Overview

Also Known As:I Lyon, I/Lyn, I/FnLn

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).

Genetic overview

Genetic Background	Generation

View Genetics

Research Applications

Reproductive Biology Research
Sensorineural Research
Neurobiology Research
Cancer Research
Immunology, Inflammation and Autoimmunity Research
Research Tools
Dermatology Research
Mouse/Human Gene Homologs

View All Research Applications

Details

Detailed 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. 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 (Ednrb^s). 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.

Control Suggestions

None Available

Additional Information

Considerations for Choosing Controls

Selected References

Albertini DF; Eppig JJ. 1995. Unusual cytoskeletal and chromatin configurations in mouse oocytes that are atypical in meiotic progression. Dev Genet 16(1):13-9PubMed: 7758242 MGI: J:109918
Bender PK; Lalley PA. 1989. I/Lyn mouse phosphorylase kinase deficiency: mutation disrupts expression of the alpha/alpha'-subunit mRNAs. Proc Natl Acad Sci U S A 86(24):9996-10000PubMed: 2602386 MGI: J:10186
Case LK; Petell L; Yurkovetskiy L; Purdy A; Savage KJ; Golovkina TV. 2008. Replication of beta- and gammaretroviruses is restricted in I/LnJ mice via the same genetic mechanism. J Virol 82(3):1438-47PubMed: 18057254 MGI: J:163153
Case LK; Purdy A; Golovkina TV. 2005. Molecular and cellular basis of the retrovirus resistance in I/LnJ mice. J Immunol 175(11):7543-9PubMed: 16301663 MGI: J:122155
Denzin LK; Khan AA; Virdis F; Wilks J; Kane M; Beilinson HA; Dikiy S; Case LK; Roopenian D; Witkowski M; Chervonsky AV; Golovkina TV. 2017. Neutralizing Antibody Responses to Viral Infections Are Linked to the Non-classical MHC Class II Gene H2-Ob. Immunity 47(2):310-322.e7PubMed: 28813660 MGI: J:254532
Doran AG; Wong K; Flint J; Adams DJ; Hunter KW; Keane TM. 2016. Deep genome sequencing and variation analysis of 13 inbred mouse strains defines candidate phenotypic alleles, private variation and homozygous truncating mutations. Genome Biol 17(1):167PubMed: 27480531 MGI: J:262923
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):1267-76PubMed: 8001159 MGI: J:22206
Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11PubMed: 15081119 MGI: J:89298
Timmermans S; Van Montagu M; Libert C. 2017. Complete overview of protein-inactivating sequence variations in 36 sequenced mouse inbred strains. Proc Natl Acad Sci U S A 114(34):9158-9163PubMed: 28784771 MGI: J:244295
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):203-14PubMed: 8174229 MGI: J:16942
Wahlsten D; Schalomon PM. 1994. A new hybrid mouse model for agenesis of the corpus callosum. Behav Brain Res 64(1-2):111-7PubMed: 7840877 MGI: J:21337

View All References

Genetics

Myo5a^d

Allele Symbol: Myo5a^d

Allele Name	dilute
Allele Type	Spontaneous
Allele Synonym(s)	blue dilution; d; d^v; 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 Myo5a^d gene. Reversions of Myo5a^d to wild-type are caused by excision of the virus leaving exactly one long terminal repeat in place.

Ednrb^s

Allele Symbol: Ednrb^s

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.

Ahr^d

Allele Symbol: Ahr^d

Allele Name	d variant
Allele Type	Not Applicable
Allele Synonym(s)	ah; Ah^d; Ah^k; 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.

Hc⁰

Allele Symbol: Hc⁰

Allele Name	deficient
Allele Type	Spontaneous
Allele Synonym(s)	C5-; C5-d; C5-def; C5-deficient; Hc^Hfib2; hc^o
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.

H2-Ob^vic1

Allele Symbol: H2-Ob^vic1

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.

Il3ra^m1

Allele Symbol: Il3ra^m1

Allele Name	mutation 1
Allele Type	Spontaneous
Allele Synonym(s)	Il3ra^A/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.

Phka1^I/FnLn

Allele Symbol: Phka1^I/FnLn

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.

Gpr84^del

Allele Symbol: Gpr84^del

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.

Mx1^s2

Allele Symbol: Mx1^s2

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 Mx1^r. The Mx1^r 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 Mx1^s1 allele which produces mRNA lacking exons 9, 10, and 11 of the Mx1^r 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 Mx1^s2 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.

