Strain Name: |
NOD/ShiLtJ |
|---|---|
Stock Number: |
001976 |
Availability: | Level 1 |
General Terms and Conditions |
| Former Name |
NOD/LtJ (Changed: 23-FEB-07
) |
| Strain Common Names | Non-obese Diabetic; |
| Genes & Alleles | Cdh23; Cdh23ahl; Hc; Hc0; |
Type Inbred Strain Additional information on Inbred Strains. Mating System Sibling x Sibling (Female x Male) Species laboratory mouse H2 Haplotype g7 Generation F120 (03-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 that is already severe by 3 months of age.Strain Description
Diabetes in NOD/ShiLtJ mice is characterized by insulitis, a leukocytic infiltrate of the pancreatic islets. Marked decreases in pancreatic insulin content occur in females at about 12 weeks of age and several weeks later in males. Onset of diabetes is marked by moderate glycosuria and by a non-fasting plasma glucose higher than 250 mg/dl. Diabetic mice are hypoinsulinemic and hyperglucagonemic, indicating a selective destruction of pancreatic islet beta cells. Susceptibility to IDDM in NOD/ShiLtJ mice is polygenic, and environment, including housing conditions, health status, and diet, exerts a strong effect on penetrance. NOD/ShiLtJ females are more widely used than males because the onset of IDDM symptoms occurs earlier and with a higher incidence (90-100% by 30 weeks of age). NOD/ShiLtJ males develop IDDM at a frequency of between 40-60% by 30-40 weeks of age. Male mice are useful for certain applications, including pharmaceutical studies, "accelerated transfer" of IDDM, and some in vitro studies. The major component of diabetes susceptibility in NOD mice is the unique MHC haplotype (H2g7 = Kd, Aad, Abg7, Enull, Db). NOD mice also exhibit multiple aberrant immunophenotypes including defective antigen presenting cell immunoregulatory functions, defects in the regulation of theT lymphocyte repertoire, defective NK cell function, defective cytokine production from macrophages (Fan et al., 2004) and impaired wound healing. They also lack hemolytic complement, C5. NOD/ShiLtJ mice also are severely hearing-impaired. A variety of mutations causing immunodeficiencies, targeted mutations in cytokine genes, as well as transgenes affecting immune functions, have been backcrossed into the NOD/ShiLt inbred strain background.Strain Development
NOD inbred mice originated early on in the inbreeding of the Cataract Shionogi (CTS) strain. These mice were originally outbred Jcl:ICR mice. At F6, the progenitors of the future NOD/Shi mice were inbred on the basis of an elevated fasting blood glucose level in cataract-free mice. At F13, the NOD progenitors were separated from what is now the NON/Shi strain. High fasting blood glucose levels continued to be the basis for selection of the latter strain, while the NOD progenitors at F13 and later were selected on the basis of a normal fasting blood glucose level. In 1974, at F20, a female in the "normoglycemic" line spontaneously developed overt insulin-dependent diabetes mellitus with insulitis (IDDM). Selective breeding of the progeny of this diabetic female produced the nonobese diabetic (NOD) strain. Originally restricted to distribution in Japan, NOD substrains were distributed during the early 1980s to Australia and the United States. NOD and NON strains were imported from a colony in Kyoto, Japan by Dr. M. Hattori to the Joslin Diabetes Ceneter in Boston in 1984. Breeder pairs from this importation were sent from The Joslin Diabetes Center to Dr. E Leiter at The Jackson Laboratory, and are the source of the production strains NOD/ShiLtJ and NON/ShiLtJ. The current generation of inbreeding is F83.
| 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, 129/ReJ, C57BR/cd, SKH2/J, BUB/Bn, MA/MyJ, LP/J, 129/ScJ, 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 | Hc0 | ||
| Allele Name | deficient | ||
| Common Name(s) | C5-; C5-d; C5-def; C5-deficient; hco; | ||
| Gene Symbol and Name | Hc, hemolytic complement | ||
| Chromosome | 2 | ||
| Gene Common Name(s) | C5; C5a; CPAMD4; FLJ17816; FLJ17822; He; MGC142298; RGD1561905; | ||
| General Note |
This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, AKR/J, DBA/2J, NZB/B1NJ, SWR/J, B10.D2/oSnJ Hc was identified as a candidate gene for Abhr2 in a microarray analysis of lung mRNA from A/J, C3H/HeJ, and (A/J x C3H/HeJ)F1 x A/J backcross animals. Hc genotype shows statistically significant correlation to allergen-induced bronchial hyperresponsive phenotype. The A/J allele contains a 2 bp deletion resulting in deficient Hc mRNA and protein production and is associated with susceptibility to allergen-induced bronchial hyperresponsiveness. (J:108211) | ||
