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).
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. 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). 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.
|Allele Name||d variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||Ahd; Ahk; AhRd; Ahhn; ah; in|
|Gene Symbol and Name||Ahr, aryl-hydrocarbon receptor|
|Gene Synonym(s)||Ah; Ah; Ahh; Ahh; Ahre; Ahre; In; In; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; bHLHe76; dioxin receptor; inflammatory reactivity|
|Strain of Origin||Not Applicable|
|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 Synonym(s)||pied spotting; s|
|Gene Symbol and Name||Ednrb, endothelin receptor type B|
|Gene Synonym(s)||ABCDS; AU022549; ET-B; ET-BR; ETB; ETB1; ETBR; ETR-b; ETRB; ETb; Ednra; Etb; HSCR; HSCR2; Sox10m1; WS4A; expressed sequence AU022549; piebald; s|
|Strain of Origin||old mutant of the mouse fancy|
|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 Synonym(s)||C5-; C5-d; C5-def; C5-deficient; hco|
|Gene Symbol and Name||Hc, hemolytic complement|
|Gene Synonym(s)||C5; C5; C5D; C5a; C5b; CPAMD4; ECLZB; He; He|
|Strain of Origin||multiple strains|
|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.|
|Allele Synonym(s)||Maltese dilution; blue dilution; d; dv|
|Gene Symbol and Name||Myo5a, myosin VA|
|Gene Synonym(s)||9630007J19Rik; 9630007J19Rik; AI413174; AI661011; D; Dbv; Dbv; Dop; GS1; MVa; MYH12; MYO5; MYR12; Myh12; Myo5; Myo5; MyoVA; RIKEN cDNA 9630007J19 gene; d; dilute; expressed sequence AI413174; expressed sequence AI661011; flail; flail; flailer; flr; myosin V; nmf244|
|Strain of Origin||old mutant of the mouse fancy|
|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.|
|Gene Symbol and Name||Phka1, phosphorylase kinase alpha 1|
|Gene Synonym(s)||9830108K24Rik; 9830108K24Rik; PHKA; Pcyt1b; Phka; Phka; RIKEN cDNA 9830108K24 gene; phosphorylase kinase alpha|
|Strain of Origin||I/FnLn|
|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 inmuscle extracts.|
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided,
their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of
each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders
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