Role of deoxyuridine incorporation and DNA repair in the expression of human chromosomal fragile sites.

This paper is a discussion of the possible roles of deoxyuridine incorporation into DNA and DNA-repair processes in the expression of the folate-sensitive, common chromosomal fragile sites. Expression of aberrations at these sites increases under conditions expected to increase deoxyuridine incorporation into the chromosome. It is likely that this abnormal base is removed by an excision-repair process that results in transient chromosome breaks; these breaks are seen as chromosome aberrations if repair is not completed before metaphase. Analogous events may account for other types of chromosome aberrations including the so-called "spontaneous" aberrations, the rare folate-sensitive fragile sites, and fragile sites induced by other means.