The relationship between cell proliferation and post-mitotic cell expansion observed in compensation could be regarded as a simple trade-off between these two developmental processes in leaf primordia. However, such a mechanism is not supported by the time-course data of leaf development in several mutants. For example, the overexpression of ANT or loss-of-function of PEAPOD (PPD) lengthens the cell proliferation phase but does not shorten the duration of post-mitotic cell expansion (Mizukami and Fischer 2000; White 2006). Therefore, compensation cannot be regarded as a simple trade-off between these processes.
However, changes in the timing of the transition from the normal cell cycle to endocycles might be another factor that causes compensation, because the endocycle is a modified cell cycle that lacks a cell division step, and there is a rough positive correlation between endopolyploidy levels and cell size (e.g., Melaragno et al. 1993). Although this correlation seems to exist in some compensation-exhibiting mutants and transgenics (such as struwwelpeter (swp) and weak lines of KRP2 overexpressers; Autran et al. 2002; Verkest et al. 2005), however, several lines of evidence have indicated that an increase in the levels of endopolyploidy is not a necessary condition for increased cell size due to compensation. For example, a strong KRP2 overexpressing line, in which both cell cycling and endocycling are inhibited, clearly shows compensation (De Veylder et al. 2001). In addition, guard cells, which always have a 2C DNA content, also exhibit compensation in transgenic tobacco lines that have reduced expression levels of ribosomal protein L3 genes, and in the Ara-bidopsis swp mutant (Autran et al. 2002; Popescu and Tumer 2004).
Moreover, we recently found more genetic evidence that an increase in en-dopolyploidy is not an essential condition for the increase in cell size that occurs in compensation. This evidence was found during the isolation and analysis of the extra-small sisters (xs) mutants, which are defective in cell expansion but have normal numbers of cells in leaves (Fujikura et al. 2007). Among the xs mutants, xs1, xs2, xs4, and xs5 showed suppressed compensation triggered by the an3 mutation. Importantly, these xs mutants differ in the levels of endocycling in leaves, showing normal, increased, or decreased ploidy. This lack of correlation between the level of endocycling and the magnitude of compensation strongly suggests that the level of endopolyploidy and the occurrence of compensation are independent (Fujikura et al. 2007).
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