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Pathways. We ordered the mutants in a number of ways. First, by how far they traversed the cycle before arresting. We analyzed the following cell cycle events: budding, DNA synthesis, nuclear division cytokinesis and cell division. The event that stopped first after a shift from the permissive to the restrictive temperature was considered the primary defect. After the primary defect, other cell cycle events would occur or not depending upon the particular mutant. Eventually, the cell would arrest development and generate a terminal phenotype, depending on which events occurred and which did not. Mutants were found with primary defects in each of the cell cycle events that we monitored. The phenotypes of the mutants suggested a relatively simple pathway of dependent events leading to cell division. The first event, controlled by the CDC28 gene, was required for initiating two pathways, one of which led to budding, nuclear migration, cytokinesis and cell division. The second led to DNA replication, nuclear division and joined the first prior to cytokinesis and cell division. We tested our conclusions by constructing all possible double mutants and, indeed, the phenotypes of double mutants was precisely that expected for the pathway.