One gene named ANTAGONIST OF LIKE HETEROCHROMATIN PROTEIN 1 ( ALP1) was isolated from both screens, indicating that it likely functions broadly in antagonizing PcG repression. To better understand the mechanisms that may counteract PcG repression, two independent suppressor screens were performed to identify mutants that could revert the developmental and transcriptional defects of the CLF and LHP1 mutants, respectively.

The enzymatic complex PRC2 contains one of the three H3K27 trimethyltransferases, MEDEA (MEA), CURLY LEAF (CLF), and SWINGER (SWN), whereas the PRC1 complex includes the H3K27me3-binding protein LIKE HETEROCHROMATIN PROTEIN 1 (LHP1). In Arabidopsis, PcG function requires two classes of protein complexes: Polycomb Repressive Complexes 1 and 2 (PRC1 and PRC2, respectively).

PcG genes play critically important roles in regulating plant development by targeting thousands of genes for transcriptional repression through trimethylation of lysine 27 on histone H3 (H3K27me3). But can immobilized TEGs fortuitously acquire cellular functions that are beneficial to the host and become a useful fixture of the genome? In a recent issue of PLOS Genetics, Turck, Goodrich, and colleagues describe a clear example of this process, in which a transposase-derived gene functions to antagonize transcriptional repression by the Polycomb group (PcG) genes in Arabidopsis thaliana. Over time, silenced TEs accumulate genetic mutations, become immobilized, and are eliminated from the genome by recombination or decay into intergenic DNA. To minimize the mutagenic effects of transposition, host organisms have evolved various mechanisms to repress TE-encoded genes (TEGs) both transcriptionally through chromatin modifications and post-transcriptionally through RNA interference. Eukaryotic genomes are littered with transposable elements (TEs)-“selfish” genetic entities capable of increasing copy numbers through transposition to account for large fractions of the nuclear DNA.

The selfish gene