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.