However, triple mutant cells exhibit extremely strong morphological defects; they form very long buds and are defective for cell separation, resulting in the formation of branched chains of elongated cells. The resulting quadruple mutant grows slightly slower than the triple mutant, as Levocetirizine judged by Megestrol acetate colony size, but this growth defect remains slight compared with wild type.Cytological analysis indicates that the elongated bud morphology of the hslD ginD kccD triple mutant are eliminated by deletion of SWE.Deletion of either HSL, KCC, orGIN alone has no striking effect on strain viability or growth.During exponential growth, the cellular morphology of each of these single mutants is similar to wild type. In contrast, introduction of the sweD allele does not alleviate the cytokinesis defect of the hslD ginD kccD triple mutant, as measured by the frequency of largebudded cells that have finished nuclear division but are not yet separated. Each of the double mutants, hslD kccD, hslD ginD, and kccD ginD, has a phenotype that is intermediate between that of the single and triple mutants.The strongest defect is observed in the ginD hslD cells, closely followed by the ginD kccD double mutant.The elongated bud morphology and cell cycle defects of each of these double mutants is suppressed by sweD. Therefore, we tested whether any of these mutations interact genetically with septin mutants.Strains carrying a cdc, hslD, ginD, orkcc D single mutation exhibit few or no morphological defects when grown at C; however, each of the cdc hslD, cdc kccD, and cdc ginD double mutants form elongated buds at this temperature. These genetic interactions are additive; the cdc hslD kccD ginD quadruple mutant displays extreme growth defects at the permissive temperature.The majority accumulate septins as elongated, irregular patches at the bud neck appear to have normal septin structures.Cdc localization is aberrant in hslD kccD ginD cells but similar to wild type in budded hslD kccD ginD sweD cells.The timing of nuclear division was monitored in synchronized populations of wildtype and cdc strains.Pheromonearrested cells were diluted into fresh medium at C and the timing of bud emergence and nuclear division were determined.The wildtype and the septin mutant strains initiate budding at the same time, but nuclear division was delayed min in the mutant relative to wild type. Thus, both the switch to isotropic growth and nuclear division are delayed as a result of the disruption of septin structures.Cell morphology and the timing of nuclear division were examined in cdc and cdc sweD strains incubated at the restrictive temperature.The cdc strain forms very elongated buds when grown at C, whereas the cdc sweD double mutant develops smaller, rounder buds. In addition to its effect on bud morphology, the deletion of SWE also abolishes the nuclear division delay due to the cdc mutation. In fact, the cdc sweD double mutant has additional defects compared with the original cdc strain.The SWE deletion greatly reduces the ability of the cdc strain to grow at a semipermissive temperature. In the cdc CDCYF mutant, the mitotic delay due to the septin mutation was also abolished.