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Strain Name:

I/LnJ

Stock Number:

000674

Availability:

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General Terms and Conditions

Strain Common Names      I Lyon;
Genes & Alleles   Ednrb;   Ednrbs;   Hc;   Hc0;   Myo5a;   Myo5ad;


Product Information

Strain Details

Type Inbred Strain
Additional information on Inbred Strains.
Mating SystemSibling x Sibling         (Female x Male)
Specieslaboratory mouse
H2 Haplotypej
GenerationF144 (22-NOV-06)

Appearance
pink-eyed dilute brown, piebald (spotted)
Related Genotype: a/a Tyrp1b/Tyrp1b Oca2p/Oca2p Myo5ad/Myo5ad Ednrbs/Ednrbs

Strain Description
I/LnJ mice were originally derived by Dr. LC Strong in 1926 from an unpedigreed stock of mice. A high proportion of mice from this strain lack a corpus callosum. This absence is associated with slow growth of the medial septum subadjacent to the cavum septi. The reproductive performance of I/LnJ mice is very poor. Further analysis indicates that oocytes from I/LnJ mice display retarded kinetics of meiotic maturation and a high frequency of metaphase I arrest. Some oocytes fail to resume meiosis. Oocytes have many very small centrosomes with an absence of microtubules. I/LnJ mice, in addition to carrying several other coat color alleles, are homozygous for the piebald mutation (Ednrbs). The piebald spontaneous mutation is the result of a mutation in the endothelin receptor type B gene, Ednrb. Mice show irregular white spotting, the amount of which is greatly influenced by minor modifying genes. They also have dark eyes. The white areas of the coat are completely lacking in neural crest-derived melanocytes, and there is a reduction in the number of melanocytes in the choroid layer of the eye.

Mammalian Phenotype Terms assigned by genotype

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

Hc0/Hc0

        Background Not Specified
  • immune system phenotype
  • abnormal C5 physiology (MGI Ref ID J:5016)
    • macrophages fail to secrete complement 5

Hc0/Hc0

        involves: A/J * C3H/HeJ
  • respiratory system phenotype
  • increased airway responsiveness (MGI Ref ID J:108211)
    • susceptibility to allergen-induced bronchial hyperresponsiveness

Hc0/Hc0

        involves: C57BL/10SnJ
  • immune system phenotype
  • increased susceptibility to bacterial infection (MGI Ref ID J:44240)
    • Hc-deficient mice display a 25-fold reduction in bacterial clearance after 1 and 3 hours after CLP compared to control mice

Hc0/Hc0

        B10.D2-Hc0
  • homeostasis/metabolism phenotype
  • decreased susceptibility to injury (MGI Ref ID J:120567)
    • mice are resistant to ischemia reperfusion-induced renal injury
    • serum urea nitrogen is reduced 35% to 40% compared to wild type mice subjected to ischemia reperfusion

Gene & Allele Details

Allele Symbol Ednrbs
Allele Name piebald
Common Name(s) s;
Strain of Originold mutant of the mouse fancy
Gene Symbol and Name Ednrb, endothelin receptor type B
Chromosome 14
Gene Common Name(s) ABCDS; AU022549; ETB; ETBR; ETRB; Ednra; HSCR; HSCR2; Sox10m1; expressed sequence AU022549; piebald; s;
General Note Also called piebald spotting. This is a very old mutation of the mouse fancy, and was described in the scientific literature as early as 1920 (J23183). Some piebalds in existing stocks may be of independent origin. Homozygotes show irregular white spotting, the amount of which is greatly influenced by minor modifying genes (J:12952). Homozygotes have dark eyes. The white areas of the coat are completely lacking in melanocytes, and there is a reduction in the number of melanocytes in the choroid layer of the eye (J:15014, J:12970). There may also be defects in the structure of the iris, suggesting that pigment cells make some structural or inductive contribution to normal development (J:13123).Homozygotes may develop megacolon which is always associatedwith lack of ganglion cells in the distal portion of the colon. The incidence of megacolon is also affected by minor modifying genes (J:15014). Pigment cells and enteric ganglion cells of the colon are both derived from the neural crest, and Mayer (J:12725) has shown by explantation of embryonic tissues that the defect leading to white spotting is in the neural crest rather than in the skin. The defect probably consists of failure of pigment cells to differentiate in certain tissue environments rather than in failure to migrate (J:5036). The distribution of white areas in the skin and other organs is probably due to normal regional differences in these tissues in capacity to support pigmentation and not to regional heterogeneity among the pigment cells themselves (J:5220, J:5036, J:5060, J:5782).The piebald mutation was shown to be linked closely with Hr (J:299), later mapped to Chr 14 (J:52911). The localization has been refined in studies of induced mutations, using an intersubspecific backcross (J:16291).
Molecular Note This mutation is allelic to a targeted mutation for this gene. Homozygous mice produce approximately 25% of the normal levels of transcript from this allele. RT-PCR analysis demonstrated that no alterations in the coding sequence would result in any alteration of the amino acid sequence. A 5.5 kb retrotransposon-like element is found in intron 1. About 75% of the mRNA produced is an aberrant 6.5 kb form lacking exons 2-6 but containing exon 1. The remaining 25% of the mRNA formed is of normal, 4.4 kb, size. [MGI Ref ID J:110573] [MGI Ref ID J:22206] [MGI Ref ID J:56133]
 
