Two protein bands, resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, account for most of the cytochrome P -450 in Drosophila melanogaster . P -450-A is ubiquitous among strains tested; whereas P -450-B is unique to certain strains. Dimethylnitrosamine demethylase activity is associated with P -450-B. Biochemical and genetic analyses showed that genes located on chromosome II were required for P -450-B expression. These genes were mapped within an interval that includes a major insecticide-resistance locus. Regulatory loci on chromosome III were required for maximum expression of P -450-B. One of these regulatory loci was mapped at another major resistance locus on chromosome III. There was a good correlation between P -450-B expression and resistance to phenylurea among the different strains tested. These results indicate that Drosophila can be a useful model to study the molecular mechanisms of insecticide resistance.

A dimethylnitrosamine (DMN) demethylase with levels of activity comparable to that in uninduced rat liver was demonstrated in both larval and adult forms of the Hikone-R strain of Drosophila. A microsomal enzyme, it has many properties of a cytochrome P-450-containing mixed-function oxidase. Kinetic analysis indicates only a single enzyme with an apparent Km of 10.5 mM DMN.

An important question facing our society is the impact of numerous chemical insults on the health of man and his environment. Faced with a staggering array of chemicals and enormous testing costs, we can test only a few chemicals for possible carcinogenic effects. Recent results with the Salmonella/mammalian microsome mutagenesis assay developed by Ames (2), demonstrating a striking correlation between carcinogenicity and mutagenicity of many chemical compounds, offer the possibility that mutagenesis assay systems can provide a quick identification of potential carcinogens. Results from microbial assays can serve as a guideline for further mutagenesis testing as well as identify those compounds requiring more extensive analysis in mammalian systems.

The biochemical evidence presented in this paper supports Baker's hypothesis, based on genetic evidence, that the lethality of scs1/0 larvae is due primarily to suppression of the genes for 18S and 28S ribosomal RNA. The levels of ribosomal RNA in scs1/0 and in y w/0 (control) larvae were determined by three different methods. The results showed a consistent reduction of about 15% in the amount of 18S and 28S ribosomal RNA in scs1/0. In addition, DNA:RNA hybridization data established that the scs1 chromosome had not lost ribosomal DNA, so that the decreased synthesis of ribosomes could not be attributed to a somatic deletion. It is suggested that the reduction in 18S and 28S ribosomal RNA in scs1/0 results from a suppression of transcription.

Aneuploids have been produced for the 5S RNA genes of Drosophila melanogaster by three different methods. Tandem duplications were produced at a frequency of about 0.05% by irradiation of oocytes and selection for “anti-Minutes.” Other Minute suppressors were recovered and localized to the region between nuDand Pu2on the genetic map. One, SuM1, reduced crossing-over as a heterozygote and is tentatively identified as a duplication. Deficiencies for the 5S RNA genes were also produced, which showed no dominant phenotype. A Minute deficiency was localized to region 56F-57A on the salivary map and was shown to be allelic to M(2) 173. The “anti-Minute” method of selection should be useful for producing tandem duplications throughout the genome.