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Journal articles on the topic 'Msh1'

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Published: 5 June 2025

Last updated: 15 July 2025

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Reenan, R. A., and R. D. Kolodner. "Characterization of insertion mutations in the Saccharomyces cerevisiae MSH1 and MSH2 genes: evidence for separate mitochondrial and nuclear functions." Genetics 132, no. 4 (1992): 975–85. http://dx.doi.org/10.1093/genetics/132.4.975.

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Abstract The MSH1 and MSH2 genes of Saccharomyces cerevisiae are predicted to encode proteins that are homologous to the Escherichia coli MutS and Streptococcus pneumoniae HexA proteins and their homologs. Disruption of the MSH1 gene caused a petite phenotype which was established rapidly. A functional MSH1 gene present on a single-copy centromere plasmid was incapable of rescuing the established msh1 petite phenotype. Analysis of msh1 strains demonstrated that mutagenesis and large-scale rearrangement of mitochondrial DNA had occurred. 4',6-Diamidino-2-phenylindole (DAPI) staining of msh1 yeast revealed an aberrant distribution of mtDNA. Haploid msh2 mutants displayed an increase of 85-fold in the rate of spontaneous mutation to canavanine resistance. Sporulation of homozygous msh2/msh2 diploids gave rise to a high level of lethality which was compounded during increased vegetative growth prior to sporulation. msh2 mutations also affected gene conversion of two HIS4 alleles. The his4x mutation, lying near the 5' end of the gene, was converted with equal frequency in both wild-type and msh2 strains. However, many of the events in the msh2 background were post-meiotic segregation (PMS) events (46.4%) while none (&lt; 0.25%) of the aberrant segregations in wild type were PMS events. The his4b allele, lying 1.6 kb downstream of his4x, was converted at a 10-fold higher frequency in the msh2 background than in the corresponding wild-type strain. Like the his4x allele, his4b showed a high level of PMS (30%) in the msh2 background compared to the corresponding wild-type strain where no (&lt; 0.26%) PMS events were observed. These results indicate that MSH1 plays a role in repair or stability of mtDNA and MSH2 plays a role in repair of 4-bp insertion/deletion mispairs in the nucleus.

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Kolas, Nadine K., Anton Svetlanov, Michelle L. Lenzi, et al. "Localization of MMR proteins on meiotic chromosomes in mice indicates distinct functions during prophase I." Journal of Cell Biology 171, no. 3 (2005): 447–58. http://dx.doi.org/10.1083/jcb.200506170.

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Mammalian MutL homologues function in DNA mismatch repair (MMR) after replication errors and in meiotic recombination. Both functions are initiated by a heterodimer of MutS homologues specific to either MMR (MSH2–MSH3 or MSH2–MSH6) or crossing over (MSH4–MSH5). Mutations of three of the four MutL homologues (Mlh1, Mlh3, and Pms2) result in meiotic defects. We show herein that two distinct complexes involving MLH3 are formed during murine meiosis. The first is a stable association between MLH3 and MLH1 and is involved in promoting crossing over in conjunction with MSH4–MSH5. The second complex involves MLH3 together with MSH2–MSH3 and localizes to repetitive sequences at centromeres and the Y chromosome. This complex is up-regulated in Pms2−/− males, but not females, providing an explanation for the sexual dimorphism seen in Pms2−/− mice. 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.

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Reenan, R. A., and R. D. Kolodner. "Isolation and characterization of two Saccharomyces cerevisiae genes encoding homologs of the bacterial HexA and MutS mismatch repair proteins." Genetics 132, no. 4 (1992): 963–73. http://dx.doi.org/10.1093/genetics/132.4.963.

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Abstract Homologs of the Escherichia coli (mutL, S and uvrD) and Streptococcus pneumoniae (hexA, B) genes involved in mismatch repair are known in several distantly related organisms. Degenerate oligonucleotide primers based on conserved regions of E. coli MutS protein and its homologs from Salmonella typhimurium, S. pneumoniae and human were used in the polymerase chain reaction (PCR) to amplify and clone mutS/hexA homologs from Saccharomyces cerevisiae. Two DNA sequences were amplified whose deduced amino acid sequences both shared a high degree of homology with MutS. These sequences were then used to clone the full-length genes from a yeast genomic library. Sequence analysis of the two MSH genes (MSH = mutS homolog), MSH1 and MSH2, revealed open reading frames of 2877 bp and 2898 bp. The deduced amino acid sequences predict polypeptides of 109.3 kD and 109.1 kD, respectively. The overall amino acid sequence identity with the E. coli MutS protein is 28.6% for MSH1 and 25.2% for MSH2. Features previously found to be shared by MutS homologs, such as the nucleotide binding site and the helix-turn-helix DNA binding motif as well as other highly conserved regions whose function remain unknown, were also found in the two yeast homologs. Evidence presented in this and a companion study suggest that MSH1 is involved in repair of mitochondrial DNA and that MSH2 is involved in nuclear DNA repair.

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Bai, Ming-Zhu, and Yan-Yan Guo. "Bioinformatics Analysis of MSH1 Genes of Green Plants: Multiple Parallel Length Expansions, Intron Gains and Losses, Partial Gene Duplications, and Alternative Splicing." International Journal of Molecular Sciences 24, no. 17 (2023): 13620. http://dx.doi.org/10.3390/ijms241713620.

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MutS homolog 1 (MSH1) is involved in the recombining and repairing of organelle genomes and is essential for maintaining their stability. Previous studies indicated that the length of the gene varied greatly among species and detected species-specific partial gene duplications in Physcomitrella patens. However, there are critical gaps in the understanding of the gene size expansion, and the extent of the partial gene duplication of MSH1 remains unclear. Here, we screened MSH1 genes in 85 selected species with genome sequences representing the main clades of green plants (Viridiplantae). We identified the MSH1 gene in all lineages of green plants, except for nine incomplete species, for bioinformatics analysis. The gene is a singleton gene in most of the selected species with conserved amino acids and protein domains. Gene length varies greatly among the species, ranging from 3234 bp in Ostreococcus tauri to 805,861 bp in Cycas panzhihuaensis. The expansion of MSH1 repeatedly occurred in multiple clades, especially in Gymnosperms, Orchidaceae, and Chloranthus spicatus. MSH1 has exceptionally long introns in certain species due to the gene length expansion, and the longest intron even reaches 101,025 bp. And the gene length is positively correlated with the proportion of the transposable elements (TEs) in the introns. In addition, gene structure analysis indicated that the MSH1 of green plants had undergone parallel intron gains and losses in all major lineages. However, the intron number of seed plants (gymnosperm and angiosperm) is relatively stable. All the selected gymnosperms contain 22 introns except for Gnetum montanum and Welwitschia mirabilis, while all the selected angiosperm species preserve 21 introns except for the ANA grade. Notably, the coding region of MSH1 in algae presents an exceptionally high GC content (47.7% to 75.5%). Moreover, over one-third of the selected species contain species-specific partial gene duplications of MSH1, except for the conserved mosses-specific partial gene duplication. Additionally, we found conserved alternatively spliced MSH1 transcripts in five species. The study of MSH1 sheds light on the evolution of the long genes of green plants.

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Elmore, Robert A., Mary K. Dick, and Poonam K. Sharma. "Muir-Torre syndrome: the curious case of wobbly microsatellites and their mucosal Lynch." International Journal of Research in Dermatology 5, no. 3 (2019): 646. http://dx.doi.org/10.18203/issn.2455-4529.intjresdermatol20193244.

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<p>MSH2 mismatch repair gene is commonly associated with Lynch syndrome; however, Lynch syndrome’s phenotypic variant, Muir-Torre syndrome is a lesser known entity comprising a spectrum of benign to malignant sebaceous neoplasms and is often the first etiology of a more significant prodromal syndrome. Both syndromes encompass gastrointestinal, genitourinary tract, and prostatic pathologies. We present a 15-year patient progression starting with new sebaceous hyperplasia and congenital melanocytic nevus skin lesions presenting in a 38-year-old caucasian male. After approximately four years additional cutaneous lesions began continuously appearing identified as: ulcerated sebaceoma, basal cell carcinoma, sebaceous hyperplasia, sebaceous adenoma, and hidradenoma. The patient went on to develop prostate adenocarcinoma and tubular adenoma of the ascending colon and rectum. Immunohistochemical staining demonstrated MSH2 and MSH6 instability and patient was recommended for Lynch Syndrome genetic testing. Later genetic analysis showed pathologic variant of MSH2 confirming Muir-Torre Syndrome. When multiple pathologies are involved that affect ectoderm differentiation, a diagnostic workup for microsatellite instability is recommended in association with a genetic counselor consultation. When a familial defect in a DNA repair enzyme (MSH1, MSH2, etc.) is known, we recommend PCR amplification for microsatellite instability in offspring between ages 5-15 to reduce morbidity and mortality in this population.</p>

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Lencina, Franco, Alejandra Landau, and Alberto R. Prina. "The Barley Chloroplast Mutator (cpm) Mutant: All Roads Lead to the Msh1 Gene." International Journal of Molecular Sciences 23, no. 3 (2022): 1814. http://dx.doi.org/10.3390/ijms23031814.

