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Rad27 and Exo1 function in different excision pathways for mismatch repair in Saccharomyces cerevisiae

Author

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  • Felipe A. Calil

    (Ludwig Institute for Cancer Research, University of California School of Medicine)

  • Bin-Zhong Li

    (Ludwig Institute for Cancer Research, University of California School of Medicine)

  • Kendall A. Torres

    (Ludwig Institute for Cancer Research, University of California School of Medicine)

  • Katarina Nguyen

    (Ludwig Institute for Cancer Research, University of California School of Medicine)

  • Nikki Bowen

    (Ludwig Institute for Cancer Research, University of California School of Medicine)

  • Christopher D. Putnam

    (Ludwig Institute for Cancer Research, University of California School of Medicine
    University of California School of Medicine)

  • Richard D. Kolodner

    (Ludwig Institute for Cancer Research, University of California School of Medicine
    Cellular and Molecular Medicine, University of California School of Medicine
    Moores-UCSD Cancer Center, University of California School of Medicine
    Institute of Genomic Medicine, University of California School of Medicine)

Abstract

Eukaryotic DNA Mismatch Repair (MMR) involves redundant exonuclease 1 (Exo1)-dependent and Exo1-independent pathways, of which the Exo1-independent pathway(s) is not well understood. The exo1Δ440-702 mutation, which deletes the MutS Homolog 2 (Msh2) and MutL Homolog 1 (Mlh1) interacting peptides (SHIP and MIP boxes, respectively), eliminates the Exo1 MMR functions but is not lethal in combination with rad27Δ mutations. Analyzing the effect of different combinations of the exo1Δ440-702 mutation, a rad27Δ mutation and the pms1-A99V mutation, which inactivates an Exo1-independent MMR pathway, demonstrated that each of these mutations inactivates a different MMR pathway. Furthermore, it was possible to reconstitute a Rad27- and Msh2-Msh6-dependent MMR reaction in vitro using a mispaired DNA substrate and other MMR proteins. Our results demonstrate Rad27 defines an Exo1-independent eukaryotic MMR pathway that is redundant with at least two other MMR pathways.

Suggested Citation

  • Felipe A. Calil & Bin-Zhong Li & Kendall A. Torres & Katarina Nguyen & Nikki Bowen & Christopher D. Putnam & Richard D. Kolodner, 2021. "Rad27 and Exo1 function in different excision pathways for mismatch repair in Saccharomyces cerevisiae," Nature Communications, Nature, vol. 12(1), pages 1-10, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-25866-z
    DOI: 10.1038/s41467-021-25866-z
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