T. Komiyama et al., PORE FORMATION ON PROLIFERATING YEAST SACCHAROMYCES-CEREVISIAE CELL BUDS BY HM-1 KILLER TOXIN, Journal of Biochemistry, 119(4), 1996, pp. 731-736
The cytocidal effect of HM-1 produced by Hansenula mrakii on yeast Sac
charomyces cerevisiae cells was studied. The HM-1 strongly inhibited t
he growth of S. cerevisiae cells at a low concentration (IC50: 2.1 X 1
0(-8) M) by reducing the number of viable cells. The killer action of
HM-1 was most efficient when cells were actively proliferating. Cells
in a resting state were resistant, but they became HM-l-sensitive afte
r about 90 min of culturing at 30 degrees C, concomitantly with the in
crement of budding index. In association with the reduction of viable
cell number, ultraviolet light-absorbing cellular components were disc
harged from sensitive cells. HRI-1 molecules appear to bind to suscept
ible cells rather loosely since cells incubated with HM-1 were able to
proliferate after having been washed. By phase-contrast light microsc
opy and scanning electron microscopy, discharge of cell material was o
bserved at the budding portions of HM-1-treated cells. Addition of sor
bitol to make the culture medium isotonic partially reduced the cell d
eath induced by HM-1. These results suggest that HM-1 acts on the budd
ing region of proliferating yeast cells, resulting in pore formation,
leakage of cell material and eventual cell death.