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hCTR1: a human gene for copper uptake identified by complementation in yeast

B Zhou1, J Gitschier

  • 1Howard Hughes Medical Institute, University of California, San Francisco, CA 94143, USA.

Proceedings of the National Academy of Sciences of the United States of America
|July 8, 1997
PubMed
Summary

Researchers identified a human gene, hCTR1, crucial for cellular copper uptake. This discovery sheds light on copper transport mechanisms in mammals and offers insights into copper homeostasis.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • The molecular mechanisms governing cellular copper uptake in mammalian cells remain largely unknown.
  • Copper is an essential trace element vital for various cellular processes, but its overload can be toxic.

Purpose of the Study:

  • To identify and characterize the human gene responsible for high-affinity copper uptake.
  • To investigate the functional role of the identified human gene in copper transport and homeostasis.

Main Methods:

  • Complementation of a high-affinity copper uptake mutant (ctr1) in yeast using a human gene.
  • Assessing the rescued growth defects, iron transport, and SOD1 function in yeast.
  • Measuring cellular copper levels in yeast overexpressing the human gene using atomic absorption spectroscopy.

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  • Identifying a second similar human gene (hCTR2) through database searches.

    • Main Results:

    • A human gene, named hCTR1, was isolated for its ability to complement the ctr1 yeast mutant's growth defect.
    • hCTR1 expression in yeast rescued not only copper uptake but also iron transport and SOD1 defects.
    • Overexpression of hCTR1 in yeast led to increased sensitivity to copper toxicity and elevated cellular copper levels.
    • A second homologous gene, hCTR2, was identified, and both genes are expressed in all human tissues and map to chromosome 9q31/32.

    Conclusions:

    • The identified human gene, hCTR1, is a strong candidate for mediating high-affinity copper uptake in humans.
    • Mammalian and yeast cells utilize conserved copper homeostatic mechanisms, evidenced by functional similarities between hCTR1 and yeast CTR1.
    • The discovery of hCTR1 and hCTR2 provides new targets for understanding copper metabolism and related disorders.