The yeast CLC chloride channel functions in cation homeostasis
- *Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge, MA 02142-1479; †The Johns Hopkins University School of Medicine, Department of Pediatrics, Baltimore, MD 21205-2185; and ‡Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development and §Office of the Director, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
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Contributed by Gerald R. Fink
Abstract
A defect in the yeast GEF1 gene, a CLC chloride channel homolog leads to an iron requirement and cation sensitivity. The iron requirement is due to a failure to load Cu2+ onto a component of the iron uptake system, Fet3. This process, which requires both Gef1 and the Menkes disease Cu2+-ATPase yeast homolog Ccc2, occurs in late- or post-Golgi vesicles, where Gef1 and Ccc2 are localized. The defects of gef1 mutants can be suppressed by the introduction of Torpedo marmorata CLC-0 or Arabidopsis thaliana CLC-c and -d chloride channel genes. The functions of Gef1 in cation homeostasis provide clues to the understanding of diseases caused by chloride channel mutations in humans and cation toxicity in plants.
Footnotes
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↵ ¶ To whom reprint requests should be addressed.
- ABBREVIATION:
- HA,
- hemagglutinin
- Copyright © 1998, The National Academy of Sciences
