Abstract

The antibiotic, mitomycin C (MC), induces non-homologous chromosomal interchanges in gonial cells of Drosophila males and females. In both males and females, the interchanges were recovered in a non-random distribution within the gonial broods of individual families. MC also increased the frequency of crossing-over in Drosophila females especially in the centromeric regions of gonial cells, yet did not induce crossing-over in males. The MC-induced increase in crossing-over in females was not a result of gonially induced events that were multiplied mitotically in stem cells as was the case with MC-induced interchanges. MC was also mutagenic in both sexes especially in those cells which had completed the first meiotic prophase. Since MC can either mono- or bifunctionally alkylate DNA, it was proposed that excision of monofunctionally alkylated bases would give rise to single-strand “nicks”, whereas excision of two bases involved in a bifunctionally alkylated crosslink would generate double-strand “cuts”. By this model, single-strand nicks could act as the precondition for crossing-over and would produce crossovers when the necessary factors for spontaneous meiotic crossing-over are present. Double-strand “cuts”, on the other hand, could generate translocation-type interchanges independently of the crossover apparatus in both males and females. A test of this prediction was made with the monofunctional alkylating agent ethyl methanesulfonate (EMS). Results were consistent with the model and revealed that gonial cells just preceding the stage at which crossing-over occurs, are most sensitive to EMS.

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