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Mutational and hyperexpression-induced disruption of bipolar budding in yeast

Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, MA 02138, USA¹
Section of Molecular Cell and Developmental Biology, The University of Texas, Austin, TX 78712, USA²
Department of Biochemistry and Molecular Biology, SUNY Upstate Medical University, 750 E. Adams St, Syracuse, NY 13210, USA³

Author for correspondence: Brian Haarer. Tel: +1 315 464 8757. Fax: +1 315 464 8750. e-mail: haarerb{at}mail.upstate.edu

Analysis of bud-site selection in the yeast Saccharomyces cerevisiae has helped to identify many genes that are generally important for eukaryotic cell polarization. Colony morphology screens were used to identify factors relevant to the process of bipolar budding in yeast. Mutants defective in bipolar budding were identified by virtue of their inability to grow as pseudohyphae in a haploid bud3 background. A mutant allele of the MYO2 gene, encoding a class-V unconventional myosin was identified that perturbs bipolar budding without affecting axial budding and without grossly affecting the role of Myo2p in secretion and maintenance of the actin cytoskeleton. Several genes were also identified whose products, when overexpressed, are capable of disrupting bipolar budding. Among these are the actin-monomer-binding protein profilin and the Aip3p/Bud6p-interacting protein Atc1p. The results strongly support involvement of the actin cytoskeleton in the establishment of bipolar budding and in the maintenance of pseudohyphal growth.

Keywords: Polarity, actin, profilin, MYO2, myosin

Abbreviations: PIP₂; phosphatidylinositol 4,5-bisphosphate

^a Present Address: SLIL Biomedical Corp., Menlo Park, CA 94025, USA.

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