Cytoplasmic dynein is a ubiquitously expressed microtubule motor involved in vesicle transport, mitosis, nuclear migration, and spindle orientation. In the filamentous fungus Aspergillus nidulans, inactivation of
cytoplasmic dynein, although not lethal, severely impairs nuclear migration. The role of
dynein in mitosis and vesicle transport in this organism is unclear. To investigate the complete range of
dynein function in A. nidulans, we searched for synthetic lethal mutations that significantly reduced growth in the absence of
dynein but had little effect on their own. We isolated 19 sld (synthetic lethality without
dynein) mutations in nine different genes. Mutations in two genes exacerbate the nuclear migration defect seen in the absence of
dynein. Mutations in six other genes, including sldA and sldB, show a strong synthetic lethal interaction with a mutation in the mitotic
kinesin bimC and, thus, are likely to play a role in mitosis. Mutations in sldA and sldB also confer
hypersensitivity to the microtubule-destabilizing
drug benomyl. sldA and sldB were cloned by complementation of their mutant phenotypes using an A. nidulans autonomously replicating vector. Sequencing revealed homology to the spindle assembly checkpoint genes BUB1 and BUB3 from Saccharomyces cerevisiae. Genetic interaction between
dynein and spindle assembly checkpoint genes, as well as other mitotic genes, indicates that A. nidulans
dynein plays a role in mitosis. We suggest a model for
dynein motor action in A. nidulans that can explain
dynein involvement in both mitosis and nuclear distribution.