Originally published as Genetics Published Articles Ahead of Print on July 29, 2007.

Genetics, Vol. 177, 281-293, September 2007, Copyright © 2007
doi:10.1534/genetics.107.076133

Cdc15 Is Required for Spore Morphogenesis Independently of Cdc14 in Saccharomyces cerevisiae

M. Evangelina Pablo-Hernando^*, Yolanda Arnaiz-Pita^*, Hideki Nakanishi, Dean Dawson, Francisco del Rey^*, Aaron M. Neiman and Carlos R. Vázquez de Aldana^*,1

^* Instituto de Microbiología Bioquímica, Departamento de Microbiología y Genética, CSIC/Universidad de Salamanca, 37007 Salamanca, Spain, Department of Biochemistry and Cell Biology, State University of New York, Stony Brook, New York 11794-5215 and Program in Molecular, Cell and Developmental Biology, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104

¹ Corresponding author: Instituto de Microbiología Bioquímica, Departamento de Microbiología y Genética, CSIC/Universidad de Salamanca, 37007 Salamanca, Spain.
E-mail: cvazquez{at}usal.es.

In Saccharomyces cerevisiae exit from mitosis requires the Cdc14 phosphatase to reverse CDK-mediated phosphorylation. Cdc14 is released from the nucleolus by the Cdc14 early anaphase release (FEAR) and mitotic exit network (MEN) pathways. In meiosis, the FEAR pathway is essential for exit from anaphase I. The MEN component Cdc15 is required for the formation of mature spores. To analyze the role of Cdc15 during sporulation, a conditional mutant in which CDC15 expression was controlled by the CLB2 promoter was used. Cdc15-depleted cells proceeded normally through the meiotic divisions but were unable to properly disassemble meiosis II spindles. The morphology of the prospore membrane was aberrant and failed to capture the nuclear lobes. Cdc15 was not required for Cdc14 release from the nucleoli, but it was essential to maintain Cdc14 released and for its nucleo-cytoplasmic transport. However, cells carrying a CDC14 allele with defects in nuclear export (Cdc14-NES) were able to disassemble the spindle and to complete spore formation, suggesting that the Cdc14 nuclear export defect was not the cause of the phenotypes observed in cdc15 mutants.

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