cross-link exposure

In bacteria, transformation is a process of gene transfer that ordinarily occurs between individual cells of the same bacterial species. Transformation involves integration of donor DNA into the recipient chromosome by recombination. This process appears to be an adaptation for repairing DNA damages in the recipient chromosome by HRR.[5] Transformation may provide a benefit to pathogenic bacteria by allowing repair of DNA damage, particularly damages that occur in the inflammatory, oxidizing environment associated with infection of a host. When two or more viruses, each containing lethal genomic damages, infect the same host cell, the virus genomes can often pair with each other and undergo HRR to produce viable progeny. This process, referred to as multiplicity reactivation, has been studied in bacteriophages T4 and lambda,[6] as well as in several pathogenic viruses. In the case of pathogenic viruses, multiplicity reactivation may be an adaptive benefit to the virus since it allows the repair of DNA damages caused by exposure to the oxidizing environment produced during host infection.[5] Meiotic recombination[edit] Molecular models of meiotic recombination have evolved over the years as relevant evidence accumulated. A major incentive for developing a fundamental understanding of the mechanism of meiotic recombination is that such understanding is crucial for solving the problem of the adaptive function of sex, a major unresolved issue in biology. A recent model that reflects current understanding was presented by Anderson and Sekelsky,[7] and is outlined in the first figure in this article. The figure shows that two of the four chromatids present early in meiosis (prophase I) are paired with each other and able to interact. Recombination, in this version of the model, is initiated by a double-strand break (or gap) shown in the DNA molecule (chromatid) at the top of the first figure in this article. However, other types of DNA damage may also initiate recombination. For instance, an inter-strand cross-link (caused by exposure to a cross-linking agent such as mitomycin C) can be repaired by HRR.

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