Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse   Donating Investigator Dr. R. M. Liskay,   Oregon Health Sciences University

Description
Mice that are homozygous for the targeted mutation are viable, but show an increased incidence of sarcomas and lymphomas. Sperm, tail and tumor cells from homozygous mice exhibit microsatellite instability. Male mice on the mixed C57BL/6 and 129S2 background are infertile with reduced numbers of spermatozoa. Spermatozoa exhibit misshapen heads, truncated, irregular flagella. This strain may be useful in the studies of spermatogenesis, cancer and DNA mismatch repair.

Development
A targeting vector was designed to replace exon 2 of the targeted gene with a neomycin resistance cassette. The construct was electroporated into 129S2/SvPas-derived D3 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts, and chimeric males were bred to C57BL/6 females. Heterozygous offspring were bred to C57BL/6 mice for greater than 10 generations prior to arrival at The Jackson Laboratory.

Control Information

	Control
	Wild-type from the colony
	000664 C57BL/6J
Considerations for Choosing Controls

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI

- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Colorectal Cancer, Hereditary Nonpolyposis, Type 4; HNPCC4   (PMS2) Mismatch Repair Cancer Syndrome; MMRCS   (PMS2)

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Pms2^tm1Lisk/Pms2⁺

        involves: 129S2/SvPas

• tumorigenesis
• increased incidence of chemically-induced tumors
  • N-methyl-N-nitrosourea (MNU)-treated mice exhibit a higher incidence and multiplicity of intestinal tumors (adenomas and adenocarcinomas) compared with similarly treated wild-type mice without loss of the wild-type allele   (MGI Ref ID J:61787)
  • however, the incidence of induced thymic lymphomas is normal   (MGI Ref ID J:61787)
• homeostasis/metabolism phenotype
• increased incidence of chemically-induced tumors
  • N-methyl-N-nitrosourea (MNU)-treated mice exhibit a higher incidence and multiplicity of intestinal tumors (adenomas and adenocarcinomas) compared with similarly treated wild-type mice without loss of the wild-type allele   (MGI Ref ID J:61787)
  • however, the incidence of induced thymic lymphomas is normal   (MGI Ref ID J:61787)

Pms2^tm1Lisk/Pms2^tm1Lisk

        involves: 129S2/SvPas * C57BL/6

• tumorigenesis
• increased lymphoma incidence   (MGI Ref ID J:27389)
• sarcoma   (MGI Ref ID J:27389)
• reproductive system phenotype
• abnormal male meiosis
  • abnormalities in chromosomal synapsis during meiotic prophase I   (MGI Ref ID J:27389)
• abnormal sperm flagellum morphology
  • truncated, irregular flagella   (MGI Ref ID J:27389)
• globozoospermia
  • misshaped heads   (MGI Ref ID J:27389)
• male infertility
  • female mice are fertile   (MGI Ref ID J:27389)
• oligozoospermia
  • spermatozoan content of the epididymis was <25% that of wild-type   (MGI Ref ID J:27389)
• cellular phenotype
• abnormal mismatch repair
  • DNA from tumors and sperm exhibits increased microsatellite instability   (MGI Ref ID J:27389)
• homeostasis/metabolism phenotype
• abnormal mismatch repair
  • DNA from tumors and sperm exhibits increased microsatellite instability   (MGI Ref ID J:27389)

