Antagonistic functions of CTL1 and SUH1 mediate cell wall assembly in Arabidopsis

Abstract

Plant genomes contain numerous genes encoding chitinase-like (CTL) proteins, which have a similar protein structure to chitinase but lack the chitinolytic activity to cleave the {beta}-1,4-glycosidic bond in chitins, polymers of N-acetylglucosamine. Mutations in CTL1 in rice and Arabidopsis have been found to cause pleiotropic developmental defects, including altered cell wall composition and decreased abiotic stress tolerance, likely due to a reduction in cellulose content. In this study, we identified suppressor of hot2-1 (suh1) as a genetic suppressor of the ctl1hot2-1 mutation in Arabidopsis. The mutation in SUH1 restored almost all ctl1hot2-1 defects examined to nearly wild-type levels, with the exception of partial recovery of cellulose content in ctl1hot2-1 mutants. SUH1 encodes a Golgi-located type II membrane protein with glycosyltransferase (GT) activity, and its mutations lead to reduction in cellulose content and hypersensitivity to cellulose biosynthesis inhibitors, although to a lesser extent than ctl1hot2-1 mutation. The SUH1 promoter fused with the GUS reporter gene exhibited GUS activity in interfascicular fibers and xylem in stems, and this activity was significantly increased by the ctl1hot2-1 mutation. Our findings provide genetic and molecular evidence that the antagonistic activities of CTL1 and SUH1 play an essential role in cell wall assembly in Arabidopsis. HighlightThis study reports mutations in suppressor of hot2-1 (SUH1) gene that rescues the defects caused by mutations in CTL1, which are characterized by stunted growth due to decreased cellulose levels.