High production of nondisjunction mutants in the offspring of Drosophila melanogaster females exposed to carbon dioxide at meiosis I.

Drosophila melanogaster females homozygous for X-linked recessive markers, y and wi, were exposed to CO2 and mated with y+ w+/Y males. The progeny were sampled and inspected for y wi/y wi/Y (XXY) and y+ w+/O (XO) mutants. The frequency of nondisjunction XXY mutants after a 90-min exposure to CO2 increased 100-fold above the control level in the first-day brood but did not increase above the control level in the second to sixth broods, showing that CO2 is an extremely potent inducer of nondisjunction in mature oocytes during meiotic metaphase I but is not harmful to immature oocytes. Nondisjunction-causing damage induced by CO2 in mature oocytes disappeared completely within one day after CO2 treatment, as evidenced by a reduction of the number of XXY mutants to the control level when the mating of CO2-treated females was delayed by one day. CO2-induced nondisjunction is probably due to damage to spindle microtubules in mature oocytes at metaphase I. N2 is a less potent inducer of nondisjunction than CO2. Maternal X-irradiation with 4 Gy did not induce XXY mutants, showing that medium-level radiation does not induce nondisjunction. The results support Gaulden's hypothesis that oxygen deficits and CO2 increases in the microenvironment of mature oocytes can be potent inducers of nondisjunction. The possible relationship to the cluster of Down syndrome seen in Berlin shortly after the Chernobyl accident is discussed.