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under different light regimes - Biology Department

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Fig. 2. Chlorophyll ¯uorescene of wild-type and sdd1-1 mutant plants. Relative electron transport rates in the photosynthetic electron transport<br />

chain and non-photochemical quenching coef®cients were obtained during stepwise increase of PFD. Plants were grown at constant PFD (A, D:<br />

80 mmol m ±2 s ±1 ; B, E: 200±250 mmol m ±2 s ±1 ; C, F: 300±400 mmol m ±2 s ±1 ). Data were obtained from the same sets of plants as results shown in<br />

Fig. 1, respectively. Each data point represents the average of 3±4 individual plants 6SE.<br />

high <strong>light</strong> conditions, contained signi®cantly increased<br />

amounts of carbohydrates when compared with plants<br />

which grew continuously <strong>under</strong> high <strong>light</strong> intensities.<br />

Factors such as carbohydrate partitioning or differences in<br />

metabolic activity could be responsible for this discrepancy.<br />

Discussion<br />

Mutation of the SDD1 gene results in a 2.5-fold increase of<br />

stomatal density in Arabidopsis rosette leaves, but no other<br />

apparent features of leaf morphology are altered (Berger<br />

and Altmann, 2000). The enhancement of stomatal density<br />

could be observed <strong>under</strong> various environmental conditions.<br />

Exposure to increasing <strong>light</strong> intensities causes a parallel<br />

Photosynthesis in Arabidopsis mutant sdd1-1 871<br />

increase in the stomatal density of the wild type and the<br />

mutant. This shows that the mechanisms responsible for<br />

<strong>light</strong>-dependent adjustment of stomatal density are still<br />

active in the mutant and are, therefore, independent of<br />

SDD1 activity. These results indicate that environmental<br />

parameters may in¯uence stomatal density through a<br />

<strong>different</strong> signalling pathway, or be downstream of SDD1<br />

within the same signalling cascade. Recently, an<br />

Arabidopsis gene (HIC for high carbon dioxide) has been<br />

identi®ed which is involved in regulation of stomatal<br />

densities <strong>under</strong> elevated CO2 (Gray et al., 2000). In<br />

contrast to SDD1 the HIC gene did not seem to be involved<br />

in mechanisms that prevent the formation of stomata that<br />

directly contact one another and no clusters occurred<br />

(Serna and Fenoll, 2000). It is, therefore, likely that SDD1<br />

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