Sequence data of sg RNA leader±body junctions from other arteriviruses are also dif®cult to reconcile with the leader-primed transcription model. For the porcine and simian arteriviruses (Meulenberg et al., 1993; Godeny et al., 1998) , the leader±body junctions of some sg RNAs mapped two nucleotides upstream of the body TRS, which again would not leave a single nucleotide to hold the putative free leader on the template after the hypothetical back trimming'. On the other hand, these ®ndings and our data can be explained readily by the discontinuous minus strand extension model ( Figure 1C ). The six-nucleotide Fig. 5 . Sequence analysis of mRNA7 leader±body junctions from position 1 TRS mutants. Sequences were determined directly from sg mRNA7-speci®c RT±PCR products. For the U 1 A and U 1 C mutants, the sequence shown corresponds to the plus strand of sg RNA7. For sequencing-related technical reasons, the minus strand sequence was determined for the U 1 G mutants; a mirror image of the electropherogram is shown with the corresponding plus strand sequence listed at the top of the panel. For every mutant, a sequence alignment of the leader (red) and body (blue) TRSs and surrounding sequences is shown (TRSs are boxed). The mRNA7 leader±body junctions detected by our sequence analysis are shown in yellow. duplex formed between the body TRS complement at the 3¢ end of the leaderless sg minus strand and the leader TRS in the genomic RNA template should suf®ce to position the nascent minus strand properly for subsequent elongation to add the complement of the leader sequence. In most cases, the nascent minus strand contains the entire body TRS complement at its 3¢ end at the moment of strand transfer, leading to a body TRS-derived leader±body junction sequence in the sg mRNA molecule. In a small number of transcripts, however, minus strand synthesis appears to be interrupted before nucleotide +1 of the body TRS is copied and, after strand transfer, resumes by incorporating the complement of the +1 nucleotide of the leader TRS. As stated above, we postulate that the detection of this phenomenon is determined by the level of crossovers between the ±1 and +1 position that is allowed by the mutations introduced at the +1 position of body TRS or leader TRS. We cannot, however, formally exclude that a`back trimming' activity degrades the 3¢-terminal nucleotide of the minus strand before or after strand transfer. However, note that in the discontinuous minus strand extension model ( Figure 1C ), such an activity would not disturb the proper positioning of the nascent minus strand on the leader template, because the TRS± TRS duplex would be shortened by one nucleotide only.