Genetic dissection of cell wall defects and the strigolactone pathway in Arabidopsis.

Abstract

Defects in the biosynthesis and/or deposition of secondary plant cell wall polymers result in the collapse of xylem vessels causing a dwarfed plant stature and an altered plant architecture termed irregular xylem (irx) syndrome. For example, reduced xylan O-acetylation causes strong developmental defects and increased freezing tolerance. Recently, we demonstrated that the irx syndrome in the trichome birefringence-like 29/eskimo1 (tbl29/esk1) mutant is dependent on the biosynthesis of the phytohormone strigolactone (SL). In this report, we show that other xylan- and cellulose-deficient secondary wall mutants exhibit increased freezing tolerance correlated with the irx syndrome. In addition, blocking SL synthesis has also a suppressor effect on these phenotypes, suggesting a more general interaction between secondary wall defects and SL biosynthesis. In contrast, SLs do not play a role in developmental defects triggered by primary wall deficiencies, suggesting that the interaction is restricted to vascular tissue.\n\nThrough a reverse genetics approach the requirement of different components of the SL pathway impacting the irx syndrome in tbl29 was evaluated. Our results are consistent with a specific role for carlactone in this process, and suggest that a MORE AXILLARY GROWTH 2 (MAX2)-independent SL perception mechanism might be involved.