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Plant Cell, Vol. 11, 1319-1336, July 1999, Copyright © 1999, American Society of Plant Physiologists
Epigenetic Interactions among Three dTph1 Transposons in Two Homologous Chromosomes Activate a New ExcisionRepair Mechanism in Petunia
Adèle van Houwelingena,
Erik Souera,
Jos Mola, and
Ronald Koesa
a Department of Genetics, Institute for Molecular Biological Sciences, Vrije Universiteit, BioCentrum Amsterdam, de Boelelaan 1087, 1081 HV, Amsterdam, The Netherlands
Correspondence to:
Ronald Koes, koes{at}bio.vu.nl (E-mail), 31-20-4447155 (fax)
Unstable anthocyanin3 (an3) alleles of petunia with insertions of the Activator/Dissociationlike transposon dTph1 fall into two classes that differ in their genetic behavior. Excision of the (single) dTph1 insertion from class 1 an3 alleles results in the formation of a footprint, similar to the "classical" mechanism observed for excisions of maize and snapdragon transposons. By contrast, dTph1 excision and gap repair in class 2 an3 alleles occurs via a newly discovered mechanism that does not generate a footprint at the empty donor site. This novel mechanism depends on the presence of two additional dTph1 elements: one located in cis, 30 bp upstream of the an3 translation start in the same an3 allele, and a homologous copy, which is located in trans in the homologous an3 allele. Absence of the latter dTph1 element causes a heritable suppression of dTph1 excisionrepair from the homologous an3 allele by the novel mechanism, which to some extent resembles paramutation. Thus, an epigenetic interaction among three dTph1 copies activates a novel recombination mechanism that eliminates a transposon insertion.
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