Physiological characterisation of acuB deletion in Aspergillus niger

Susan Lisette Meijer, Willem Adriaan De Jongh, Lisbeth Olsson, J. Nielsen

    Research output: Contribution to journalJournal articleResearchpeer-review

    Abstract

    The acuB gene of Aspergillus niger is an ortholog of facB in Aspergillus nidulans. Under carbon-repression conditions, facB is repressed, thereby preventing acetate metabolism when the repressing carbon source is present. Even though facB is reported to be repressed directly by CreA, it is believed that a basal level of FacB activity exists under glucose-repressive conditions. In the present study, the effect of deletion of acuB on the physiology of A. niger was assessed. Differences in organic acid and acetate production, enzyme activities and extracellular amino and non-amino organic acid production were determined under glucose-repressing and -derepressing conditions. Furthermore, consumption of alternative carbon sources (e.g. xylose, citrate, lactate and succinate) was investigated. It was shown that AcuB has pleiotropic effects on the physiology of A. niger. The results indicate that metabolic pathways that are not directly involved in acetate metabolism are influenced by acuB deletion. Clear differences in organic acid consumption and production were detected between the a dagger acuB and reference strain. However, the hypothesis that AcuB is responsible for basal AcuA activity necessary for activation of acetate metabolic pathways, even during growth on glucose, could not be confirmed. The experiments demonstrated that also when acuB was deleted, no acetate was formed. Therefore, AcuB cannot be the only activator of AcuA, and another control mechanism has to be available for activating AcuA.
    Original languageEnglish
    JournalApplied Microbiology and Biotechnology
    Volume84
    Issue number1
    Pages (from-to)157-167
    ISSN0175-7598
    DOIs
    Publication statusPublished - 2009

    Keywords

    • AcuB deletion
    • Organic acids
    • Acetate
    • Signal transduction pathways

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