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Homologous recombination : ウィキペディア英語版
Homologous recombination

Homologous recombination is a type of genetic recombination in which nucleotide sequences are exchanged between two similar or identical molecules of DNA. It is most widely used by cells to accurately repair harmful breaks that occur on both strands of DNA, known as double-strand breaks. Homologous recombination also produces new combinations of DNA sequences during meiosis, the process by which eukaryotes make gamete cells, like sperm and egg cells in animals. These new combinations of DNA represent genetic variation in offspring, which in turn enables populations to adapt during the course of evolution. Homologous recombination is also used in horizontal gene transfer to exchange genetic material between different strains and species of bacteria and viruses.
Although homologous recombination varies widely among different organisms and cell types, most forms involve the same basic steps. After a double-strand break occurs, sections of DNA around the 5' ends of the break are cut away in a process called ''resection''. In the ''strand invasion'' step that follows, an overhanging 3' end of the broken DNA molecule then "invades" a similar or identical DNA molecule that is not broken. After strand invasion, the further sequence of events may follow either of two main pathways discussed below (see Models); the DSBR (double-strand break repair) pathway or the SDSA (synthesis-dependent strand annealing) pathway. Homologous recombination that occurs during DNA repair tends to result in non-crossover products, in effect restoring the damaged DNA molecule as it existed before the double-strand break.
Homologous recombination is conserved across all three domains of life as well as viruses, suggesting that it is a nearly universal biological mechanism. The discovery of genes for homologous recombination in protists—a diverse group of eukaryotic microorganisms—has been interpreted as evidence that meiosis emerged early in the evolution of eukaryotes. Since their dysfunction has been strongly associated with increased susceptibility to several types of cancer, the proteins that facilitate homologous recombination are topics of active research. Homologous recombination is also used in gene targeting, a technique for introducing genetic changes into target organisms. For their development of this technique, Mario Capecchi, Martin Evans and Oliver Smithies were awarded the 2007 Nobel Prize for Physiology or Medicine.
== History and discovery ==

In the early 1900s, William Bateson and Reginald Punnett found an exception to one of the principles of inheritance originally described by Gregor Mendel in the 1860s. In contrast to Mendel's notion that traits are independently assorted when passed from parent to child—for example that a cat's hair color and its tail length are inherited independent of each other—Bateson and Punnett showed that certain genes associated with physical traits can be inherited together, or genetically linked.〔(【引用サイトリンク】 publisher=NAHSTE, University of Edinburgh )〕 In 1911, after observing that linked traits could on occasion be inherited separately, Thomas Hunt Morgan suggested that "crossovers" can occur between linked genes, where one of the linked genes physically crosses over to a different chromosome. Two decades later, Barbara McClintock and Harriet Creighton demonstrated that chromosomal crossover occurs during meiosis, the process of cell division by which sperm and egg cells are made. Within the same year as McClintock's discovery, Curt Stern showed that crossing over—later called "recombination"—could also occur in somatic cells like white blood cells and skin cells that divide through mitosis.〔
In 1947, the microbiologist Joshua Lederberg showed that bacteria—which had been assumed to reproduce only asexually through binary fission—are capable of genetic recombination, which is more similar to sexual reproduction. This work established ''E. coli'' as a model organism in genetics, and helped Lederberg win the 1958 Nobel Prize in Physiology or Medicine.〔(【引用サイトリンク】 publisher=Nobelprize.org )〕 Building on studies in fungi, in 1964 Robin Holliday proposed a model for recombination in meiosis which introduced key details of how the process can work, including the exchange of material between chromosomes through Holliday junctions. In 1983, Jack Szostak and colleagues presented a model now known as the DSBR pathway, which accounted for observations not explained by the Holliday model.〔 During the next decade, experiments in ''Drosophila'', budding yeast and mammalian cells led to the emergence of other models of homologous recombination, called SDSA pathways, which do not always rely on Holliday junctions.〔

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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