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Involvement of cell wall β‐glucan in the action of HM‐1 killer toxin
Author(s) -
Kasahara Shin,
Inoue Shunsuke Ben,
Mio Toshiyuki,
Yamada Toshiko,
Nakajima Tasuku,
Ichishima Eiji,
Furuichi Yasuhiro,
Yamada Hisafumi
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)00575-3
Subject(s) - toxin , mannan , glucan , cell wall , biology , clostridium difficile toxin a , microbiology and biotechnology , chemistry , biochemistry , polysaccharide , clostridium difficile , antibiotics
HM‐1 killer toxin secreted from Hansenula mrakii inhibits the growth of Saccharomyces cerevisiae cells by interfering with β‐1,3‐glucan synthesis. We found that HM‐1 killer toxin killed intact cells but not protoplasts. In addition, cells lacking the functional KRE 6 allele ( kre6Δ ) 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 KPE6 had a reduced level of the cell wall β‐1,6‐glucan compared to that in cells harboring the normal KRE6 . These results suggest that the cell wall ⨿‐glucan is involved in the action of HM‐1 killer toxin. Addition of HM‐1 killer toxin with several kinds of oligosaccharides revealed that either ⨿‐1,3‐ or β‐1,6‐glucan blocked the cytocidal action of HM‐1 killer toxin whereas α‐1,4‐glucan and chitin did not. Mannan also interfered with HM‐1 killer toxin action, but this inhibitory effect was much weaker than that observed with β‐1,3‐ or β‐1,6‐glucans. Thus, it appears that the cell wall β‐glucan interacts with HM‐1 killer toxin, and that this toxin‐β‐glucan commitment is required for the action of HM‐1 killer toxin.