INVOLVEMENT OF CELL-WALL BETA-GLUCAN IN THE ACTION OF HM-1 KILLER TOXIN

HM-1 killer toxin secreted from Hansenula mrakii inhibits the growth o f Saccharomyces cel cerevisiae cells by interfering with beta-1,3-gluc an synthesis. We found that HM-1 killer toxin killed intact cells but not protoplasts. In addition, cells lacking the functional KRE6 allele (kre6 Delta) became resistant to higher concentration of HM-1 killer toxin. As reported by Roemer and Bussey [(1991) Proc. Natl. Acad. Sci. 88 11295-11299], cells lacking functional KRE6 had a reduced level of the cell wall beta-1,6-glucan compared to that in cells harboring the normal KRE6. These results suggest that the cell wall beta-glucan is involved in the action of HM-1 killer toxin. Addition of HM-1 killer t oxin with several kinds of oligosaccharides revealed that either beta- 1,3- or beta-1,6-glucan blocked the cytocidal action of HM-1 killer to xin whereas alpha-1,4-glucan and chitin did not. Mannan also interfere d with HM-1 killer toxin action, but this inhibitory effect was much w eaker than that observed with beta-1,3- or beta-1,6-glucans. Thus, it appears that the cell wall beta-glucan interacts with HM-1 killer toxi n, and that this toxin-beta-glucan commitment is required for the acti on of HM-1 killer