Plant organs are organised and demarcated by boundary domains, which display reduced growth and regulate the patterning of adjacent tissues. Although boundary-specific genes, such as CUP-SHAPED COTYLEDON (CUC) transcription factors CUC2 and CUC3, are known, how boundary domain function is achieved remains unclear. Now, Nicolas Arnaud and colleagues employ morphometric analyses across scales to understand the function of Arabidopsis leaf boundaries. Focussing on SPINDLY (SPY), an O-fucosyltransferase, the loss of which causes smoother leaf serrations, the authors use 2D and 3D morphometrics to analyse spy-3 mutant leaves. They determine that serration changes may result from defects in boundary-domain formation, likely caused by unrestricted cell growth of sinus cells. Through loss- and gain-of-function experiments, the researchers show that SPY, CUC2 and CUC3 act redundantly during boundary domain development. Moreover, SPY and CUC2 act through a common pathway implicated in cell wall loosening. Indeed, using atomic force microscopy to measure the stiffness of cell walls with or without CUC2 expression, the authors show that cells lacking CUC2 or SPY are less stiff. Together, these data link genetic factors to a mechanical framework, showing that SPY and CUC2 restrict sinus cell growth in the boundary by regulating cell wall stiffness.