Epigenetic interactions among three dTph1 transposons in two homologous chromosomes activate a new excision-repair mechanism in petunia

Unstable anthocyanin3 (an3) alleles of petunia with insertions of the Activ ator/Dissociation-like transposon dTph1 fall into two classes that differ i n their genetic behavior. Excision of the (single) dTph1 insertion from cla ss 1 an3 alleles results in the formation of a footprint, similar to the "c lassical" mechanism observed for excisions of maize and snapdragon transpos ons. By contrast, dTph1 excision and gap repair in class 2 an3 alleles occu rs via a newly discovered mechanism that does not generate a footprint at t he empty donor site. This novel mechanism depends on the presence of two ad ditional dTph1 elements: one located in cis, 30 bp upstream of the an3 tran slation start in the same an3 allele, and a homologous copy, which is locat ed in trans in the homologous an3 allele. Absence of the latter dTph1 eleme nt causes a heritable suppression of dTph1 excision-repair from the homolog ous an3 allele by the novel mechanism, which to some extent resembles param utation. Thus, an epigenetic interaction among three dTph1 copies activates a novel recombination mechanism that eliminates a transposon insertion.