| Standard Name | MLH2 |
|---|---|
| Systematic Name | YLR035C |
| Feature Type | ORF, Verified |
| Description | Protein involved in the mismatch repair of certain frameshift intermediates and involved in meiotic recombination; forms a complex with Mlh1p (1, 2, 3 and see Summary Paragraph) |
| Chromosomal Location | |
|---|---|
| Note: this feature is encoded on the Crick strand. | |
| View Computational GO annotations for MLH2 | |
| Molecular Function | |
| Manually curated |
|
| Biological Process | |
| Manually curated | |
| Cellular Component | |
| Manually curated |
| Large-scale survey | |
|---|---|
| null |
|
| Resources |
| 25 total interaction(s) for 19 unique genes/features. | |
| Physical Interactions |
|
| Genetic Interactions |
|
| Resources |
|
|
| |
| Resources |
| Localization | |
|---|---|
| Phosphorylation | PhosphoGRID | PhosphoPep Database |
| Structure | |
| Homologs |
| Note: this feature is encoded on the Crick strand. | |||||||||||||
|
| |||||||||||||
| Last Update | Coordinates: 2011-02-03 | Sequence: 1996-07-31 | ||||||||||||
| Subfeature details |
| ||||||||||||
| Retrieve sequences | |||||||||||||
| S288C only | |
|---|---|
| S288C vs. other species | |
| S288C vs. other strains |
| External Links | All Associated Seq | Entrez Gene | Entrez RefSeq Protein | MIPS | Search all NCBI (Entrez) | UniProtKB |
|---|
| Primary SGDID | S000004025 |
|---|
MLH2, one of four MutL homologs in S. cerevisiae, is involved in mismatch repair during mitosis and meiosis and plays a role in correcting mismatches that arise during the formation of heteroduplex DNA between two homologous chromosomes during meiotic recombination (reviewed in 4, 5). Like Pms1p and Mlh3p, two other MutL homologs, Mlh2p forms a heterodimer with Mlh1p, the fourth MutL homolog (6, 7, 8, 2). Although mlh2 single mutants are resistant to some anticancer compounds (9) and are involved in the repair of specific types of mismatches (1), its role in general mismatch repair appears to be limited. In mlh2 single mutants, there is an increase in events where the 4:4 Mendelian segregation pattern of the 8 single-strands of DNA is altered to a 5:3 non-Mendelian segregation pattern, suggesting mlh2 mutants fail to repair these mismatches during meiosis (2, 3). Although mlh2 single mutants do not display a decrease in the level of cross-overs like an mlh3 single mutant, an mlh2 mlh3 double mutant displays an increase in the level of cross-overs compared to the mlh3 single mutant, suggesting that Mlh2p may play a role in the formation of heteroduplexes that lead to cross-overs (3).
| 1) | Harfe BD, et al. (2000) Discrete in vivo roles for the MutL homologs Mlh2p and Mlh3p in the removal of frameshift intermediates in budding yeast. Curr Biol 10(3):145-8 |
| 2) | Wang TF, et al. (1999) Functional specificity of MutL homologs in yeast: evidence for three Mlh1-based heterocomplexes with distinct roles during meiosis in recombination and mismatch correction. Proc Natl Acad Sci U S A 96(24):13914-9 |
| 3) | Abdullah MF, et al. (2004) A role for the MutL homologue MLH2 in controlling heteroduplex formation and in regulating between two different crossover pathways in budding yeast. Cytogenet Genome Res 107(3-4):180-90 |
| 4) | Kolodner RD and Marsischky GT (1999) Eukaryotic DNA mismatch repair. Curr Opin Genet Dev 9(1):89-96 |
| 5) | Borts RH, et al. (2000) The many faces of mismatch repair in meiosis. Mutat Res 451(1-2):129-50 |
| 6) | Prolla TA, et al. (1994) MLH1, PMS1, and MSH2 interactions during the initiation of DNA mismatch repair in yeast. Science 265(5175):1091-3 |
| 7) | Pang Q, et al. (1997) Functional domains of the Saccharomyces cerevisiae Mlh1p and Pms1p DNA mismatch repair proteins and their relevance to human hereditary nonpolyposis colorectal cancer-associated mutations. Mol Cell Biol 17(8):4465-73 |
| 8) | Flores-Rozas H and Kolodner RD (1998) The Saccharomyces cerevisiae MLH3 gene functions in MSH3-dependent suppression of frameshift mutations. Proc Natl Acad Sci U S A 95(21):12404-9 |
| 9) | Durant ST, et al. (1999) Dependence on RAD52 and RAD1 for anticancer drug resistance mediated by inactivation of mismatch repair genes. Curr Biol 9(1):51-4 |