Cox7a2l^l

Allele Symbol: Cox7a2l^l

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⁺ Itpr3^tf/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.

B2m^a

Allele Symbol: B2m^a

Allele Name	a variant
Allele Type	Spontaneous (Not Applicable)
Allele Synonym(s)
Gene Symbol and Name	B2m, beta-2 microglobulin
Gene Synonym(s)
Strain of Origin	multiple strains
Chromosome	2
Molecular Note	The a variant is slightly slower running on SDS PAGE and was found to have an aspartic acid at amino acid position 85. This allele is found in A, BALB/c, LP and most other strains.

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

glycogen storage disease IXd

Research Areas By Phenotype

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

Reproductive Biology Research
- Developmental Defects Affecting Gonads
- Fertility Defects
Sensorineural Research
- Hearing Defects
  - Age related hearing loss, control
Neurobiology Research
- Neurodevelopmental Defects
  - acallosal
- Hearing Defects
  - Age related hearing loss, control
- Angelman syndrome

Genotype: H2-Ob^vic1 related

Cancer Research
Virology Research
Immunology, Inflammation and Autoimmunity Research

Genotype: Hc⁰ related

Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - specific complement deficiency
Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - specific complement deficiency, C5 complement

Genotype: Il3ra^m1 related

Immunology, Inflammation and Autoimmunity Research
- CD Antigens, Antigen Receptors, and Histocompatibility Markers
  - genes regulating susceptibility to infectious disease and endotoxin

Genotype: Myo5a^d related

Dermatology Research
- Color and White Spotting Defects
Mouse/Human Gene Homologs
- Griscelli Syndrome

Genotype: Ednrb^s related

Neurobiology Research
- Receptor Defects
- Hearing Defects
- Neurodevelopmental Defects
Sensorineural Research
- Hearing Defects
Mouse/Human Gene Homologs
- Hirschsprung disease
Dermatology Research
- Color and White Spotting Defects
Developmental Biology Research
- Neural Crest Defects
- Neurodevelopmental Defects

Genotype: Ahr^d related

Metabolism Research
Research Tools
- Toxicology Research

Mammalian Phenotype Terms by Genotype

The following phenotype relates to a compound genotype created using this strain

Genotype: Phka1^I/FnLn/Y
I/FnLn

homeostasis/metabolism phenotype

increased skeletal muscle glycogen level
- the glycogen content of resting skeletal muscle in hemizygous males is three fold higher than that in C57BL/FnLn controls, with a mean of 13.1mg/g tissue versus 4mg/g

muscle phenotype

increased skeletal muscle glycogen level
- the glycogen content of resting skeletal muscle in hemizygous males is three fold higher than that in C57BL/FnLn controls, with a mean of 13.1mg/g tissue versus 4mg/g

Genotype: Phka1^I/FnLn/Phka1^I/FnLn
I/FnLn

homeostasis/metabolism phenotype

increased skeletal muscle glycogen level
- the glycogen content of resting skeletal muscle is two to three fold higher than that in C57BL/FnLn controls, with a mean of 11.5mg/g tissue versus 4.4mg/g, and epinephrine does not induce phosphorylase kinase activity

muscle phenotype

increased skeletal muscle glycogen level
- the glycogen content of resting skeletal muscle is two to three fold higher than that in C57BL/FnLn controls, with a mean of 11.5mg/g tissue versus 4.4mg/g, and epinephrine does not induce phosphorylase kinase activity

Genotype: H2-Ob^vic1/H2-Ob^vic1
I/LnJ

immune system phenotype

decreased susceptibility to viral infection
- toxic immune responses, but not interleukin 12
- although MMTV and MuLV infection can occur, MMTV transmission and mammary tumor induction are blocked and MuLV transmission and virally induced disease are blocked, and these responses are mediated by anti-virion antibodies, require gamma interferon, cytotoxic immune responses, but not interleukin 12

decreased susceptibility to Retroviridae infection
- although MMTV and MuLV infection can occur, MMTV transmission and mammary tumor induction are blocked and MuLV transmission and virally induced disease are blocked, and these responses are mediated by anti-virion antibodies, require gamma interferon, cytotoxic immune responses, but not interleukin 12

neoplasm

decreased incidence of induced tumors
- mammary glands become infected with MMTV but at 1.5 years zero of 24 infected females develop tumors

