Our laboratory cloned the Spm element some years ago and we have explored the molecular basis of Spm inactivation and reactivation. We�ve done this genetically in maize and we�ve used reconstructed transgenic systems with introduced cloned element-encoded genes and Spm promoter-reporter gene fusions. The essential findings are these:
1. When the element is inactive, its promoter sequence is methylated.
2. The heritability of the inactive or silenced state is correlated with the methylation level of a downstream, very GC-rich seqence.
3. The promoter is rapidly methylated in transgenic plants, but only if it contains the GC-rich downstream sequence.
4. The element encodes two proteins that are necessary for transposition and one of these, TnpA, is both a transposition protein and a regulator.
5. TnpA binds to multiple sites present in both direct and inverted orientations at both element ends.
6. TnpA can reactivate a silenced, methylated element both transiently and heritably, identifying it a sequence-specific epigenetic regulatory protein.