The mitotic NIM A kinase shows synthetic lethal interactions with genes potentially involved in septation and cell tip growth in Aspergillus nidulans.

Meera Govindaraghavan 1*, Sarah Lea McGuire 2 and Stephen A. Osmani 1

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1Department of Molecular Genetics, The Ohio State University, Columbus, OH 2Department of Biology, Millsaps College, Jackson, MS


In Aspergillus nidulans the transition from G2 into mitosis requires the NIMA kinase. In yeast, a synthetic lethal screen using KIN3, the non essential NIMA orthologue, identified twelve genes, not involved with the cell cycle (S.L. McGuire, unpublished). Since KIN3 does not have mitotic functions, if these synthetic interactions where conserved in A. nidulans this might reveal additional non-mitotic roles for NIMA. W e therefore determined if NIMA interacts with the orthologues of the yeast genes that are synthetically lethal with KIN3. Of the ten orthologues identified, synthetic lethal/sick temperature sensitive interactions with nimA7 were identified for only four, An-swd1, An- vps23, An-vps25 and An-ypt7. W e characterized the nuclear morphology and septation of the double mutants which revealed temperature sensitive synthetic growth defects linked to abnormal branching, septation and DNA segregation. Because we additionally discovered a defect in the tip morphology of nimA ts cells, collectively the results indicate that NIM A plays roles in septation and tip growth. This hypothesis is strengthened by the observation that NIMA localizes to septa and cell tips (C. De-Souza, K-F. Shen and S.A. Osmani unpublished). Further characterization of these interactions will lead to a better understanding of these previously unrealized non mitotic functions of NIMA. *Student poster

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6th International Aspergillus Meeting
    • Asperfest 6 (2009)