Pms2^tm1Lisk/Pms2^tm1Lisk

        involves: 129S2/SvPas

• mortality/aging
• premature death
  • median survival is 13 months   (MGI Ref ID J:162378)
  • median survival is reduced compared to in wild-type mice   (MGI Ref ID J:125218)
• reproductive system phenotype
• abnormal seminiferous tubule morphology
  • severely depleted in spermatogenic cells   (MGI Ref ID J:162378)
• decreased male germ cell number
  • severe depletion of spermatogenic cells   (MGI Ref ID J:162378)
• male infertility   (MGI Ref ID J:162378)
• small testis
  • about 70% the size of wild-type testes   (MGI Ref ID J:162378)
• teratozoospermia
  • mature sperm have misshapen heads and truncated or coiled flagella   (MGI Ref ID J:162378)
• • abnormal sperm head morphology   (MGI Ref ID J:162378)
  • coiled sperm flagellum   (MGI Ref ID J:162378)
  • short sperm flagellum   (MGI Ref ID J:162378)
• cellular phenotype
• abnormal cell physiology
  • sister chromatid exchange in mouse embryonic fibroblasts is increased compared to in wild-type cells   (MGI Ref ID J:125218)
• • abnormal DNA repair
    • increase in microsatellite instability and mutation frequencies   (MGI Ref ID J:162378)
  • • abnormal mismatch repair
      • absence of MMR in MEFs   (MGI Ref ID J:162378)
  • abnormal class switch recombination
    • decrease in ex vivo class switch recombination   (MGI Ref ID J:162378)
  • chromosomal instability
    • mouse embryonic fibroblasts (MEFs) exhibit in increase in microsatellite instability compared with wild-type cells   (MGI Ref ID J:125218)
    • end-to-end chromosome fusions in MEFs are slightly increased compared to in wild-type cells   (MGI Ref ID J:125218)
    • MEFs exhibit an increase in chromosome breaks, fragments, bivalent recombination figures, chromatid cross-links, chromosome fusions, and minichromosomes compared with wild-type cells   (MGI Ref ID J:125218)
    • however, telomere length is normal   (MGI Ref ID J:125218)
• tumorigenesis
• carcinoma   (MGI Ref ID J:125218)
• increased lymphoma incidence   (MGI Ref ID J:125218)
• • B cell derived lymphoma   (MGI Ref ID J:162378)
• sarcoma
  • histiocytic sarcomas   (MGI Ref ID J:125218)
• immune system phenotype
• abnormal class switch recombination
  • decrease in ex vivo class switch recombination   (MGI Ref ID J:162378)
• hematopoietic system phenotype
• abnormal class switch recombination
  • decrease in ex vivo class switch recombination   (MGI Ref ID J:162378)
• homeostasis/metabolism phenotype
• abnormal DNA repair
  • increase in microsatellite instability and mutation frequencies   (MGI Ref ID J:162378)
• • abnormal mismatch repair
    • absence of MMR in MEFs   (MGI Ref ID J:162378)
• endocrine/exocrine gland phenotype
• abnormal seminiferous tubule morphology
  • severely depleted in spermatogenic cells   (MGI Ref ID J:162378)
• small testis
  • about 70% the size of wild-type testes   (MGI Ref ID J:162378)

View Research Applications

Research Applications

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

Cancer Research
Increased Tumor Incidence
      Lymphomas
      Other Tissues/Organs
      Other Tissues/Organs: multiple
Other
      DNA Repair

Reproductive Biology Research
Fertility Defects
      males only

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Pms2tm1Lisk
Allele Name		targeted mutation 1, Michael Liskay
Allele Type		Targeted (knock-out)
Common Name(s)		Pms2-;
Mutation Made By		Dr. Sean Baker,   Oregon Health Sciences University
Strain of Origin		129S2/SvPas
ES Cell Line Name		D3
ES Cell Line Strain		129S2/SvPas
Gene Symbol and Name		Pms2, postmeiotic segregation increased 2 (S. cerevisiae)
Chromosome		5
Gene Common Name(s)		AW555130; DNA mismatch repair; HNPCC4; PMS2CL; PMSL2; expressed sequence AW555130; mismatch repair;
Molecular Note		A neomycin cassette was inserted into exon 2, replacing a highly conserved region of the gene. Protein was not detectable by Western analysis in fibroblast cultures from homozygous mutant animals. [MGI Ref ID J:27389]

