Abstract
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. 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. Over time, silenced TEs accumulate genetic mutations, become immobilized, and are eliminated from the genome by recombination or decay into intergenic DNA. 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 [1].
Highlights
In addition to ANTAGONIST OF LIKE HETEROCHROMATIN PROTEIN 1 (ALP1), a number of TPase-derived genes have been described in eukaryotes
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
Can immobilized TE-encoded genes (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 [1]
Summary
In addition to ALP1, a number of TPase-derived genes have been described in eukaryotes (for excellent recent reviews, see [10,11]). 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. 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 [1].
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