Light quality and intensity has a profound effect on plant growth. Changes to the red-far red ratio trigger the photoreceptor-dependent shade avoidance response, which involves increased cell expansion and, in extreme cases, an acceleration of plant development (Franklin and Whitelam 2005). Here, I will focus on the effects of light quantity on plant growth, specifically leaf organ growth, and the emphasis will be on Arabidopsis. It should be noted that most Arabidopsis experiments are performed in laboratory growth chamber conditions, where "high light" corresponds to 150-250 ^molm-2 s-1, and "low light" corresponds to 15-75 ^molm-2 s-1. However, in nature, exposure to sunlight corresponds to 150-2000 ^molm-2 s-1, and "shade" in nature can span the whole high-light/low-light range examined in the laboratory. Therefore, the relevance of the observations described below remains to be validated for natural conditions.
Leaf organ growth responds to light intensity in several ways: In constant conditions, leaf initiation rate is reduced by low light (Cookson et al. 2005); blade anatomy is altered such that in "sun" leaves, two layers of palisade cells are produced (Kim et al. 2005); and the density of stomata is increased (Lake et al. 2001) in high light. In low light, leaf blade area is decreased, mediated by a reduction in cell number, but it is not yet known whether this is caused by reduced cell division, or whether cell growth (and as a consequence, cell division) is reduced (Cookson et al. 2005; Granier and Tardieu 1999). However, reduced proliferation is compensated for in part by increased cell expansion (Cookson et al. 2005; Cookson and Granier 2006) Moreover, the growth characteristics of the leaf organs are altered in low light so that maximal organ expansion rates are reduced and delayed (Cookson et al. 2005). Interestingly, a strong correlation was observed between leaf initiation rates and leaf epidermal cell number (Cookson et al. 2005). This raises the intriguing possibility that light intensity generates a signal that acts directly on the meristem to control the rate of primordium formation and the number of cells committed to a primordium. Such a possibility is consistent with the observation that all early processes in leaf organ development are correlated with each other (Cookson et al. 2005), implying that they are co-regulated.
Non-stressing levels of high light also increase photosynthesis and carbon assimilation and are therefore likely to also affect whole plant growth. Increased root growth (and an associated improved ability for mineral nu trient assimilation), would positively affect leaf growth. Such indirect effects on Arabidopsis leaf growth parameters in different light intensities have not been reported.
Overall growth of most plants, including Arabidopsis, is promoted in elevated CO2 concentrations (Pritchard et al. 1999; Tocquin et al. 2006). Leaf organ growth in Arabidopsis is stimulated, and this effect is more pronounced when nitrogen is not limiting (Tocquin et al. 2006). Kinematic analysis of Arabidopsis leaf growth under these conditions has not yet been reported. However, in monocot leaves such analysis is more straightforward. In a detailed analysis of leaf growth kinetics in two wheat cultivars, elevated CO2 concentration led to enhanced cell production and increased meristem size, but no change of cell size at cytokinesis or of final expanded cell size was observed (Masle 2000). Together, this suggests that cell cycle entry is directly stimulated by CO2 and that control of this parameter mediates CO2 concentration-dependent organ growth changes. Interestingly, growth in elevated CO2 concentration leads to significantly increased foliar concentrations of cytokinins, gibberellins, and auxin, while concentrations of growth-inhibitory ABA are reduced in Arabidopsis (Teng et al. 2006). If leaf growth control in dicotyledonous leaves mirrors that in mono-cots, then Arabidopsis CYCD3;1, which is one of the D3-type cyclins that limits cell cycle entry (Menges et al. 2006) and is also involved in mediating cytokinin-dependent stimulation of cell division (Riou-Khamlichi et al. 1999), may be a direct target of CO2 concentration-dependent organ growth control.
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