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The barley chloroplast mutator (cpm) is a nuclear gene mutant that induces a wide spectrum of cytoplasmically inherited chlorophyll deficiencies. Plastome instability of cpm seedlings was determined by identification of a particular landscape of polymorphisms that suggests failures in a plastome mismatch repair (MMR) protein. In Arabidopsis, MSH genes encode proteins that are in charge of mismatch repair and have anti-recombination activity. In this work, barley homologs of these genes were identified, and their sequences were analyzed in control and cpm mutant seedlings. A substitution, leading to a premature stop codon and a truncated MSH1 protein, was identified in the Msh1 gene of cpm plants. The relationship between this mutation and the presence of chlorophyll deficiencies was established in progenies from crosses and backcrosses. These results strongly suggest that the mutation identified in the Msh1 gene of the cpm mutant is responsible for the observed plastome instabilities. Interestingly, comparison of mutant phenotypes and molecular changes induced by the barley cpm mutant with those of Arabidopsis MSH1 mutants revealed marked differences.

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Chi Mai, Nguyen, NinhThi Ngoc, Nguyen Xuan Cuong, et al. "PHYLOGENETIC ANALYSIS AND SPECIES IDENTIFICATION OF 11 GORGONIAN CORALS (OCTOCORALLIA: ALCYONACEA) IN THE NORTH CENTRAL COAST OF VIETNAM BASED ON MSH1MTDNA AND 28S RDNA MARKERS." International Journal of Advanced Research 9, no. 08 (2021): 505–14. http://dx.doi.org/10.21474/ijar01/13298.

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Vietnam contains diverse marine ecosystems with the high biodiversity of marine organisms, including gorgonian corals of Alcyonacea order. In order to support traditional classification of these corals, in this study mitochondrial barcoding markers msh1 and nuclear 28S rDNA were developed for analysis of 11 specimens collected in 2015 and 2016 from different islands and bays along the North Central coast of Vietnam. Phylogenetic analyses based on msh1 and 28S sequence polymorphism showed that all specimens belonged to Anthozoa class, Octocorallia sub-class and Alcyonacea order. At lower taxa levels, they were divided into 4 sub-orders, 7 families and 7 genera according to 7 distinct clades with bootstrap values from 99-100%.The identifications of 7 out of 11 specimens including Sinularia brassica (2 specimens)and Sinularialeptoclados, Dichotellagemmacea, Annella reticulata, S. conferta and S. nanolobata were in concordance between morphological and molecular methods. The other 4 specimens were only identified at genus levels of Astrogorgia sp., Melithaea sp. Scleronephthya sp. and Muricella sp. by either msh1-morphology or msh1-28S markers. These results highlight the importance of molecular markers to elucidate patterns of biodiversity and species identification of soft coral.

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Broz, Amanda K., Mychaela M. Hodous, Yi Zou, Patricia C. Vail, Zhiqiang Wu, and Daniel B. Sloan. "Flipping the switch on some of the slowest mutating genomes: Direct measurements of plant mitochondrial and plastid mutation rates in msh1 mutants." PLOS Genetics 21, no. 6 (2025): e1011764. https://doi.org/10.1371/journal.pgen.1011764.

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Plant mitochondrial and plastid genomes have exceptionally slow rates of sequence evolution, and recent work has identified an unusual member of the MutS gene family (“plant MSH1”) as being instrumental in preventing point mutations in these genomes. However, the effects of disrupting MSH1-mediated DNA repair on “germline” mutation rates have not been quantified. Here, we used Arabidopsis thaliana mutation accumulation (MA) lines to measure mutation rates in msh1 mutants and matched wild type (WT) controls. We detected 124 single nucleotide variants (SNVs: 49 mitochondrial and 75 plastid) and 668 small insertions and deletions (indels: 258 mitochondrial and 410 plastid) in msh1 MA lines at a heteroplasmic frequency of ≥ 20%. In striking contrast, we did not find any organelle mutations in the WT MA lines above this threshold, and reanalysis of data from a much larger WT MA experiment also failed to detect any variants. The observed number of SNVs in the msh1 MA lines corresponds to estimated mutation rates of 6.1 × 10-7 and 3.2 × 10-6 per bp per generation in mitochondrial and plastid genomes, respectively. These rates exceed those of species known to have very high mitochondrial mutation rates (e.g., nematodes and fruit flies) by an order of magnitude or more and are on par with estimated rates in humans despite the generation times of A. thaliana being nearly 100-fold shorter. Therefore, disruption of a single plant-specific genetic factor in A. thaliana is sufficient to erase or even reverse the enormous difference in organelle mutation rates between plants and animals.

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Wiesendanger, Margrit, Burkhard Kneitz, Winfried Edelmann, and Matthew D. Scharff. "Somatic Hypermutation in Muts Homologue (Msh)3-, Msh6-, and Msh3/Msh6-Deficient Mice Reveals a Role for the Msh2–Msh6 Heterodimer in Modulating the Base Substitution Pattern." Journal of Experimental Medicine 191, no. 3 (2000): 579–84. http://dx.doi.org/10.1084/jem.191.3.579.

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Although the primary function of the DNA mismatch repair (MMR) system is to identify and correct base mismatches that have been erroneously introduced during DNA replication, recent studies have further implicated several MMR components in somatic hypermutation of immunoglobulin (Ig) genes. We studied the immune response in mice deficient in MutS homologue (MSH)3 and MSH6, two mutually exclusive partners of MSH2 that have not been examined previously for their role in Ig hypermutation. In Msh6−/− and Msh3−/−/Msh6−/− mice, base substitutions are preferentially targeted to G and C nucleotides and to an RGYW hot spot, as has been shown previously in Msh2−/− mice. In contrast, Msh3−/− mice show no differences from their littermate controls. These findings indicate that the MSH2–MSH6 heterodimer, but not the MSH2–MSH3 complex, is responsible for modulating Ig hypermutation.

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Chua, Melvin, Emilie Lalonde, Osman Mahamud, et al. "Copy number alterations of DNA mismatch repair (MMR) genes as novel prognostic markers in localised prostate cancer (CaP)." Journal of Clinical Oncology 34, no. 2_suppl (2016): 96. http://dx.doi.org/10.1200/jco.2016.34.2_suppl.96.

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96 Background: To investigate the prognostic significance of CNA of genes involved in the MMR pathway in localised CaP. Methods: We studied CNA of genes involved in MMR, namely MSH2, MSH3, MSH6, MLH1, PMS2, in 284 patients with intermediate-risk CaP (Toronto cohort), and compared our findings against three public databases (MSKCC and Cambridge cohorts) that included 375 low- to high-risk CaP. The Toronto cohort comprised of 143 and 141 individuals who underwent image-guided radiotherapy (IGRT) and radical prostatectomy (RadP), respectively, while all patients from the public databases underwent RadP. Information on genome-wide copy number alterations (Toronto) was obtained using Affymetrix Oncoscan array. Biochemical relapse-free survival (bRFS) was assessed for clinical outcome. Results: CNA of MSH2, MSH3, MSH6, MLH1, PMS2 were observed in 3.9% (n = 11), 7.7% (n = 22), 3.9% (n = 11), 4.6% (n = 13) and 13.0% (n = 37) of the Toronto cohort, respectively. Distinct patterns of allelic gain and loss were observed for the gene set; gains only for MLH1 and PMS2, and losses only, in all but 1 case, for MSH2, MSH3 and MSH6. In the Toronto cohort, allelic losses of MSH2, MSH3 and MSH6 were determined to be prognostic for poorer bRFS in IGRT patients (HR 2.04, 95% CI 1.01, 4.12, p = 0.048), but not for patients who underwent RadP (HR 1.08, 95% CI 0.49, 2.39, p = 0.84); while gains in MLH1 and PMS2 were not prognostic in either IGRT or RadP patients. A pooled analysis of these genes for all RadP patients from the Toronto and public databases (n = 516) did however indicate that allelic losses of MSH2, MSH3 and MSH6 were significant predictors of poorer bRFS (HR 2.48, 95% CI 1.64-3.77, p < 0.001), but not MLH1 and PMS2 gains. On multi-variable modelling that includes percent genome aberration and pre-treatment PSA levels, allelic losses of MSH2, MSH3 and MSH6remained significant predictors of bRFS for the pooled RadP cohort (HR 1.96, 95% CI 1.27, 3.01, Wald's p < 0.001), but not for IGRT patients (HR 1.50, 95% CI 0.72, 3.12, p = 0.28). Conclusions: We identified a distinct pattern of copy number loss of MSH2, MSH3 and MSH6 genes in localised CaP that appears to be a novel biomarker of failure to definitive treatment.

