Involvement of cell wall β-glucan in the action of HM-1 killer toxin

Shin Kasahara, Shunsuke Ben Inoue, Toshiyuki Mio, Toshiko Yamada, Tasuku Nakajima, Eiji Ichishima, Yasuhiro Furuichi, Hisafumi Yamada

    Research output: Contribution to journalArticlepeer-review

    48 Citations (Scopus)


    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 {amalgamation}-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 {amalgamation}-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.

    Original languageEnglish
    Pages (from-to)27-32
    Number of pages6
    JournalFEBS Letters
    Issue number1
    Publication statusPublished - 1994 Jul 4


    • Cell wall
    • HM-1 killer toxin
    • KRE6
    • β-Glucan

    ASJC Scopus subject areas

    • Biophysics
    • Structural Biology
    • Biochemistry
    • Molecular Biology
    • Genetics
    • Cell Biology


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