MutL: conducting the cell's response to mismatched and misaligned DNA
| Autor: | Claire G. Cupples, Yaroslava Y. Polosina |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
DNA Replication
DNA Bacterial Protein Conformation Biology DNA Mismatch Repair Models Biological General Biochemistry Genetics and Molecular Biology DNA Glycosylases MutL Proteins Adenosine Triphosphate MutS-1 Escherichia coli Animals Adenosine Triphosphatases Endodeoxyribonucleases Escherichia coli Proteins DNA replication MutS Proteins DNA Helicases Base excision repair MutS DNA Mismatch-Binding Protein Cell biology Biochemistry Coding strand DNA mismatch repair Somatic Hypermutation Immunoglobulin Nucleotide excision repair Signal Transduction |
| Zdroj: | BioEssays : news and reviews in molecular, cellular and developmental biology. 32(1) |
| ISSN: | 1521-1878 |
| Popis: | Base pair mismatches in DNA arise from errors in DNA replication, recombination, and biochemical modification of bases. Mismatches are inherently transient. They are resolved passively by DNA replication, or actively by enzymatic removal and resynthesis of one of the bases. The first step in removal is recognition of strand discontinuity by one of the MutS proteins. Mismatches arising from errors in DNA replication are repaired in favor of the base on the template strand, but other mismatches trigger base excision or nucleotide excision repair (NER), or non-repair pathways such as hypermutation, cell cycle arrest, or apoptosis. We argue that MutL homologues play a key role in determining biologic outcome by recruiting and/or activating effector proteins in response to lesion recognition by MutS. We suggest that the process is regulated by conformational changes in MutL caused by cycles of ATP binding and hydrolysis, and by physiologic changes which influence effector availability. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text