Structure and maintenance of the cell wall are determined, in part, by balanced function of cell wall biosynthesis and degradation. We hypothesized that the abnormally-thick cell walls and septa of the N.crassa NDR kinase cot-1 mutant may be a result of altered expression of the cell wall remodeling machinery. Inactivation of gul-1 (a homologue of the yeast Ssd1 RNA-binding protein involved in translational regulation of cell wall remodeling proteins) partially suppresses the cot-1 phenotype, accompanied by improved characteristics of the cell wall and septa. A 40% increase in chitin content in the cell wall of cot-1 (when compared to the wild type) was almost completely abolished in the gul-1;cot-1strain. Furthermore, the gul-1 mutant was also found to be almost 2-fold more sensitive to chitin synthase inhibition, when compared to the wild type. We have determined that gul-1 is involved in regulation of the expression of cell wall remodeling genes such as glucan synthase, chitin synthases and a chitinasein a manner which is at least partially independent of the classic cell wall integrity pathway. Overall, expression of at least 25 genes involved in cell-wall remodeling was GUL-1-dependent. Moreover, based on GO analysis, GUL-1 was also found to regulate additional pathways such as transmembrane transport (34 genes) andamino acid metabolism (8 genes).We conclude that GUL1 is a regulator of cell wall remodeling and that the suppressive effect on cot-1 is conferred via this capacity.