The transgenic petunia line 17-R contains one copy of the maize A1 gene which mediates brick-red pelargonidin pigmentation of the flower. A white derivative, 17-W, was isolated from homozygous progeny of this line in which no pelargonidin pigmentation was observed. In 17-W the 35S promoter driving the A1 gene was hypermethylated, in contrast to its hypomethylated state in 17-R. Progeny plants carrying both the 17-R and 17-W allele did not show the expected A1 phenotype. Predominantly white progeny and variable plants were observed which showed a continuous change in pattern and intensity of pelargonidin pigmentation. This reduction of A1 activity argues for a semidominant effect of the 17-W allele which inhibits the activity of its homologue, 17-R. This system shows striking similarities to some paramutation phenomena in plants which represent a heritable change in gene function of a paramutable allele directed by a paramutagenic homologue. The analysis of the methylation patterns of the A1 alleles suggests that interactions between differentially methylated alleles are responsible for the paramutation-like effect which is mediated by somatic pairing. The analogy of this system to other phenomena based on homology-dependent interlocus trans-inactivation supports the assumption that those may be based on a related mechanism which includes an interaction between ectopic homologues.