Induction of chromosome aberrations by chemical mutagens in neural ganglia of Drosophila melanogaster

Marco, A. De; Polani, Stefania

doi:10.1016/0027-5107(83)90080-5

Cited by 3 publications

(1 citation statement)

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“…Since Merz [1961] first reported breakage of chromosomes by mitomycin C (MMC), the induction of chromosome aberrations and sister chromatid exchanges by this bifunctional alkylating agent has been documented in a wide variety of cells [eg, Nowell, 1964;Morad et al, 1973;Au et al, 1980;Gupta and Sharma, 1982;Kocan et al, 1982;Sandberg, 1982;Wolff, 1982;Cervenka and Hirsch, 1983;De Marco and Polani, 1983;Dulout and Olivero, 19841. As a consequence, MMC is now generally viewed as a good positive control chemical in tests with chromosome change as the mutagenic endpoint.…”

Section: Introductionmentioning

confidence: 99%

Chromosome fragments and other abnormalities induced by mitomycin C in the neuroblast of chortophaga viridifasciata

1985

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Mitomycin C (MMC) induces acentric chromosome fragments in the neuroblast (Nb) of the grasshopper embryo (Chortophaga viridifasciata) after acute and chronic exposure to concentrations ranging from 10(-8) to 10(-4) M, the dose response being essentially linear up to 10(-5) M. Because Colcemid is not used in the Nb assay, it was possible to detect two additional effects of MMC: (1) Prolonged retardation of many cells occurs when they reach very late prophase; the chromosomes continue condensing and lose their orderly prophase orientation, and the nuclear envelope becomes increasingly fragile. Such cells, which were observed after both acute and chronic exposure, give the false impression of being c-metaphases when they are fixed and squashed. The frequency of retarded very late prophases and the duration of retardation are related to MMC concentration and time of exposure. A rationale is presented supporting the idea that the events associated with retarded very late prophase result from MMC effects on the nuclear envelope. (2) MMC significantly increases the frequency of Nb's with attenuated centromeres at the beginning of early anaphase, an effect that appears to be caused by a delay in the repulsion of sister chromatids that usually occurs immediately after centromere separation begins.

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