Our study of pedicel development in er demonstrates that the ER gene influences the growth rate but not the overall duration of growth. As evidenced from a histological analysis, ER controls the cell cycle duration in the 3,4,5-Trimethoxyphenylacetic acid epidermis and cortex. This function is connected to the regulation of cell growth during the proliferative phase as the size at which cells divide is unchanged in the mutant. Multiple factors contribute to efficient cellular growth; the ability to increase the cytoplasmic content, proper expansion of the cell wall, and availability of space to grow. Any of these factors might be regulated by ER. The consistency of cell size at division between the wild type and er is an interesting finding, as the existence of a threshold for plant cell division is an undecided issue. Another interesting observation is that the acceleration of the cortex cell cycle, which we observed in the wild type is absent in er. If proliferation in the epidermis and cortex is indeed coordinated by a common proliferative factor, the absence of this acceleration could be due to a longer period of asymmetric cell divisions in er. It has been previously reported that in er mature epidermis cells are much smaller, and cortex cells are bigger, compared to the wild type. Based on our data, ER is important early on for controlling the rate of cellular growth, but it does not directly regulate the size of mature cells or the rate of cell elongation after cells differentiate. The decreased size of epidermal cells in er may be a consequence of the different ratio of epidermal cells to cortex cells and the limited space for epidermal cell elongation. This is consistent with ER expression only in young organ primordia before the cell elongation stage. Recently, the reduced stature of er plants was attributed to the function of the gene in the phloem, where it perceives a signal from the endodermis. Some of the vasculature defects caused by er mutation are radial expansion of xylem and premature vasculature differentiation. At this point it is difficult to conclusively determine whether ER directly regulates growth in the epidermis and cortex during the proliferative stage, or if the reduction of growth in those tissues is a secondary consequence of reduced cellular growth in the vasculature. The second function of ER is to regulate stomata and pavement cell differentiation in the epidermis by prolonging the proliferative phase and inhibiting premature cell differentiation. We not only observed premature formation of meristemoids in er, but also an early onset of pavement cell elongation. The simultaneous shift to early cell differentiation suggests that there is a correlation between onset of the stomata differentiation pathway and the transition to cell elongation in cells that did not become MMCs. While in wild type leaves and pedicels stomata differentiation slightly precedes cell elongation, in the er mutant it appears that, at least in pedicel, cell elongation happens first. Therefore, the differentiation of stomata is not a requirement for induction of pavement cell elongation. We hypothesize that cell differentiation in the epidermis is a complex 
and synchronized event, with some cells differentiating in the stomata pathway and others exiting the mitotic cell cycle and transitioning to expansion. In this way, once the epidermis switches to the differentiation phase, cells have a very limited ability to proliferate unless they are part of the stomata differentiation pathway. More precise temporal Catharanthine sulfate analysis of the correlation between cell elongation and stomata differentiation in the wild type and stomata differentiation mutants is needed to verify this hypothesis. The enhancement of cellular growth by ER during the proliferative stage is limited specifically to the proximodistal axis.