Coupling of Cell Growth and Division

There is increasing evidence that cell growth and division are co-regulated: rapidly dividing cells in young leaf primordia and in roots are remarkably uniform in size and recently, possible effector pathways for co-regulation of cell growth and division were identified. The best mechanistic evidence for co-regulation of cell division and cell growth currently comes from the analysis of Arabidopsis TCP20. TCP20, which belongs to a plant-specific class of transcription factors and is thought to promote gene expression, binds in vivo to the promoters of ribosomal protein genes as well as to the promoter of the mitotic cyclin B1;1 (Li et al. 2005). Elevated expression of cyclin B1;1 has been shown to promote organ growth (Doerner et al. 1996). However, the biological function of class I TCP genes in control of organ growth has not been reported yet.

EBP1 genes, identified in potato and Arabidopsis, are a further type of effector gene that affect phase I growth (Horvath et al. 2006). Putative orthologs have been identified in other eukaryotes, where they are thought to regulate ribosome biogenesis (Squatrito et al. 2004), modulate translational activity (Squatrito et al. 2006), as well as DNA replication by binding to the Rb protein (Zhang et al. 2003). This wide range of activities raises the interesting possibility that plant EBP1 genes are involved in promoting phase I growth (by promoting cell growth), as well as phase II growth (by regulating E2F activity). Over-expression of plant EBP1 leads to larger leaves with more cells, while reduced expression results in the opposite (Horvath et al. 2006). In this work, cell size at birth and ploidy were not analyzed and so the direct effects of EBP1 on cell growth and the phase I/II switch are not yet known.

Altered expression of many additional genes has been reported to enhance organ growth, including: ARGOS (Hu et al. 2003), AINTEGUMENTA (Mizukami and Fischer 2000), PEAPOD (White 2006), and BIG BROTHER (Disch et al. 2006). All these genes have opposing effects on organ size when either over- or under-expressed. Elevated expression (ARGOS, AINTEGU-MENTA) or reduced expression (PEAPOD, BIG BROTHER) leads to extended phase I growth, with little or no effect on final cell size. However, cell size at birth in these plants (i.e., during phase I growth) was not reported, and therefore it is presently not clear whether these genes specifically control the timing of the phase I/II transition, or also affect the rate of cell growth.

Enhanced expression of some activating cyclin subunits of the CDK complexes that are rate-limiting regulators of cell cycle progression has led to accelerated organ growth without affecting the final size of the plant (Cock-croft et al. 2000; Doerner et al. 1996; Li et al. 2005). These observations raise several intriguing possibilities: It is possible (although there is no experimental evidence yet) that CDK activity feeds back on cell growth control. This could be a parsimonious regulatory mechanism, in which for example, developmental pathways could directly regulate cell cycle activity. This would then suffice to entrain appropriate levels of cell growth activity. Alternatively, it is possible that cell division onset in meristems and organ primordia only occurs significantly later than the attainment of a minimal cell size in plants. In this scenario, CDK activity limits organ growth and the plant can cope with increased proliferation because cell mass is sufficient to sustain division at an earlier time. A third possibility is that a specific CDK activity could be required for mitosis and therefore become limiting at the phase I/II boundary. A delay of the phase I/II transition would enhance the growth capacity of the affected organ or meristem by increasing the size of the dividing cell population. In this scenario, CDK mitotic activity limits organ growth by controlling the switch in cellular growth mechanisms.

There is good evidence that cell division activity positively correlates with organ growth rates: High levels of CDK activity are associated with high proliferation (Granier et al. 2000). Enhanced expression of activating cyclin sub-units of the cyclin-dependent kinase (CDK) complexes that are rate-limiting regulators of cell cycle progression has led to accelerated organ growth without affecting the final size of the plant (Cockcroft et al. 2000; Doerner et al. 1996; Li et al. 2005). Further, careful quantitative analysis of CDK kinase activity in relation to root organ growth rates support the notion that the level of CDK activity is a good predictor for the magnitude of organ growth rate (Beemster et al. 2002). Therefore, it appears possible that regulatory networks directly regulate CDK activity as a mechanism for plant growth control.

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