Promoting Factors

Compared to proliferation, our knowledge of the molecular control of growth by cell expansion is more limited. Cell expansion in developing organs is driven by water uptake into the central vacuole and involves a massive enlargement of the cell wall through biosynthesis and deposition of new wall material (Menand and Robaglia 2004). During this process, the cell wall must be made extensible in a finely tuned manner to allow it to yield to the turgor pressure while maintaining its integrity. Members of the expansin family of proteins are prime candidates for controlling cell wall extensibility and are presumed to act by breaking noncovalent bonds between cell wall components to allow them to slide relative to each other (Cosgrove 2005). Regulating expansin activity is therefore a plausible mechanism for determining the extent of organ growth through cell expansion. Indeed, downregulating members of the alpha class of expansins in Arabidopsis, rice and petunia leads to smaller organs because of reduced cell enlargement. By contrast, overexpression of these genes in Ara-bidopsis and rice is sufficient to increase organ size as a result of larger cells (Cho and Cosgrove 2000; Choi et al. 2003; Zenoni et al. 2004). Thus, expansin activity may indeed be limiting for organ growth by expansion.

Cell expansion in developing organs is promoted by the ARGOS homolog ARGOS-LIKE (ARL) (Hu et al. 2006). Reduced ARL expression leads to smaller organs with less expanded cells, while increased ARL activity is sufficient to cause organ enlargement due to larger cells. In contrast to ARGOS

mediating auxin effects on growth, ARL appears to function downstream of brassinosteroids, and ARL overexpression can partially rescue the dwarfism of brassinosteroid-insensitive mutants. The contrasting effects of ARGOS and ARL on cell proliferation and expansion, respectively, are reminiscent of the different functions of members of the GRF-family (Horiguchi et al. 2005; Kim et al. 2003; Kim and Kende 2004) (see above). It is intriguing that members of homologous gene pairs or families are involved in the two seemingly very different cellular processes that drive overall organ growth. Unraveling the modes of action of ARGOS and ARL should indicate whether fundamentally similar mechanisms are involved in controlling growth by proliferation and by post-mitotic expansion, with the two genes potentially influencing the process of cellular expansion at different scales, i.e., the limited expansion during the proliferation phase and the large-scale expansion afterwards.

As mentioned before, cell expansion is often accompanied by an increase in ploidy due to endoreduplication. The identification of a topoisomerase VI complex (topo VI) in Arabidopsis suggests that endoreduplication is an essential prerequisite for growth by expansion (Sugimoto-Shirasu et al. 2002, 2005). Mutations in any of the presumed topo VI components block endoreduplication beyond a DNA content of 8C (i.e., eight times the DNA amount of the haploid genome) and lead to severe dwarfing, because cells fail to expand. Pharmacological studies with specific inhibitors of topo II and topo VI indicate that they fulfil distinct yet partly overlapping roles in decatenating chromosomes during mitotic cell cycles and endoreduplication (Sugimoto-Shirasu et al. 2005). However, despite the clear requirement for topo VI activity in permitting endoreduplication and cell expansion, it is unlikely that topo VI determines the final ploidy level and thus, due to the correlation of DNA content and cell size, the extent to which organ cells enlarge.

The final ploidy level of hypocotyl and leaf cells as well as the timing of the switch from proliferation to endoreduplication can be influenced by overex-pressing or eliminating critical cell cycle regulators (for example De Veylder et al. 2001,2002; del Pozo et al. 2006). These manipulations can affect final cell size and in some cases also overall organ size, as discussed in more detail by Magyar in this volume.

The phytohormone classes of brassinosteroids and gibberellins are known to promote cell expansion (Clouse and Sasse 1998; Richards et al. 2001; Szek-eres et al. 1996). Both brassinosteroid- and gibberellin-insensitive mutants are dwarfed because of insufficient cell expansion, whereas constitutive gib-berellin signaling leads to increased cell enlargement, particularly in the stem (Jacobsen and Olszewski 1993). For brassinosteroids, overproduction has been reported to increase overall plant growth, both by proliferation and expansion (Choe et al. 2001), suggesting that brassinosteroids can stimulate both modes of organ growth. The molecular mechanisms of brassinosteroid and gibberellin signaling have been elucidated in considerable detail, as described in recent reviews (Fleet and Sun 2005; Vert et al. 2005).

The extent of cell expansion depends to some degree on the total number of organ cells that have been generated during the preceding proliferation phase: In mutants with reduced cell numbers, such as ant or an3, organ cells enlarge more strongly than in wild-type, and thus partially compensate for the insufficient cell numbers (Horiguchi et al. 2006; Mizukami and Fischer 2000). This fascinating issue is discussed further by Tsukaya in this volume, whose chapter will also highlight the pathways that determine organ shape.

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