The yeast 'killer' system is composed of the L-A helper and M 1 satellite dsRNA viruses (35) . The L-A dsRNA viral genome encodes a capsid protein (Gag), and an RNA-dependent RNA polymerase (Pol) that is synthesized as a Gag-pol fusion protein consequent to a À1 Programmed Ribosomal Frameshifting (PRF) event (36) . The M 1 satellite dsRNA is encapsidated and replicated in L-A encoded viral particles, and the M 1 (+) strand encodes a secreted toxin that kills uninfected yeast through its interactions with the GPI-anchored Kre1p cell wall assembly protein (37) . Changes in À1 PRF efficiency alter the ratio of Gag to Gag-pol, and inhibit the ability of cells to maintain M 1 (19) . To monitor the effects of the mutants on Killer virus maintenance, colonies of JD1313 cells expressing either wild-type or mutant rpl11B alleles were spotted onto a lawn of diploid, Killer À indicator cells. Cells expressing wild-type RPL11B were Killer + as demonstrated by their ability to inhibit growth of the indicator cells ( Figure 2C ). In contrast, isogenic cells expressing the 51-4A, 54-7A and F57A mutants were Killer À . A weak killer phenotype, defined by decreased zones of growth inhibition, was observed in mutants Y52E, Y52N, Y52H and F57A.