Genetic recombination : understanding the mechanisms / Harold L.K. Whitehouse.
- Harold Leslie Keer Whitehouse
- Date:
- [1982]
Licence: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)
Credit: Genetic recombination : understanding the mechanisms / Harold L.K. Whitehouse. Source: Wellcome Collection.
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![and Parag (1975) and in Saccharomyces by Boram and Roman (1976). It thus seems likely that a repair process requiring recombination may be of general occurrence in fungi, and that damage to DNA of a mitotic cell derepresses recom bination. Repression of mitotic recombination seems to be associated with repression of sister-chromatid exchange. Such exchanges were first detected by Taylor, Woods and Hughes (1957) in their investigation of chromosome replication in Vicia faba. As described in Section 1, they used autoradiography, following 3 H-labelling of newly synthesized strands of DNA. They found that sister chromatids sometimes underwent exchange, revealed as a label switch in the autoradiograph. There has been much debate as to how far sister-chromatid exchanges are a consequence of the presence of the label needed to detect them (review: Wolff, 1977). It seems clear that many, perhaps a majority, do result from the labelling. This applies also to the harlequin staining described in Section 1, using a fluorescent dye and Giemsa stain after two rounds of replication in the presence of 5-bromo- deoxyuridine. Thus, Schvartzman et al. (1979) concluded that most of the sister- chromatid exchanges observed in this way in Allium cepa (Onion) root tips were induced by the bromodeoxyuridine. In marked contrast to this low spontaneous exchange rate, Chaganti, Schonberg and German (1974) discovered that in the rare human disease called Bloom’s syndrome, which is caused by a single reces sive gene, bl, sister-chromatid exchanges were frequent. Using harlequin staining, their frequency in lymphocytes in culture was found to be about 13 times the normal rate (Plate 6 ). This discovery is of particular interest because lymphocytes from bl homozygotes also show a high frequency of quadriradial chromosome configurations at mitosis (German, 1964). As pointed out in Section 2, these imply mitotic crossing over. It seems as if the recessive gene responsible for Bloom’s syndrome leads to derepression of recombination both between homologous chromosomes and between sister chromatids. Tice, Windier and Rary (1978) studied a mixed culture of normal human fibroblast cells and those from a Bloom's patient. They found that the bl bl cells produced an agent capable of increasing the frequency of sister-chromatid exchanges in normal cells. Rommelaere, Susskind and Errera (1973) found that ultraviolet irradiation increased the frequency of both mitotic crossing over and sister-chromatid exchange in cultured cells of Cricetulus griseus (Chinese Hamster). The mitotic crossing over was observed by inducing fusion between cells labelled with 1 3 H Ithymidine and others labelled with [ l 4 C]thymidine, and finding chromosomes carrying both labels. Schvartzman et al. (1979) favoured the Meselson-Radding hypothesis as the mechanism of sister-chromatid exchange, since they found exchanges in Allium root tips when only one of the four polynucleotide chains contained bromodeoxyuridine. They inferred from this that a break in only one strand was needed to initiate sister-chromatid exchange. (See also Section 7.) On present evidence it is reasonable to suppose a common mechanism for recombination between sister chromatids and between homologous chromosomes, both at mitosis and meiosis. The differences seem to be in regulation, sister-](https://iiif.wellcomecollection.org/image/b18020768_0362.JP2/full/800%2C/0/default.jpg)
