Brassinosteroid coordinates cell layer interactions in plants via cell wall and tissue mechanics.

Growth coordination between cell layers is essential for development of most multicellular organisms. Coordination may be mediated by molecular signaling and/or mechanical connectivity between cells, but how genes modify mechanical interactions between layers is unknown. Here we show that genes driving brassinosteroid synthesis promote growth of internal tissue, at least in part, by reducing mechanical epidermal constraint. We identified a brassinosteroid-deficient dwarf mutant in the aquatic plant Utricularia gibba with twisted internal tissue, likely caused by mechanical constraint from a slow-growing epidermis. We tested this hypothesis by showing that a brassinosteroid mutant in Arabidopsis enhances epidermal crack formation, indicative of increased tissue stress. We propose that by remodeling cell walls, brassinosteroids reduce epidermal constraint, showing how genes can control growth coordination between layers by means of mechanics.

Localization of stomatal lineage proteins reveals contrasting planar polarity patterns in Arabidopsis cotyledons.

Many plant cells exhibit polarity, revealed by asymmetric localization of specific proteins within each cell.1,2,3,4,5,6 Polarity is typically coordinated between cells across a tissue, raising the question of how coordination is achieved. One hypothesis is that mechanical stresses provide cues.7 This idea gains support from experiments in which cotyledons were mechanically stretched transversely to their midline.8 These previously published results showed that without applied tension, the stomatal lineage cell polarity marker, BREVIS RADIX-LIKE 2 (BRXL2), exhibited no significant excess in the transverse orientation. By contrast, 7 h after stretching, BRXL2 polarity distribution exhibited transverse excess, aligned with the stretch direction. These stretching experiments involved statistical comparisons between snapshots of stretched and unstretched cotyledons, with different specimens being imaged in each case.8 Here, we image the same cotyledon before and after stretching and find no evidence for reorientation of polarity. Instead, statistical analysis shows that cotyledons contain a pre-existing transverse excess in BRXL2 polarity orientation that is not significantly modified by applied tension. The transverse excess reflects BRLX2 being preferentially localized toward the medial side of the cell, nearer to the cotyledon midline, creating a weak medial bias. A second polarity marker, BREAKING OF ASYMMETRY IN THE STOMATAL LINEAGE (BASL), also exhibits weak medial bias in stomatal lineages, whereas ectopic expression of BASL in non-stomatal cells exhibits strong proximal bias, as previously observed in rosette leaves. This proximal bias is also unperturbed by applied tension. Our findings therefore show that cotyledons contain two near-orthogonal coordinated biases in planar polarity: mediolateral and proximodistal.