A Role for NIMA in the Nuclear Localization of Cyclin B in Aspergillus nidulans

NIMA promotes entry into mitosis in late G2 by some mechanism that is after activation of the Aspergillus nidulans G2 cyclin-dependent kinase, NIMX^CDC2/NIME^{Cyclin B}. Here we present two independent lines of evidence which indicate that this mechanism involves control of NIMX^CDC2/NIME^{Cyclin B} localization. First, we found that NIME^{Cyclin B} localized to the nucleus and the nucleus-associated organelle, the spindle pole body, in a NIMA-dependent manner. Analysis of cells from asynchronous cultures, synchronous cultures, and cultures arrested in S or G2 showed that NIME^{Cyclin B} was predominantly nuclear during interphase, with maximal nuclear accumulation in late G2. NIMX^CDC2 colocalized with NIME^{Cyclin B} in G2 cells. Although inactivation of NIMA using either the nimA1 or nimA5 temperature-sensitive mutations blocked cells in G2, NIMX^CDC2/NIME^{Cyclin B} localization was predominantly cytoplasmic rather than nuclear. Second, we found that nimA interacts genetically with sonA, which is a homologue of the yeast nucleocytoplasmic transporter GLE2/RAE1. Mutations in sonA were identified as allele-specific suppressors of nimA1. The sonA1 suppressor alleviated the nuclear division and NIME^{Cyclin B} localization defects of nimA1 cells without markedly increasing NIMX^CDC2 or NIMA kinase activity. These results indicate that NIMA promotes the nuclear localization of the NIMX^CDC2/ NIME^{Cyclin B} complex, by a process involving SONA. This mechanism may be involved in coordinating the functions of NIMX^CDC2 and NIMA in the regulation of mitosis.