One or two sites of +1 frameshifting have been documented in animal mt genes (for review, see [40] ), but such extensive +1 and +2 frameshifts are unique. In retroviruses, a -1 frameshift is corrected by tRNA back-slippage over homopolymeric codons adjacent to a local secondary structure that may include a pseudoknot (for review, see [41] ). Masuda et al. [20] suggest two feasible mechanisms for the translational frameshifts in Perkinsus: a ribosomal frameshift in which stalled ribosomes skip the first bases of these codons (similar to the model hypothesized by Beckenbach et al. [42] ), or specialized tRNAs recognizing non-triplet codons AGGY and CCCCU to code for glycine and proline, respectively. In this study, we add cox1 for P. chesapeaki and cob sequences for P. marinus and P. chesapeaki, which share the unusual AGGY codon with cox1 and use other unusual codons (UAGGC and UCGGU) to encode glycine as well. Specialized tRNAs in the Perkinsus mitochondrial system recognizing non-triplet AGGY and CCCCU codons, and likely UMGGY as well, may be more likely than the ribosomal frameshifting scenario, as naturally occurring tRNA mutants suppress +1 frameshifts via an extended anticodon loop in Escherichia coli (e.g. [43] ), and quadruplet codons are used in protein mutagenesis [44] .