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Martomo, Stella A., William W. Yang, and Patricia J. Gearhart. "A Role for Msh6 But Not Msh3 in Somatic Hypermutation and Class Switch Recombination." Journal of Experimental Medicine 200, no. 1 (2004): 61–68. http://dx.doi.org/10.1084/jem.20040691.

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Somatic hypermutation is initiated by activation-induced cytidine deaminase (AID), and occurs in several kilobases of DNA around rearranged immunoglobulin variable (V) genes and switch (S) sites before constant genes. AID deaminates cytosine to uracil, which can produce mutations of C:G nucleotide pairs, and the mismatch repair protein Msh2 participates in generating substitutions of downstream A:T pairs. Msh2 is always found as a heterodimer with either Msh3 or Msh6, so it is important to know which one is involved. Therefore, we sequenced V and S regions from Msh3- and Msh6-deficient mice and compared mutations to those from wild-type mice. 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. This establishes a role for the Msh2-Msh6 heterodimer in hypermutation and switch recombination. When the positions of mutation were mapped, several focused peaks were found in Msh6−/− clones, whereas mutations were dispersed in Msh3−/− and wild-type clones. The peaks occurred at either G or C in WGCW motifs (W = A or T), indicating that C was mutated on both DNA strands. This suggests that AID has limited entry points into V and S regions in vivo, and subsequent mutation requires Msh2-Msh6 and DNA polymerase.

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Bowen, Nikki, та Richard D. Kolodner. "Reconstitution of Saccharomyces cerevisiae DNA polymerase ε-dependent mismatch repair with purified proteins". Proceedings of the National Academy of Sciences 114, № 14 (2017): 3607–12. http://dx.doi.org/10.1073/pnas.1701753114.

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Mammalian and Saccharomyces cerevisiae mismatch repair (MMR) proteins catalyze two MMR reactions in vitro. In one, mispair binding by either the MutS homolog 2 (Msh2)–MutS homolog 6 (Msh6) or the Msh2–MutS homolog 3 (Msh3) stimulates 5′ to 3′ excision by exonuclease 1 (Exo1) from a single-strand break 5′ to the mispair, excising the mispair. In the other, Msh2–Msh6 or Msh2–Msh3 activate the MutL homolog 1 (Mlh1)–postmeiotic segregation 1 (Pms1) endonuclease in the presence of a mispair and a nick 3′ to the mispair, to make nicks 5′ to the mispair, allowing Exo1 to excise the mispair. DNA polymerase δ (Pol δ) is thought to catalyze DNA synthesis to fill in the gaps resulting from mispair excision. However, colocalization of the S. cerevisiae mispair recognition proteins with the replicative DNA polymerases during DNA replication has suggested that DNA polymerase ε (Pol ε) may also play a role in MMR. Here we describe the reconstitution of Pol ε-dependent MMR using S. cerevisiae proteins. A mixture of Msh2–Msh6 (or Msh2–Msh3), Exo1, RPA, RFC-Δ1N, PCNA, and Pol ε was found to catalyze both short-patch and long-patch 5′ nick-directed MMR of a substrate containing a +1 (+T) mispair. When the substrate contained a nick 3′ to the mispair, a mixture of Msh2–Msh6 (or Msh2–Msh3), Exo1, RPA, RFC-Δ1N, PCNA, and Pol ε was found to catalyze an MMR reaction that required Mlh1–Pms1. These results demonstrate that Pol ε can act in eukaryotic MMR in vitro.

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Li, Ziqiang, Stefan J. Scherer, Diana Ronai, et al. "Examination of Msh6- and Msh3-deficient Mice in Class Switching Reveals Overlapping and Distinct Roles of MutS Homologues in Antibody Diversification." Journal of Experimental Medicine 200, no. 1 (2004): 47–59. http://dx.doi.org/10.1084/jem.20040355.

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Somatic hypermutation and class switch recombination (CSR) contribute to the somatic diversification of antibodies. 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. However, their roles in CSR have not yet been reported. Here we show that Msh6−/− mice have a decrease in CSR, whereas Msh3−/− mice do not. When switch regions were analyzed for mutations, deficiency in Msh6 was associated with an increase in transition mutations at G/C basepairs, mutations at RGYW/WRCY hotspots, and a small increase in the targeting of G/C bases. In addition, Msh6−/− mice exhibited an increase in the targeting of recombination sites to GAGCT/GGGGT consensus repeats and hotspots in Sγ3 but not in Sμ. In contrast to Msh2−/− mice, deficiency in Msh6 surprisingly did not change the characteristics of Sμ-Sγ3 switch junctions. However, Msh6−/− mice exhibited a change in the positioning of Sμ and Sγ3 junctions. Although none of these changes were seen in Msh3−/− mice, they had a higher percentage of large inserts in their switch junctions. Together, our data suggest that MutS homologues Msh2, Msh3, and Msh6 play overlapping and distinct roles during antibody diversification processes.

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Newton, Gerald L., Nancy Buchmeier, and Robert C. Fahey. "Biosynthesis and Functions of Mycothiol, the Unique Protective Thiol of Actinobacteria." Microbiology and Molecular Biology Reviews 72, no. 3 (2008): 471–94. http://dx.doi.org/10.1128/mmbr.00008-08.

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SUMMARY Mycothiol (MSH; AcCys-GlcN-Ins) is the major thiol found in Actinobacteria and has many of the functions of glutathione, which is the dominant thiol in other bacteria and eukaryotes but is absent in Actinobacteria. MSH functions as a protected reserve of cysteine and in the detoxification of alkylating agents, reactive oxygen and nitrogen species, and antibiotics. MSH also acts as a thiol buffer which is important in maintaining the highly reducing environment within the cell and protecting against disulfide stress. The pathway of MSH biosynthesis involves production of GlcNAc-Ins-P by MSH glycosyltransferase (MshA), dephosphorylation by the MSH phosphatase MshA2 (not yet identified), deacetylation by MshB to produce GlcN-Ins, linkage to Cys by the MSH ligase MshC, and acetylation by MSH synthase (MshD), yielding MSH. Studies of MSH mutants have shown that the MSH glycosyltransferase MshA and the MSH ligase MshC are required for MSH production, whereas mutants in the MSH deacetylase MshB and the acetyltransferase (MSH synthase) MshD produce some MSH and/or a closely related thiol. Current evidence indicates that MSH biosynthesis is controlled by transcriptional regulation mediated by σB and σR in Streptomyces coelicolor. Identified enzymes of MSH metabolism include mycothione reductase (disulfide reductase; Mtr), the S-nitrosomycothiol reductase MscR, the MSH S-conjugate amidase Mca, and an MSH-dependent maleylpyruvate isomerase. Mca cleaves MSH S-conjugates to generate mercapturic acids (AcCySR), excreted from the cell, and GlcN-Ins, used for resynthesis of MSH. The phenotypes of MSH-deficient mutants indicate the occurrence of one or more MSH-dependent S-transferases, peroxidases, and mycoredoxins, which are important targets for future studies. Current evidence suggests that several MSH biosynthetic and metabolic enzymes are potential targets for drugs against tuberculosis. The functions of MSH in antibiotic-producing streptomycetes and in bioremediation are areas for future study.

