Viruses with single stranded, positive sense RNA genomes are among the most economically important plant pathogens. Turnip crinkle virus (TCV) is a commonly used model for studying the genome replication of this group of viruses. In our previous study, we found p28, one of the two TCV replication proteins, repressed the replication of a TCV replicon encoding wildtype p28. The other replication protein p88 contains the entire p28 at its N terminus. Here we further examined the effect of p88 on the replication of TCV replicons encoding either wildtype or mutated forms of p88. We found that transient, replication-independent expression of p88 permitted the complementation of a p88-defective replicon, but repressed the replication of another replicon encoding intact p88. Surprisingly, lowering p88 protein levels enhanced trans-complementation, but weakened repression. Testing a series of N-terminal deletion mutants of p88 demonstrated that repression by p88 can be attributed to multiple domains within p88, including those outside p28. Finally, both trans-complementation and repression by p88 were accompanied by preferential accumulation of subgenomic RNA2, and a novel class of small TCV RNAs. Our results suggest that repression of TCV replication by p88 may manifest a viral mechanism that regulates the ratio of genomic and subgenomic RNAs based on p88 abundance.