Summary Roots form highly complex systems varying in growth direction and branching pattern to forage for nutrients efficiently. Here mutations in the KAI2 (KARRIKIN INSENSITIVE) α/β‐fold hydrolase and the MAX2 (MORE AXILLARY GROWTH 2) F‐box leucine‐rich protein, which together perceive karrikins (smoke‐derived butenolides), caused alteration in root skewing in Arabidopsis thaliana. This phenotype was independent of endogenous strigolactones perception by the D14 α/β‐fold hydrolase and MAX2. Thus, KAI2/MAX2 effect on root growth may be through the perception of endogenous KAI2‐ligands (KLs), which have yet to be identified. Upon perception of a ligand, a KAI2/MAX2 complex is formed together with additional target proteins before ubiquitination and degradation through the 26S proteasome. Using a genetic approach, we show that SMAX1 (SUPPRESSOR OF MAX2‐1)/SMXL2 and SMXL6,7,8 (SUPPRESSOR OF MAX2‐1‐LIKE) are also likely degradation targets for the KAI2/MAX2 complex in the context of root skewing. In A. thaliana therefore, KAI2 and MAX2 act to limit root skewing, while kai2's gravitropic and mechano‐sensing responses remained largely unaffected. Many proteins are involved in root skewing, and we investigated the link between MAX2 and two members of the SKS/SKU family. Though KLs are yet to be identified in plants, our data support the hypothesis that they are present and can affect root skewing.

Mechanosensitive (MS) channels behave as microprobes that transduce mechanical tension into electric and ion signals. The plasma membrane anion-permeable channel AtMSL10 belongs to the first family of MS channels (MscS-LIKE) that has been characterized in Arabidopsis thaliana. In the same membrane, a rapidly activated calcium MS channel activity (RMA) associated with the presence of the DEFECTIVE KERNEL1 (AtDEK1) protein has been recently described. In this Review, based on the comparison of the specific properties of AtMSL10 and RMA, we put forward hypotheses on the mechanism of activation of these two channels, their respective roles in signalling and also raise the question of the molecular identity of RMA. Finally, we propose functions for these two channels within the context of plant mechanotransduction.