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Candida albicans is a major fungal pathogen whose virulence is associated with its ability to transition from a budding yeast form to invasive hyphal filaments. The kinesin-14 family memberCa Kar3 is required for transition between these morphological states, as well as for mitotic progression and karyogamy. While kinesin-14 proteins are ubiquitous,Ca Kar3 homologs in hemiascomycete fungi are unique because they form heterodimers with noncatalytic kinesin-like proteins. Thus,Ca Kar3-based motors may represent a novel antifungal drug target. We have identified and examined the roles of a kinesin-like regulator ofCa Kar3. We show thatorf19.306 (dubbedCaCIK1 ) encodes a protein that forms a heterodimer withCa Kar3, localizesCa Kar3 to spindle pole bodies, and can bind microtubules and influenceCa Kar3 mechanochemistry despite lacking an ATPase activity of its own. Similar toCa Kar3 depletion, loss ofCa Cik1 results in cell cycle arrest, filamentation defects, and an inability to undergo karyogamy. Furthermore, an examination of the spindle structure in cells lacking either of these proteins shows that a large proportion have a monopolar spindle or two dissociated half-spindles, a phenotype unique to theC. albicans kinesin-14 homolog. These findings provide new insights into mitotic spindle structure and kinesin motor function inC. albicans and identify a potentially vulnerable target for antifungal drug development.

eukaryotic cell

Candida albicans Kinesin Kar3 Depends on a Cik1-Like Regulatory Partner Protein for Its Roles in Mating, Cell Morphogenesis, and Bipolar Spindle Formation