Routine Q-banding chromosome analysis detected the jumping behaviour of bright fluorescent chromosome 22 satellites (22s+) in two unrelated males (case 1 ascertained for recurrent abortions and case 2 for infertility), and in the mother of one of them, all with a normal karyotype. The 22s+ was present in more than 90% of the cells. In a minority of the cells the polymorphism was present alternatively on another acrocentric, on one chromosome 22 and on another acrocentric, on both chromosomes 22 or it was absent. We take these findings as evidence of mitotic exchanges between the short arms of the acrocentric chromosomes. The presence of a stable 22s+ in the fibroblasts of case 1 and in the lymphocytes of his son indicates that acrocentric short arm exchanges depend both on the type of tissue and on the genetic content of all the other acrocentrics.

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SORB (selected observed residual breakpoints) induced by ionizing radiation or endonucleases are often non-randomly distributed in mammalian chromosomes. However, the role played by chromatin structure in the localization of chromosome SORB is not well understood. Anti-topoisomerase drugs such as etoposide are potent clastogens and unlike endonucleases or ionizing radiation, induce DNA double-strand breaks (DSB) by an indirect mechanism. Topoisomerase II (Topo II) is a main component of the nuclear matrix and the chromosome scaffold. Since etoposide leads to DSB by influencing the activity of Topo II, this compound may be a useful tool to study the influence of the chromatin organization on the distribution of induced SORB in mammalian chromosomes. In the present work, we compared the distribution of SORB induced during S-phase by etoposide or X-rays in the short euchromatic and long heterochromatic arms of the CHO9 X chromosome. The S-phase stage (early, mid or late) at which CHO9 cells were exposed to etoposide or X-rays was marked by incorporation of BrdU during treatments and later determined by immunolabeling of metaphase chromosomes with an anti-BrdU FITC-coupled antibody. The majority of treated cells were in late S-phase during treatment either with etoposide or X-rays. SORB induced by etoposide mapped preferentially to Xq but random localization was observed for SORB produced by X-rays. Possible explanations for the uneven distribution of etoposide-induced breakpoints along Xq are discussed.