Extragenic Suppressors of the nimX2^cdc2 Mutation of Aspergillus nidulans Affect Nuclear Division, Septation and Conidiation

Corresponding author: Sarah Lea McGuire, Millsaps College, P.O. Box 150305, 1701 N. State St., Jackson, MS 39210., mcguisl{at}millsaps.edu (E-mail)

Communicating editor: M. D. ROSE

The Aspergillus nidulans NIMX^CDC2 protein kinase has been shown to be required for both the G₂/M and G₁/S transitions, and recent evidence has implicated a role for NIMX^CDC2 in septation and conidiation. While much is understood of its G₂/M function, little is known about the functions of NIMX^CDC2 during G₁/S, septation, and conidiophore development. In an attempt to better understand how NIMX^CDC2 is involved in these processes, we have isolated four extragenic suppressors of the A. nidulans nimX2^cdc2 temperature-sensitive mutation. Mutation of these suppressor genes, designated snxA-snxD for suppressor of nimX, affects nuclear division, septation, and conidiation. The cold-sensitive snxA1 mutation leads to arrest of nuclear division during G₁ or early S. snxB1 causes hyperseptation in the hyphae and sensitivity to hydroxyurea, while snxC1 causes septation in the conidiophore stalk and aberrant conidiophore structure. snxD1 leads to slight septation defects and hydroxyurea sensitivity. The additional phenotypes that result from the suppressor mutations provide genetic evidence that NIMX^CDC2 affects septation and conidiation in addition to nuclear division, and cloning and biochemical analysis of these will allow a better understanding of the role of NIMX^CDC2 in these processes.