129 inbred mice are characterized by a high incidence of spontaneous testicular teratomas, though the incidence differs between substrains. 129/SvJ mice, as well as mice from other 129 sublines, are widely used in the production of targeted mutations due to the availability of multiple embryonic stem cell lines derived from them. Major genetic variation exists between various sublines of the 129 "family".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.
In response to challenge, 129X1/SvJ mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease (Xie et al. 2004).
White et al. reported a variation in thioglycolate medium-induced peritoneal leukocyte recruitment in 4 analyzed strains. The response of total leukocyte recruitment, from greatest to least, was C57BL/6J>BALB/c>CD1>129X1/SvJ. Variations were also found in the timeline of response and cell types most impacted.
129X1/SvJ mice were transferred from the laboratory of Dr. Roy Stevens (Sv) at The Jackson Laboratory to the production colonies in 1982. Historical data and genetic analysis indicate that an accidental outcrossing of 129X1/Sv occurred prior to that transfer, sometime between 1977 and 1978, resulting in a change in coat color from Aw to a (white-bellied agouti to nonagouti) in the 129/Sv substrain.
|Allele Type||Spontaneous (Null/Knockout)|
|Gene Symbol and Name||Astn2, astrotactin 2|
|Gene Synonym(s)||1d8; Astnl; Astnl; astrotactin-like; bA67K19.1|
|Strain of Origin||129X1/SvJ|
|Molecular Note||The molecular lesion is a a ~30 kb deletion that encompasses exon 5 and has endpoints within a pair of LINE elements. PCR typing showed that the ~30 kb deletion is present in both R1 ES cells and in 129X1/SvJ mice, but not in the closely related 129S1/SvlmJ or 129S6/SvEvTac strains.|
|Allele Name||age related hearing loss 1|
|Allele Synonym(s)||Cdh23753A; mdfw|
|Gene Symbol and Name||Cdh23, cadherin 23 (otocadherin)|
|Gene Synonym(s)||4930542A03Rik; 4930542A03Rik; CDHR23; PITA5; RIKEN cDNA 4930542A03 gene; USH1D; W; age related hearing loss 1; ahl; ahl; bob; bob; bobby; bus; bustling; mdfw; mdfw; modifier of deaf waddler; neuroscience mutagenesis facility, 112; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; nmf112; nmf112; nmf181; nmf181; nmf252; nmf252; sals; sals; salsa; v; waltzer|
|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: CD1, 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 Synonym(s)||Disc1129S6; Disc1delta6|
|Gene Symbol and Name||Disc1, disrupted in schizophrenia 1|
|Gene Synonym(s)||C1orf136; SCZD9|
|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||polymerase iota deficient|
|Allele Synonym(s)||Poli-; Poli129|
|Gene Symbol and Name||Poli, polymerase (DNA directed), iota|
|Gene Synonym(s)||RAD30 (S. cerevisiae) homolog B; RAD30B; RAD3OB; Rad30b; 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.|
pink-eyed, light-bellied, light chinchilla
Related Genotype: Aw/Aw Oca2p Tyrc-ch/Oca2p Tyrc
Related Genotype: Aw/Aw Oca2p Tyrc/Oca2p Tyrc
pink-eyed, light-bellied, chinchilla
Related Genotype: Aw/Aw Oca2p Tyrc-ch/Oca2p Tyrc-ch
When using the 129X1 mouse strain in a publication, please include JAX stock #000691 in your Materials and Methods section.
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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