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Gene Review

Msh3  -  mutS homolog 3 (E. coli)

Mus musculus

Synonyms: D13Em1, DNA mismatch repair protein Msh3, Protein repair-1, Protein repair-3, REP-1, ...
 
 
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Disease relevance of Msh3

  • Somatic expansion behaviour of the (CTG)n repeat in myotonic dystrophy knock-in mice is differentially affected by Msh3 and Msh6 mismatch-repair proteins [1].
  • The mutation rate of the herpes simplex virus thymidine kinase 1 (HSV-tk1) gene was unchanged in Msh3-deficient ES cell lines but markedly elevated in Msh2-deficient and Msh3 Msh2 double-mutant cells [2].
  • Remodeling of the human retina in choroideremia: rab escort protein 1 (REP-1) mutations [3].
  • The loss of REP1 in CHM patients may trigger retinal degeneration through its effects on Rab proteins [4].
 

High impact information on Msh3

  • Here we show that Msh6(-)(/)(-) mice have a decrease in CSR, whereas Msh3(-)(/)(-) mice do not [5].
  • It has been shown that MutS homologue (Msh)6 (in conjunction with Msh2) but not Msh3 is involved in generating A/T base substitutions in somatic hypermutation [5].
  • Msh6-deficient mice had fewer substitutions of A and T bases in both regions and reduced heavy chain class switching, whereas Msh3-deficient mice had normal antibody responses [6].
  • Subsequently, both alleles of mMsh2, another mutS homolog, were disrupted in the same fashion to obtain cell lines homozygous for targeted mutations at both the Rep-3 and mMsh2 loci and devoid of selectable markers [7].
  • Analysis of the mouse Dhfr/Rep-3 major promoter region by using linker-scanning and internal deletion mutations and DNase I footprinting [8].
 

Biological context of Msh3

  • The association of MLH3 with repetitive DNA sequences is coincident with MSH2-MSH3 and is decreased in Msh2-/- and Msh3-/- mice, suggesting a novel role for the MMR family in the maintenance of repeat unit integrity during mammalian meiosis [9].
  • Our analysis therefore has revealed distinct mutational spectra and clarified the roles of Msh3 and Msh6 in DNA repair and intestinal tumorigenesis [10].
  • However, in Msh3(-/-)Msh6(-/-)Apc1638N tumors, we observed a mixture of base substitutions (46%) and frameshifts (54%), indicating that in Msh6(-/-)Apc1638N mice frameshift mutations in the Apc gene were suppressed by Msh3 [10].
  • Examination of Msh6- and Msh3-deficient mice in class switching reveals overlapping and distinct roles of MutS homologues in antibody diversification [5].
  • Msh3-deficient cells displayed a modest (16-fold) elevation in the instability of a dinucleotide repeat, whereas Msh2-deficient and Msh2 Msh3 double-mutant cells displayed markedly increased levels of repeat instability [2].
 

Anatomical context of Msh3

 

Other interactions of Msh3

  • However, when Msh3 deficiency is combined with Msh6 deficiency (Msh3(-/-)Msh6(-/-)Apc1638N), the survival rate of the mice was further reduced compared to Msh6(-/-)Apc(1638N) mice because of a high multiplicity of intestinal tumors at a younger age [10].
 

Analytical, diagnostic and therapeutic context of Msh3

  • METHODS: CHM hemizygotes with REP-1 mutations, spanning an age range of 7 decades, were studied with in vivo microscopy by optical coherence tomography [3].

References

  1. Somatic expansion behaviour of the (CTG)n repeat in myotonic dystrophy knock-in mice is differentially affected by Msh3 and Msh6 mismatch-repair proteins. van den Broek, W.J., Nelen, M.R., Wansink, D.G., Coerwinkel, M.M., te Riele, H., Groenen, P.J., Wieringa, B. Hum. Mol. Genet. (2002) [Pubmed]
  2. Genetic analysis of mouse embryonic stem cells bearing Msh3 and Msh2 single and compound mutations. Abuin, A., Zhang, H., Bradley, A. Mol. Cell. Biol. (2000) [Pubmed]
  3. Remodeling of the human retina in choroideremia: rab escort protein 1 (REP-1) mutations. Jacobson, S.G., Cideciyan, A.V., Sumaroka, A., Aleman, T.S., Schwartz, S.B., Windsor, E.A., Roman, A.J., Stone, E.M., MacDonald, I.M. Invest. Ophthalmol. Vis. Sci. (2006) [Pubmed]
  4. Rapid degradation of dominant-negative Rab27 proteins in vivo precludes their use in transgenic mouse models. Ramalho, J.S., Anders, R., Jaissle, G.B., Seeliger, M.W., Huxley, C., Seabra, M.C. BMC Cell Biol. (2002) [Pubmed]
  5. Examination of Msh6- and Msh3-deficient mice in class switching reveals overlapping and distinct roles of MutS homologues in antibody diversification. Li, Z., Scherer, S.J., Ronai, D., Iglesias-Ussel, M.D., Peled, J.U., Bardwell, P.D., Zhuang, M., Lee, K., Martin, A., Edelmann, W., Scharff, M.D. J. Exp. Med. (2004) [Pubmed]
  6. A role for Msh6 but not Msh3 in somatic hypermutation and class switch recombination. Martomo, S.A., Yang, W.W., Gearhart, P.J. J. Exp. Med. (2004) [Pubmed]
  7. Recycling selectable markers in mouse embryonic stem cells. Abuin, A., Bradley, A. Mol. Cell. Biol. (1996) [Pubmed]
  8. Analysis of the mouse Dhfr/Rep-3 major promoter region by using linker-scanning and internal deletion mutations and DNase I footprinting. Smith, M.L., Mitchell, P.J., Crouse, G.F. Mol. Cell. Biol. (1990) [Pubmed]
  9. 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]
  10. The distinct spectra of tumor-associated Apc mutations in mismatch repair-deficient Apc1638N mice define the roles of MSH3 and MSH6 in DNA repair and intestinal tumorigenesis. Kuraguchi, M., Yang, K., Wong, E., Avdievich, E., Fan, K., Kolodner, R.D., Lipkin, M., Brown, A.M., Kucherlapati, R., Edelmann, W. Cancer Res. (2001) [Pubmed]
 
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