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#MutH

2 public questions tagged with this topic.

Repair Pathway

Mismatch repair in eukaryotes lacks

Eukaryotic mismatch repair retains conserved MutS homologs MSH2/MSH6 for mismatch recognition and MutL homologs MLH1/PMS2 for coordination, but lacks MutH ortholog entirely. Strand discrimination does not depend on Dam methylation, absent in eukaryotes. Instead, naturally occurring nicks associated with lagging strand Okazaki fragment termini, leading strand replication discontinuities, or PCNA-bound MutL endonuclease activity create entry points for EXO1 exonuclease. MutLα itself displays latent endonuclease regulated by PCNA and ATP. Therefore, eukaryotic system achieves directionality witho

Ref: NCBI Bookshelf DNA Mismatch Repair in Eukaryotes No MutH; Lodish Molecular Cell Biology 9th ed. Chapter 11 Eukaryotic MMR differences

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Repair Pathway

MutH introduces a nick in the

MutH is methylation-sensitive endonuclease whose nicking activity is licensed by MutS-MutL complex bound at mismatch. Parental strands carry N6-methyladenine at GATC sites due to Dam methylase, whereas newly synthesized strands remain unmethylated for several minutes post-replication. MutH senses this chemical asymmetry and introduces single-strand break 5' to GATC on unmethylated strand. This incision creates entry point for helicase II UvrD and single-strand exonucleases ExoI, ExoVII, RecJ. Selective cleavage ensures degradation targets error-containing nascent strand while methylated templa

Ref: Berg et al., Biochemistry, 9th ed., Section 28.3: MutH endonuclease hemimethylated incision mechanism; J Biol Chem 2020 strand-specific nicking

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