Originally published as Genetics Published Articles Ahead of Print on June 1, 2009.

Genetics, Vol. 182, 955-966, August 2009, Copyright © 2009
doi:10.1534/genetics.109.104414

The Ccr4-Pop2-NOT mRNA Deadenylase Contributes to Septin Organization in Saccharomyces cerevisiae

Ana Traven^*,1,2, Traude H. Beilharz, Tricia L. Lo^*,1, Franziska Lueder, Thomas Preiss and Jörg Heierhorst^*,

^* St. Vincent's Institute of Medical Research, Fitzroy, Victoria 3065, Australia, Molecular Genetics Division, Victor Chang Cardiac Research Institute, Darlinghurst (Sydney), NSW 2010, Australia; School of Biotechnology and Biomolecular Sciences and St. Vincent's Clinical School, University of New South Wales, Sydney, NSW 2052, Australia Department of Biochemistry and Molecular Biology and Department of Medicine, St. Vincent's Hospital, University of Melbourne, Parkville, Victoria 3010, Australia

² Corresponding author: Department of Biochemistry and Molecular Biology, Building 76 (STRIP2) Monash University, Clayton Campus, Wellington Rd., Victoria 3800, Australia.
E-mail: ana.traven{at}med.monash.edu.au

In yeast, assembly of the septins at the cell cortex is required for a series of key cell cycle events: bud-site selection, the morphogenesis and mitotic exit checkpoints, and cytokinesis. Here we establish that the Ccr4-Pop2-NOT mRNA deadenylase contributes to septin organization. mRNAs encoding regulators of septin assembly (Ccd42, Cdc24, Rga1, Rga2, Bem3, Gin4, Cla4, and Elm1) presented with short poly(A) tails at steady state in wild-type (wt) cells, suggesting their translation could be restricted by deadenylation. Deadenylation of septin regulators was dependent on the major cellular mRNA deadenylase Ccr4-Pop2-NOT, whereas the alternative deadenylase Pan2 played a minor role. Consistent with deadenylation of septin regulators being important for function, deletion of deadenylase subunits CCR4 or POP2, but not PAN2, resulted in septin morphology defects (e.g., ectopic bud-localized septin rings), particularly upon activation of the Cdc28-inhibitory kinase Swe1. Aberrant septin staining was also observed in the deadenylase-dead ccr4-1 mutant, demonstrating the deadenylase activity of Ccr4-Pop2 is required. Moreover, ccr4, pop2, and ccr4-1 mutants showed aberrant cell morphology previously observed in septin assembly mutants and exhibited genetic interactions with mutations that compromise septin assembly (shs1, cla4, elm1, and gin4). Mutations in the Not subunits of Ccr4-Pop2-NOT, which are thought to predominantly function in transcriptional control, also resulted in septin organization defects. Therefore, both mRNA deadenylase and transcriptional functions of Ccr4-Pop2-NOT contribute to septin organization in yeast.

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