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. [MGI Ref ID J:23983]
 
Allele Symbol Myo5ad
Allele Name dilute
Common Name(s) d; dv; maltese dilution;
Strain of Originold mutant of the mouse fancy
Gene Symbol and Name Myo5a, myosin Va
Chromosome 9
Gene Common Name(s) 9630007J19Rik; AI413174; AI661011; D; Dbv; Dop; GS1; MVa; MYH12; MYO5; MYR12; Myo5; MyoVA; RIKEN cDNA 9630007J19 gene; d; dilute; expressed sequence AI413174; expressed sequence AI661011; flail; flailer; flr; myosin V; nmf244;
General Note Mutations at the Myo5a locus lighten coat color through an abnormal morphology of melanocytes that causes uneven pigmentation of the hair shaft (J:11005). Most of these mutations also cause severe neurological defects; in some mutant forms, these defectslead to early death (J:12978), while in others life span is normal, but convulsions and loss of equilibrium occur after about four months of age (J:16915).

Maltese dilution, as this mutation was originally called, is an old mutation of the mouse fancy. The blue-gray color of the hair produced by this mutation in nonagouti (a/a) mice is caused by clumping of the melanin pigment into a few large masses (J:12958). The melanocytes are misshapen, with fewer and thinner dendritic processes than wild-type melanocytes, and melanin granules are largely clumped around the nucleus (J:12970). Incorporation of tyrosine into melanin proceeds at a normal rate (J:12173), and the fine structure of the melanin granules is normal (J:5346). Cultured primary melanocytesfrom dilute homozygotes are normal in morphology but display clustering of melanosomes (J:37976).

Griscelli disease (Chediak-Higashi-like syndrome, OMIM 214450) is a human autosomal recessive disorder whose symptoms include pigment dilution, immunodeficiency, and acute lethal lymphocyte and macrophage activation. Melanocyte malformation is characteristic of the pigment abnormality. The immunological abnormality includes absence of cutaneous hypersensitivity and impaired function of natural-killer cells. Griscelli disease resembles the dilute-lethal mouse mutant, except for the neurological disorder in the mouse. The locus for Griscelli disease colocalizes with the locus for myosin Va, which is mutated in at least some Griscelli patients. Griscelli disease is thus the homolog of mouse Maltese dilution (J:41253).

The original Myo5ad mutation which identified the locuswas caused by insertion of an ecotropic murine leukemia virus (see Emv3) (J:6844, J:6587). All other mutations examined lack the virus. Reversions of Myo5ad to wild-type, which have been reported frequently, are caused by excision of the virusleaving exactly one long terminal repeat in place (J:7092). The virus is integrated into a noncoding region of the DNA (J:7751).

Colony Maintenance

Diet Information LabDiet® 5K52/5K67

Related Strains

Strains carrying   Ednrbs allele
000577   B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J
000676   LP/J
000308   SSL/LeJ
000275   V/LeJ
View Strains carrying   Ednrbs     (4 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
001976   NOD/ShiLtJ
000684   NZB/BlNJ
000682   RF/J
000688   ST/bJ
000689   SWR/J
View Strains carrying   Hc0     (17 strains)

Strains carrying   Myo5ad allele
001005   AKXD1/TyJ
001003   AKXD11/TyJ
000765   AKXD13/TyJ
000779   AKXD14/TyJ
000954   AKXD15/TyJ
001093   AKXD18/TyJ
000776   AKXD2/TyJ
001062   AKXD21/TyJ
000947   AKXD22/TyJ
000949   AKXD25/TyJ
000764   AKXD27/TyJ
000959   AKXD3/TyJ
000285   B6.Cg-Rorasg + +/+ Myo5ad Bmp5se/J
000652   BDP/J
000036   BXD1/TyJ
000013   BXD16/TyJ
000015   BXD18/TyJ
000010   BXD19/TyJ
000077   BXD21/TyJ
000043   BXD22/TyJ
000081   BXD25/TyJ
006255   BXD25/TyJRwwJ
000029   BXD29/TyJ
000037   BXD5/TyJ
000007   BXD6/TyJ
000084   BXD8/TyJ
000105   BXD9/TyJ
000284   CWD/LeJ
000670   DBA/1J
000671   DBA/2J
000963   DBA/2J-Myo5ad+17J/Myo5ad/J
000964   DBA/2J-Myo5ad+18J/Myo5ad/J
000067   DBA/2J-Myo5ad+2J/Myo5ad/J
000673   HRS/J
001850   MEV-Q/TyJ
001855   MEV-V/TyJ
003345   MEV/2Ty-Emv64/J
000679   P/J
000644   SEA/GnJ
000390   STOCK Myo5ad Ds/J
000994   STOCK a Myo5ad Mregdsu/J
000286   STOCK a/a Myo5ad fd/+ +/J
View Strains carrying   Myo5ad     (42 strains)