Genotyping

Genotyping Information

Genotyping Protocols

Pms2^tm1Lisk, Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Baker SM; Bronner CE; Zhang L; Plug AW; Robatzek M; Warren G; Elliott EA; Yu J; Ashley T; Arnheim N; Flavell RA; Liskay RM. 1995. Male mice defective in the DNA mismatch repair gene PMS2 exhibit abnormal chromosome synapsis in meiosis. Cell 82(2):309-19. [PubMed: 7628019]  [MGI Ref ID J:27389]

Additional References

Pms2^tm1Lisk related

Andrew SE; Xu XS; Baross-Francis A; Narayanan L; Milhausen K; Liskay RM; Jirik FR; Glazer PM. 2000. Mutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts Carcinogenesis 21(7):1291-6. [PubMed: 10874005]  [MGI Ref ID J:63445]

Baker SM; Harris AC; Tsao JL; Flath TJ; Bronner CE; Gordon M ; Shibata D ; Liskay RM. 1998. Enhanced intestinal adenomatous polyp formation in Pms2-/-;Min mice. Cancer Res 58(6):1087-9. [PubMed: 9515784]  [MGI Ref ID J:46419]

Baross-Francis A; Makhani N; Liskay RM; Jirik FR. 2001. Elevated mutant frequencies and increased C : G-->T : A transitions in Mlh1-/- versus Pms2-/- murine small intestinal epithelial cells. Oncogene 20(5):619-25. [PubMed: 11313994]  [MGI Ref ID J:68922]

Baross-Francis A; Milhausen MK; Andrew SE; Jevon G; Jirik FR. 2000. Tumors arising in DNA mismatch repair-deficient mice show a wide variation in mutation frequency as assessed by a transgenic reporter gene. Carcinogenesis 21(6):1259-62. [PubMed: 10837019]  [MGI Ref ID J:62878]

Bourn RL; De Biase I; Pinto RM; Sandi C; Al-Mahdawi S; Pook MA; Bidichandani SI. 2012. Pms2 suppresses large expansions of the (GAA.TTC)n sequence in neuronal tissues. PLoS One 7(10):e47085. [PubMed: 23071719]  [MGI Ref ID J:192085]

Cascalho M; Wong J; Steinberg C; Wabl M. 1998. Mismatch repair co-opted by hypermutation. Science 279(5354):1207-10. [PubMed: 9469811]  [MGI Ref ID J:124315]

Chen PC; Dudley S; Hagen W; Dizon D; Paxton L; Reichow D; Yoon SR; Yang K; Arnheim N; Liskay RM; Lipkin SM. 2005. Contributions by MutL homologues Mlh3 and Pms2 to DNA mismatch repair and tumor suppression in the mouse. Cancer Res 65(19):8662-70. [PubMed: 16204034]  [MGI Ref ID J:102704]

Chen PC; Kuraguchi M; Velasquez J; Wang Y; Yang K; Edwards R; Gillen D; Edelmann W; Kucherlapati R; Lipkin SM. 2008. Novel roles for MLH3 deficiency and TLE6-like amplification in DNA mismatch repair-deficient gastrointestinal tumorigenesis and progression. PLoS Genet 4(6):e1000092. [PubMed: 18551179]  [MGI Ref ID J:137189]

Clarke AR; Sansom OJ. 2003. Analyzing tumor suppressor activities in the murine small intestine. Oncol Res 13(6-10):333-7. [PubMed: 12725522]  [MGI Ref ID J:83056]

Dobrovolsky VN; McKinzie PB; Shaddock JG; Mittelstaedt RA; Heflich RH; Parsons BL. 2003. Pms2 deficiency results in increased mutation in the Hprt gene but not the Tk gene of Tk(+/-) transgenic mice. Mutagenesis 18(4):365-70. [PubMed: 12840110]  [MGI Ref ID J:133813]

Ehrenstein MR; Rada C; Jones AM; Milstein C; Neuberger MS. 2001. Switch junction sequences in PMS2-deficient mice reveal a microhomology-mediated mechanism of Ig class switch recombination. Proc Natl Acad Sci U S A 98(25):14553-8. [PubMed: 11717399]  [MGI Ref ID J:73124]

