Gene repair mechanisms

Which is the most correct sequence of events in gene repair mechanisms in patients without a mutated repair process ... 

Heteroduplex recombination involves preparing single-stranded DNA from two different homologous genes and mixing them to form heteroduplexes. These heteroduplexes are then transformed into a host that then creates hybrid homoduplexes through in vivo mismatch repair mechanisms [22]. 

Burch (1983) suggests that repair mechanisms cause a non neglectible complication for extrapolation from high to low doses and presents a modification of the linear-quadratic formula given above. Katz and Hofmann (1982) carried out an analysis of particle tracks with the result that they find no basis for a linear or linear-quadratic extrapolation to low doses. Van Bekkum and Bentvelzen (1982) present a hypothesis of the gene transfer-... 

Ultraviolet light induces the formation of dimers between adjacent thymines in DNA (also occasionally between other adjacent pyrimidines). The formation of thymine dimers interferes with DNA rephcation and normal gene expression. Thymine dimers are eliminated from DNA by a nucleotide excision-repair mechanism (Figure 1-2-4). 

Multiple mutations that activate oncogenes or inactivate tumor suppressor genes accumulate due to progressive loss of DNA repair mechanisms and cell cycle control. 

Ultraviolet light produces pyrimidine dimers in human DNA, as it does in E. coli DNA. Furthermore, the repair mechanisms are similar. Studies of skin fibroblasts from patients with xeroderma pigmentosum have revealed a biochemical defect in one form of this disease. In normal fibro-blasts, half the pyrimidine dimers produced by ultraviolet radiation are excised in less than 24 hours. In contrast, almost no dimers are excised in this time interval in fibroblasts derived from patients with xeroderma pigmentosum. The results of these studies show that xeroderma pigmentosum can be produced by a defect in the excinuclease that hydrolyzes the DNA backbone near a pyrimidine dimer. The drastic clinical consequences of this enzymatic defect emphasize the critical importance of DNA-repair processes. The disease can also be caused by mutations in eight other genes for DNA repair, which attests to the complexity of repair processes. 

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