We have identified the direction of replication of a bacteriophage P1 lytic replicon. This was accomplished by constructing lambda P1 lysogens that contain a functional P1 lytic replicon and analysing which of two nearby bacterial DNA markers flanking the lambda prophage were amplified when that replicon was activated. We demonstrate that both DNA markers are coordinately amplified, a result consistent with lytic replication proceeding in a bidirectional fashion. To analyze the role of various elements comprising the lytic replicon, we assessed the ability of a wild type replicon to complement a defective replicon that contains a transposon inserted between an essential lytic replication gene (repL) and the promoter (P53) at which transcription of that gene is initiated. We show that the wild type replicon cannot complement the mutant replicon. The simplest hypothesis to explain this result is that either P53 or repL protein functions primarily in cis for the replicon to operate.