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Arturo Arias, Brenda Lucia, Natalia García Restrepo, Paula Tatiana Uribe Echeverry, and Jhon Fredy Betancur Pérez. "Cáncer colorrectal: una mirada clínica, genética y molecular./Colorectal cancer: clinical, molecular and genetics view." Archivos de Medicina (Manizales) 13, no. 2 (2013): 208–19. http://dx.doi.org/10.30554/archmed.13.2.14.2013.

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El cáncer Colorrectal (CCR) ocupa la cuarta causa de muerte por cáncer en Estados Unidos de América y la quinta causa de muerte por cáncer en Colombia y de esta forma se convierte en un problema de salud pública. El 98 % de los cánceres Colorrectales son adenocarcinomas y el otro 2% corresponden a linfomas, carcinoides y tumores estromales gastrointestinales. Las manifestaciones clínicas se relacionan con el tamaño y la localización de la lesión, el 80% de los casos reportados de CCR no presentan un componente hereditario convirtiéndolos en CCR esporádicos. El CCR está asociado con la acumulación de mutaciones en genes supresores de tumores (p53, APC, SMAD, SCC, NM23), oncogenes (MYC y RAS) y genes reparadores del ADN (MSH1, MSH6 y MLH2) estas alteraciones genéticas hacen de este tipo de cáncer un desorden poligenético, convirtiéndolo en un modelo clásico para estudiar las bases genéticas del cáncer. Colorectal cancer took the fourth leading cause of cancer death in the United Statesof America and the fifth leading cause of cancer death in Colombia and thus becomesa public health problem. 98% of colorectal cancers are adenocarcinomas and theother 2% are lymphomas, carcinoids, and gastrointestinal stromal tumors, the clinicalmanifestations are related to the size and location of the lesion, 80% of reported casesof CRC not present a hereditary component making them sporadic CRC. The CRC isassociated with the accumulation of mutations in tumor suppressor genes (p53, APC,SMAD, SCC, NM23), oncogenes (MYC and RAS) and DNA repair genes (MSH1, MSH6and MLH2) these genetic alterations make this type of cancer a polygenic disorder,making it a classic model for studying the genetic basis of cancer.

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Sørensen, Sebastian R., Maria S. Holtze, Allan Simonsen, and Jens Aamand. "Degradation and Mineralization of Nanomolar Concentrations of the Herbicide Dichlobenil and Its Persistent Metabolite 2,6-Dichlorobenzamide by Aminobacter spp. Isolated from Dichlobenil-Treated Soils." Applied and Environmental Microbiology 73, no. 2 (2006): 399–406. http://dx.doi.org/10.1128/aem.01498-06.

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ABSTRACT 2,6-Dichlorobenzamide (BAM), a persistent metabolite from the herbicide 2,6-dichlorobenzonitrile (dichlobenil), is the pesticide residue most frequently detected in Danish groundwater. A BAM-mineralizing bacterial community was enriched from dichlobenil-treated soil sampled from the courtyard of a former plant nursery. A BAM-mineralizing bacterium (designated strain MSH1) was cultivated and identified by 16S rRNA gene sequencing and fatty acid analysis as being closely related to members of the genus Aminobacter, including the only cultured BAM degrader, Aminobacter sp. strain ASI1. Strain MSH1 mineralized 15 to 64% of the added [ring-U-14C]BAM to 14CO2 with BAM at initial concentrations in the range of 7.9 nM to 263.1 μM provided as the sole carbon, nitrogen, and energy source. A quantitative enzyme-linked immunoassay analysis with antibodies against BAM revealed residue concentrations of 0.35 to 18.05 nM BAM following incubation for 10 days, corresponding to a BAM depletion of 95.6 to 99.9%. In contrast to the Aminobacter sp. strain ASI1, strain MSH1 also mineralized the herbicide itself along with several metabolites, including ortho-chlorobenzonitrile, ortho-chlorobenzoic acid, and benzonitrile, making it the first known dichlobenil-mineralizing bacterium. Aminobacter type strains not previously exposed to dichlobenil or BAM were capable of degrading nonchlorinated structural analogs. Combined, these results suggest that closely related Aminobacter strains may have a selective advantage in BAM-contaminated environments, since they are able to use this metabolite or structurally related compounds as a carbon and nitrogen source.

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Tornier, Carine, Stéphanie Bessone, Isabelle Varlet, Claudia Rudolph, Michel Darmon, and Oliver Fleck. "Requirement for Msh6, but Not for Swi4 (Msh3), in Msh2-Dependent Repair of Base-Base Mismatches and Mononucleotide Loops inSchizosaccharomyces pombe." Genetics 158, no. 1 (2001): 65–75. http://dx.doi.org/10.1093/genetics/158.1.65.

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AbstractThe msh6 mismatch repair gene of Schizosaccharomyces pombe was cloned, sequenced, and inactivated. Strains bearing all combinations of inactivated msh6, msh2, and swi4 (the S. pombe MSH3 ortholog) alleles were tested for their defects in mitotic and meiotic mismatch repair. Mitotic mutation rates were similarly increased in msh6 and msh2 mutants, both for reversion of a base-base substitution as well as of an insertion of one nucleotide in a mononucleotide run. Tetrad analysis and intragenic two-factor crosses revealed that meiotic mismatch repair was affected in msh6 to the same extent as in msh2 background. In contrast, loss of Swi4 likely did not cause a defect in mismatch repair, but rather resulted in reduced recombination frequency. Consistently, a mutated swi4 caused a two- to threefold reduction of recombinants in intergenic crosses, while msh2 and msh6 mutants were not significantly different from wild type. In summary, our study showed that Msh6 plays the same important role as Msh2 in the major mismatch repair pathway of S. pombe, while Swi4 rather functions in recombination.

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Wagner, Daniel-Christoph, Johanna, Isabelle Glocke, et al. "Object-based analysis of astroglial reaction and astrocyte subtype morphology after ischemic brain injury." Acta Neurobiologiae Experimentalis 73, no. 1 (2013): 79–87. http://dx.doi.org/10.55782/ane-2013-1923.

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The astrocytic response to ischemic brain injury is characterized by specific alterations of glial cell morphology and function. Various studies described both beneficial and detrimental aspects of activated astrocytes, suggesting the existence of different subtypes. We investigated this issue using a novel object-based approach to study characteristics of astrogliosis after stroke. Spontaneously hypertensive rats received permanent middle cerebral artery occlusion. After 96 h, brain specimens were removed, fixed and stained for GFAP, glutamine synthetase (GS), S100Beta and Musashi1 (Msh1). Three regions of interest were defined (contralateral hemisphere, ipsilateral remote zone and infarct border zone), and confocal stacks were acquired (n=5 biological with each n=4 technical replicates). The stacks were background-corrected and colocalization between the selected markers and GFAP was determined using an automated thresholding algorithm. The fluorescence and colocalization channels were then converted into 3D-objects using both intensity and volume as filters to ultimately determine the final volumes of marker expression and colocalization, as well as the morphological changes of astrocyte process arborisation. We found that both S100Beta and Msh1 determined the same GFAP-positive astroglial cell population albeit the cellular compartments differed. GFAP stained most of the astrocyte processes and is hence suitable for the analysis of qualitative characteristics of astrogliosis. Due to its peri-nuclear localization, Msh1 is appropriate to estimate the total number of astrocytes even in regions with severe reactive astrogliosis. GS expression in GFAP-positive astrocytes was high in the remote zone and low at the infarct border, indicating the existence of astrocyte subclasses.

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Olkinuora, Alisa, Annette Gylling, Henrikki Almusa, et al. "Molecular Basis of Mismatch Repair Protein Deficiency in Tumors from Lynch Suspected Cases with Negative Germline Test Results." Cancers 12, no. 7 (2020): 1853. http://dx.doi.org/10.3390/cancers12071853.

