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A role for HEM2 in cadmium tolerance

T C Hunter¹, R K Mehra

¹Environmental Toxicology Graduate Program, University of California, Riverside 92521, USA.

Journal of Inorganic Biochemistry

|July 9, 1998

Summary

Researchers identified a gene in Candida glabrata crucial for cadmium tolerance. This gene restores cadmium detoxification by enabling the production of glutathione and phytochelatins, essential for heavy metal resistance.

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Area of Science:

Microbiology
Molecular Biology
Biochemistry

Background:

Cadmium (Cd) is a toxic heavy metal.
Candida glabrata possesses mechanisms for Cd tolerance, involving glutathione and phytochelatins.
Understanding the genetic basis of Cd tolerance is vital for managing heavy metal exposure.

Purpose of the Study:

To clone and characterize a gene responsible for cadmium tolerance in Candida glabrata.
To investigate the role of this gene in the biosynthesis of protective compounds against cadmium toxicity.

Main Methods:

Construction and screening of a C. glabrata genomic library.
Transformation of a Cd-sensitive mutant with the genomic library.
Complementation analysis of a Saccharomyces cerevisiae hem2 mutant.
Biochemical assays for enzyme activity and metabolite levels.

Main Results:

A gene restoring Cd tolerance was cloned from C. glabrata.
The cloned gene encodes a protein homologous to porphobilinogen synthase (HEM2).
The Cd-sensitive mutant showed reduced porphobilinogen synthase and sulfite reductase activity.
Cysteine supplementation enhanced Cd tolerance, while hemin chloride and methionine restored it, suggesting a link to heme biosynthesis and transsulfuration.

Conclusions:

The cloned gene is essential for Cd tolerance in C. glabrata, likely by maintaining the heme biosynthesis pathway.
Dysfunction in this pathway affects glutathione and phytochelatin production, crucial for detoxifying cadmium.
Heme availability and the transsulfuration pathway are critical for cadmium detoxification in C. glabrata.

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