Ezzatizadeh V; Pinto RM; Sandi C; Sandi M; Al-Mahdawi S; Te Riele H; Pook MA. 2012. The mismatch repair system protects against intergenerational GAA repeat instability in a Friedreich ataxia mouse model. Neurobiol Dis 46(1):165-71. [PubMed: 22289650]  [MGI Ref ID J:182296]

Frey S; Bertocci B; Delbos F; Quint L; Weill JC; Reynaud CA. 1998. Mismatch repair deficiency interferes with the accumulation of mutations in chronically stimulated B cells and not with the hypermutation process. Immunity 9(1):127-34. [PubMed: 9697842]  [MGI Ref ID J:48833]

Gurtu VE; Verma S; Grossmann AH; Liskay RM; Skarnes WC; Baker SM. 2002. Maternal effect for DNA mismatch repair in the mouse. Genetics 160(1):271-7. [PubMed: 11805062]  [MGI Ref ID J:74547]

Hegan DC; Narayanan L; Jirik FR; Edelmann W; Liskay RM; Glazer PM. 2006. Differing patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6. Carcinogenesis 27(12):2402-8. [PubMed: 16728433]  [MGI Ref ID J:115827]

Jahid S; Sun J; Edwards RA; Dizon D; Panarelli NC; Milsom JW; Sikandar SS; Gumus ZH; Lipkin SM. 2012. miR-23a promotes the transition from indolent to invasive colorectal cancer. Cancer Discov 2(6):540-53. [PubMed: 22628407]  [MGI Ref ID J:193067]

Kim N; Bozek G; Lo JC; Storb U. 1999. Different mismatch repair deficiencies all have the same effects on somatic hypermutation: intact primary mechanism accompanied by secondary modifications. J Exp Med 190(1):21-30. [PubMed: 10429667]  [MGI Ref ID J:115296]

Kolas NK; Svetlanov A; Lenzi ML; Macaluso FP; Lipkin SM; Liskay RM; Greally J; Edelmann W; Cohen PE. 2005. Localization of MMR proteins on meiotic chromosomes in mice indicates distinct functions during prophase I. J Cell Biol 171(3):447-58. [PubMed: 16260499]  [MGI Ref ID J:104493]

Larson JS; Stringer SL; Stringer JR. 2004. Impact of mismatch repair deficiency on genomic stability in the maternal germline and during early embryonic development. Mutat Res 556(1-2):45-53. [PubMed: 15491631]  [MGI Ref ID J:93781]

Narayanan L; Fritzell JA; Baker SM; Liskay RM; Glazer PM. 1997. Elevated levels of mutation in multiple tissues of mice deficient in the DNA mismatch repair gene Pms2. Proc Natl Acad Sci U S A 94(7):3122-7. [PubMed: 9096356]  [MGI Ref ID J:39399]

Prolla TA; Baker SM; Harris AC; Tsao JL; Yao X; Bronner CE; Zheng B ; Gordon M ; Reneker J ; Arnheim N ; Shibata D ; Bradley A ; Liskay RM. 1998. Tumour susceptibility and spontaneous mutation in mice deficient in Mlh1, Pms1 and Pms2 DNA mismatch repair. Nat Genet 18(3):276-9. [PubMed: 9500552]  [MGI Ref ID J:46382]

Qin J; Baker S; Te Riele H; Liskay RM; Arnheim N. 2002. Evidence for the lack of mismatch-repair directed antirecombination during mouse meiosis. J Hered 93(3):201-5. [PubMed: 12195036]  [MGI Ref ID J:102776]

Qin X; Liu L; Gerson SL. 1999. Mice defective in the DNA mismatch gene PMS2 are hypersensitive to MNU induced thymic lymphoma and are partially protected by transgenic expression of human MGMT. Oncogene 18(30):4394-400. [PubMed: 10439048]  [MGI Ref ID J:56767]

