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The process of homologous recombination plays essential roles in the mitotic and meiotic cell cycles of most eukaryotic organisms. During meiosis, the programmed formation and processing of double strand breaks by homologous recombination is obligatory to establish the mechanical force between chromosome homologues essential for their segregation. The absence of homologous recombination in meiosis leads to random segregation of homologues at the first meiotic division and formation of aneuploid gametes (spores in yeast).
Meiotic recombination also contributes to genetic diversity by creating new linkage arrangements between genes, or parts of genes. In mitotic cells, double strand breaks form during S-phase by the convergence of replication forks with transient single-strand lesions. These breaks are repaired by homologous recombination to restore the collapsed replication fork. The absence of homologous recombination functions in vertebrates results in the accumulation of chromosome and chromatid breaks during S-phase triggering apoptosis and cell death.
The recent discovery that several human cancer prone syndromes, for example, Nijmegin Breakage Syndrome and A-TLD, are caused by defects in double-strand break repair has highlighted the importance of this pathway in maintaining genome integrity and cancer avoidance. The genes required for the repair of double-strand breaks by homologous recombination in eukaryotes are members of the RAD52 group and most were identified in yeast by the sensitivity of mutants to ionizing radiation. Mutations in the RAD52 group genes lead to defects in meiotic and/or mitotic recombination providing evidence for a link between double-strand break (DSB) repair and homologous recombination. Homologues of the RAD52 group of genes have been identified in many other eukaryotes, and in some cases in prokaryotes and archaea, indicating that the recombinational repair pathway is highly conserved.
The focus of research in my laboratory during the last decade has been to identify new genes involved in homologous recombination and further characterization of the RAD52 group genes using budding yeast as a model system.
The process of homologous recombination plays essential roles in the mitotic and meiotic cell cycles of most eukaryotic organisms. During meiosis, the programmed formation and processing of double strand breaks by homologous recombination is obligatory to establish the mechanical force between chromosome homologues essential for their segregation. The absence of homologous recombination in meiosis leads to random segregation of homologues at the first meiotic division and formation of aneuploid gametes (spores in yeast).
Meiotic recombination also contributes to genetic diversity by creating new linkage arrangements between genes, or parts of genes. In mitotic cells, double strand breaks form during S-phase by the convergence of replication forks with transient single-strand lesions. These breaks are repaired by homologous recombination to restore the collapsed replication fork. The absence of homologous recombination functions in vertebrates results in the accumulation of chromosome and chromatid breaks during S-phase triggering apoptosis and cell death.
The recent discovery that several human cancer prone syndromes, for example, Nijmegin Breakage Syndrome and A-TLD, are caused by defects in double-strand break repair has highlighted the importance of this pathway in maintaining genome integrity and cancer avoidance. The genes required for the repair of double-strand breaks by homologous recombination in eukaryotes are members of the RAD52 group and most were identified in yeast by the sensitivity of mutants to ionizing radiation. Mutations in the RAD52 group genes lead to defects in meiotic and/or mitotic recombination providing evidence for a link between double-strand break (DSB) repair and homologous recombination. Homologues of the RAD52 group of genes have been identified in many other eukaryotes, and in some cases in prokaryotes and archaea, indicating that the recombinational repair pathway is highly conserved.
The focus of research in my laboratory during the last decade has been to identify new genes involved in homologous recombination and further characterization of the RAD52 group genes using budding yeast as a model system.
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Methods in Cell Biology (2024): 35-48
Lorenzo Galanti,Martina Peritore,Robert Gnugge,Elda Cannavo, Johannes Heipke, Maria Dilia Palumbieri,Barbara Steigenberger,Lorraine S. Symington,Petr Cejka,Boris Pfander
NATURE COMMUNICATIONSno. 1 (2024): 2890-2890
Michael T Kimble, Aakanksha Sane, Robert Jd Reid, Matthew J Johnson,Rodney Rothstein,Lorraine S Symington
bioRxiv : the preprint server for biology (2024)
Genes & developmentno. 7-8 (2024): 354-354
Nature Communicationsno. 1 (2023): 1-16
Molecular cellno. 8 (2023): 1237-1250.e15
Nature Communicationsno. 1 (2023): 1-15
bioRxiv (Cold Spring Harbor Laboratory) (2023)
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