This strain is currently unavailable due to replenishing of cryopreserved stocks. Customers who register interest will be contacted when the strain is available again.
I inbred mice are a piebald strain that lacks a corpus callosum and exhibits behaviors consistent with attention deficit hyperactivity disorder (ADHD). They are resistant to mouse mammary tumor virus (MMTV) and generate neutralizing antibodies to MMTV and Murine Leukemia Virus (MuLv).
Read More +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. I/LnJ mice are resistant to MMTV induced mammary tumor development and generate neutralizing antibodies to MMTV and MuLv virions that effectively block viral transmission. This phenotype was traced to the I/LnJ loss-of-function allele, vic1, in H2-Ob (Denzin et al., 2017). Due to a frameshift mutation in alpha 1 phosphorylase kinase these mice have increased glycogen content in resting skeletal muscle. 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). Thus, these 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. Although kinked tail is not a phenotype noted at birth, approximately 10% of pups at wean age and 20% of breeders have a single kink in the tail. This phenotype was recorded in 2006, and whether this strain characteristic was part of the original phenotype of this inbred strain or arose subsequent to inbreeding is not known.
Allele Name | dilute |
---|---|
Allele Type | Spontaneous |
Allele Synonym(s) | blue dilution; d; dv; Maltese dilution |
Gene Symbol and Name | Myo5a, myosin VA |
Gene Synonym(s) | |
Strain of Origin | old mutant of the mouse fancy |
Chromosome | 9 |
Molecular Note | This mutation is the result of the integration of ecotropic murine leukemia virus Emv-3 into a noncoding region of the Myo5ad gene. Reversions of Myo5ad to wild-type are caused by excision of the virus leaving exactly one long terminal repeat in place. |
Allele Name | piebald |
---|---|
Allele Type | Spontaneous |
Allele Synonym(s) | pied spotting; s |
Gene Symbol and Name | Ednrb, endothelin receptor type B |
Gene Synonym(s) | |
Strain of Origin | old mutant of the mouse fancy |
Chromosome | 14 |
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. |
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. |
Allele Name | d variant |
---|---|
Allele Type | Not Applicable |
Allele Synonym(s) | ah; Ahd; Ahk; Ahhn; AhRd; in |
Gene Symbol and Name | Ahr, aryl-hydrocarbon receptor |
Gene Synonym(s) | |
Strain of Origin | Not Applicable |
Chromosome | 12 |
General Note | Strain of origin - this allele was found in DBA/2J, AKR/J, 129, SWR, RF, NZB strains |
Molecular Note | This allele encodes a 104 kDa receptor that is stabilized by molybdate and has an affinity for ligand 10-100 fold lower than that of the receptor produced by the C57BL/6J allele. PCR sequencing of cDNA revealed ten nucleotide differences between the coding sequences of the DBA/2J and C57BL/6J receptors. Five of the ten differences would cause amino acid changes. One of these, an apparent T to C transition replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the DBA/2J allele. This change would extend translation of the DBA/2J mRNA by 43 amino acids, accounting for the larger size of the peptide produced by this allele (104 kDa vs 95 kDa for the C57BL/6J allele). A second T to C transition changes a leucine codon in the C57BL/6J allele to a proline codon in the DBA/2J allele, and would likely change secondary structure of the peptide and thus ligand affinity. |
Allele Name | deficient |
---|---|
Allele Type | Spontaneous |
Allele Synonym(s) | C5-; C5-d; C5-def; C5-deficient; HcHfib2; hco |
Gene Symbol and Name | Hc, hemolytic complement |
Gene Synonym(s) | |
Strain of Origin | multiple strains |
Chromosome | 2 |
General Note | This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, A/J, 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, A/J, AKR/J, DBA/2J, I/LnJ, KK/HlJ, MOLF/EiJ, NZB/B1NJ, RF/J, ST/bJ 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. |
Allele Name | virus infectivity controller 1 |
---|---|
Allele Type | Spontaneous (Null/Knockout) |
Allele Synonym(s) | |
Gene Symbol and Name | H2-Ob, histocompatibility 2, O region beta locus |
Gene Synonym(s) | |
Strain of Origin | I/LnJ |
Chromosome | 17 |
Molecular Note | This I/LnJ loss-of-function variant has eight nucleotide substitutions in the 5-prime and four nucleotide substitutions in the 3-prime non-coding regions and four coding mutations that cause the amino acid substitutions S128N, V148I, L167H, and E239K. |
Allele Name | mutation 1 |
---|---|
Allele Type | Spontaneous |
Allele Synonym(s) | Il3raA/J; Il3ran |
Gene Symbol and Name | Il3ra, interleukin 3 receptor, alpha chain |
Gene Synonym(s) | |
Strain of Origin | multiple strains |
Chromosome | 14 |
General Note | This allele has been identified in A/J, A/WySnJ, A/HeJ, C58/J, RF/J, AKR/J, SM/J, BUB/BnJ, CE/J, and NZB/B1NJ. see J:24918. |
Molecular Note | Sequence analysis revealed A/J mice lack the sequence corresponding to exon 8, which encodes 10 amino acid residues in the extracellular domain. Aberrant splicing was due to a 5 base pair deletion at the branch point in intron 7. |
Allele Name | I/FnLn |
---|---|
Allele Type | Spontaneous |
Allele Synonym(s) | |
Gene Symbol and Name | Phka1, phosphorylase kinase alpha 1 |
Gene Synonym(s) | |
Strain of Origin | I/FnLn |
Chromosome | X |
