S. Zimmering

The repair-deficient mei-9a drosophila female potentiates chromosome loss induced in the paternal genome by diethylnitrosamine

Abstract Following matings of DEN-treated X c2 / B S Y y + males with repair-deficient mei -9 a females and ordinary females, significant increases in complete and partial sex chromosome loss as well as dramatic shifts in sex ratio were found with mei -9 a but not ordinary females. Accordingly, the mei -9 a female enhances the detection of chromosome lesions leading to chromosome loss induced in the male genome by DEN. To date, the 4 compounds tested in this way (DMN, DEN, MMS and procarbazine) exhibit strong potentiation of chromosome loss with mei -9 a females suggesting the possibility that a protocol involving treatment (or not) of X c2 / B s Y y + males mated with mei -9 a females may hold promise as an alternative to traditional tests for chromosome loss using repair-proficient females. Comparison with published translocation data on the 4 compounds indicated above suggests an overall greater sensitivity of the described mei -9 a chromosome-loss test compared with the traditional translocation test in the detection of chemically induced chromosome lesions.

Dose-response relationship for ethyl nitrosourea-induced sex-linked recessive lethals in germ cells of the female Drosophila melanogaster at relatively low doses

The present authors have begun to explore the dose-reponse relationship of ENU-induced sexlinked recessive lethals in immature germ cells of Drosophila melanogaster employing relatively low doses

Note on the utility of the st mus302 test for chromosome loss in a blind test of an environmental compound for chromosome breakage in Drosophila.

Under the auspices of the National Institute of Environmental Health Sciences (NIEHS) and in conjunction with other Drosophila laboratories, we are assaying environmental compounds for mutagenic activity in a blind test evaluating initially for gene/point mutations in the sex-linked recessive lethal test and, if positive, for chromosome breakage in the heritable translocation test to detect translocations between chromosomes 2 and 3 and between the Y chromosome and chromosome 2 and/or 3. One of the first compounds tested proved positive in both assays. The compound bears the code designation 024474 or 623474. For the recessive lethal test, males 24 h old and starved 6 h were permitted to feed for 72 h (solutions renewed at 24-h intervals) on 0.0, 2.5, 5.0 and 7.5 mg/ml of the compound in 5% sucrose. Results were, respectively (number of lethals/numbers of tests), 1/3349 (0.03%), 10/1040 (0.96%), 16/1088 (1.47%) and 39/2509 (1.55%). Only males treated with 7.5 mg/ml were tested for translocations. No translocations were found in 8335 control genomes and 4/6210 and 7.5 mg/ml distributed as follows: 0/2645 following 7-9 days of sperm storage, 4/3416 (10-12 days) and 0,/149 (13-15 days); shorter periods of storage (1-6 days) were not tested. Regarding tests for chromosome breakage, Zimmering and co-workers have demonstrated improved chromosome-breakage detection capability of conventional F1 tests for chromosome loss by substituting repair-deficient mei-9 a for ordinary repair-proficient PI females in mutagenicity assays of 5 monofunctional alkylating agents including MMS, DMN, DEN, procarbazine (see Zimmering, 1981) and MNU (Zimmering and Moberg, unpublished). More recently, females from the repair-deficient strain designated s t mus302 have been employed and shown to confer even greater sensitivity on the chromosome loss test in assays of the above compounds (Zimmering, 1982, and unpublished). Accordingly, X c2, y f / B S y y +