. "10 Transposons and Genome Evolution in Plants." Variation and Evolution in Plants and Microorganisms: Toward a New Synthesis 50 Years after Stebbins. Washington, DC: The National Academies Press, 2000.
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Variation and Evolution in Plants and Microorganisms: TOWARD A NEW SYNTHESIS 50 YEARS AFTER STEBBINS
THE ORIGIN OF TRANSPOSONS AND METHYLATION
Although it is popular to assert that transposons are genomic “parasites” and that DNA methylation evolved to control them, I suggest that the evidence supports neither notion (Yoder et al., 1997). The idea that transposons as parasitic, selfish DNA comes from a couple of essays written two decades ago, one by Doolittle and Sapienza (1980) and one by Orgel and Crick (1980). These essays sought rightly to free us from the then prevalent notion that genome structure is optimized by phenotypic selection. But the persistence of the moniker “selfish DNA” has become an impediment to further understanding of the origin, historical contribution, and contemporary role of transposons in chromosome structure.
Transposons may be an inevitable by-product of the evolution of sequence-specific endonucleases. Complete transposons have been shown to arise from a single cleavage site and an endonuclease gene (Morita etal., 1999). Although the successful constitution of a transposon from the recognition sequences used in Ig gene rearrangement and the RAG1 and RAG2 proteins was interpreted as evidence that the V(D)J recombination system evolved from an ancient mobile DNA element, the fact is that the critical components of a transposon and a site-specific rearrangement system are the same (Hiom et al., 1998). Thus questions about the origin of certain kinds of transposons may devolve to questions about the association of sequence-specific DNA binding domains with endonuclease domains.
Although the majority of methylated sequences in a genome can be transposable elements, the view that DNA methylation evolved to control transposons seems implausible in the light of evidence that duplications of any kind trigger methylation in organisms that methylate DNA (Yoder et al., 1997; Garrick et al., 1998; Selker, 1999). And organisms that do not methylate DNA also have mechanisms for detecting duplications and sequestering repeats (Pirrotta, 1997; Sherman and Pillus, 1997; Henikoff, 1998). Genome expansion by duplication is predicated on preventing illegitimate recombination between duplicated sequences. Although different eukaryotic lineages appear to have invented different mechanisms, what is common to repeat-induced silencing in all eukaryotes is the stable packaging of DNA into “repressive” chromatin. It may be that the evolution of mechanisms that recognize, mark, and sequester duplications into repressive chromatin structures, among which some involve DNA methylation, were the prerequisites for expansion of genomes by endore-duplication at all scales. The additional benefit of such “repressive” mechanisms in minimizing spurious transcription could be secondary sequelae. Because sequence duplication is inherent in transposition, the ability to recognize and repress duplications would serve to minimize