Over the last 10 years, we have focussed on the study of yeast cell proliferation, particularly in response to zymocin which is a trimeric (abg) toxin complex from Kluyveromyces lactis that kills Saccharomyces cerevisiae. The overall goal of our research into this yeast pathosystem has been to use the power of budding yeasts as eukaryotic models to provide insights into organismic interaction and microbial competition. Using molecular techniques, we have genetically dissected the lethal response towards zymocin, which results in a G1 cell cycle arrest, into a multi-step pathway that involves ~30 genes. It initiates with docking of zymocin onto cell wall chitin and chitinolysis by zymocin's a-subunit. Subsequently, early events that mediate import and activation of zymocin's lethal g-toxin subunit require plasma membrane sphingolipid synthesis and the proton pump Pma1. Intracellularly, g-toxicity requires the Elongator complex (Elp1-6), Elongator-related proteins (Kti11-14: killer toxin insensitive) and tRNA methylase Trm9. These zymocin players were isolated in our group using genome-wide transposon mutagenesis to identify toxin resistant S. cerevisiae mutants or single-copy complementation of existing kti mutants generated in the group of Stark at Dundee. As shown by the Svejstrup group, Elongator is a histone acetylase (HAT) that partners with RNA polymerase II. By virtue of its HAT activity, Elongator is thought to assist transcription by RNA polymerase II through chromatin. In further support of a transcriptional role, Elongator binds unspliced nascent mRNAs that emanate from the transcription machinery in the nucleus.