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Unveiling fungal controls of dimorphic switching

Objectif

Fungal pathogens represent an ever-increasing public health problem, being responsible for nearly 40% of deaths from hospital-acquired infections. These fungal infections are particularly devastating for AIDS patients and other immuno compromised individuals where treatment is rarely curative. Fungal infections are not restricted to animals. Around 10% of the known fungal species are phytopathogens, representing an economic threat causing millions of euros worth of loss to crops. Many pathogenic fungi are dimorphic, that is they can alternate between a unicellular, yeast growth form and a multi-cellular filamentous growth form.

Little is known about the molecular mechanisms, which control dimorphic switching, and maintain each growth form. Until recently, the absence of defined genetic tools in dimorphic fungi has meant that investigation of the mechanisms controlling dimorphism has been restricted to model fungi which undertake the multi-cellular touni-cellular switch as part of a broader developmental programme.

Pénicillium marneffei displays temperature-dependent dimorphism, being predominantly hyphalin form; as opposed to Candida albicans, which is predominantly yeast. The pathogenic form of P.marneffei is strictly yeast-like. DNA micro-arrays and promoter tagging screen s will allow theidentification of genes responsible for the dimorphic switch and the maintenance of the hyphal and yeast growth forms. Selected genes identified in this project will be 'knocked out' to determine their role in development and pathogenicity.

Ustilago mayáis is a phytopathogenic fungus very valuable as a system to study fungaldimorphism and virulence. Contrary to P. marneffei, the pathogenic form of U. mayáis is the filamentous growth. Recently, the crkl gene has been identified to control morphogenesis.

Appel à propositions

FP6-2002-MOBILITY-6
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Coordinateur

CONSEJO SUPERIOR DE INVESTIGACIONES CIENTIFICAS
Contribution de l’UE
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Adresse
Calle Serrano 117
MADRID
Espagne

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