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Some 10–50% of Lynch-suspected cases with abnormal immunohistochemical (IHC) staining remain without any identifiable germline mutation of DNA mismatch repair (MMR) genes. MMR proteins form heterodimeric complexes, giving rise to distinct IHC patterns when mutant. Potential reasons for not finding a germline mutation include involvement of an MMR gene not predicted by the IHC pattern, epigenetic mechanism of predisposition, primary mutation in another DNA repair or replication-associated gene, and double somatic MMR gene mutations. We addressed these possibilities by germline and tumor studies in 60 Lynch-suspected cases ascertained through diagnostics (n = 55) or research (n = 5). All cases had abnormal MMR protein staining in tumors but no point mutation or large rearrangement of the suspected MMR genes in the germline. In diagnostic practice, MSH2/MSH6 (MutS Homolog 2/MutS Homolog 6) deficiency prompts MSH2 mutation screening; in our study, 3/11 index individuals (27%) with this IHC pattern revealed pathogenic germline mutations in MSH6. Individuals with isolated absence of MSH6 are routinely screened for MSH6 mutations alone; we found a predisposing mutation in MSH2 in 1/7 such cases (14%). Somatic deletion of the MSH2-MSH6 region, joint loss of MSH6 and MSH3 (MutS Homolog 3) proteins, and hindered MSH2/MSH6 dimerization offered explanations to misleading IHC patterns. Constitutional epimutation hypothesis was pursued in the MSH2 and/or MSH6-deficient cases plus 38 cases with MLH1 (MutL Homolog 1)-deficient tumors; a primary MLH1 epimutation was identified in one case with an MLH1-deficient tumor. We conclude that both MSH2 and MSH6 should be screened in MSH2/6- and MSH6-deficient cases. In MLH1-deficient cases, constitutional epimutations of MLH1 warrant consideration.

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Li, Yan, Ishita Mukerji, and Manju Hingorani. "Investigation of the Binding Interaction of S. cerevisiae MutS Homologs MSH2-MSH6 and MSH4-MSH5 with Holliday Junctions." Biophysical Journal 100, no. 3 (2011): 243a. http://dx.doi.org/10.1016/j.bpj.2010.12.1543.

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Dislich, Bastian, Kirsten D. Mertz, Beat Gloor, and Rupert Langer. "Interspatial Distribution of Tumor and Immune Cells in Correlation with PD-L1 in Molecular Subtypes of Gastric Cancers." Cancers 14, no. 7 (2022): 1736. http://dx.doi.org/10.3390/cancers14071736.

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(1) Background: EBV-positive and mismatch repair-deficient (MMRd) gastric cancers (GCs) show higher levels of tumor-infiltrating lymphocytes (TILs) and PD-L1 expression and thus a more profound response to immunotherapy. However, the majority of GCs are EBV-negative (EBV−) and MMR proficient (MMRp). We analyzed PD-L1 expression and TILs in EBV-MMRpGCs in comparison to EBV-positive (EBV+) and MMRdGCs to identify an immunogenic phenotype susceptible to immunotherapy. (2) Methods: A next-generation tissue microarray of 409 primary resected GCs was analyzed by Epstein-Barr encoding region (EBER) in situ hybridization for MSH1, PMS2, MSH2, MSH6, PD-L1, and CD8 immunohistochemistry. PD-L1 positivity was defined as a combined positive score (CPS) of ≥1. CD8+ TILs and their proximity to cancer cells were digitally analyzed on the HALO™ image analysis platform. (3) Results: Eleven cases were EBV+, 49 cases MMRd, and 349 cases EBV-MMRpGCs. The highest rate of PD-L1 positivity was seen in EBV+GCs, followed by MMRdGCs and EBV-MMRpGCs (81.8%, 73.5%, and 27.8%, respectively). EBV+ and MMRdGCs also demonstrated increased numbers and proximity of CD8+ TILs to tumor cells compared to EBV-MMRpGCs (p < 0.001 each). PD-L1 status positively correlated with the total numbers of CD8+ TILs and their proximity to tumor cells in all subtypes, including EBV-MMRpGCs (p < 0.001 each). A total of 28.4% of EBV-MMRpGCs showed high CD8+ TILs independent of PD-L1. (4) Conclusions: PD-L1 and CD8 immunohistochemistry, supplemented by digital image analysis, may identify EBV-MMRpGCs with high immunoreactivity indices, indicating susceptibility to immunotherapy.

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Korzun, V., A. Börner, R. Siebert, et al. "Chromosomal location and genetic mapping of the mismatch repair gene homologs MSH2, MSH3, and MSH6 in rye and wheat." Genome 42, no. 6 (1999): 1255–57. http://dx.doi.org/10.1139/g99-081.

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The efficiency of homeologous recombination is influenced by mismatch repair genes in bacteria, yeast, and mammals. To elucidate a possible role of these genes in homeologous pairing and cross-compatibility in plants, gene probes of wheat (Triticum aestivum) specific for the mismatch repair gene homologues MSH2, MSH3, and MSH6 were used to map them to their genomic positions in rye (Secale cereale). Whereas MSH2 was mapped to the short arm of chromosome 1R, MSH3 was mapped to the long arm of chromosome 2R and MSH6 to the long arm of chromosome 5R. Southern blots with nullisomic-tetrasomic (NT) lines of wheat indicated the presence of the sequences on the respective homeologous group of wheat chromosomes. Additionally, an MSH6-specific homologue could also be detected on homoeologous group 3 of wheat. However, in the well-known, highly homoeologous pairing wheat mutant ph1b the MSH6-specific sequence is not within the deleted part of chromosome 5BL, indicating that the pairing phenotype is not due to a loss of one of the mismatch repair genes tested.Key words: mismatch repair genes, chromosomal location, RFLP mapping, wheat, rye.

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Harrington, Jill M., and Richard D. Kolodner. "Saccharomyces cerevisiae Msh2-Msh3 Acts in Repair of Base-Base Mispairs." Molecular and Cellular Biology 27, no. 18 (2007): 6546–54. http://dx.doi.org/10.1128/mcb.00855-07.

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ABSTRACT DNA mismatch repair is thought to act through two subpathways involving the recognition of base-base and insertion/deletion mispairs by the Msh2-Msh6 heterodimer and the recognition of insertion/deletion mispairs by the Msh2-Msh3 heterodimer. Here, through genetic and biochemical approaches, we describe a previously unidentified role of the Msh2-Msh3 heterodimer in the recognition of base-base mispairs and the suppression of homology-mediated duplication and deletion mutations. Saccharomyces cerevisiae msh3 mutants did not show an increase in the rate of base substitution mutations by the CAN1 forward mutation assay compared to the rate for the wild type but did show an altered spectrum of base substitution mutations, including an increased accumulation of base pair changes from GC to CG and from AT to TA; msh3 mutants also accumulated homology-mediated duplication and deletion mutations. The mutation spectrum of mlh3 mutants paralleled that of msh3 mutants, suggesting that the Mlh1-Mlh3 heterodimer may also play a role in the repair of base-base mispairs and in the suppression of homology-mediated duplication and deletion mutations. Mispair binding analysis with purified Msh2-Msh3 and DNA substrates derived from CAN1 sequences found to be mutated in vivo demonstrated that Msh2-Msh3 exhibited robust binding to specific base-base mispairs that was consistent with functional mispair binding.

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Kenchanmane Raju, Sunil Kumar, Mon-Ray Shao, Yashitola Wamboldt, and Sally Mackenzie. "Epigenomic plasticity of Arabidopsis msh1 mutants under prolonged cold stress." Plant Direct 2, no. 8 (2018): e00079. http://dx.doi.org/10.1002/pld3.79.

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Martín, A. C., S. G. Atienza, M. C. Ramírez, F. Barro, and A. Martín. "Male fertility restoration of wheat in Hordeum chilense cytoplasm is associated with 6HchS chromosome addition." Australian Journal of Agricultural Research 59, no. 3 (2008): 206. http://dx.doi.org/10.1071/ar07239.

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We report a new cytoplasmic male sterility (CMS) source in bread wheat (Triticum aestivum L.) designated as msH1. CMS has been identified during the process of obtaining alloplasmic bread wheat in different Hordeum chilense Roem. Schultz. cytoplasms. It was observed that when using the H. chilense H1 accession, the corresponding alloplasmic line was male sterile. This alloplasmic wheat is stable under different environmental conditions and it does not exhibit developmental or floral abnormalities, showing only slightly reduced height and some delay in heading. On examining microsporogenesis in the alloplasmic line, it was found that different stages of meiosis were completed normally, but abnormal development occurred at the uninucleate-pollen stage at the first mitosis, resulting in failure of anther exertion and pollen abortion. Fertility restoration of the CMS phenotype caused by the H. chilense cytoplasm was associated with the addition of chromosome 6HchS from H. chilense accession H1. Thus, some fertility restoration genes appear to be located in this chromosome arm. Considering the features displayed by the msH1 system, we consider that it has a great potential for the development of viable technology for hybrid wheat production.

