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RTA2 is involved in calcineurin-mediated azole resistance and sphingoid long-chain base release in Candida albicans

X M Jia1, Y Wang, Y Jia

  • 1Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai 200433, China.

Cellular and Molecular Life Sciences : CMLS
|November 13, 2008
PubMed

Insights

The calcineurin pathway regulates azole resistance in Candida albicans via RTA2. RTA2 controls sphingolipid release, impacting cell membrane integrity against azoles.

Area of Science:

  • Mycology
  • Molecular Biology
  • Biochemistry

Background:

  • The calcineurin pathway is crucial for azole resistance in *Candida albicans*.
  • RTA2's role in this pathway and its impact on fungal resistance are not fully understood.

Purpose of the Study:

  • To investigate the role of RTA2 in calcineurin-mediated azole resistance in *Candida albicans*.
  • To elucidate the relationship between RTA2, sphingolipid metabolism, and azole susceptibility.

Main Methods:

  • Genetic manipulation of RTA2 (depletion and overexpression) in *C. albicans*.
  • Assessment of azole susceptibility under various conditions, including CaCl(2) treatment and calcineurin inhibition.
  • Analysis of RTA2 gene expression and sphingolipid (dihydrosphingosine) levels.

Main Results:

  • RTA2 is upregulated by calcineurin and modulates azole resistance.
  • RTA2 depletion increases susceptibility to azoles and damages the cell membrane.
  • RTA2 overexpression decreases azole-induced cell membrane damage.
  • Disruption of RTA2 leads to increased dihydrosphingosine accumulation due to reduced release.

Conclusions:

  • RTA2 is a key mediator of calcineurin-dependent azole resistance in *C. albicans*.
  • RTA2 influences fungal cell membrane integrity and sphingoid long-chain base release.

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