The hfa (high frequency of aneuploidy) mutants of Aspergillus nidulans carry conditional lethal (temperature-sensitive) defects which cause an increased frequency of aneuploids to be produced amongst their asexual progeny. When examined microscopically, most of the mutants grew and divided their nuclei at restrictive temperature, albeit more slowly than the wild-type, and aneuploidy was not attributable to an obvious cell cycle lesion. Exceptions were hfaB3 and hfaL1 which exhibited defects in nuclear division, although neither mutant arrested at a specific point in the cell cycle. Cells carrying hfaB3 contained only a single enlarged nucleus which was often transected (‘cut’) by the first septum and temperature-shift experiments showed that the mutation triggers aneuploidy by causing failure to properly exit mitosis. Although the hfaD1 mutant underwent nuclear division, it differed morphologically from wild-type by exhibiting a hyper-branching phenotype. The original hfaD1 isolate was shown also to carry a second unlinked mutation (designated hurA1) which confers resistance to hydroxyurea and partly alleviates the growth defects imposed by hfaD1.