Functional study of the Na+, K+/H+antiporter Cnh1p in the pathogenic yeast Candida albicans
Project goals
Intracellular pH and K+ content belong among factors controlling morphology of a diploid fungus Candida albicans. The C. albicans CNH1 gene encodes a Na+/H+-antiporter with substrate specificity for four alkalimetal cations (Na+, Li+, K+, Rb+). Heterologous expression of CNH1 in Saccharomyces cerevisiae revealed that Cnh1p could be involved in the regulation of internal H+ and K+ concentrations . The main task of this project is to elucidate whether the activity of Cnh1p could be one of the factors involved in switch from the yeast budding form to the pathogenic mycelium. Within the project C. albicans strains lacking one or both CNH1 alleles will be constructed and the cell morphology and internal K+ content will be compared tostrains overexpressing the Cnh1p localization and transport activity at different conditions will be determined. Obtained results should bring new knowledge about the regulation of K+ and pH homeostasis in C. albicans in relation to its pathogenity.
Keywords
Candida albicansNa+,K+/H+-antiporterK+ homeostasiscell volumeintracellular pHpathogenesis
Public support
Provider
Academy of Sciences of the Czech Republic
Programme
The research grant projects for juniors
Call for proposals
Juniorské badatelské grantové projekty 1 (SAV02003-XJ)
Main participants
Fyziologický ústav AV ČR, v. v. i.
Contest type
VS - Public tender
Contract ID
—
Alternative language
Project name in Czech
Studium funkce Na+, K+/H+-antiportního systému Cnh1p v patogenní kvasince Candida albicans
Annotation in Czech
Mezi faktory kontrolující morfologii diploidní kvasinky Candida albicans patří vnitrobuněčné pH a obsah K+. Gen CNH1 z C. albicans kóduje Na+/H+-antiportní systém se substrátovou specifitou nejméně pro čtyři alkalické kationty (Na+, Li+, K+, Rb+). Heterogenní exprese CNH1 v Saccharomyces cerevisiae ukázala, že v jC. albicans by se Cnh1p mohl podílet na regulaci vnitrobuněčné koncentrace H+ a K+. Hlavním cílem předkládaného projektu je zjistit, zda aktivita Cnh1p může ovlivňovat morfologii buněk C. albicans (změnu z jednobuněčné na patogenní vláknitou formu). V rámci projektu budou zkonstruovány kmeny C. albicans s deletovanou jednou nebo oběma alelami genu CNH1. Morfologie buněk a vnitrobuněčný obsah K+ budou porovnány s kmenem se zvýšenou expresí Cnh1p. Zároveň bude stanovena lokalizace a transportní aktivita přenašeče CNH1p za různých podmínek. Získané výsledky by mohly přinést nové poznatky o regulaci moheostáze K+ a pH buňkách C. albicans ve vztahu k patogenitě této kvasinky.
Scientific branches
R&D category
ZV - Basic research
CEP classification - main branch
EB - Genetics and molecular biology
CEP - secondary branch
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CEP - another secondary branch
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10603 - Genetics and heredity (medical genetics to be 3)
10604 - Reproductive biology (medical aspects to be 3)
10605 - Developmental biology
10608 - Biochemistry and molecular biology
10609 - Biochemical research methods
30101 - Human genetics
Completed project evaluation
Provider evaluation
N - Nesplněno zadání
Project results evaluation
It was proved that Cnh1 antiporter is localized in the plasma membrane in C.albicans cells, is not important for the tolerance to Na, Li and Cs cations, plays the role in the maintenance of K and Rb homeostasis. The results haven't been published yet.
Solution timeline
Realization period - beginning
Jan 1, 2003
Realization period - end
Jan 1, 2004
Project status
U - Finished project
Latest support payment
—
Data delivery to CEP
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data delivery code
CEP/2005/AV0/AV05KJ/U/N/4:2
Data delivery date
Sep 26, 2007
Finance
Total approved costs
597 thou. CZK
Public financial support
329 thou. CZK
Other public sources
268 thou. CZK
Non public and foreign sources
0 thou. CZK
Recognised costs
597 CZK thou.
Public support
329 CZK thou.
0%
Provider
Academy of Sciences of the Czech Republic
CEP
EB - Genetics and molecular biology
Solution period
01. 01. 2003 - 01. 01. 2004