Antagonistic functions of CTL1 and SUH1 mediate cell wall assembly inArabidopsis

Abstract

AbstractPlant genomes contain numerous genes encoding chitinase-like (CTL) proteins, which have a similar protein structure to chitinase but lack the chitinolytic activity to cleave theβ-1,4-glycosidic bond in chitins, polymers ofN-acetylglucosamine. Mutations inCTL1in rice andArabidopsishave 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 identifiedsuppressor of hot2-1(suh1) as a genetic suppressor of thectl1hot2-1mutation inArabidopsis. The mutation inSUH1restored almost allctl1hot2-1defects examined to nearly wild-type levels, with the exception of partial recovery of cellulose content inctl1hot2-1mutants.SUH1encodes 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 thanctl1hot2-1mutation. TheSUH1promoter fused with the GUS reporter gene exhibited GUS activity in interfascicular fibers and xylem in stems, and this activity was significantly increased by thectl1hot2-1mutation. Our findings provide genetic and molecular evidence that the antagonistic activities of CTL1 and SUH1 play an essential role in cell wall assembly inArabidopsis.HighlightThis study reports mutations insuppressor of hot2-1(SUH1) gene that rescues the defects caused by mutations inCTL1, which are characterized by stunted growth due to decreased cellulose levels.