We have sampled a London population of Drosophila melanogaster for null alleles at twenty-five allozyme loci. The same loci and biochemical techniques were used as in our previous survey of a North Carolina population (Voelker et al. 1980). This second survey is completely concordant with the first. No nulls were detected among the five X-linked loci. The mean frequency of nulls at the twenty autosomal loci was 0.0023. Although there is significant interlocus heterogeneity, the two populations appear to have the same frequencies at each locus. This suggests that null alleles at these allozyme loci are in mutation-selection balance, and we estimate the average heterozygous effect of an allozyme null to be 0.0015. Consideration of allozyme null-allele frequencies, the effects of allozyme null alleles on viability and fertility and the generally greater amount of genetic variability at allozyme loci determined by electrophoresis lead us to doubt the validity of generalizing from allozyme data to the whole genome.

A Raleigh, NC, population of Drosophila melanogaster was sampled for the presence of enzyme null alleles at 25 loci. No nulls were found at any of five X-linked loci. Nulls were recovered at 13 of 20 autosomal loci; the weighted mean frequency for all 20 autosomal loci was estimated to be 0.0025. A consideration of the effects of these null alleles on viability strongly suggests that, although they may contribute to so-called polygenic variation, they are not representative of the entire genome.

We previously described an alpha-amanitin-resistant mutant of D. melanogaster (AmaC4 or simply C4) with an altered, amanitin-resistant RNA polymerase II. We have now more fully characterized this mutant genetically and biochemically. We genetically mapped C4 to position 35.66 on the X chromosome and cytogenetically localized it to the polytene chromosome band interval 10C2-10D4. We then demonstrated that C4 is allelic to a previously known lethal-mutable locus I(1)L5 in this chromosomal region. Several known lethal alleles of L5 in fact affected the properties of RNA polymerase II in vitro. Following EMS mutagenesis of the C4-bearing chromosome we recovered new lethal L5 alleles, some of which were shown biochemically to have an altered amanitin-resistance polymerase II component. Furthermore, we induced mutants of C4 that had lost amanitin-resistance and showed that these mutants were also lethal alleles of L5. All the lethal alleles of L5 failed to completely complement each other genetically, and when analyzed biochemically their polymerase II displayed altered enzymatic properties. We conclude that C4 is an allele of the L5 locus and that this locus is most probably a structural gene for a subunit of RNA polymerase II. Some of the mutants at this locus display developmental abnormalities.