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How do polyploids create novel variation?

Although polyploids initially attracted attention because of their unique cytogenetics, it was soon apparent that polyploids can have distinctive phenotypes and hybrid vigor useful for agriculture (Randolph, 1941; Levin, 2002; Ramsey and Schemske, 2002). Hybrid vigor, also known as heterosis, is an agriculturally important phenomenon describing the observation that the hybrid offspring of two inbred genetically different varieties produces higher yields than either one of the two parental lines. Judging from the success of many allopolyploid crop plants it may appear as if a state of allopolyploidy generally allowed the plant greater vigor. In contrast to hybrid vigor, some allopolyploids show decreased vigor compared to their diploid progenitors for some traits. An example of this is seed lethality for resynthesized Arabidopsis suecica (Comai et al., 2000; Madlung et al., 2002). Natural A. suecica does not show seed lethality, suggesting that this trait changed over generation of natural selection. This and other lines of evidence indicate that the genomes of new allopolyploids can be unstable, perhaps due to the phenomena of “genome shock” that may result from the union of different genomes (McClintock, 1985). The changes in response to this “genomic shock” may be the first steps in the diploidization process, and they could involve changes in gene expression.

Over the last decade, it has become apparent that polyploid genomes are not always a simple sum of their constituent genomes, but products of dynamic genetic and epigenetic changes that occur upon, or shortly after, polyploid formation. Epigenetic changes, which involve alterations of gene expression without a change in DNA sequence, are particularly intriguing because they play essential roles in plant development and plant defense against viruses and transposons. In nascent polyploids, observed epigenetic phenomena include nucleolar dominance, changes in DNA methylation and chromatin structure, triggering silencing or activation of genes and (retro)transposons, and novel phenotypes (reviewed in Matzke et al., 1999; Comai, 2000; Wendel, 2000; Liu and Wendel, 2002, 2003; Osborn et al. 2003).

Since the immediate consequences of polyploidization can best be studied in either synthetic or natural polyploids of recent ancestry, research on polyploidy and epigenetics has taken place primarily in experimental organisms. In addition, research in polyploidy has undergone a renaissance because of the available genomic and genetic resources in model organisms. Collectively, these studies have documented that the degree of genetic and epigenetic changes in recent natural and synthetic allopolyploids varies across taxa. For example, Arabidopsis (Mittelsten Scheid et al. 1996; Lee and Chen 2001; Madlung et al. 2002; Chen et al. 2003; Mittelsten Scheid et al. 2003), Brassica (Song et al. 1995; Chen and Pikaard 1997; Pires et al. 2003), Triticum (Ozkan et al. 2001; Shaked et al. 2001; Kashkush et al. 2003), and Nicotiana (Kenton et al. 1993; Lim et al. 2000; Mette et al. 2002) demonstrate rapid genomic and epigenetic changes. In contrast, synthetic Gossypium polyploids show few changes in overall genome sequences, yet they display differential expression of genes in different tissue types (Liu et al. 2001; Adams et al. 2003). These and other recent studies suggest that genetic and epigenetic changes contribute to the potentially dynamic nature of polyploids (Soltis and Soltis 1995). Studies of recent natural polyploids are now revealing the link between these epigenetic changes and the evolutionarily success of polyploid speciation.

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Figure legend: Potential causes of novel variation in polyploids. The merger of chromosomes from two diploid genomes (red and blue) into a tetraploid genome can cause (1) increased variation of dosage-regulated gene effects and expression (magnitudes of allelic effects and expression shown by size of blocks for three loci); (2) altered regulatory interactions (trans-acting regulatory factors shown as dimeric proteins, with heterodimers not functioning properly); (3) genetic changes affecting gene expression (e.g., insertions, deletions, translocations and gene conversions); and (4) epigenetic changes (repression or derepression of gene expression caused by genome interaction of chromatin modeling factors, which could also trigger movement of transposable elements).

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