Growth‐ and stress‐related defects associated with wall hypoacetylation are strigolactone‐dependent

Mutants affected in the Arabidopsis TBL 29/ ESK 1 xylan O‐acetyltransferase display a strong reduction in total wall O ‐acetylation accompanied by a dwarfed plant stature, collapsed xylem morphology, and enhanced freezing tolerance. A newly identified tbl29/esk1 suppressor mutation reduces the expression of the MAX 4 gene, affecting the biosynthesis of methyl carlactonoate (Me CLA ), an active strigolactone ( SL ). Genetic and biochemical evidence suggests that blocking the biosynthesis of this SL is sufficient to recover all developmental and stress‐related defects associated with the TBL 29/ ESK 1 loss of function without affecting its direct effect—reduced wall O ‐acetylation. Altered levels of the MAX 4 SL biosynthetic gene, reduced branch number, and higher levels of Me CLA , were also found in tbl29/esk1 plants consistent with a constitutive activation of the SL pathway. These results suggest that the reduction in O ‐acetyl substituents in xylan is not directly responsible for the observed tbl29/esk1 phenotypes. Alternatively, plants may perceive defects in the structure of wall polymers and/or wall architecture activating the SL hormonal pathway as a compensatory mechanism.