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Morak, Monika, Sarah Käsbauer, Martina Kerscher, et al. "Loss of MSH2 and MSH6 due to heterozygous germline defects in MSH3 and MSH6." Familial Cancer 16, no. 4 (2017): 491–500. http://dx.doi.org/10.1007/s10689-017-9975-z.

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Clark, Alan B., Frank Valle, Karin Drotschmann, Ronald K. Gary, and Thomas A. Kunkel. "Functional Interaction of Proliferating Cell Nuclear Antigen with MSH2-MSH6 and MSH2-MSH3 Complexes." Journal of Biological Chemistry 275, no. 47 (2000): 36498–501. http://dx.doi.org/10.1074/jbc.c000513200.

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Fordham, Sarah E., Elizabeth C. Matheson, Kathryn Scott, Julie Irving, and James M. Allan. "Cellular Response to Cytarabine Is Modulated by the DNA Mismatch Repair Pathway: Implications for Treatment of Acute Myeloid Leukemia." Blood 116, no. 21 (2010): 1819. http://dx.doi.org/10.1182/blood.v116.21.1819.1819.

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Abstract Abstract 1819 The DNA mismatch repair (MMR) pathway is responsible for repair of spontaneous errors arising during DNA replication, thus maintaining the integrity of the genome. DNA MMR is frequently dysregulated in some forms of leukemia. We and others have shown that microsatellite instability, the hallmark of dysfunctional DNA MMR, is present in up to 90% of therapy-related myeloid leukemia, 50% of relapsed myeloid leukemia, but is rarely seen in de novo leukemia. Paradoxically, functional MMR mediates the cytotoxicity of certain chemotherapeutic agents, particularly methylating agents and the nucleoside analogue 6-thioguanine (6-TG), and dysregulation of the MMR pathway confers tolerance to these agents. In the present study, using cell lines harboring defects in MMR components, we show that MMR status also modulates response to the nucleoside analogue cytarabine (Ara-C) and to other therapeutic nucleoside analogues commonly used in the treatment of leukemia. We initially determined gene and protein expression levels of the major MMR components (MSH2, MSH3, MSH6, MLH1 and PMS2) in two psuedo-isogenic cell line pairs, and investigated the ability of cell extracts to bind to defined mismatches in electrophoretic mobility shift assays. In cytotoxicity assays, the cell lines HL-60R (which demonstrates 200-fold overexpression of MSH3) and MT-1 (which lacks functional MSH6 due to bi-allelic gene mutation) were tolerant to the cytotoxic effects of a methylating agent, methylnitrosourea (MNU), and 6-TG, relative to their respective parental cell lines. We also generated a panel of fully isogenic MMR-defective cell lines in which either MSH2, MSH3 or MSH6 protein was reduced to almost negligible levels using short hairpin RNA-mediated gene knockdown. Knockdown of either MSH2 or MSH6 conferred tolerance to the killing effects of MNU and 6-TG by virtue of loss of MutSα activity (a heterodimer of MSH2 and MSH6 responsible for recognition of base:base mispairs), whereas knockdown of MSH3 did not affect cellular response to these agents. Consistent with a role for MMR in affecting cellular response to other nucleoside analogues used to treat leukemia, the cell lines also displayed differential toxicity to the killing effects of Ara-C, clofarabine, cladribine and fludarabine compared to their MMR-proficient parental counterparts, however the exact response was dependent on the specific nature of the MMR defect. Cell lines with a reduction in MSH2 protein demonstrated hypersensitivity to cytotoxicity induced by these nucleoside analogues. Conversely, MSH3 knockdown conferred resistance to the cytotoxic effects of these agents. These data suggest that DNA MMR can affect response to nucleoside analogues via multiple mechanisms, and may also involve interaction of DNA MMR components with other DNA repair pathways. One possibility is that these agents induce base lesions in DNA recognized by DNA MMR components. Consistent with this model, we have shown that Ara-C induces DNA polymerase slippage in vitro, generating a substrate potentially recognized by MutSβ (a heterodimer of MSH2 and MSH3 responsible for recognition of small insertions and extrahelical loops). Furthermore, we have also shown that Ara-C is mutagenic at the thymidine kinase and hypoxanthine-guanine phosphoribosyltransferase loci in the TK6 cell line. Taken together, these data suggest that cellular MMR status affects response to nucleoside analogues and furthermore, the specific nature of the defect is important in determining the exact response. These findings have implications for the use of nucleoside analogues in the treatment of cancers where MMR dysfunction has been identified to occur with high frequency, such as therapy-related and relapsed acute myeloid leukemia. Disclosures: No relevant conflicts of interest to declare.

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Petes, Thomas D., Patricia W. Greenwell, and Margaret Dominska. "Stabilization of Microsatellite Sequences by Variant Repeats in the Yeast Saccharomyces cerevisiae." Genetics 146, no. 2 (1997): 491–98. http://dx.doi.org/10.1093/genetics/146.2.491.

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We examined the effect of a single variant repeat on the stability of a 51-base pair (bp) microsatellite (poly GT). We found that the insertion stabilizes the microsatellite about fivefold in wild-type strains. The stabilizing effect of the variant base was also observed in strains with mutations in the DNA mismatch repair genes pms1, msh2 and msh3, indicating that this effect does not require a functional DNA mismatch repair system. Most of the microsatellite alterations in the pms1, msh2 and msh3 strains were additions or deletions of single GT repeats, but about half of the alterations in the wild-type and msh6 strains were large (&gt;8 bp) deletions or additions.

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Terao, Y., and J. Imamura. "EFFECTS OF SUPPRESSION OF MSH1 ON MITOCHONDRIAL GENOME IN BRASSICA NAPUS." Acta Horticulturae, no. 1005 (September 2013): 111–16. http://dx.doi.org/10.17660/actahortic.2013.1005.9.

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Floer, Martin, David G. Binion, Victoria M. Nelson, et al. "Role of MutS homolog 2 (MSH2) in intestinal myofibroblast proliferation during Crohn's disease stricture formation." American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no. 3 (2008): G581—G590. http://dx.doi.org/10.1152/ajpgi.90311.2008.

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Tissue remodeling and mesenchymal cell accumulation accompanies chronic inflammatory disorders involving joints, lung, vasculature, and bowel. Chronic inflammation may alter DNA-mismatch repair (MMR) systems in mesenchymal cells, but is not defined in Crohn's disease (CD) and its associated intestinal remodeling and stricture formation. We determined whether DNA-MMR alteration plays a role in the pathogenesis of CD tissue remodeling. Control and CD bowel tissues were used to generate primary cultures of muscularis mucosa myofibroblasts, which were assessed directly or following stimulation with TNF-α/LPS or H2O2. MutS homolog (MSH)2, MSH3, and MSH6 expression in tissues and myofibroblasts was determined. Immunohistochemical staining revealed an increased expression of MSH2 in CD muscularis mucosa and submucosal tissues compared with controls or uninvolved CD tissue, and MSH2 expression was increased in CD myofibroblasts compared with control cells. TNF-α/LPS and H2O2 further enhanced MSH2 expression in both control and CD cells, which were decreased by simvastatin. There were no significant changes in MSH3 and MSH6 expression. Proliferating cell nuclear antigen and Ki67 staining of CD tissue revealed increased proliferation in the muscularis mucosa and submucosa of chronically inflamed tissues, and enhanced proliferation was seen in CD myofibroblasts compared with controls. Simvastatin reversed the effects of inflammatory stress on the DNA-MMR and inhibited proliferation of control and CD myofibroblasts. Gene silencing with MSH2 siRNA selectively decreased CD myofibroblast proliferation. These data demonstrate a potential role for MSH2 in the pathogenesis of nonneoplastic mesenchymal cell accumulation and intestinal remodeling in CD chronic inflammation.

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Guervilly, Jean-Hugues, Marion Blin, Luisa Laureti, Emilie Baudelet, Stéphane Audebert та Pierre-Henri Gaillard. "SLX4 dampens MutSα-dependent mismatch repair". Nucleic Acids Research 50, № 5 (2022): 2667–80. http://dx.doi.org/10.1093/nar/gkac075.

