Genome alignments permit us to deduce positional correspondence between genes or groups of genes, but provide no direct information about gene function. Indeed, whole-genome duplication and the associated adaptation of the new gene set to the duplicated state may be closely associated with changes in functionality, particularly of those genes that do persist in duplicate. Gene duplication often leads to over expression of some genes and silencing of others, as has been found in synthetic allopolyploids of wheat and cotton (Adams et al. 2003; Kashkush et al. 2003). Retention of duplicated genes following polyploidy might be due to genomic buffering of dosage-sensitive genes (Chapman et al. 2006; Thomas et al. 2006), or to differential expression and/or sub-functionalization of other paralogs (Lynch and Force 2000).
Allopolyploidy addition to internal chromosomal rearrangements also changes the gene expression in different plant taxa including triticale (Chen 2007). Polyploidy is associated with a host of non-additive phenotypes that may be a result of changes in gene regulation and expression. For example, each of the allotetra-ploids B. napus (n = 19) (Udall et al. 2006) and G. hirsutum (Jiang et al. 1998) yield more than their diploid progenitors, possibly due in part to a relative increase in number of regulators, controlling gene expression in polyploids (Osborn et al. 2003). Genome-wide expression profiling in synthetic allotetraploid A. thaliana x A. arenosa has shown non-additive gene regulation (Wang et al. 2006). Delay in flowering time is attributed to epistatic interactions between two loci, one for flowering from A. thaliana and the other from A. arenosa (Wang et al. 2006). There is an important need to better understand the radical changes occurring after poly-ploidization, and their relationship to the evolution of genetic novelty.
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