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Phosphate Transport and Sensing in Saccharomyces cerevisiae
Dennis D. Wykoffa and Erin K. O'Sheaaa Howard Hughes Medical Institute, Department of Biochemistry and Biophysics, University of California, San Francisco, California 94143
Corresponding author: Erin K. O'Shea, Howard Hughes Medical Institute, Department of Biochemisty and Biophysics, University of California, 513 Parnassus Ave., San Francisco, CA 94143-0448., oshea{at}biochem.ucsf.edu (E-mail)
Communicating editor: M. JOHNSTON
strains have defects in phosphate signaling; they constitutively express PHO5, a phosphate starvation-inducible gene. We began these studies to determine the role of phosphate transporters in signaling phosphate starvation. Previous experiments demonstrated a defect in phosphate uptake in phosphate-starved pho84
cells; however, the pho84
strain expresses PHO5 constitutively when grown in phosphate-replete media. We determined that pho84
cells have a significant defect in phosphate uptake even when grown in high phosphate media. Overexpression of unrelated phosphate transporters or a glycerophosphoinositol transporter in the pho84
strain suppresses the PHO5 constitutive phenotype. These data suggest that PHO84 is not required for sensing phosphate. We further characterized putative phosphate transporters, identifying two new phosphate transporters, PHO90 and PHO91. A synthetic lethal phenotype was observed when five phosphate transporters were inactivated, and the contribution of each transporter to uptake in high phosphate conditions was determined. Finally, a PHO84-dependent compensation response was identified; the abundance of Pho84p at the plasma membrane increases in cells that are defective in other phosphate transporters.
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