The origin of such a relationship as in equations 1 and 2 could be traced to mutational changes in a sequence, where we restrict our analysis for the moment to transitional types of mutations since this is the dominant mode. Consider a mutation of a cytosine to thymine in one strand of a DNA in a GC-rich sequence. The opposite strand, calling it strand 2 for convenience, will initially have a bulge for the original paired guanine, and the event leads to following possibilities [31] : (a) the DNA repair mechanism reverse mutates the thymine to cytosine in strand 1, thus negating the effect of the original mutation; (b) the guanine in strand 2 is replaced by an adenine; and (c) a third possibility in case the damage repair coincides with replication, that the DNA is elongated by pairing the mutated thymine in strand 1 with a new adenine in strand 2 and addition of a cytosine in strand 1 to match the guanine in strand 2 left over after the original mutation, i.e. creation of a T-A pair and addition of a new C-G pair. Such an event would be quite rare, especially in coding regions since it will alter the reading frames unless the total change leads to addition of three base pairs; several intronless gene sequences indeed show very small contribution from the quadratic term compared to the interrupted genes, e.g. petunia hsp70G ( Table 1 ). The example of the mutation event of cytosine to thymine in strand 1 can be considered to change the intra-pyrimidine difference, n C-T , in strand 1 and trigger a change in the intrapurine difference, n G-A , in strand 2. The two changes can be related by