Alteration of
Saccharomyces cerevisiae plasma membrane fluidity is accompanied with
the reduced sensitivity of cells to the killer toxin K1.
Drahomíra Novotná (1), Hana Flegelová (1), Roman Chaloupka (2), Jan Malác (2),
Dana Gásková (2), Blanka Janderová (1), Karel Sigler (3)
(1) Dept. Genet. Microbiol., Fac. Sci., Charles University, Vinicná 5, Prague
2, 128 44, Czech Republic (dranov@natur.cuni.cz); (2) Institute of Physics,
Charles University, Ke Karlovu 5, 121 16 Prague 2, Czech Republic; (3)
Institute of Microbiology, Czech Academy of Sciences, Videnská 1083, 142 20
Prague 4, Czech Republic
The yeast Saccharomyces cerevisiae produces K1 killer toxin that is able to kill sensitive yeast cells by inducing uncontrolled leakage of ions through their plasma membrane. This phenomenon can be caused either by incorporation of oligomerized toxin molecules into the membrane, where they form de novo ion channels, or by the opening of native ion channels. It can be assumed that both these processes can be affected by membrane fluidity. We increased or decreased membrane fluidity by precultivating of S. cerevisiae cells at non-optimal temperatures, in the presence of ethanol or polyunsaturated linoleic (18:2) or linolenic (18:3) fatty acids. The sensitivity of cells precultivated under these conditions to K1 killer toxin was in all cases decreased, albeit with different intensities -increased fluidity had a small effect on cell survival while decreased fluidity had a marked effect. The most significant differences were observed for cells with membrane fluidity lowered by cultivation at 38°C. We suggest that these results could reflect reduction of killer toxin contacts with membrane protein receptor at non-optimal membrane microviscosity and disprove the hypothesis that killer toxin K1 could interact directly with plasma membrane lipids. This work was supported by grants: GACR 204/00/0629, GAUK 130/2000, MSM 113100003