Opposing effects of <i>trans</i>‐ and <i>cis</i>‐cinnamic acid during rice coleoptile elongation

<jats:title>Abstract</jats:title><jats:p>The phenylpropanoid cinnamic acid (CA) is a plant metabolite that can occur under a <jats:italic>trans</jats:italic>‐ or <jats:italic>cis</jats:italic>‐form. In contrast to the proven bioactivity of the <jats:italic>cis</jats:italic>‐form (<jats:italic>c</jats:italic>‐CA), the activity of <jats:italic>trans</jats:italic>‐CA (<jats:italic>t</jats:italic>‐CA) is still a matter of debate. We tested both compounds using a submerged rice coleoptile assay and demonstrated that they have opposite effects on cell elongation. Notably, in the tip of rice coleoptile <jats:italic>t</jats:italic>‐CA showed an inhibiting and <jats:italic>c</jats:italic>‐CA a stimulating activity. By combining transcriptomics and (untargeted) metabolomics with activity assays and genetic and pharmacological experiments, we aimed to explain the underlying mechanistic processes. We propose a model in which <jats:italic>c</jats:italic>‐CA treatment activates proton pumps and stimulates acidification of the apoplast, which in turn leads to the loosening of the cell wall, necessary for elongation. We hypothesize that <jats:italic>c</jats:italic>‐CA also inactivates auxin efflux transporters, which might cause a local auxin accumulation in the tip of the coleoptile. For <jats:italic>t</jats:italic>‐CA, the phenotype can partially be explained by a stimulation of cell wall polysaccharide feruloylation, leading to a more rigid cell wall. Metabolite profiling also demonstrated that salicylic acid (SA) derivatives are increased upon <jats:italic>t</jats:italic>‐CA treatment. As SA is a known antagonist of auxin, the shift in SA homeostasis provides an additional explanation of the observed <jats:italic>t</jats:italic>‐CA‐mediated restriction on cell growth.</jats:p>