| Molecular Note | A 2 base "TA" deletion at positions 62 and 63 of an 83 base pair exon near the 5' end of the gene is found in the following mouse strains: A/HeJ, AKR/J, DBA/2J, NZB/B1NJ, SWR/J, B10.D2/oSnJ. The consequence of this deletion is the creation of a stop codon starting four bases after the deletion. A truncated product of 216 amino acids is predicted as a result although contradictory reports exist that a larger pro-C5 protein may be synthesized. Nevertheless, macrophages from mouse strains carrying this allele do not secrete complement 5. [J:23983] | ||
| Diet Information | LabDiet® 5K52/5K67 |
|---|
NOD Strains
001289 NOD/ShiLt 006778 NOD/ShiLt-Tg(GFAP-Cd80)9Mdos/MdosJ 004939 NOD/ShiLtJ-Leprdb-5J/LtJ View NOD Strains (3 strains)
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 003072 ALS/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 002050 NOR/LtJ 000679 P/J 002747 SENCARB/PtJ 002335 SKH2/J 003392 STOCK Crb1rd8/J View Strains carrying Cdh23ahl (41 strains)
Strains carrying Hc0 allele
000645 A/HeJ 000646 A/J 000647 A/WySnJ 000648 AKR/J 000460 B10.D2-Hc0 H2d H2-T18c/o2SnJ 000461 B10.D2-Hc0 H2d H2-T18c/oSnJ 000657 CE/J 000671 DBA/2J 007048 DBA/2J-Gpnmb+/SjJ 001800 FVB/NJ 001491 FVB/NMob 001303 NOD.CB17-Prkdcscid/J 000684 NZB/BlNJ 000682 RF/J 000688 ST/bJ 000689 SWR/J View Strains carrying Hc0 (16 strains)
Strains carrying other alleles of Cdh23
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 (7 strains)
Strains carrying other alleles of Hc
000470 AK.M-H2m H2-T18a/nSnJ 005308 B10.Cg-H2d Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ 000463 B10.D2-Hc1 H2d H2-T18c/nSnJ 003147 B10.D2-Hc1 H2d H2-T18c/nSnJ-Tg(DO11.10)10Dlo/J 004306 NOD.CBALs-Hc1/LtJ View Strains carrying other alleles of Hc (5 strains)
Body Weight Information - JAX® Mice Strain NOD/ShiLtJ (001976)Mouse Phenome Database
(This chart reflects the typical correlation between body weight and age for mice maintained in production colonies at The Jackson Laboratory.)
Festing Inbred Strain Characteristics: NOD
NEW -- JAX® Physiological Data Summary
NEW -- JAX® Physiological Data Protocol
NEW -- JAX® Physiological Data Protocol
NEW -- JAX® Physiological Data Summary
Genetic Quality Control Annual Report
JAX Notes, Spring 1999; 477. Control Strains for NOD/LtJ Mice in Diabetes Research.
JAX Notes, Spring 2003; 489. Malocclusion in the Laboratory Mouse.
JAX Notes, Spring 2003; 489. Role of NK and NKT Cells in Immunity and Disease.
JAX Notes, Spring 2007; 505. Research Using NOD/ShiLtJ Mouse Suggests Novel Therapies for Type 1 Diabetes.
JAX Notes, Summer 1992; 450. Myoepitheliomas in Inbred Laboratory Mice.
JAX Notes, Summer 2003; 490. Hydrocephalus in Laboratory Mice.
JAX Notes, Winter 1993; 452. NOD/LtJ Mice Available.
JAX Notes, Winter 1999; 476. Using NOD/LtJ Males in Diabetes Research.
JAX Notes, Winter 2006; 504. JAX® Mice: the Gold Standard Just Got Better.
Room Number AX8
Cdh23ahl relatedDevelopmental Biology Research
Lymphoid Tissue Defects (hematopoietic defects)
Diabetes and Obesity Research
Hyperglycemia
Hypoinsulinemia
Impaired Wound Healing
Islet Transplantation Studies
Type 1 Diabetes (IDDM)
Immunology and Inflammation Research
Autoimmunity (Type 1 Diabetes)
Internal/Organ Research
Wound Healing (delayed/impaired)
Neurobiology Research
Vestibular and Hearing Defects (Age related hearing loss)
Research Tools
Immunology and Inflammation Research (NK Cell Deficiency)
Sensorineural Research
Vestibular and Hearing Defects (Age related hearing loss)
Hc0 relatedNeurobiology Research
Vestibular and Hearing Defects (Age related hearing loss)
Sensorineural Research
Vestibular and Hearing Defects (Age related hearing loss)
Immunology and Inflammation Research
Immunodeficiency (specific complement deficiency)
Research Tools
Immunology and Inflammation Research (specific complement deficiency) (C5 complement)
Selected Reference(s)
Additional ReferencesMakino S; Kunimoto K; Muraoka Y; Mizushima Y; Katagiri K; Tochino Y. 1980. Breeding of a non-obese, diabetic strain of mice. Jikken Dobutsu 29(1):1-13. [PubMed: 6995140] [J:25411]
Serreze DV; Chapman HD; Varnum DS; Gerling I; Leiter EH; Shultz LD. 1997. Initiation of autoimmune diabetes in NOD/Lt mice is MHC class I-dependent. J Immunol 158(8):3978-86. [PubMed: 9103469] [J:39473]
| Strain Name: | NOD/ShiLtJ |
| Stock Number: | 001976 |
IMPORTANT NOTE: Prices are based on shipping destination. To view prices, select your shipping destination.
| Standard Supply | Level 1. JAX Ready Strain® (readily available). |
|---|---|
| Supply Notes |
Mice are not available above eight weeks of age. Shipped at a specific age in weeks. Mice at a precise age in days and littermates are also available. Strains that must be genotyped are not available until five to seven weeks of age. Genomic DNA is available for this strain from the Mouse DNA Resource. |
| Licensing | See General Terms and Conditions below |
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