Control of Ammonium Permease Expression and Filamentous Growth by the GATA Transcription Factors <i>GLN3</i> and <i>GAT1</i> in <i>Candida albicans</i>

  • Neelam Dabas
    Institut für Molekulare Infektionsbiologie, Universität Würzburg, Röntgenring 11, D-97070 Würzburg, Germany
  • Joachim Morschhäuser
    Institut für Molekulare Infektionsbiologie, Universität Würzburg, Röntgenring 11, D-97070 Würzburg, Germany

抄録

<jats:title>ABSTRACT</jats:title> <jats:p> In response to nitrogen starvation, the human fungal pathogen <jats:italic>Candida albicans</jats:italic> switches from yeast to filamentous growth. This morphogenetic switch is controlled by the ammonium permease Mep2p, whose expression is induced under limiting nitrogen conditions. In order to understand in more detail how nitrogen starvation-induced filamentous growth is regulated in <jats:italic>C. albicans</jats:italic> , we identified the <jats:italic>cis</jats:italic> -acting sequences in the <jats:italic>MEP2</jats:italic> promoter that mediate its induction in response to nitrogen limitation. We found that two putative binding sites for GATA transcription factors have a central role in <jats:italic>MEP2</jats:italic> expression, as deletion of the region containing these sites or mutation of the GATAA sequences in the full-length <jats:italic>MEP2</jats:italic> promoter strongly reduced <jats:italic>MEP2</jats:italic> expression. To investigate whether the GATA transcription factors <jats:italic>GLN3</jats:italic> and <jats:italic>GAT1</jats:italic> regulate <jats:italic>MEP2</jats:italic> expression, we constructed mutants of the <jats:italic>C. albicans</jats:italic> wild-type strain SC5314 lacking one or both of these transcription factors. Expression of Mep2p was strongly reduced in <jats:italic>gln3</jats:italic> Δ and <jats:italic>gat1</jats:italic> Δ single mutants and abolished in <jats:italic>gln3</jats:italic> Δ <jats:italic>gat1</jats:italic> Δ double mutants. Deletion of <jats:italic>GLN3</jats:italic> strongly inhibited filamentous growth under limiting nitrogen conditions, but the filamentation defect of <jats:italic>gln3</jats:italic> Δ mutants could be rescued by constitutive expression of <jats:italic>MEP2</jats:italic> from the <jats:italic>ADH1</jats:italic> promoter. In contrast, inactivation of <jats:italic>GAT1</jats:italic> had no effect on filamentation, and we found that filamentation became independent of the presence of a functional <jats:italic>MEP2</jats:italic> gene in the <jats:italic>gat1</jats:italic> Δ mutants, indicating that the loss of <jats:italic>GAT1</jats:italic> function results in the activation of other pathways inducing filamentous growth. These results demonstrate that the GATA transcription factors <jats:italic>GLN3</jats:italic> and <jats:italic>GAT1</jats:italic> control expression of the <jats:italic>MEP2</jats:italic> ammonium permease and that <jats:italic>GLN3</jats:italic> is also an important regulator of nitrogen starvation-induced filamentous growth in <jats:italic>C. albicans</jats:italic> . </jats:p>

収録刊行物

  • Eukaryotic Cell

    Eukaryotic Cell 6 (5), 875-888, 2007-05

    American Society for Microbiology

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