The gene pn was found to be active already in larvae 30 h old, long before eye-pteridines accumulated. At this developmental stage pn interacts with the gene K-pn. From studies with induced somatic recombination, gynandromorphs, and induced pn mutations, in a K-pn background it was concluded that the interaction pn-K-pn is non-autonomous in the epidermis, but in some internal organs it is apparently autonomous and causes the death of pn–K-pn flies. It is proposed that pn mutants interfere with an early step of the conversion of guanosine to pteridine, so that a deficiency of drosopterines, but not of the competing sepiapterine and biopterine, is caused. The accumulated precursor is presumably the substrate for a poisonous reaction triggered by K-pn.