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Abstract The tumour suppressor SLX4 plays multiple roles in the maintenance of genome stability, acting as a scaffold for structure-specific endonucleases and other DNA repair proteins. It directly interacts with the mismatch repair (MMR) protein MSH2 but the significance of this interaction remained unknown until recent findings showing that MutSβ (MSH2-MSH3) stimulates in vitro the SLX4-dependent Holliday junction resolvase activity. Here, we characterize the mode of interaction between SLX4 and MSH2, which relies on an MSH2-interacting peptide (SHIP box) that drives interaction of SLX4 with both MutSβ and MutSα (MSH2-MSH6). While we show that this MSH2 binding domain is dispensable for the well-established role of SLX4 in interstrand crosslink repair, we find that it mediates inhibition of MutSα-dependent MMR by SLX4, unravelling an unanticipated function of SLX4.

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Greene, C. N., and S. Jinks-Robertson. "Frameshift intermediates in homopolymer runs are removed efficiently by yeast mismatch repair proteins." Molecular and Cellular Biology 17, no. 5 (1997): 2844–50. http://dx.doi.org/10.1128/mcb.17.5.2844.

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A change in the number of base pairs within a coding sequence can result in a frameshift mutation, which almost invariably eliminates the function of the encoded protein. A frameshift reversion assay with Saccharomyces cerevisiae that can be used to examine the types of insertions and deletions that are generated during DNA replication, as well as the editing functions that remove such replication errors, has been developed. Reversion spectra have been obtained in a wild-type strain and in strains defective for defined components of the postreplicative mismatch repair system (msh2, msh3, msh6, msh3 msh6, pms1, and mih1 mutants). Comparison of the spectra reveals that yeast mismatch repair proteins preferentially remove frameshift intermediates that arise in homopolymer tracts and indicates that some of the proteins have distinct substrate or context specificities.

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Pal, Arumay, Harry M. Greenblatt, and Yaakov Levy. "Prerecognition Diffusion Mechanism of Human DNA Mismatch Repair Proteins along DNA: Msh2-Msh3 versus Msh2-Msh6." Biochemistry 59, no. 51 (2020): 4822–32. http://dx.doi.org/10.1021/acs.biochem.0c00669.

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Schultz-Jensen, Nadja, Berith E. Knudsen, Zuzana Frkova, et al. "Large-scale bioreactor production of the herbicide-degrading Aminobacter sp. strain MSH1." Applied Microbiology and Biotechnology 98, no. 5 (2013): 2335–44. http://dx.doi.org/10.1007/s00253-013-5202-5.

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Ekelund, Flemming, Christoffer Bugge Harder, Berith Elkær Knudsen, and Jens Aamand. "Aminobacter MSH1-Mineralisation of BAM in Sand-Filters Depends on Biological Diversity." PLOS ONE 10, no. 6 (2015): e0128838. http://dx.doi.org/10.1371/journal.pone.0128838.

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Marsischky, G. T., N. Filosi, M. F. Kane, and R. Kolodner. "Redundancy of Saccharomyces cerevisiae MSH3 and MSH6 in MSH2-dependent mismatch repair." Genes & Development 10, no. 4 (1996): 407–20. http://dx.doi.org/10.1101/gad.10.4.407.

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Wang, Aifen, Robert W. Holloway, Jinsong Yang, Zhe Pei, Yan Sun, and Yingyan Zhao. "Clinicopathologic analysis of MMR gene mutations and uterine adenocarcinomas: An updated population-based study." Journal of Clinical Oncology 38, no. 15_suppl (2020): e18100-e18100. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e18100.

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e18100 Background: Endometrial carcinoma frequently harbors genetic alterations in genes encoding mismatch repair (MMR) enzymes, a finding which has important implications for adjuvant therapy. The aim of this study is to determine an optimal screening strategy to detect MMR mutations for each histologic subtype of endometrial carcinoma (EC). Methods: We performed a comparative analysis of the demographic, clinical, pathologic, and molecular data, including MLH1, MLH3, PMS1, PMS2, MSH2, MSH3, MSH6, and EPCAM, for 562 patients from The Cancer Genome Atlas database (TCGA), stratified by tumor histologic subtype. Results: Molecular data was available for 562 patients, of which 162 (28.8%) had tumors that were positive for MMR mutations. We did not separate somatic and germline mutation. Of these tumors, the penetrate rate of FIGO grade 3 endometrioid endometrial carcinoma (EEC G3) (84/184, 45.7%) was significantly higher than the one of uterine serous carcinoma (USC) (35/156, 22.4%) ( p < 0.001), grade 2 (EEC G2) (26/129, 20.2%) ( p < 0.001), and grade 1 (EEC G1) (17/93, 18.3%) ( p < 0.001). Of EEC G3 tumors, patients with MMR gene mutations were significantly older ( p = 0.024) or had lower BMI's than MMR mutation noncarriers ( p = 0.028). Of 562 endometrial carcinomas, alterations in MSH2 (n = 55), MSH6 (n = 54), MSH3 (n = 50) were the most frequent mutations. There were no differences in overall survival and progression-free interval between MMR mutation carriers and nonmutation carriers (p > 0.05) except that PFI with MMR gene mutation was higher than with MMR proficiency in EEC G3 ( p = 0.014). Conclusions: EEC G3 harbored the most MMR mutations among EC. EEC G3 and USC could be more considered to screen MMR mutation due to more MMR mutations occurred in EEC G3 and USC than did among EEC G2 and EEC G1. Besides MLH1, MSH2, MSH6, PMS2 and EPCAM mutation , MLH3, MSH3, PMS1 mutation could be screened in patients with newly diagnosed endometrial carcinoma. [Table: see text]

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Martín, Azahara C., Sergio G. Atienza, María C. Ramírez, Francisco Barro, and Antonio Martín. "Chromosome engineering in wheat to restore male fertility in the msH1 CMS system." Molecular Breeding 24, no. 4 (2009): 397–408. http://dx.doi.org/10.1007/s11032-009-9301-z.

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Sia, E. A., R. J. Kokoska, M. Dominska, P. Greenwell, and T. D. Petes. "Microsatellite instability in yeast: dependence on repeat unit size and DNA mismatch repair genes." Molecular and Cellular Biology 17, no. 5 (1997): 2851–58. http://dx.doi.org/10.1128/mcb.17.5.2851.

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We examined the stability of microsatellites of different repeat unit lengths in Saccharomyces cerevisiae strains deficient in DNA mismatch repair. The msh2 and msh3 mutations destabilized microsatellites with repeat units of 1, 2, 4, 5, and 8 bp; a poly(G) tract of 18 bp was destabilized several thousand-fold by the msh2 mutation and about 100-fold by msh3. The msh6 mutations destabilized microsatellites with repeat units of 1 and 2 bp but had no effect on microsatellites with larger repeats. These results argue that coding sequences containing repetitive DNA tracts will be preferred target sites for mutations in human tumors with mismatch repair defects. We find that the DNA mismatch repair genes destabilize microsatellites with repeat units from 1 to 13 bp but have no effect on the stability of minisatellites with repeat units of 16 or 20 bp. Our data also suggest that displaced loops on the nascent strand, resulting from DNA polymerase slippage, are repaired differently than loops on the template strand.

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Pante, Eric, and Les Watling. "Chrysogorgia from the New England and Corner Seamounts: Atlantic–Pacific connections." Journal of the Marine Biological Association of the United Kingdom 92, no. 5 (2011): 911–27. http://dx.doi.org/10.1017/s0025315411001354.

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Recent exploration of the New England and Corner Seamounts revealed four new species of Chrysogorgia, described here using a combination of molecular and morphological data. These four species are characterized by a sinistral spiral, a character that, with one known exception, has only been reported for Pacific species. In addition, two species have a sclerite composition typical of the Pacific (‘squamosae typicae’). This faunal connection between the Atlantic and the Pacific is confirmed by analysis of the mitochondrial msh1 gene. The exceptional preservation of specimens collected with remotely operated vehicles allows us to discuss the effect of growth on some morphological characters.

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Mansour, Ahmed A., Carine Tornier, Elisabeth Lehmann, Michel Darmon, and Oliver Fleck. "Control of GT Repeat Stability in Schizosaccharomyces pombe by Mismatch Repair Factors." Genetics 158, no. 1 (2001): 77–85. http://dx.doi.org/10.1093/genetics/158.1.77.

