Synthesia 10.1
cerevisiae mutants resistant to killer toxins K1 and K2 at the plasma membrane level. In this report we present the results of our attempt to isolate S.
In addition, K1 toxin can also damage yeast cells via another mechanism: TOK1-deleted cells die after prolonged exposure to killer cells or concentrated toxin. This channel could therefore be the putative plasma membrane receptor for K1 toxin. Recently it was found that killer toxin K1 increases the probability of the open state (via reversible destabilization of closed states) of the plasma membrane potassium channel Tok1p. The mutant was found to have a lowered content of three membrane proteins but the mutated gene was not identified. In an attempt to identify a K1 killer toxin receptor on the plasma membrane, mutant kre12 with resistant spheroplasts was isolated. The structure and properties of the plasma membrane receptors for killer toxins are still unclear. The mechanism of action of K28 killer toxin is quite different – it involves an independent blockage of both DNA synthesis and cell budding, thereby causing a loss of cell viability. The electrical potential across the cell membrane is disrupted as a consequence of formation of ion-conductive channels and subsequently pores in the plasma membrane of sensitive cells through which important cell constituents – potassium ions, ATP and others – leak out of the cell into the outer medium. It is assumed that the mode of action of K1 and K2 toxins on the plasma membrane is very similar. These findings, together with kinetic studies indicating that susceptible cells contain two populations of toxin-binding sites, suggest that there are also some receptors for killer toxins on the plasma membrane. The cell wall is not necessarily needed for the next step, toxin interaction with the plasma membrane, since wall-less spheroplasts of sensitive strains but also of kre mutants succumb to the toxin as well. Mutants with a reduced amount of β-1,6-glucan ( kre mutants) are resistant to killer toxin K1. The first step requires binding of the toxin to cell wall receptors containing β-1,6-glucan (for K1 toxin) or mannan proteins (for K28 toxin). The presumed mode of their action involves two steps. Saccharomyces cerevisiae produces four types of killer toxin, K1, K2, K3 and K28, which are encoded by double-stranded (ds) RNA encapsidated in virus-like particles localized in the cytoplasm. The killer phenomenon discovered in yeasts in 1963 involves the production of proteinaceous killer toxins that kill other susceptible yeast strains. Killer toxin, Toxin K1 and K2, Resistance, Saccharomyces cerevisiae 1 Introduction