Strains carrying other alleles of Ednrb
003295   B6;129-Ednrbtm1Ywa/J
000308   SSL/LeJ
004711   STOCK Ednrbs-52Pub
View Strains carrying other alleles of Ednrb     (3 strains)

View Strains carrying other alleles of Hc     (5 strains)

Strains carrying other alleles of Myo5a
005012   A.B6 Tyr+-Myo5ad-l31J/J
001013   B10.D2/nSnJ-Myo5ad-n/J
000502   B6 x B6CBCa Aw-J/A-Myo5aflr Gnb5flr/J
000963   DBA/2J-Myo5ad+17J/Myo5ad/J
000964   DBA/2J-Myo5ad+18J/Myo5ad/J
000067   DBA/2J-Myo5ad+2J/Myo5ad/J
000253   DLS/LeJ
View Strains carrying other alleles of Myo5a     (7 strains)

Phenotypic Data

Mouse Phenome Database
Festing Inbred Strain Characteristics: I

Additional Web Information

Genetic Quality Control Annual Report
JAX® NOTES, April 1988; 433. H-2 Haplotypes of Mice from Jackson Laboratory Production Colonies.

Animal Health Reports

Room Number           FGB29

Research Applications

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

Neurobiology Research
Angelman syndrome
Neurodevelopmental Defects (acallosal)
Vestibular and Hearing Defects (Age related hearing loss, control)

Reproductive Biology Research
Developmental Defects Affecting Gonads
Fertility Defects

Sensorineural Research
Vestibular and Hearing Defects (Age related hearing loss, control)

Ednrbs related

Dermatology Research
Color and White Spotting Defects

Developmental Biology Research
Neural Crest Defects
Neurodevelopmental Defects

Mouse/Human Gene Homologs
Hirschsprung disease

Neurobiology Research
Neurodevelopmental Defects
Receptor Defects
Vestibular and Hearing Defects

Sensorineural Research
Vestibular and Hearing Defects

Hc0 related

Immunology and Inflammation Research
Immunodeficiency (specific complement deficiency)

Research Tools
Immunology and Inflammation Research (specific complement deficiency) (C5 complement)

Myo5ad related

Dermatology Research
Color and White Spotting Defects

Mouse/Human Gene Homologs
Griscelli Syndrome

References

Selected Reference(s)

Albertini DF; Eppig JJ. 1995. Unusual cytoskeletal and chromatin configurations in mouse oocytes that are atypical in meiotic progression. Dev Genet 16(1):13-9. [PubMed: 7758242]  [MGI Ref ID J:109918]

Hosoda K; Hammer RE; Richardson JA; Baynash AG; Cheung JC; Giaid A; Yanagisawa M. 1994. Targeted and natural (piebald-lethal) mutations of endothelin-B receptor gene produce megacolon associated with spotted coat color in mice. Cell 79(7):1267-76. [PubMed: 8001159]  [MGI Ref ID J:22206]

Wahlsten D; Bulman-Fleming B. 1994. Retarded growth of the medial septum: a major gene effect in acallosal mice. Brain Res Dev Brain Res 77(2):203-14. [PubMed: 8174229]  [MGI Ref ID J:16942]

Wahlsten D; Ozaki HS; Livy D. 1992. Deficient corpus callosum in hybrids between ddN and three other abnormal mouse strains. Neurosci Lett 136(1):99-101. [PubMed: 1635672]  [MGI Ref ID J:2581]

Wahlsten D; Schalomon PM. 1994. A new hybrid mouse model for agenesis of the corpus callosum. Behav Brain Res 64(1-2):111-7. [PubMed: 7840877]  [MGI Ref ID J:21337]

Additional References

Price and Supply Information

Strain Name: I/LnJ
Stock Number: 000674

Price Details

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Supply Details

Standard SupplyRepository-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 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.
LicensingSee General Terms and Conditions below  

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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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