Interplay of brassinosteroids, strigolactones, and <scp>CLE44</scp> in modulating Arabidopsis stem architecture in response to mechanical stress

Vascular tissues are crucial to providing plants with physical support and transporting water, nutrients, and signaling metabolites. Mechanical stress produced by wind, insects, and other external factors affects plant growth and development. Mechanical load weight treatments, simulating these stressors, are known to induce specific changes in vascular tissues, leading to increased stem diameter and a higher number of vascular bundles (VBs). In this work, brassinosteroids (BRs) and strigolactones (SLs) are shown as essential for the anatomical changes provoked in the Arabidopsis thaliana stem architecture in response to weight-induced mechanical stress. Unlike wild-type plants, BR signaling mutants (bes1 and bzr1) and plants treated with the BR synthesis inhibitor brassinazole failed to exhibit the characteristic increase in stem diameter and VB number after mechanical weight treatment. The SL synthesis gene MAX4 and the SL-responsive gene BRC1 play a crucial role in stem widening and increasing VB number. Supporting this, max4 and brc1 mutants neither showed increased stem diameter nor VB number in response to weight treatment. Moreover, CLE44, a downstream target of BRC1, also plays a necessary role, as cle44 mutants failed to respond to the weight stimulus. Interestingly, CLE44 expression is induced by the synthetic SL analogue GR24 but not by BRs. These findings underscore the convergent and essential roles of BRs and SLs in adapting stem architecture in response to mechanical stress.