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.