Experimental evidence suggests that Mid2p acts to negatively influence cell growth in response to cell wall damage. Absence of Mid2p in cells deficient for one or more genes involved in Beta-1,6 glucan synthesis, such as KRE6, results in significant restoration of growth rate without apparent restoration of cell wall Beta-1,6 glucan content. In contrast, over expression of Mid2p in a kre6 background causes cells to grow significantly slower than kre6 cells. Altered expression of Mid2p also has effects in mutants deficient for Beta-1,3 glucan production. mid2 cells are resistant to calcofluor white, and over expression of Mid2p results in hypersensitivity to this microfibril intercalating dye. Taken together, these results suggest that Mid2p activity is influenced by the presence of a variety of cell wall polymers. Consistent with computer-aided predictions, experimental analysis suggests that Mid2p is a Type I integral membrane protein. Experimental evidence demonstrates that Mid2p is localized to the plasma membrane, is highly glycosylated, and is covalently associated with the cell wall. The structure, localization and genetic interactions exhibited by Mid2p suggest that it influences cell growth in response to cell wall damage effected by mutation or calcofluor white. These observations may be extended to form the hypothesis that Mid2p is a component of a growth control mechanism that responds to cell wall state.