The main characteristic of the hub1-1 (ang4-1) mutant of Arabidopsis is its small plant size and narrow leaf lamina (Figures 1   and 2A   , Table 1   ). The reduced leaf area in the hub1-1 mutant was confirmed by morphological measurements of the fully expanded leaves 1 and 2 that had a significantly decreased lamina length and width, petiole length, and total lamina and petiole lengths (Table 1). The lamina area of mature first and second leaves of hub1-1 was reduced to 55% of that of the wild-type Landsberg erecta (Ler) (Table 1). The length:width ratio was significantly increased, reflecting a much stronger reduction in width than in length of the blade (Table 1). Similar observations were made on leaf 6 (Cookson et al., 2005). The hub1-1 mutation also affected rosette growth, reducing fresh and dry weight at flowering by 40 and 39%, respectively (Figure 2B). To investigate whether a defect of cell proliferation and/or cell expansion is responsible for the growth defects of the hub1-1 mutant leaves, the number of palisade cells was counted in serial sections at the widest position of mature first and second leaves. The number of palisade cells across hub1-1 lamina (31 ± 4 cells; average ± sd, n = 3) was 44% that of those in Ler (70 ± 4 cells), resulting in narrow leaf shape of the hub1-1 mutant (Figure 2C). In addition to reduced cell numbers, distribution and size of the mesophyll cells were irregular with some enlarged cells and the air spaces were increased (Figure 2D). In leaf 6, similarly reduced cell numbers had been observed in the epidermal cell layer (Cookson et al., 2005). Thus, the main cause of the reduced leaf size in hub1-1 was a decrease in cell numbers. To verify whether the hub1-1 mutation influenced the growth of other organs, the length of the primary roots was measured in vitro during early seedling development. The hub1-1 primary roots grew much more slowly than those of the wild-type Ler (Figure 2E). To investigate whether the effect was due to morphogenetic defects, the root apical meristems were stained with propidium iodide and 4′,6-diamidino-2-phenylindole and analyzed by confocal microscopy. No differences between hub1-1 and Ler were seen regarding cellular organization or cell wall formation (see Supplemental Figures 1A to 1D online). A promoter–β-glucuronidase fusion construct with the B-type cyclin CYCB1;1 is a powerful tool to monitor mitotic activity in roots (Himanen et al., 2002) and was transformed into hub1-1 and Ler to evaluate the meristem size and activity of hub1-1 roots. The area of the β-glucuronidase staining in the root tips had a clearly reduced meristem size (by 50%) for hub1-1 (see Supplemental Figures 1E and 1F online). To investigate the cause of this growth reduction, root growth was analyzed kinematically. The root growth of young seedlings is often accelerated because of the increment of the number of dividing cells in the growth zone (Beemster and Baskin, 1998). As expected from the reduced meristem size, the root growth rate of hub1-1 was severely reduced and no acceleration of growth took place (Figure 3A   ). To verify whether the reduction of root growth rate was caused by reduced cell production as suggested by the reduced meristem size or by reduced cell expansion, the length of cortex cells was measured. The average mature cortex cell length was significantly (P < 0.001) reduced from 171 μm in Ler to 104 μm in hub1-1, whereas the cell production per hour had decreased by 65%, from 1.26 in Ler to 0.44 in hub1-1 (Figure 2F). Thus, hub1-1 affected root growth by altering both cell production in meristem and postmitotic cell expansion.