Abstract text: Xylan O-acetylation is a major determinant of secondary cell wall integrity, and its reduction leads to severe developmental defects, including dwarfism and collapsed xylem. Surprisingly, these defects can be genetically suppressed by mutations in the strigolactone biosynthesis pathway without restoration of xylan O-acetylation. The molecular mechanism underlying this suppression remains unclear.

Here, we show through genetic interaction analyses that strigolactone deficiency suppresses growth and vascular defects associated with xylan hypoacetylation through transcription factors typically involved in hormonal crosstalk. Cell wall compositional analyses and mass spectrometry profiling reveal that the phenotypic rescue tightly correlates with a compensatory polysaccharide substitution pattern. Mechanistically, these transcriptional factors regulate specific glycosytransferase genes, fine-tuning wall polymer modification under hypoacetylation conditions. Disruption of this regulatory module abolishes suppression, highlighting its functional importance.

Together, our findings point to a mechanism involving hormonal crosstalk that can maintain secondary cell wall integrity when xylan O-acetylation is compromised, providing new insight into the plasticity of secondary wall regulation.