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Abstract The mismatch repair (MMR) system ensures genome integrity by removing mispaired and unpaired bases that originate during replication. A major source of mutational changes is strand slippage in repetitive DNA sequences without concomitant repair. We established a genetic assay that allows measuring the stability of GT repeats in the ade6 gene of Schizosaccharomyces pombe. In repair-proficient strains most of the repeat variations were insertions, with addition of two nucleotides being the most frequent event. GT repeats were highly destabilized in strains defective in msh2 or pms1. In these backgrounds, mainly 2-bp insertions and 2-bp deletions occurred. Surprisingly, essentially the same high mutation rate was found with mutants defective in msh6. In contrast, a defect in swi4 (a homologue of Msh3) caused only slight effects, and instability was not further increased in msh6 swi4 double mutants. Also inactivation of exo1, which encodes an exonuclease that has an MMR-dependent function in repair of base-base mismatches, caused only slightly increased repeat instability. We conclude that Msh2, Msh6, and Pms1 have an important role in preventing tract length variations in dinucleotide repeats. Exo1 and Swi4 have a minor function, which is at least partially independent of MMR.

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Rawat, Mamta, Svetozar Kovacevic, Helen Billman-Jacobe, and Yossef Av-Gay. "Inactivation of mshB, a key gene in the mycothiol biosynthesis pathway in Mycobacterium smegmatis." Microbiology 149, no. 5 (2003): 1341–49. http://dx.doi.org/10.1099/mic.0.26084-0.

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The mshB gene encoding N-acetyl-1-d-myo-inosityl-2-amino-2-deoxy-α-d-glucopyranoside deacetylase (MshB) is a key enzyme in mycothiol biosynthesis. Disruption of mshB in Mycobacterium smegmatis resulted in decreased production of mycothiol (5–10 % of the parent strain mc2155) but did not abolish mycothiol synthesis completely. Complementation of the MshB− mutants with the mshB gene resulted in increased mycothiol production towards the exponential and stationary phases of the bacterial growth cycle. These results suggest that another enzyme is capable of mycothiol biosynthesis by providing N-acetylglucosaminylinositol deacetylation activity in the absence of MshB. One of the candidate enzymes capable of carrying out such reactions is the MshB orthologue mycothiol amide hydrolase, MCA. However, epichromosomal expression of mca in the MshB− mutants did not restore mycothiol levels to the level of the parent strain. Unlike other mutants, which have little or no detectable levels of mycothiol, the MshB− mutant did not exhibit increased resistance to isoniazid. However, the MshB− mutant was resistant to ethionamide. Phenotypic analysis of other mutants lacking mycothiol revealed that MshA− mutants also exhibit ethionamide resistance but that a MshC−mutant was sensitive to ethionamide, suggesting that mycothiol or its early intermediates influence ethionamide activation.

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Chi, N. W., and R. D. Kolodner. "Purification and characterization of MSH1, a yeast mitochondrial protein that binds to DNA mismatches." Journal of Biological Chemistry 269, no. 47 (1994): 29984–92. http://dx.doi.org/10.1016/s0021-9258(18)43978-6.

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Sia, Elaine A., and David T. Kirkpatrick. "The yeast MSH1 gene is not involved in DNA repair or recombination during meiosis." DNA Repair 4, no. 2 (2005): 253–61. http://dx.doi.org/10.1016/j.dnarep.2004.10.002.

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de la Rosa Santamaria, Roberto, Mon-Ray Shao, Guomei Wang, et al. "MSH1-Induced Non-Genetic Variation Provides a Source of Phenotypic Diversity in Sorghum bicolor." PLoS ONE 9, no. 10 (2014): e108407. http://dx.doi.org/10.1371/journal.pone.0108407.

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Bai, Lanlan, Tomoya Hirose, Wlaa Assi, Satoshi Wada, Shin-nosuke Takeshima, and Yoko Aida. "Bovine Leukemia Virus Infection Affects Host Gene Expression Associated with DNA Mismatch Repair." Pathogens 9, no. 11 (2020): 909. http://dx.doi.org/10.3390/pathogens9110909.

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Bovine leukemia virus (BLV) causes enzootic bovine leukosis, a malignant form of B-cell lymphoma, and is closely related to human T-cell leukemia viruses. We investigated whether BLV infection affects host genes associated with DNA mismatch repair (MMR). Next-generation sequencing of blood samples from five calves experimentally infected with BLV revealed the highest expression levels of seven MMR genes (EXO1, UNG, PCNA, MSH2, MSH3, MSH6, and PMS2) at the point of peak proviral loads (PVLs). Furthermore, MMR gene expression was only upregulated in cattle with higher PVLs. In particular, the expression levels of MSH2, MSH3, and UNG positively correlated with PVL in vivo. The expression levels of all seven MMR genes in pig kidney-15 cells and the levels of PMS2 and EXO1 in HeLa cells also increased tendencies after transient transfection with a BLV infectious clone. Moreover, MMR gene expression levels were significantly higher in BLV-expressing cell lines compared with those in the respective parental cell lines. Expression levels of MSH2 and EXO1 in BLV-infected cattle with lymphoma were significantly lower and higher, respectively, compared with those in infected cattle in vivo. These results reveal that BLV infection affects MMR gene expression, offering new candidate markers for lymphoma diagnosis.

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Lee, Susan D., Jennifer A. Surtees, and Eric Alani. "Saccharomyces cerevisiae MSH2–MSH3 and MSH2–MSH6 Complexes Display Distinct Requirements for DNA Binding Domain I in Mismatch Recognition." Journal of Molecular Biology 366, no. 1 (2007): 53–66. http://dx.doi.org/10.1016/j.jmb.2006.10.099.

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Duan, Jinlin, Tao Chen, Qiwei Li, et al. "Protein arginine methyltransferase 6 enhances immune checkpoint blockade efficacy via the STING pathway in MMR-proficient colorectal cancer." Journal for ImmunoTherapy of Cancer 13, no. 3 (2025): e010639. https://doi.org/10.1136/jitc-2024-010639.

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BackgroundThe emergence of immunotherapy has revolutionized the paradigm of cancer treatment with immune checkpoint blockades (ICB) in solid cancers, including colorectal cancer (CRC). However, only a small subset of CRC patients harboring deficient mismatch repair (dMMR) or microsatellite instability-high (MSI-H) benefits from ICB therapy. A very limited response to ICB therapy has been achieved in MMR-proficient CRC, representing a significant challenge limiting the clinical application of immunotherapy. MMR is the critical DNA repair pathway that maintains genomic integrity by correcting DNA mismatches, which is mediated by the MutSα or MutSβ complex consisting of MSH2 with MSH6 and MSH3, respectively. Given that MMR status directs effective immune response, we sought to determine whether targeting MMR capacity boosts ICB efficacy.MethodsAzoxymethane/dextran sodium sulfate (AOM/DSS)‐induced CRC and xenograft model were used to evaluate the function of PRMT6 and response to PRMT6 inhibitor EPZ020411 and combination therapy of PD1 and EPZ020411. Biochemical assays were performed to elucidate the underlying mechanism of PRMT6-mediated MSH2 methylation and immune evasion.ResultsWe have identified PRMT6 as a crucial regulator of MMR capacity via MSH2 dimethylation at R171 and R219. Such a modification abrogates its MMR capacity and prevents the recruitment of MSH3 and MSH6. PRMT6 loss or inhibition triggers cytosolic DNA accumulation and cGAS-STING signaling activation, leading to enhanced immune response in PRMT6-deficient colon tumors or xenografts. Pharmacological inhibition of PRMT6 using EPZ020411 promotes mutagenesis and destabilizes MutSα or MutSβ assembly, and prolonged EPZ020411 exposure maintains an MSI-like phenotype in microsatellite stability (MSS) cells. EPZ020411 treatment sensitizes ICB efficacy of MSS cells, but not MSI cells in vivo. Similar effects have been observed in MSS colon tumors induced by AOM/DSS.ConclusionsOur study provides a preclinical proof of concept to overcome resistance to immunotherapy by targeting PRMT6 in CRC with MSS.

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Raes, Bart, Benjamin Horemans, Daniel Rentsch, et al. "Aminobacter sp. MSH1 Mineralizes the Groundwater Micropollutant 2,6-Dichlorobenzamide through a Unique Chlorobenzoate Catabolic Pathway." Environmental Science & Technology 53, no. 17 (2019): 10146–56. http://dx.doi.org/10.1021/acs.est.9b02021.

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