AN EXTRA COPY OF NIMECYCLINB ELEVATES PRE-MPF LEVELS AND PARTIALLY SUPPRESSES MUTATION OF NIMTCDC25 IN ASPERGILLUS-NIDULANS

Previous work has shown that nimA encodes a cell cycle regulated protein kinase that is required along with the p34cdc2 histone H1 kinase (MPF) for mitosis in Aspergillus nidulans. We have now identified two other gene products required for mitosis in A. nidulans. nimT encodes a protein similar to the fission yeast cdc25 tyrosine phosphatase and is required for the conversion of pre-MPF to MPF and nimE encodes a B-type cyclin which is a subunit of MPF. A new genetic interaction between nimE(cyclinB) and nimT(cdc25) type genes is reported. Increased copy number of nimE(cyclinB) can suppress mutation of nimT(cdc25) and also lead to increased accumulation of tyrosine phosphorylated p34cdc2 (pre-MPF). This biochemical observation suggests an explanation for the genetic complementation. If nimE(cyclinB) recruits p34cdc2 for tyrosine phosphorylation to form pre-MPF it follows that increased expression of nimE(cyclinB) would increase the level of pre-MPF. The increased level of pre-MPF generated may then allow the mutant nimT(cdc25) protein to convert enough pre-MPF to MPF and thus permit some mitotic progression. We also demonstrate that correct cell cycle regulation by the p34cdc2 protein kinase pathway is essential for correct developmental progression in A. nidulans.