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

Article

Authorship

RAMINGER, BETINA LORENA ; Muñoz-Gasca, Aitor ; Cubas, Pilar ; CHAN, RAQUEL LIA ; CABELLO, JULIETA VIRGINIA

Date

2025

Publishing House and Editing Place

WILEY-BLACKWELL PUBLISHING, INC

Magazine

PLANT JOURNAL, vol. 123 (pp. 1-16) - ISSN 0960-7412
WILEY-BLACKWELL PUBLISHING, INC

ISSN

0960-7412

Summary Information provided by the agent in SIGEVA

Vascular tissues are crucial to providing plants with physical support and transporting water, nutrients, andsignaling metabolites. Mechanical stress produced by wind, insects, and other external factors affects plantgrowth and development. Mechanical load weight treatments, simulating these stressors, are known toinduce speci?c changes in vascular tissues, leading to increased stem diameter and a higher number of vas-cular bundles (VBs). In this work, brassinosteroids (BRs) and strigolactones ... Vascular tissues are crucial to providing plants with physical support and transporting water, nutrients, andsignaling metabolites. Mechanical stress produced by wind, insects, and other external factors affects plantgrowth and development. Mechanical load weight treatments, simulating these stressors, are known toinduce speci?c changes in vascular tissues, leading to increased stem diameter and a higher number of vas-cular bundles (VBs). In this work, brassinosteroids (BRs) and strigolactones (SLs) are shown as essential forthe anatomical changes provoked in the Arabidopsis thaliana stem architecture in response toweight-induced mechanical stress. Unlike wild-type plants, BR signaling mutants (bes1 and bzr1) and plantstreated with the BR synthesis inhibitor brassinazole failed to exhibit the characteristic increase in stemdiameter and VB number after mechanical weight treatment. The SL synthesis gene MAX4 and theSL-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 weighttreatment. Moreover, CLE44, a downstream target of BRC1, also plays a necessary role, as cle44 mutantsfailed to respond to the weight stimulus. Interestingly, CLE44 expression is induced by the synthetic SL ana-logue GR24 but not by BRs. These ?ndings underscore the convergent and essential roles of BRs and SLs inadapting stem architecture in response to mechanical stress.