Growth- and stress-related defects associated to wall hypoacetylation are strigolactone-dependent

Abstract

Mutants affected in the Arabidopsis TBL29/ESK1 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 affects the biosynthesis of strigolactones (SL) due to the reduced expression of the MAX4 gene. Genetic and biochemical evidence suggests that blocking the biosynthesis of SL is sufficient to recover all developmental and stress-related defects associated with the TBL29/ESK1 loss of function without affecting its direct effect - reduced wall O-acetylation. Altered levels of the MAX4 SL biosynthetic gene, reduced branch number, and higher levels of methyl carlactonoate, an active SL, were also found in tbl29/esk1 plants consistent with a constitutive activation of the SL pathway. These results indicate that the reduction of 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.