Regulation of Copper Toxicity by Candida albicans GPA2
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| Published in | Eukaryotic Cell Vol. 12; no. 7; pp. 954 - 961 |
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| Language | English |
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American Society for Microbiology
01.07.2013
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| AbstractList | ABSTRACT
Copper is an essential nutrient that is toxic to cells when present in excess. The fungal pathogen
Candida albicans
employs several mechanisms to survive in the presence of excess copper, but the molecular pathways that govern these responses are not completely understood. We report that deletion of
GPA2
, which specifies a G-protein α subunit, confers increased resistance to excess copper and propose that the increased resistance is due to a combination of decreased copper uptake and an increase in copper chelation by metallothioneins. This is supported by our observations that a
gpa2
Δ/Δ mutant has reduced expression of the copper uptake genes,
CTR1
and
FRE7
, and a marked decrease in copper accumulation following exposure to high copper levels. Furthermore, deletion of
GPA2
results in an increased expression of the copper metallothionein gene,
CRD2
. Gpa2p functions upstream in the cyclic AMP (cAMP)-protein kinase A (PKA) pathway to govern hyphal morphogenesis. The copper resistance phenotype of the
gpa2
Δ/Δ mutant can be reversed by artificially increasing the intracellular concentration of cAMP. These results provide evidence for a novel role of the PKA pathway in regulation of copper homeostasis. Furthermore, the connection between the PKA pathway and copper homeostasis appears to be conserved in the pathogen
Cryptococcus neoformans
but not in the nonpathogenic
Saccharomyces cerevisiae
. Copper is an essential nutrient that is toxic to cells when present in excess. The fungal pathogen Candida albicans employs several mechanisms to survive in the presence of excess copper, but the molecular pathways that govern these responses are not completely understood. We report that deletion of GPA2, which specifies a G-protein α subunit, confers increased resistance to excess copper and propose that the increased resistance is due to a combination of decreased copper uptake and an increase in copper chelation by metallothioneins. This is supported by our observations that a gpa2Δ/Δ mutant has reduced expression of the copper uptake genes, CTR1 and FRE7, and a marked decrease in copper accumulation following exposure to high copper levels. Furthermore, deletion of GPA2 results in an increased expression of the copper metallothionein gene, CRD2. Gpa2p functions upstream in the cyclic AMP (cAMP)-protein kinase A (PKA) pathway to govern hyphal morphogenesis. The copper resistance phenotype of the gpa2Δ/Δ mutant can be reversed by artificially increasing the intracellular concentration of cAMP. These results provide evidence for a novel role of the PKA pathway in regulation of copper homeostasis. Furthermore, the connection between the PKA pathway and copper homeostasis appears to be conserved in the pathogen Cryptococcus neoformans but not in the nonpathogenic Saccharomyces cerevisiae. Copper is an essential nutrient that is toxic to cells when present in excess. The fungal pathogen Candida albicans employs several mechanisms to survive in the presence of excess copper, but the molecular pathways that govern these responses are not completely understood. We report that deletion of GPA2, which specifies a G-protein alpha subunit, confers increased resistance to excess copper and propose that the increased resistance is due to a combination of decreased copper uptake and an increase in copper chelation by metallothioneins. This is supported by our observations that a gpa2 Delta / Delta mutant has reduced expression of the copper uptake genes, CTR1 and FRE7, and a marked decrease in copper accumulation following exposure to high copper levels. Furthermore, deletion of GPA2 results in an increased expression of the copper metallothionein gene, CRD2. Gpa2p functions upstream in the cyclic AMP (cAMP)-protein kinase A (PKA) pathway to govern hyphal morphogenesis. The copper resistance phenotype of the gpa2 Delta / Delta mutant can be reversed by artificially increasing the intracellular concentration of cAMP. These results provide evidence for a novel role of the PKA pathway in regulation of copper homeostasis. Furthermore, the connection between the PKA pathway and copper homeostasis appears to be conserved in the pathogen Cryptococcus neoformans but not in the nonpathogenic Saccharomyces cerevisiae. Copper is an essential nutrient that is toxic to cells when present in excess. The fungal pathogen Candida albicans employs several mechanisms to survive in the presence of excess copper, but the molecular pathways that govern these responses are not completely understood. We report that deletion of GPA2 , which specifies a G-protein α subunit, confers increased resistance to excess copper and propose that the increased resistance is due to a combination of decreased copper uptake and an increase in copper chelation by metallothioneins. This is supported by our observations that a gpa2 Δ/Δ mutant has reduced expression of the copper uptake genes, CTR1 and FRE7 , and a marked decrease in copper accumulation following exposure to high copper levels. Furthermore, deletion of GPA2 results in an increased expression of the copper metallothionein gene, CRD2 . Gpa2p functions upstream in the cyclic AMP (cAMP)-protein kinase A (PKA) pathway to govern hyphal morphogenesis. The copper resistance phenotype of the gpa2 Δ/Δ mutant can be reversed by artificially increasing the intracellular concentration of cAMP. These results provide evidence for a novel role of the PKA pathway in regulation of copper homeostasis. Furthermore, the connection between the PKA pathway and copper homeostasis appears to be conserved in the pathogen Cryptococcus neoformans but not in the nonpathogenic Saccharomyces cerevisiae . Classifications Services EC Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue EC About EC Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy EC RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 1535-9778 Online ISSN: 1535-9786 Copyright © 2014 by the American Society for Microbiology. For an alternate route to EC .asm.org, visit: EC |
| Author | Sarah L. J. Michel Jennifer A. Schwartz Jamie L. Michalek Gurjinder S. Jandu Karen T. Olarte Vincent M. Bruno |
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Reddit... Copper is an essential nutrient that is toxic to cells when present in excess. The fungal pathogen Candida albicans employs several mechanisms to survive in... ABSTRACT Copper is an essential nutrient that is toxic to cells when present in excess. The fungal pathogen Candida albicans employs several mechanisms to... Copper is an essential nutrient that is toxic to cells when present in excess. The fungal pathogen Candida albicans employs several mechanisms to survive in... |
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| SubjectTerms | Cadmium - toxicity Candida albicans Candida albicans - cytology Candida albicans - drug effects Candida albicans - genetics Candida albicans - metabolism Cisplatin - pharmacology Copper - toxicity Cryptococcus neoformans Cyclic AMP - pharmacology Cyclic AMP-Dependent Protein Kinases - metabolism Fungal Proteins - genetics Fungal Proteins - metabolism Gene Deletion Gene Expression Regulation, Fungal - drug effects Genes, Fungal - genetics GTP-Binding Protein alpha Subunits - genetics GTP-Binding Protein alpha Subunits - metabolism Homeostasis - drug effects Homeostasis - genetics Iron - toxicity Saccharomyces cerevisiae Signal Transduction - drug effects Signal Transduction - genetics Silver - toxicity |
| Title | Regulation of Copper Toxicity by Candida albicans GPA2 |
| URI | http://ec.asm.org/content/12/7/954.abstract https://www.ncbi.nlm.nih.gov/pubmed/23584994 https://search.proquest.com/docview/1399923252 https://pubmed.ncbi.nlm.nih.gov/PMC3697471 |
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