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

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 exo1?440-702 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 rad27? mutations. Analyzing the effect of different combinations of the exo1?440-702 mutation, a rad27? 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.
Mesh Terms:
DNA Ligases, DNA Mismatch Repair, DNA, Fungal, Exodeoxyribonucleases, Flap Endonucleases, MutL Proteins, Mutation, Proliferating Cell Nuclear Antigen, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins
Nat Commun
Date: Sep. 22, 2021
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