Phenotype Information

Festing Inbred Strain Characteristics: I

References

Albertini DF; Eppig JJ. 1995. Unusual cytoskeletal and chromatin configurations in mouse oocytes that are atypical in meiotic progression. Dev Genet 16(1):13-9PubMed: 7758242 MGI: J:109918
Bender PK; Lalley PA. 1989. I/Lyn mouse phosphorylase kinase deficiency: mutation disrupts expression of the alpha/alpha'-subunit mRNAs. Proc Natl Acad Sci U S A 86(24):9996-10000PubMed: 2602386 MGI: J:10186
Case LK; Petell L; Yurkovetskiy L; Purdy A; Savage KJ; Golovkina TV. 2008. Replication of beta- and gammaretroviruses is restricted in I/LnJ mice via the same genetic mechanism. J Virol 82(3):1438-47PubMed: 18057254 MGI: J:163153
Case LK; Purdy A; Golovkina TV. 2005. Molecular and cellular basis of the retrovirus resistance in I/LnJ mice. J Immunol 175(11):7543-9PubMed: 16301663 MGI: J:122155
Denzin LK; Khan AA; Virdis F; Wilks J; Kane M; Beilinson HA; Dikiy S; Case LK; Roopenian D; Witkowski M; Chervonsky AV; Golovkina TV. 2017. Neutralizing Antibody Responses to Viral Infections Are Linked to the Non-classical MHC Class II Gene H2-Ob. Immunity 47(2):310-322.e7PubMed: 28813660 MGI: J:254532
Doran AG; Wong K; Flint J; Adams DJ; Hunter KW; Keane TM. 2016. Deep genome sequencing and variation analysis of 13 inbred mouse strains defines candidate phenotypic alleles, private variation and homozygous truncating mutations. Genome Biol 17(1):167PubMed: 27480531 MGI: J:262923
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):1267-76PubMed: 8001159 MGI: J:22206
Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11PubMed: 15081119 MGI: J:89298
Timmermans S; Van Montagu M; Libert C. 2017. Complete overview of protein-inactivating sequence variations in 36 sequenced mouse inbred strains. Proc Natl Acad Sci U S A 114(34):9158-9163PubMed: 28784771 MGI: J:244295
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):203-14PubMed: 8174229 MGI: J:16942
Wahlsten D; Schalomon PM. 1994. A new hybrid mouse model for agenesis of the corpus callosum. Behav Brain Res 64(1-2):111-7PubMed: 7840877 MGI: J:21337

Additional References

Baynash AG; Hosoda K; Giaid A; Richardson JA; Emoto N; Hammer RE; Yanagisawa M. 1994. Interaction of endothelin-3 with endothelin-B receptor is essential for development of epidermal melanocytes and enteric neurons. Cell 79(7):1277-85PubMed: 8001160 MGI: J:22207
Golovkina TV. 2000. A novel mechanism of resistance to mouse mammary tumor virus infection. J Virol 74(6):2752-9PubMed: 10684291 MGI: J:60602
International Nomenclature Committee. 1952. COMMITTEE on Standardized Nomenclature for Inbred Strains of Mice Cancer Res 12(8):602-13PubMed: 14945054 MGI: J:166288
Lyon JB Jr. 1970. The X-chromosome and the enzymes controlling muscle glycogen: phosphorylase kinase. Biochem Genet 4(1):169-85PubMed: 5444100 MGI: J:5156
Michaelson J. 1983. Genetics of beta-2 microglobulin in the mouse. Immunogenetics 17(3):219-60PubMed: 6187676 MGI: J:7014
Poland A; Glover E. 1990. Characterization and strain distribution pattern of the murine Ah receptor specified by the Ahd and Ahb-3 alleles. Mol Pharmacol 38(3):306-12PubMed: 2169579 MGI: J:34840
Purdy A; Case L; Duvall M; Overstrom-Coleman M; Monnier N; Chervonsky A; Golovkina T. 2003. Unique Resistance of I/LnJ Mice to a Retrovirus Is Due to Sustained Interferon gamma-dependent Production of Virus-neutralizing Antibodies. J Exp Med 197(2):233-43PubMed: 12538662 MGI: J:81554
Schneider A; Davidson JJ; Wullrich A; Kilimann MW. 1993. Phosphorylase kinase deficiency in I-strain mice is associated with a frameshift mutation in the alpha subunit muscle isoform. Nat Genet 5(4):381-5PubMed: 8298647 MGI: J:15833
Wahlsten D; Ozaki HS; Livy D. 1992. Deficient corpus callosum in hybrids between ddN and three other abnormal mouse strains. Neurosci Lett 136(1):99-101PubMed: 1635672 MGI: J:2581

