A Role for NIMA in the Nuclear Localization of Cyclin B in <em>Aspergillus nidulans</em>

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