Although a complex pattern of interspersed cell proliferation and cell differentiation is known to occur during leaf blade development in eudicot plants, the genetic mechanisms coordinating this growth are unclear. In Arabidopsis , deletion of the PEAPOD ( PPD ) locus increases leaf lamina size and results in dome-shaped rather than flat leaves. Siliques are also altered in shape because of extra lamina growth. The curvature of a Δ ppd leaf reflects the difference between excess growth of the lamina and a limitation to the extension capacity of its perimeter. Excess lamina growth in Δ ppd plants is due to a prolonged phase of dispersed meristematic cell (DMC) proliferation (for example, the meristemoid and procambium cells that form stomatal stem cells and vascular cells, respectively) during blade development. The PPD locus is composed of two homologous genes, PPD1 and PPD2 , which encode plant-specific putative DNA-binding proteins. Overexpression of PPD reduces lamina size by promoting the early arrest of DMC proliferation during leaf and silique development. Therefore, by regulating the arrest of DMC proliferation, the PPD genes coordinate tissue growth, modulate lamina size, and limit curvature of the leaf blade. I propose a revised model of leaf development with two cell-cycle arrest fronts progressing from the tip to the base: the known primary front, which determines arrest of general cell proliferation, followed by a secondary front that involves PPD and arrests DMC division.