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Vol. 13, Issue 4, 1158-1174, April 2002

Yeast Genes Controlling Responses to Topogenic Signals in a Model Transmembrane Protein

Donald J. Tipper, and Carol A Harley^*

Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester Massachusetts 01655

Yeast protein insertion orientation (PIO) mutants were isolated by selecting for growth on sucrose in cells in which the only source of invertase is a C-terminal fusion to a transmembrane protein. Only the fraction with an exocellular C terminus can be processed to secreted invertase and this fraction is constrained to 2-3% by a strong charge difference signal. Identified pio mutants increased this to 9-12%. PIO1 is SPF1, encoding a P-type ATPase located in the endoplasmic reticulum (ER) or Golgi. spf1-null mutants are modestly sensitive to EGTA. Sensitivity is considerably greater in an spf1 pmr1 double mutant, although PIO is not further disturbed. Pmr1p is the Golgi Ca²⁺ ATPase and Spf1p may be the equivalent ER pump. PIO2 is STE24, a metalloprotease anchored in the ER membrane. Like Spf1p, Ste24p is expressed in all yeast cell types and belongs to a highly conserved protein family. The effects of ste24- and spf1-null mutations on invertase secretion are additive, cell generation time is increased 60%, and cells become sensitive to cold and to heat shock. Ste24p and Rce1p cleave the C-AAX bond of farnesylated CAAX box proteins. The closest paralog of SPF1 is YOR291w. Neither rce1-null nor yor291w-null mutations affected PIO or the phenotype of spf1- or ste24-null mutants. Mutations in PIO3 (unidentified) cause a weaker Pio phenotype, enhanced by a null mutation in BMH1, one of two yeast 14-3-3 proteins.

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^* Corresponding author. E-mail address: donald.tipper{at}umassmed.edu.

Present address: Department of Developmental and Molecular biology, Albert Einstein College of Medicine, Bronx, NY 10461.

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Molecular Biology of the Cell
Vol. 13, 1158-1174, April 2002
Copyright © 2002 by The American Society for Cell Biology

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