Saccharomyces cerevisiae checkpoint genes MEC1, RAD17 and RAD24 are required for normal meiotic recombination partner choice
| Autor: | Teresa M. Holzen, Jeremy M. Grushcow, Douglas K. Bishop, Ted Weinert, Ken J. Park, Michael Lichten |
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| Rok vydání: | 1999 |
| Předmět: |
Mitotic crossover
Saccharomyces cerevisiae Proteins DNA Repair Genotype Genes Fungal Cell Cycle Proteins Saccharomyces cerevisiae Biology Protein Serine-Threonine Kinases Genetic recombination Fungal Proteins Genetics Ectopic recombination Crossing Over Genetic Recombination Genetic Endodeoxyribonucleases Models Genetic Synapsis Intracellular Signaling Peptides and Proteins Nuclear Proteins G2-M DNA damage checkpoint Meiotic recombination checkpoint DNA-Binding Proteins Meiosis Mutagenesis Insertional Mutagenesis DMC1 Chromosomes Fungal Homologous recombination DNA Damage Research Article |
| Zdroj: | Europe PubMed Central |
| ISSN: | 0016-6731 |
| Popis: | Checkpoint gene function prevents meiotic progression when recombination is blocked by mutations in the recA homologue DMC1. Bypass of dmc1 arrest by mutation of the DNA damage checkpoint genes MEC1, RAD17, or RAD24 results in a dramatic loss of spore viability, suggesting that these genes play an important role in monitoring the progression of recombination. We show here that the role of mitotic checkpoint genes in meiosis is not limited to maintaining arrest in abnormal meioses; mec1-1, rad24, and rad17 single mutants have additional meiotic defects. All three mutants display Zip1 polycomplexes in two- to threefold more nuclei than observed in wild-type controls, suggesting that synapsis may be aberrant. Additionally, all three mutants exhibit elevated levels of ectopic recombination in a novel physical assay. rad17 mutants also alter the fraction of recombination events that are accompanied by an exchange of flanking markers. Crossovers are associated with up to 90% of recombination events for one pair of alleles in rad17, as compared with 65% in wild type. Meiotic progression is not required to allow ectopic recombination in rad17 mutants, as it still occurs at elevated levels in ndt80 mutants that arrest in prophase regardless of checkpoint signaling. These observations support the suggestion that MEC1, RAD17, and RAD24, in addition to their proposed monitoring function, act to promote normal meiotic recombination. |
| Databáze: | OpenAIRE |
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