TY - JOUR
T1 - Involvement of cell wall β-glucan in the action of HM-1 killer toxin
AU - Kasahara, Shin
AU - Inoue, Shunsuke Ben
AU - Mio, Toshiyuki
AU - Yamada, Toshiko
AU - Nakajima, Tasuku
AU - Ichishima, Eiji
AU - Furuichi, Yasuhiro
AU - Yamada, Hisafumi
N1 - Funding Information:
AcknowledgemenTthsi:s work wass upportedin part by a Grant in Aid (Glyco-technologyP rogram)f rom the Ministry of Agriculture.F or-estrya nd Fisherieso f Japan to T.N.
PY - 1994/7/4
Y1 - 1994/7/4
N2 - 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.
AB - 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.
KW - Cell wall
KW - HM-1 killer toxin
KW - KRE6
KW - β-Glucan
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U2 - 10.1016/0014-5793(94)00575-3
DO - 10.1016/0014-5793(94)00575-3
M3 - Article
C2 - 8026578
AN - SCOPUS:0028275528
VL - 348
SP - 27
EP - 32
JO - FEBS Letters
JF - FEBS Letters
SN - 0014-5793
IS - 1
ER -