Molecular Note | An insertion of a T residue after codon 429 results in a frameshift and premature termination 17 codons downstream which is only approximately one third of the normal protein length. Northern blot analysis reveals a great reduction of this transcript in muscle extracts. |
Allele Name | deletion |
---|---|
Allele Type | Spontaneous (Null/Knockout) |
Allele Synonym(s) | |
Gene Symbol and Name | Gpr84, G protein-coupled receptor 84 |
Gene Synonym(s) | |
Strain of Origin | multiple strains |
Chromosome | 15 |
Molecular Note | This spontaneously arising frameshift deletion is located in exon 2 at position 103308576 bp (NCBI Build 37) and results in a premature stop codon. The mutation is predicted to result in a truncated protein lacking the transmembrane domains 4-7. The inbred strains BDP/J, DBA/1J, DBA/2J, I/LnJ, FVB/NJ, LG/J, MRL/MpJ, NODShi/LtJ, NOR/LtJ, P/J, PL/J, SKHIN/Sprd, SJL/J, SM/J are homozygous for the deletion. The allele is segregating in the outbred stocks ICR and CD-1. |
Allele Name | myxovirus susceptibility 2 |
---|---|
Allele Type | Spontaneous (Null/Knockout) |
Allele Synonym(s) | |
Gene Symbol and Name | Mx1, MX dynamin-like GTPase 1 |
Gene Synonym(s) | |
Strain of Origin | multiple strains |
Chromosome | 16 |
General Note | The Mx genes determine resistance to the lethal effects of various myxoviruses including neurotropic avian influenza A virus injected intracerebrally, pneumotropic strains injected intranasally, and a hepatotropic strain injected intraperitoneally (J:5645, J:13136). Resistance is not dependent on presence of the thymus and is not abolished by immunosuppression or by inhibitors of macrophage function (J:5735, J:5478, J:5645). Resistance is specific for the orthomyxoviruses (J:6265). It is dependent on the presence of interferon-alpha and -beta but not -gamma (J:7365). The resistance allele at the Mx1 locus, under induction by alpha/beta interferon, produces the 75 kDa protein MX-1, which confers resistance to the influenza virus, in the nuclei of cells carrying the allele. Susceptibility alleles do not produce the protein (J:8273). The protein is located in the nucleus (J:7703) and produces its antiviral effect by preventing synthesis of viral mRNA in the nucleus (J:7992). Nuclear localization is necessary for anti-influenza virus activity (J:1417), but mutations induced in Mx1 showed that nuclear position was not sufficient for the effect; mutations in several domains can cause its loss (J:11840). The MX-1 protein is a GTPase containing a GTP binding domain (J:1417) and this binding core is also necessary (J:21243). Resistance is expressed by macrophages and other cells in vitro (J:6649, J:5940) but could not be transferred to susceptible animals by transfer of macrophages from resistant mice (J:6149). Resistance to infection with two tick-borne viruses, Thogoto virus (J:8273) and Dhori virus (J:27760), is also conferred by Mx1r. The Mx1r allele occurs only in strains A2G, SL/NiA, and T9, the latter being a strain derived from an influenza-resistant wild stock, and CAST/Ei, derived from Mus musculus castaneus. Most inbred strains, including C57BL/6J, C3H/HeJ, and BALB/cJ, carry an influenza susceptible Mx1s1 allele which produces mRNA lacking exons 9, 10, and 11 of the Mx1r allele. This large deletion apparently renders the protein incapable of providing resistance to influenza. The CBA/J, CE/J, I/LnJ, and PERA/Ei strains, also susceptible to the virus, have another form of the Mx1s2 allele in which there is a nonsense mutation (J:9452). Interferon is induced by viral infection and in turn induces the Mx protein (J:7703). Although some interferon-induced genes respond directly to virus invasion as well as indirectly through induction by virus-induced interferon, this primary response is very weak for the MX-1 protein in response to either influenza or Newcastle disease viruses (J:1892). |
Molecular Note | CBA/J, CE/J, I/LnJ and PERA/Ei strains have a nonsense mutation that results in a null allele and susceptibility to myxoviruses. |
Allele Name | long |
---|---|
Allele Type | Not Applicable (Not Specified) |
Allele Synonym(s) | SCAF1113 |
Gene Symbol and Name | Cox7a2l, cytochrome c oxidase subunit 7A2 like |
Gene Synonym(s) | |
Strain of Origin | multiple strains |
Chromosome | 17 |
General Note | Querying the sequences of the Sanger Mouse Genomes Project reveals that the short allele with its 6 bp deletion exists in C57BL/6J, C57BL/10J, C57BL/6NJ, C58/J, BALB/cJ, C3H/HeH, 129S5/SvEvBrd, NZW/LacZ, and SEA/GnJ, but the long allele lacking the deletion exists in 129S1/SvImJ, A/J, AKR/J, BTBR T+ Itpr3tf/J, BUB/BnJ, C3H/HeJ, C57BR/cdJ, C57L/J, CAST/EiJ, CBA/J, DBA/1J, DBA/2J, FVB/NJ, I/LnJ, KK/HiJ, LEWES/EiJ, LP/J, MOLF/EiJ, NOD/ShiLtJ, NZB/BlNJ, NZO/HlLtJ, PWK/PhJ, RF/J, SPRET/EiJ, ST/bJ, WSB/EiJ, ZALENDE/EiJ. |
Molecular Note | This allele encodes the long isoform with 113 amino acids. It is found in 129S2/SvPasCrl, CBA/CaOlaHsd, Hsd:ICR, and NZB/OlaHsd. |
When using the I Lyon mouse strain in a publication, please include JAX stock #000674 in your Materials and Methods section.
What information were you hoping to find through your search?
How easy was it to find what you were looking for?
We may wish to follow up with you. Enter your email if you are happy for us to connect and reachout to you with more questions.
Please Enter a Valid Email Address
Thank you for sharing your feedback! We are working on improving the JAX Mice search. Come back soon for exciting changes.