The acuM gene from Aspergillus nidulans was previously shown to be essential for growth on non- fermentable carbon sources by regulating the expression of gluconeogenic genes. Here we describe the construction of an A. fumigatus mutant containing a partial deletion of the acuM gene. The mutants were phenotypically characterised for their growth behaviour on different glycolytic and gluconeogenic carbon sources. As expected, the mutant was unable to grow on olive oil, acetate, ethanol and glutamate. Intermediate growth was observed on glycerol. Interestingly, the mutant was also unable to grow on albumin, whereas only a slight growth defect was observed on casamino acids and no phenotype was visible during growth on peptone. Even more, the ability to grow on albumin was restored by the addition of low amounts of glucose (2 5 mM) to the growth medium. The mutant was subsequently tested in a murine infection model using cortisone acetate treated mice. Survival curves revealed no significant differences between wild type and mutant and also the lesions within the lung tissues were highly similar. These results imply that non-hydrolysed proteins (such as albumin) cannot provide the sole carbon source during A. fumigatus pathogenesis in corticosteroid treated mice. It rather points to the (co-)metabolism of glucose or peptide fragments, which may represent major growth substituting nutrients during the infection process.
Full conference title:
6th International Aspergillus Meeting
- Asperfest 6 (2009)