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thousands of transposable elements are as stable as chromosomes containing few. By what means are such sequences prevented from transposing, recombining, deleting, and rearranging?

The transposon problem can be viewed as one aspect of a larger problem in genome evolution: why does duplicated DNA persist? Duplications are a by-product of the properties of the DNA replication and recombination machinery. Short stretches of homology suffice to give rise to duplications by slippage during replication, homology-dependent unequal crossing-over, and double-strand breakage/repair (Gorbunova and Levy, 1997; Liang et al., 1998). But duplications are problematical. Once a duplication exists, the mechanisms that generated it also permit unequal crossing over between identical repeats (Anderson and Roth, 1977; Perelson and Bell, 1977; Koch, 1979). Prokaryotes readily duplicate genetic material, but do not retain duplications (Perelson and Bell, 1977; Romero and Palacios, 1997). Thus the ability of genomes to expand by duplication is predicated on their ability to sequester homologous sequences from the cell's recombination machinery and retain them, which may necessitate the invention of mechanisms to recognize and differentially mark duplications. Some lower eukaryotes, including Neurospora crassa (Selker and Garrett, 1988; Selker, 1997) and Ascobolus immersus (Rossignol and Faugeron, 1994, 1995), have the capacity to recognize and mark duplicated sequences by methylating them. Sequence methylation silences transcription, enhances the mutability of the duplicated sequence, and inhibits recombination (Selker, 1997; Maloisel and Rossignol, 1998).

Some years ago, Adrian Bird pointed out that there are two evolutionary discontinuities in the average number of genes per genome (Bird, 1995). The first is an increase between prokaryotes and eukaryotes and the second is between invertebrates and vertebrates. He suggests that with a given cellular organization there may be an upper limit on the tolerable gene numbers imposed by the imprecision of the biochemical mechanisms controlling gene expression. He suggested that the transcriptional “noise reduction” mechanisms that arose at the prokaryote/eukaryote boundary were the nuclear envelope, chromatin, and separation of the transcriptional and translational machinery, as well as RNA processing, capping, and polyadenylation to discriminate authentic from spurious transcripts. He proposed that genome-wide DNA methylation is the novel “noise reduction” mechanism that has permitted the additional quantal leap in gene numbers characteristic of vertebrates.

HOMOLOGY-DEPENDENT GENE SILENCING

The results of both classical and contemporary studies on the silencing of redundant gene copies in plants suggests that both methylation



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