COORDINATE SUPPRESSION OF MUTATIONS CAUSED BY ROBERTSONS MUTATOR TRANSPOSONS IN MAIZE

Transposable elements from the Robertson's Mutator family are highly a ctive insertional mutagens in maize. However, mutations caused by the insertion of responder (non-autonomous) elements frequently depend on the presence of active regulator (autonomous) elements for their pheno typic effects. The hcf106::Mu1 mutation has been previously shown to d epend on Mu activity in this way. The dominant Lesion-mimic 28 mutatio n also requires Mu activity for its phenotypic effects. We have used d ouble mutants to show that the loss of Mu activity results in the coor dinate suppression of both mutant phenotypes. This loss can occur soma tically resulting in large clones of cells that have a wild-type pheno type. Autonomous and non-autonomous Mutator elements within these clon es are insensitive to digestion with methylation-sensitive enzymes, su ggesting extensive methylation of CG and non-CC cytosine residues. Our data are consistent with the sectors being caused by the cycling of M uDR regulatory elements between active and inactive phases. The patter n of sectors suggests that they are clonal and that they are derived f rom the apical cells of the vegetative shoot meristem. We propose that these cells are more likely to undergo epigenetic loss of Mu activity because of their longer cell division cycle during shoot growth. Coor dinate suppression of unlinked mutations can be used to perform mosaic analysis in maize.