During the development of the leaf lamina, the leaf margins (edges) may form lateral outgrowths called serrations (Web Figure 19.3.A, left). Although marginal serrations are modified by many genes, the key components are auxin and CUC2 (Web Figure 19.3.A, right). Loss-of-function mutations in CUC2 result in reduced serrations, and overexpression of CUC2 results in highly serrated leaves, a phenotype that is dependent on PIN1 and auxin signaling.

Web Figure 19.3.A Development of serrated leaves. (A) Arabidopsis rosette leaves have a regular arrangement of marginal outgrowths or serrations (yellow arrows). (B) Genetic and hormonal interactions involved in the formation of leaf serrations. PIN1 convergence, reinforced by auxin feedback on PIN1 localization, directs auxin flow (red arrows) toward auxin maxima along the leaf margin. CUC2 activity is required for directing PIN1 convergence. Auxin represses CUC2 expression, and CUC2 expression becomes restricted to regions between serrations.

Early in development, CUC2 is expressed evenly along the leaf margin. CUC2 functions to relocalize PIN1 auxin efflux carriers so that their orientations converge on a subset of leaf margin cells. This reorientation of PIN1 enhances polar transport of auxin toward those margin cells, eventually establishing auxin gradients with maxima more-or-less evenly spaced along the leaf margin. Growth is stimulated at these auxin maxima. Subsequently, CUC2 expression becomes restricted to the regions between the auxin maxima, where CUC2 may be involved in repressing lamina growth. Thus, the extent of leaf serration may be a consequence of the balance between growth promotion by auxin and growth repression by CUC2.