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Gene Review

Pms2  -  postmeiotic segregation increased 2 (S....

Mus musculus

Synonyms: AW555130, DNA mismatch repair, DNA mismatch repair protein PMS2, Mismatch repair endonuclease PMS2, PMS1 protein homolog 2, ...
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Disease relevance of Pms2


High impact information on Pms2

  • Mice that are deficient in either the Pms2 or Msh2 DNA mismatch repair genes have microsatellite instability and a predisposition to tumours [1].
  • Mice homozygous for a disrupted allele of the mismatch repair gene Pms2 have a mutator phenotype [6].
  • Mismatch repair deficiency interferes with the accumulation of mutations in chronically stimulated B cells and not with the hypermutation process [7].
  • By contrast, 23% of junctions from Mlh1- and Pms2-deficient cells occurred at unusually long stretches of microhomology [8].
  • DNA mismatch repair in mammals: role in disease and meiosis [9].

Biological context of Pms2

  • Previous nucleotide sequence analyses of switch recombination junctions indicated that the roles of Msh2 and the MutL homologues, Mlh1 and Pms2, differ [10].
  • However, certain changes in mutation patterns and frequency of point mutations were observed in Msh2 (MutS homologue) and Pms2 (MutL homologue) MMR-deficient mice (for review see Kim, N., and U. Storb. 1998. J. Exp. Med. 187:1729-1733) [11].
  • The data indicate that MMR proteins are directly involved in class switching and that the role of Msh2 differs from that of Mlh1 and Pms2 [8].
  • The data also suggest a mechanistic basis for the more severe mismatch repair-related phenotypes and cancer susceptibility in Mlh1- versus Mlh3- or Pms2-deficient mice [12].
  • However, when compared with Msh2(-/-) mice, lacI and cII mutants from Pms2-deficient mice revealed an increased proportion of +/-1 bp frameshift mutations and a corresponding decrease in transversion mutations [13].

Anatomical context of Pms2

  • The data demonstrate clear differences in the sequences of switch junctions in wild-type B cells in comparison with Msh2-, Mlh1-, and Pms2-deficient B cells [8].
  • Here, we extend these studies to the MutL homologues (MLH) Mlh1 and Pms2 by analysing the apoptotic response within the small intestine of gene targeted strains [14].
  • Cells with either p53 or Pms2 separately disrupted showed reduced levels of apoptosis after IR in comparison with wild type, but the double null cells showed even lower levels, consistent with nonoverlapping roles for p53 and PMS2 in the X-ray response [15].
  • In comparison to wild-type cell lines from related mice, the Pms2-, Mlh1-, or Msh2-nullizygous cell lines were found to exhibit higher levels of clonogenic survival following exposure to ionizing radiation [16].
  • In transformed cell lines established from the primary cells at early passage, similar differences in the apoptotic response to IR were seen, and clonogenic survival assays following low dose rate IR further showed that nullizygosity for Pms2 confers increased survival on cells in both wild-type and p53 null backgrounds [15].

