The creation of novel proteins is not simply ascribed to duplication of homologous sequences, but can be largely explained by frameshift translation. A deficiency of the TpA dinucleotide in protein-coding deoxyribonucleic acid (DNA) sequences renders them tolerant of frameshift mutations by minimizing the opportunity for premature stop codons, and involvement of both strands can increase genomic complexity. This supports the suggestion that new coding sequences evolve from existing or ancestral exons rather than from nonexonic sequences.
Keywords: protein-coding sequence; frameshift; TpA dinucleotide; termination codon; intrastrand parity in DNA






