The compound eyes of fruit flies are made up of hundreds of individual ommatidia, each one of which contains a lens. The outer surface of each ommatidium is called a facet, and the color of each facet is genetically determined. A somatic mutation occurring during mitosis early in the development of an eye can change the color of a single facet or, if it occurs very early in the cell line of a particular facet, a contiguous group of facets. In evaluating his experiments, Patterson assumed that the average numbers of ommatidia in male and female fruit flies were 1700 and 1720, respectively (based on Krafka 1920a, b), or approximately 855 per eye.

Numerous mutations have been discovered–and propagated in stocks–that determine the color of all the facets and thus of the entire surface of the eye. Many such mutations are in genes that are located on the X chromosome and are referred to as sex-linked. (The X chromosome is called the sex chromosome because female flies have two X chromosomes while males have only one). A wild-type fruit fly has red eyes because of a dominant mutation in one particular gene on the X chromosome. The wild-type allele at the gene of interest for Patterson's experiment is designated here as R (with R indicating a dominant mutation causing a red phenotype). A recessive mutation (symbolized here as wh) at that same gene produces a white eye unless it is in a fly carrying R. Females of genotype R/R and R/wh and males that are R all have wild-type (red) eyes. Females of genotype wh/wh and males of genotype wh have white eyes.

Patterson mated R/R females with wh males so that, in the absence of any spontaneous mutation in the reproductive cells, all female progeny would be R/wh and all male progeny would be R. Patterson then exposed the eggs, larvae, or pupal stages of those progeny to X-rays. If one of the R alleles in the cell lineage of one of the ommatidia mutated in such a way that it lost its function, the resulting ommatidium would be white. If that mutation occurred early enough in development, it might result in a whole group of congruent ommatidia becoming white.

In his papers on somatic mutations (Patterson 1928, 1929a, b), Patterson never reported anything about the dosimetry of the doses of X-rays that he administered. It was only stated that the X-ray machine was operated at 50 kV and 5 mA with the irradiated eggs, larvae, or pupae being at a distance of 12 cm and protected by an aluminum filter one mm thick. Numerically, the doses were then presented merely as ten different durations of exposure ranging from D-1 to D-10 (designated D1 to D10 in the present paper). D1 was a 5-min exposure, and each remaining exposure in the series increased by 5 min.

Reference to a later paper (Patterson 1931) on induction of sex-linked lethal mutations in reproductive cells of male fruit flies almost certainly reveals what doses were used in his experiments discussed in the present paper (Patterson 1928, 1929a, b). That paper presented doses in “r” units that were calculated from sample readings on a Victoreen dosimeter. Paul Selby notes that this dosimetry method is similar to what was used for measuring R (Roentgens) as ionizations in air for the massive mouse experiments at Oak Ridge National Laboratory starting in 1947. Patterson (1931) reported that his flies were exposed “with the machine operated at 50 kv., peak 10 ma, target distance 12 cm., and a 1-mm. aluminum filter.” These treatment details were reported to yield a total dose of 1654 r units in 16 min for a dose rate of 103.4 r/min. Five different treatments were administered with the same machine setting with different durations or fractionation regimen. The calculated dose rates for the five treatments were 103.4 (three times), 108.0, and 109.0, for a mean of 105.4 r/min. Keep in mind that this dose rate was for the machine being set at 10 mA instead of the 5 mA reported to have been used in the experiments on somatic mutations.

With reference to the above information on dosimetry, it is important to note the following quotation from the Journal of Experimental Zoology (Patterson 1929b) regarding his X-ray machine:

“In the more recent series of experiments the milli-amperage was increased from 5 to 10, but the machine was operated at the same voltage and target distance as before. This change in the method of running the machine allows a reduction to one-half the time for a given dose, and is a great advantage in any series of experiments requiring the treatment of many cultures. The effect of variations in dosage in the production of mutations in eye color is a matter of considerable importance.”

Since there is uncertainty raised by not knowing what Patterson meant by the wording “the more recent series of experiments”, it will be assumed that the dose rate in his experiments on somatic mutations (Patterson 1928, 1929a, b) was 53 r/min based on the use of 5 mA and not the ~ 106 r/min reported for 10 mA. He discusses many experiments in his (Patterson 1929b) paper and continues to identify the doses as being from D1 through D10 in all of them, those being of 5 min (or multiples thereof) duration. Presumably, if he had made the shift in milliamperage from 5 to 10 mA within the set of experiments described in that paper, he would have shifted to treatments lasting only 2 1/2 min. Therefore, assuming a dose rate of 53 r/min for durations of 5 min (or multiples thereof), the doses that were used ranged from 265 to 2650 r. The dose rate of 53 r/min is ~ 170 million times background.