THE transcriptional mapping method1 makes possible the detection of polycistronic operons in systems which are not amenable to fine structure genetic mapping. The theory behind transcriptional mapping is that a defined interference with the travel of the genetic transcribing enzyme can be used for genetic analysis in a variety of ways. For example, a series of random blocks can be introduced along the genome, allowing detection of size differences among separate cistrons or operons as well as the order of genes read by the transcribing enzyme. The agent used to interfere with the transcription process in the series of experiments reported here was actino-mycin D, an antibiotic with a well defined mode of action2. The fact that the actinomycin D interferes with the travel of RNA polymerase by introducing a random block(s) along the DNA was used by Bleyman and Woese1 and by Perry3 to demonstrate that this interruption of transcription can be described by a target theory model, in which the synthesis of RNA from larger cistrons is more sensitive to inhibition than synthesis from smaller cistrons. The data presented here extend the method to the translational level.