Additional - Ahr^d related

Additional - B2m^a related

Additional - Cox7a2l^l related

Additional - Ednrb^s related

Additional - Gpr84^del related

Additional - H2-Ob^vic1 related

Additional - Hc⁰ related

Additional - Il3ra^m1 related

Additional - Mx1^s2 related

Additional - Myo5a^d related

Additional - Phka1^I/FnLn related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Genotyping resources and troubleshooting
Mating System
- Sibling x Sibling
Appearance
- pink-eyed dilute brown, piebald (spotted)
  Related Genotype: a/a Tyrp1^b/Tyrp1^b Oca2^p/Oca2^p Myo5a^d/Myo5a^d Ednrb^s/Ednrb^s
Citation
When using the I Lyon mouse strain in a publication, please include JAX stock #000674 in your Materials and Methods section.

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Overview

Also Known As:I Lyon, I/Lyn, I/FnLn

Genetic overview

Research Applications

Details

Detailed Description

Control Suggestions

Additional Information

Selected References

Genetics

Myo5ad

Allele Symbol: Myo5ad

Ednrbs

Allele Symbol: Ednrbs

Ahrd

Allele Symbol: Ahrd

Hc0

Allele Symbol: Hc0

H2-Obvic1

Allele Symbol: H2-Obvic1

Il3ram1

Allele Symbol: Il3ram1

Phka1I/FnLn

Allele Symbol: Phka1I/FnLn

Gpr84del

Allele Symbol: Gpr84del

Mx1s2

Allele Symbol: Mx1s2

Cox7a2ll

Allele Symbol: Cox7a2ll

B2ma

Allele Symbol: B2ma

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Research Areas By Phenotype

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

Genotype: H2-Obvic1 related

Genotype: Hc0 related

Genotype: Il3ram1 related

Genotype: Myo5ad related

Genotype: Ednrbs related

Genotype: Ahrd related

Mammalian Phenotype Terms by Genotype

Genotype: Phka1I/FnLn/YI/FnLn

homeostasis/metabolism phenotype

muscle phenotype

Genotype: Phka1I/FnLn/Phka1I/FnLnI/FnLn

homeostasis/metabolism phenotype

muscle phenotype

Genotype: H2-Obvic1/H2-Obvic1I/LnJ

immune system phenotype

neoplasm

Phenotype Information

References

Additional References

Additional - Ahrd related

Additional - B2ma related

Additional - Cox7a2ll related

Additional - Ednrbs related

Additional - Gpr84del related

Additional - H2-Obvic1 related

Additional - Hc0 related

Additional - Il3ram1 related

Additional - Mx1s2 related

Additional - Myo5ad related

Additional - Phka1I/FnLn related

Technical Support

Genotyping Protocols

Mating System

Appearance

Citation

Strain Interest Registration

Contact Information

Interest

Terms Of Use

Terms Of Use

Licensing Information

Related Strains

Myo5a^d

Allele Symbol: Myo5a^d

Ednrb^s

Allele Symbol: Ednrb^s

Ahr^d

Allele Symbol: Ahr^d

Hc⁰

Allele Symbol: Hc⁰

H2-Ob^vic1

Allele Symbol: H2-Ob^vic1

Il3ra^m1

Allele Symbol: Il3ra^m1

Phka1^I/FnLn

Allele Symbol: Phka1^I/FnLn

Gpr84^del

Allele Symbol: Gpr84^del

Mx1^s2

Allele Symbol: Mx1^s2

Cox7a2l^l

Allele Symbol: Cox7a2l^l

B2m^a

Allele Symbol: B2m^a

Genotype: H2-Ob^vic1 related

Genotype: Hc⁰ related

Genotype: Il3ra^m1 related

Genotype: Myo5a^d related

Genotype: Ednrb^s related

Genotype: Ahr^d related

Genotype: Phka1^I/FnLn/Y
I/FnLn

Genotype: Phka1^I/FnLn/Phka1^I/FnLn
I/FnLn

Genotype: H2-Ob^vic1/H2-Ob^vic1
I/LnJ

Additional - Ahr^d related

Additional - B2m^a related

Additional - Cox7a2l^l related

Additional - Ednrb^s related

Additional - Gpr84^del related

Additional - H2-Ob^vic1 related

Additional - Hc⁰ related

Additional - Il3ra^m1 related

Additional - Mx1^s2 related

Additional - Myo5a^d related

Additional - Phka1^I/FnLn related