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Published online January 8, 2007
doi:10.1083/jcb.200609182
The Journal of Cell Biology, Vol. 176, No. 2, 209-222
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Heiman et al.
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Article

 The Golgi-resident protease Kex2 acts in conjunction with Prm1 to facilitate cell fusion during yeast mating

Maxwell G. Heiman, Alex Engel, and Peter Walter

1 Howard Hughes Medical Institute and 2 Department of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, CA 94158

Correspondence to Peter Walter: pwalter{at}biochem.ucsf.edu

The molecular machines that mediate cell fusion are unknown. Previously, we identified a multispanning transmembrane protein, Prm1 (pheromone-regulated membrane protein 1), that acts during yeast mating (Heiman, M.G., and P. Walter. 2000. J. Cell Biol. 151:719–730). Without Prm1, a substantial fraction of mating pairs arrest with their plasma membranes tightly apposed yet unfused. In this study, we show that lack of the Golgi-resident protease Kex2 strongly enhances the cell fusion defect of Prm1-deficient mating pairs and causes a mild fusion defect in otherwise wild-type mating pairs. Lack of the Kex1 protease but not the Ste13 protease results in similar defects. {Delta}kex2 and {Delta}kex1 fusion defects were suppressed by osmotic support, a trait shared with mutants defective in cell wall remodeling. In contrast, other cell wall mutants do not enhance the {Delta}prm1 fusion defect. Electron microscopy of {Delta}kex2-derived mating pairs revealed novel extracellular blebs at presumptive sites of fusion. Kex2 and Kex1 may promote cell fusion by proteolytically processing substrates that act in parallel to Prm1 as an alternative fusion machine, as cell wall components, or both.

M.G. Heiman's present address is The Rockefeller University, New York, NY 10021.

Abbreviations used in this paper: PRM, pheromone-regulated membrane protein; WT, wild type.


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