(d) Theoretically, each molecule of any colicin is capable of killing one sensitive
bacterial cell.
(e) The spectrum of the lethal effect of colicins is limited. Colicin-synthetizing
bacteria are immune against the effect, although these bacteria do possess colicin
binding receptors, they are not affected by it.
There exist three molecular mechanisms that make bacteria insensitive to a given
colicin: resistance, tolerance, and immunity. Each bacterium that does not have a
colicin receptor on its surface is resistant to the colicin. Colicin-tolerant describes a
bacterium that is not sensitive to it, although it has functional receptors in its outer
membrane and can specifically bind the colicin. Tolerance is caused by a loss
mutation of the sensitive strain, which blocks some of the stages that follow after
the colicin binds to the receptor.
Immunity constitutes the most specific mechanism of non-sensitivity. It emerges
when a colicinogenic bacterium produces—along with colicin—a specific low
molecular protein of acidic nature, the so called immune substance. The immune
substance is capable of binding to the C-terminal region of the respective colicin and
forms with it an inactive complex. Some strains of Shigella sonnei also have the
ability to synthetize colicin.
15.4.3 Yeasts and Zymocins
Some yeasts of certain species or genera can form toxic products, which kill sensitive
yeasts of the same species or genus. From Greek, these have been named zymocins
meaning zyme ¼ yeast, and from Latin caedere ¼ to kill. Zymocins are also called
either killer factors (toxins) or killer proteins. Another proposed term is mycocin as a
certain analogy to bacteriocins. The ability of certain yeasts to produce zymocins is
referred to as a killer phenomon. Nevertheless, other yeast cells of its own strain are
immune to those zymocins. These substances were first detected by M. Makower
and E. A. Bevan in 1963 (Bevan and Makower 1963) in Saccharomyces cerevisiae.
From the point of view of zymocin production Saccharomyces cerevisiae is the most
intensively studied species. Four different killer toxins have been described in this
microorganism, designated as K1, K2, K3, and K28 and coded by double-stranded
RNA (ds RNA) of the viruses ScV-L (so called L-virus S. cerevisiae), and ScV-M.
The killer protein can link to beta-1,6 glucan in the cellular wall of a sensitive yeast
cell. No energy is needed for this reaction. The killer protein then penetrates to the
plasma membrane. It is assumed that eight molecules of killer protein mutually join
together and form a circular octamer that causes a pore in the membrane. This pore
impairs the function of the yeast’s membrane so much so that various ions and
molecules, including those of ATP, can leak out. This leakage actually causes the
cell’s death. However, it was also discovered that killer strains can be “cured”—to
deprive them of their ability to kill sensitive cells. That successful curing can be
250
V. Klaban
bacterial cell.
(e) The spectrum of the lethal effect of colicins is limited. Colicin-synthetizing
bacteria are immune against the effect, although these bacteria do possess colicin
binding receptors, they are not affected by it.
There exist three molecular mechanisms that make bacteria insensitive to a given
colicin: resistance, tolerance, and immunity. Each bacterium that does not have a
colicin receptor on its surface is resistant to the colicin. Colicin-tolerant describes a
bacterium that is not sensitive to it, although it has functional receptors in its outer
membrane and can specifically bind the colicin. Tolerance is caused by a loss
mutation of the sensitive strain, which blocks some of the stages that follow after
the colicin binds to the receptor.
Immunity constitutes the most specific mechanism of non-sensitivity. It emerges
when a colicinogenic bacterium produces—along with colicin—a specific low
molecular protein of acidic nature, the so called immune substance. The immune
substance is capable of binding to the C-terminal region of the respective colicin and
forms with it an inactive complex. Some strains of Shigella sonnei also have the
ability to synthetize colicin.
15.4.3 Yeasts and Zymocins
Some yeasts of certain species or genera can form toxic products, which kill sensitive
yeasts of the same species or genus. From Greek, these have been named zymocins
meaning zyme ¼ yeast, and from Latin caedere ¼ to kill. Zymocins are also called
either killer factors (toxins) or killer proteins. Another proposed term is mycocin as a
certain analogy to bacteriocins. The ability of certain yeasts to produce zymocins is
referred to as a killer phenomon. Nevertheless, other yeast cells of its own strain are
immune to those zymocins. These substances were first detected by M. Makower
and E. A. Bevan in 1963 (Bevan and Makower 1963) in Saccharomyces cerevisiae.
From the point of view of zymocin production Saccharomyces cerevisiae is the most
intensively studied species. Four different killer toxins have been described in this
microorganism, designated as K1, K2, K3, and K28 and coded by double-stranded
RNA (ds RNA) of the viruses ScV-L (so called L-virus S. cerevisiae), and ScV-M.
The killer protein can link to beta-1,6 glucan in the cellular wall of a sensitive yeast
cell. No energy is needed for this reaction. The killer protein then penetrates to the
plasma membrane. It is assumed that eight molecules of killer protein mutually join
together and form a circular octamer that causes a pore in the membrane. This pore
impairs the function of the yeast’s membrane so much so that various ions and
molecules, including those of ATP, can leak out. This leakage actually causes the
cell’s death. However, it was also discovered that killer strains can be “cured”—to
deprive them of their ability to kill sensitive cells. That successful curing can be
250
V. Klaban