Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. 129P3/J is one of the parental substrains.Read More +
This strain is homozygous for Cdh23ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss with onset prior to three months of age.
Historically, the 129 inbred mice are known for the high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. (1-3% in 129 parental substrains; 30% in teratoma substrains.) More recently, 129 mice are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. There is major genetic variation within the 129 "family", which has led to an update of the nomenclature and a division of the substrains into three major groups: parental substrains (129P), steel substrains (129S) and "teratoma" substrains (129T). Investigators using 129 substrains for targeted mutagenesis should be careful in the selection of the appropriate 129 substrain to match the embryonic stem cell line. For a complete history of the numerous 129 substrains, see Simpson et al. 1997.
Derivative of strain 101 (L.C. Dunn) when mice from two sublines maintained by Hunt (Tyrc-ch Oca2p / Tyrc-ch Oca2p) and Wynder (Tyrc Oca2p / Tyrc Oca2p) respectively were sent to The Jackson Laboratory in 1948 after the 1947 fire and a cross was made between them. Offspring of the cross gave rise to the Rl, Re, and Rr sublines, the latter giving rise to the 129P3/J substrain, which is maintained as a segregating inbred for Tyrc-ch and Tyrc.
|Allele Name||MCF resistant|
|Allele Synonym(s)||Rmcfr; MCF resistant|
|Gene Symbol and Name||Rmcf, resistance to MCF virus|
|Strain of Origin||multiple strains|
|General Note|| |
This locus controls resistance and susceptibility of cells in tissue culture to infection by mink cell focus-forming murine leukemia viruses. The allele Rmcfr determines resistance and occurs in strains DBA/1, DBA/2, and CBA/Ca; the allele Rmcfs determines susceptibility and occurs in strains AKR/J, C57BL/6, BALB/c, CBA/J, NFS, NZB, 129/J, and many others. Heterozygotes are as resistant as the resistant parent or nearly so. Rmcf is different from and independent of Fv1, a locus that controls susceptibility to infection by ecotropic viruses. Rmcf is located on Chr 5 close to Hm near the centromeric end (J:7108). Rmcfr protects (AKR x CBA/Ca)F1 and (AKR x DBA/2)F1 hybrids from development of spontaneous thymic lymphomas and reduces the incidence of MCF-induced thymic lymphomas (J:7175). It also reduces susceptibility of cells of Sxvs/Sxvr mice to exogenous xenotropic viruses (J:7951). In addition, in strains susceptible to Friend virus-induced erythroleukemia, a condition thought to be due to the replication of MCF virus, Rmcfr increases resistance to the virus-induced erythroleukemia. It may cause resistance by coding for or regulating the production of an MCF-related envelope glycoprotein that blocks the receptor for MCF viruses (J:8074). This conclusion is reinforced by the findings of Buller et al. (J:8497), who showed that the Rmcfr allele contains an endogenous MCF gp70 env gene and that the Rmcfs allele, at least in some strains (C57BL/6, CBA/J, and A/WySn), contains a xenotropic gp70 env gene. Presumably the MCF gp70 inhibits exogenous MCF infection in vitro by a mechanism of viral interference.
|Molecular Note||This locus controls resistance of cells to infection by mink cell focus-forming murine leukemia viruses. The dominant r (resistance) allele is found in strains DBA/1, DBA/2 and CBA/Ca.|
|Allele Synonym(s)||deletion; Disc1del|
|Gene Symbol and Name||Disc1, disrupted in schizophrenia 1|
|Gene Synonym(s)||SCZD9; C1orf136|
|Strain of Origin||various|
|General Note||This deletion appears in multiple strains of the 129 superfamily, 101/RI, BTBR T+ tf/J, LP/J, FVB/NJ, SJL/J, SWR/J and DDY/JclSidSeyFrkJ (J:111837, J:195189).|
|Molecular Note||A 25 bp deletion of the locus causes a frame shift in the reading frame, resulting in 13 novel amino acids and a premature stop codon at exon 7.|
|Allele Name||age related hearing loss 1|
|Allele Synonym(s)||age related hearing loss 1; Cdh23ahl|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|Gene Synonym(s)||bob; bustling; bobby; nmf112; nmf252; nmf252; 4930542A03Rik; ahl; 4930542A03Rik; W; sals; mdfw; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; modifier of deaf waddler; age related hearing loss 1; v; USH1D; nmf181; RIKEN cDNA 4930542A03 gene; CDHR23; sals; waltzer; nmf112; nmf181; mdfw; neuroscience mutagenesis facility, 112; bus; ahl; bob; salsa; PITA5|
|Strain of Origin||multiple strains|
|Molecular Note||Genetic complementation tests have shown allelism between the mdfw (modifier of deaf waddler) locus and the ahl locus. Further analysis has shown this is caused by a G to A transition at nucleotide position 753 of Cdh23. This hypomorphic allele causes in frame skipping of exon 7, which is predicted to delete part of the 2nd and 3rd ectodomains, and cause reduced message stability. Twenty-seven strains classified with ahl and carrying the 753A allele include: CD-1, RBF/DnJ, PL/J, AKR/J, RF/J, BALB/cBy, A/WySnJ, P/J, SENCARA/PtJ, DBA/1J, ALS/LtJ, C58/J, C57BLKS/J, 129P1/ReJ, C57BR/cd, SKH2/J, BUB/Bn, MA/MyJ, LP/J, 129X1/SvJ, NOR/LtJ, A/J, C57BL/6, NOD/LtJ, 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.|
|Allele Name||d variant|
|Allele Type||Not Applicable|
|Allele Synonym(s)||Ahrd; d variant|
|Gene Symbol and Name||Ahr, aryl-hydrocarbon receptor|
|Gene Synonym(s)||bHLHe76; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; Ahh; dioxin receptor; In; Ah; Ahre; 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 Name||polymerase iota deficient|
|Allele Synonym(s)||Polid; polymerase iota deficient|
|Gene Symbol and Name||Poli, polymerase (DNA directed), iota|
|Gene Synonym(s)||Rad30b; RAD30B; RAD3OB; RAD30 (S. cerevisiae) homolog B; Rad30b; eta2|
|Strain of Origin||129|
|Molecular Note||A nonsense mutation changes codon 27 from serine (TCG) to an amber stop codon (TAG), and results in a truncated protein lacking any catalytic function. The allele was present in every 129 strain analyzed, including 129P3/J, 129X1/SvJ, 129P1/ReJ and 129P2/Ola. C57BL/6J and BALB/c mice did not contain the mutation.|
When using the 129P3/J mouse strain in a publication, please include JAX stock #000690 in your Materials and Methods section.
|Inbred, 1 pair minimum will be supplied|
We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.
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