Qin X; Shibata D; Gerson SL. 2000. Heterozygous DNA mismatch repair gene PMS2-knockout mice are susceptible to intestinal tumor induction with N-methyl-N-nitrosourea. Carcinogenesis 21(4):833-8. [PubMed: 10753224]  [MGI Ref ID J:61787]

Qin X; Zhou H; Liu L; Gerson SL. 1999. Transgenic expression of human MGMT blocks the hypersensitivity of PMS2-deficient mice to low dose MNU thymic lymphomagenesis. Carcinogenesis 20(9):1667-73. [PubMed: 10469609]  [MGI Ref ID J:57292]

Sansom OJ; Bishop SM; Court H; Dudley S; Liskay RM; Clarke AR. 2003. Apoptosis and mutation in the murine small intestine: loss of Mlh1- and Pms2-dependent apoptosis leads to increased mutation in vivo. DNA Repair (Amst) 2(9):1029-39. [PubMed: 12967659]  [MGI Ref ID J:85600]

Schrader CE; Edelmann W; Kucherlapati R; Stavnezer J. 1999. Reduced isotype switching in splenic B cells from mice deficient in mismatch repair enzymes [see comments] J Exp Med 190(3):323-30. [PubMed: 10430621]  [MGI Ref ID J:56764]

Schrader CE; Guikema JE; Linehan EK; Selsing E; Stavnezer J. 2007. Activation-induced cytidine deaminase-dependent DNA breaks in class switch recombination occur during G1 phase of the cell cycle and depend upon mismatch repair. J Immunol 179(9):6064-71. [PubMed: 17947680]  [MGI Ref ID J:152998]

Schrader CE; Vardo J; Stavnezer J. 2002. Role for mismatch repair proteins Msh2, Mlh1, and Pms2 in immunoglobulin class switching shown by sequence analysis of recombination junctions. J Exp Med 195(3):367-73. [PubMed: 11828012]  [MGI Ref ID J:124827]

Siegl-Cachedenier I; Munoz P; Flores JM; Klatt P; Blasco MA. 2007. Deficient mismatch repair improves organismal fitness and survival of mice with dysfunctional telomeres. Genes Dev 21(17):2234-47. [PubMed: 17785530]  [MGI Ref ID J:125218]

Winter DB; Phung QH; Umar A; Baker SM; Tarone RE; Tanaka K; Liskay RM; Kunkel TA; Bohr VA; Gearhart PJ. 1998. Altered spectra of hypermutation in antibodies from mice deficient for the DNA mismatch repair protein PMS2. Proc Natl Acad Sci U S A 95(12):6953-8. [PubMed: 9618520]  [MGI Ref ID J:48081]

Xu XS; Narayanan L; Dunklee B; Liskay RM; Glazer PM. 2001. Hypermutability to ionizing radiation in mismatch repair-deficient, Pms2 knockout mice. Cancer Res 61(9):3775-80. [PubMed: 11325851]  [MGI Ref ID J:69130]

Yao X; Buermeyer AB; Narayanan L; Tran D; Baker SM; Prolla TA ; Glazer PM ; Liskay RM ; Arnheim N. 1999. Different mutator phenotypes in Mlh1- versus Pms2-deficient mice. Proc Natl Acad Sci U S A 96(12):6850-5. [PubMed: 10359802]  [MGI Ref ID J:55724]

van Oers JM; Roa S; Werling U; Liu Y; Genschel J; Hou H Jr; Sellers RS; Modrich P; Scharff MD; Edelmann W. 2010. PMS2 endonuclease activity has distinct biological functions and is essential for genome maintenance. Proc Natl Acad Sci U S A 107(30):13384-9. [PubMed: 20624957]  [MGI Ref ID J:162378]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & Husbandry	While maintaining a live colony, these mice are bred as heterozygotes. Male mice homozygous for the mutation are infertile.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

Control Information

	Control
	Wild-type from the colony
	000664 C57BL/6J
Considerations for Choosing Controls
Control Pricing Information for Genetically Engineered Mutant Strains.

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Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX^® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX^® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX^® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.

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