untreated)
Obesity With Diabetes (moderate, adult onset)
Type 1 Diabetes (IDDM) (males: alloxan induced)
Type 1 Diabetes (IDDM) Analysis Strains (Related Inbred Strains)
Type 2 Diabetes (NIDDM) (males: spontaneous, alloxan untreated)
Metabolism Research
Free Radical Research
Neurobiology Research
Vestibular and Hearing Defects (Age related hearing loss)
Research Tools
Toxicology Research (free radical research)
Sensorineural Research
Vestibular and Hearing Defects (Age related hearing loss)
Neurobiology Research
Vestibular and Hearing Defects (Age related hearing loss)
Sensorineural Research
Vestibular and Hearing Defects (Age related hearing loss)
Selected Reference(s)
Additional ReferencesGraser RT; Mathews CE; Leiter EH; Serreze DV. 1999. MHC characterization of ALR and ALS mice: respective similarities to the NOD and NON strains. Immunogenetics 49(7-8):722-6. [PubMed: 10369935] [J:56048]
Mathews CE; Bagley R; Leiter EH. 2004. ALS/Lt: a new type 2 diabetes mouse model associated with low free radical scavenging potential. Diabetes 53 Suppl 1:S125-9. [PubMed: 14749277] [J:88014]
Mathews CE; Dunn BD; Hannigan MO; Huang CK; Leiter EH. 2002. Genetic control of neutrophil superoxide production in diabetes-resistant ALR/Lt mice. Free Radic Biol Med 32(8):744-51. [PubMed: 11937300] [J:76108]
Mathews CE; Leiter EH. 1999. Resistance of ALR/Lt islets to free radical-mediated diabetogenic stress is inherited as a dominant trait. Diabetes 48(11):2189-96. [PubMed: 10535453] [J:109893]
Mathews CE; Leiter EH. 1999. Constitutive differences in antioxidant defense status distinguish alloxan-resistant and alloxan-susceptible mice. Free Radic Biol Med 27(3-4):449-55. [PubMed: 10468221] [J:57552]
Sekiguchi F; Ishibashi K; Katoh H; Kawamoto Y; Ino T. 1990. Genetic profile of alloxan-induced diabetes-susceptible mice (ALS) and-resistant mice (ALR). Exp Anim 39(2):269-72. [PubMed: 2361527] [J:109930]
Ueda H; Ikegami H; Yamato E; Fu J; Fukuda M; Shen G; Kawaguchi Y; Takekawa K; Fujioka Y; Fujisawa T; Nakagawa Y; Hamada Y; Shibata M; Ogihara T. 1995. The NSY mouse: a new animal model of spontaneous NIDDM with moderate obesity. Diabetologia 38(5):503-8. [PubMed: 7489831] [J:25653]
| Strain Name: | ALS/LtJ |
| Stock Number: | 003072 |
IMPORTANT NOTE: Prices are based on shipping destination. The shipping destinations are:
| Price(s) in US dollars ($) | Genotype(s) Provided | ||||
|---|---|---|---|---|---|
| Individual Mouse Price | $60.70 | ||||
| Standard Supply | Repository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of ~nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within 48 hours of order placement. |
|---|---|
| Supply Notes |
Histology and Tissue Collection Services are available for all JAX® Mice strains. For more information, please contact Customer Service at orderquest@jax.org or 1-800-422-6423. Usually shipped between four and six weeks of age. This strain is included in the Mouse Mutant Resource collection. Genomic DNA is available for this strain from the Mouse DNA Resource. |
| Licensing | See General Terms and Conditions below |
Purchasing Information
JAX® Mice Orders
Surgical Services
Contact Information
Orders & Technical Support
Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
Technical Support Email Form