In phase I, cell growth alternates with division in mitotic cells. Cell growth is a prerequisite for division in meristems and organ primordia, and is driven by the increase of cell mass by synthesis of macromolecular cell constituents (Jorgensen and Tyers 2004). Ribosomes limit macromolecular synthesis and, therefore, their synthesis and its regulation is at the nexus of growth control. For example, yeast cells commit ~50% of their total transcription activity and a large fraction of their energy budget towards building ribosomes (Warner 1999) and quantitative studies reveal a strong positive correlation of ribo-some synthesis with cell growth (Planta 1997; Warner 1999). There is good evidence that impaired ribosome biosynthesis reduces plant growth (Van Li-jsebettens et al. 1994; Weijers et al. 2001; Horvath and Bogre, this volume), but no detailed information is yet available on how well ribosome biosynthesis correlates with growth activity in plants. The expression of many components of the plant ribosome is regulated transcriptionally (McIntosh and Bonham-Smith 2006), but it is still poorly understood how ribosomal RNA and protein synthesis for ribosome production are coordinated mechanistically (for review, see McIntosh and Bonham-Smith 2006).
Cell growth is under control of the target of rapamycin (TOR) pathway, which couples nutritional cues to the regulation of ribosome biosynthesis, the rates of protein synthesis and proliferation. The TOR pathway interacts with the PI-3-kinase pathway, which mediates growth factor cues, and this interaction insures coordinate cellular growth responses (Arsham and Neufeld 2006; Jorgensen and Tyers 2004). The TOR pathway has been well characterized in animal and yeast systems, but much detail remains to be uncovered in plants: Orthologs of the TOR kinase, and of some additional components of the TOR signaling pathway have been identified in plants (Bogre et al. 2003; Menand et al. 2002; Wang et al. 2003), but their functional significance for plant cell growth control, specifically for coupling environmental change to growth responses, are only beginning to be examined in detail (Mahfouz et al. 2006). Likewise, plant homologs of PI-3-kinases and their effectors, the AGC kinases have been identified (Wang et al. 2003). At least one AGC kinase has been shown to be responsive to auxin and cytokinin growth regulator inputs (Anthony et al. 2004), and IRE (an AGC kinase) positively regulates root hair tip growth (Oyama et al. 2002). However, many gaps need to be filled until we understand the mechanisms of how growth regulator and nutrient inputs converge on cell growth control in plants.
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