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  1. Meiotic recombination: A mechanism for tracking and eliminating mutations?Bruce D. McKee - 1996 - Bioessays 18 (5):411-419.
    The function of meiotic recombination has remained controversial, despite recent inroads into mechanisms. Ideas concerning a possible role of recombination in the elimination or efficient incorporation of mutations have been backed by theoretical studies but have lacked empirical support. Recent investigations into the basis for local variations in recombination frequency in yeast have uncovered a strong association between recombination initiation sites and transcriptional regulatory sequences. Other recent studies indicate a strong correlation between transcription and mutation rates in yeast genes. Taken (...)
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  • Post‐replication repair in DT40 cells: translesion polymerases versus recombinases.Helfrid Hochegger, Eichiro Sonoda & Shunichi Takeda - 2004 - Bioessays 26 (2):151-158.
    Replication forks inevitably stall at damaged DNA in every cell cycle. The ability to overcome DNA lesions is an essential feature of the replication machinery. A variety of specialized polymerases have recently been discovered, which enable cells to replicate past various forms of damage by a process termed translesion synthesis. Alternatively, homologous recombination can be used to restart DNA replication across the lesion. Genetic and biochemical studies have shed light on the impact of these two post‐replication repair pathways in bacteria (...)
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  • Roadblocks and detours during DNA replication: Mechanisms of mutagenesis in mammalian cells.Hanspeter Naegeli - 1994 - Bioessays 16 (8):557-564.
    Mutations in specific genes result in birth defects, cancer, inherited diseases or lethality. The frequency with which DNA damage is converted to mutations increases dramatically when the cellular genome is replicated. Although DNA damage poses special problems to the fidelity of DNA replication, efficient mechanisms exist in mammalian cells which function to replicate their genome despite the presence of many damaged sites. These mechanisms operate in either error‐prone or error‐free modes of DNA synthesis, and frequently involve DNA strand‐pairing reactions. Genetic (...)
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