Associations of Pms2 with chemical compounds


Other interactions of Pms2


Analytical, diagnostic and therapeutic context of Pms2


  1. Involvement of mouse Mlh1 in DNA mismatch repair and meiotic crossing over. Baker, S.M., Plug, A.W., Prolla, T.A., Bronner, C.E., Harris, A.C., Yao, X., Christie, D.M., Monell, C., Arnheim, N., Bradley, A., Ashley, T., Liskay, R.M. Nat. Genet. (1996) [Pubmed]
  2. Loss of heterozygosity and point mutation at Aprt locus in T cells and fibroblasts of Pms2-/- mice. Shao, C., Yin, M., Deng, L., Stambrook, P.J., Doetschman, T., Tischfield, J.A. Oncogene (2002) [Pubmed]
  3. Elevated mutant frequencies and increased C : G-->T : A transitions in Mlh1-/- versus Pms2-/- murine small intestinal epithelial cells. Baross-Francis, A., Makhani, N., Liskay, R.M., Jirik, F.R. Oncogene (2001) [Pubmed]
  4. MLH3: a DNA mismatch repair gene associated with mammalian microsatellite instability. Lipkin, S.M., Wang, V., Jacoby, R., Banerjee-Basu, S., Baxevanis, A.D., Lynch, H.T., Elliott, R.M., Collins, F.S. Nat. Genet. (2000) [Pubmed]
  5. Selective radiosensitization of drug-resistant MutS homologue-2 (MSH2) mismatch repair-deficient cells by halogenated thymidine (dThd) analogues: Msh2 mediates dThd analogue DNA levels and the differential cytotoxicity and cell cycle effects of the dThd analogues and 6-thioguanine. Berry, S.E., Davis, T.W., Schupp, J.E., Hwang, H.S., de Wind, N., Kinsella, T.J. Cancer Res. (2000) [Pubmed]
  6. Mismatch repair co-opted by hypermutation. Cascalho, M., Wong, J., Steinberg, C., Wabl, M. Science (1998) [Pubmed]
  7. Mismatch repair deficiency interferes with the accumulation of mutations in chronically stimulated B cells and not with the hypermutation process. Frey, S., Bertocci, B., Delbos, F., Quint, L., Weill, J.C., Reynaud, C.A. Immunity (1998) [Pubmed]
  8. Role for mismatch repair proteins Msh2, Mlh1, and Pms2 in immunoglobulin class switching shown by sequence analysis of recombination junctions. Schrader, C.E., Vardo, J., Stavnezer, J. J. Exp. Med. (2002) [Pubmed]
  9. DNA mismatch repair in mammals: role in disease and meiosis. Arnheim, N., Shibata, D. Curr. Opin. Genet. Dev. (1997) [Pubmed]
  10. Mlh1 can function in antibody class switch recombination independently of Msh2. Schrader, C.E., Vardo, J., Stavnezer, J. J. Exp. Med. (2003) [Pubmed]
  11. Different mismatch repair deficiencies all have the same effects on somatic hypermutation: intact primary mechanism accompanied by secondary modifications. Kim, N., Bozek, G., Lo, J.C., Storb, U. J. Exp. Med. (1999) [Pubmed]
  12. Contributions by MutL homologues Mlh3 and Pms2 to DNA mismatch repair and tumor suppression in the mouse. Chen, P.C., Dudley, S., Hagen, W., Dizon, D., Paxton, L., Reichow, D., Yoon, S.R., Yang, K., Arnheim, N., Liskay, R.M., Lipkin, S.M. Cancer Res. (2005) [Pubmed]
  13. Mutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts. Andrew, S.E., Xu, X.S., Baross-Francis, A., Narayanan, L., Milhausen, K., Liskay, R.M., Jirik, F.R., Glazer, P.M. Carcinogenesis (2000) [Pubmed]
  14. Apoptosis and mutation in the murine small intestine: loss of Mlh1- and Pms2-dependent apoptosis leads to increased mutation in vivo. Sansom, O.J., Bishop, S.M., Court, H., Dudley, S., Liskay, R.M., Clarke, A.R. DNA Repair (Amst.) (2003) [Pubmed]
  15. Ionizing radiation-induced apoptosis via separate Pms2- and p53-dependent pathways. Zeng, M., Narayanan, L., Xu, X.S., Prolla, T.A., Liskay, R.M., Glazer, P.M. Cancer Res. (2000) [Pubmed]
  16. Role of DNA mismatch repair in the cytotoxicity of ionizing radiation. Fritzell, J.A., Narayanan, L., Baker, S.M., Bronner, C.E., Andrew, S.E., Prolla, T.A., Bradley, A., Jirik, F.R., Liskay, R.M., Glazer, P.M. Cancer Res. (1997) [Pubmed]
  17. A role for mismatch repair in control of DNA ploidy following DNA damage. Strathdee, G., Sansom, O.J., Sim, A., Clarke, A.R., Brown, R. Oncogene (2001) [Pubmed]
  18. A mouse kidney cell line with a G:C --> C:G transversion mutator phenotype. Shin, C.Y., Ponomareva, O.N., Connolly, L., Turker, M.S. Mutat. Res. (2002) [Pubmed]
  19. DNA mismatch repair deficiency stimulates N-ethyl-N-nitrosourea-induced mutagenesis and lymphomagenesis. Claij, N., van der Wal, A., Dekker, M., Jansen, L., te Riele, H. Cancer Res. (2003) [Pubmed]
  20. Mismatch repair in methylated DNA. Structure and activity of the mismatch-specific thymine glycosylase domain of methyl-CpG-binding protein MBD4. Wu, P., Qiu, C., Sohail, A., Zhang, X., Bhagwat, A.S., Cheng, X. J. Biol. Chem. (2003) [Pubmed]
  21. Localization of MMR proteins on meiotic chromosomes in mice indicates distinct functions during prophase I. Kolas, N.K., Svetlanov, A., Lenzi, M.L., Macaluso, F.P., Lipkin, S.M., Liskay, R.M., Greally, J., Edelmann, W., Cohen, P.E. J. Cell Biol. (2005) [Pubmed]
  22. Altered spectra of hypermutation in antibodies from mice deficient for the DNA mismatch repair protein PMS2. Winter, D.B., Phung, Q.H., Umar, A., Baker, S.M., Tarone, R.E., Tanaka, K., Liskay, R.M., Kunkel, T.A., Bohr, V.A., Gearhart, P.J. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
  23. Levels of H-ras codon 61 CAA to AAA mutation: response to 4-ABP-treatment and Pms2-deficiency. Parsons, B.L., Delongchamp, R.R., Beland, F.A., Heflich, R.H. Mutagenesis (2006) [Pubmed]
  24. A:T --> G:C base pair substitutions occur at a higher rate than other substitution events in Pms2 deficient mouse cells. Shin, C.Y., Turker, M.S. DNA Repair (Amst.) (2002) [Pubmed]
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