Abstract
Plant genomes contain numerous genes encoding chitinase-like (CTL) proteins, which have a similar protein structure to chitinase belonging to the glycoside hydrolase (GH) family but lack the chitinolytic activity to cleave the β-1,4-glycosidic bond in chitins, polymers of N-acetylglucosamine. CTL1 mutations found in rice and Arabidopsis have caused pleiotropic developmental defects, including altered cell wall composition and decreased abiotic stress tolerance, likely due to reduced cellulose content. In this study, we identified suppressor of hot2 1 (suh1) as a genetic suppressor of the ctl1 (hot2-1) mutation in Arabidopsis. The mutation in SUH1 restored almost all examined ctl1 (hot2-1) defects to nearly wild-type levels or at least partially. SUH1 encodes a Golgi-located type II membrane protein with glycosyltransferase (GT) activity, and its mutations lead to a reduction in cellulose content and hypersensitivity to cellulose biosynthesis inhibitors, although to a lesser extent than ctl1 (hot2-1) mutation. The SUH1 promoter fused with the GUS reporter gene exhibited GUS activity in interfascicular fibers and xylem in stems; meanwhile, the ctl1 (hot2-1) mutation significantly increased this activity. Our findings provide genetic and molecular evidence that the antagonistic activities of CTL1 and SUH1 play an essential role in assembling the cell wall in Arabidopsis.