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Yeasts in Biotechnology and Human Health pp 135–153Cite as

Emerging Mechanisms of Drug Resistance in Candida albicans

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Part of the book series: Progress in Molecular and Subcellular Biology ((PMSB,volume 58))

Abstract

Drug resistance mechanisms in the commensal human pathogen Candida albicans are continually evolving. Over time, Candida species have implemented diverse strategies to vanquish the effects of various classes of drugs, thereby emanating as a serious life threat. Apart from the repertoire of well-established strategies, which predominantly comprise permeability constraints, increased drug efflux or compromised drug import, alteration, overexpression of drug targets, and chromosome duplication, C. albicans has evolved novel regulatory mechanisms of drug resistance. For instance, recent evidences point to newer circuitry involving different mediators of the stress-responsive machinery of oxidative, osmotic, thermal, nitrosative, and nutrient limitation, which contribute to the emergence of drug resistance. Contemporary advances in genome-wide studies of transcription factors, for instance, the Zn2Cys6 transcription factors, TAC1 (transcriptional activator of CDR) in Candida albicans, or YRR1 in yeast have made it feasible to dissect their involvement for the elucidation of unexplored regulatory network of drug resistance. The coordination of implementers of the conventional and nonconventional drug resistance strategies provides robustness to this commensal human pathogen. In this review, we shed light not only on the established strategies of antifungal resistance but also discuss emerging cellular circuitry governing drug resistance of this human pathogen.

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Notes

  1. 1.

    Three stresses described in Fig. 6.2:

    1. (1)

      Oxidative Stress

      Oxidative stress regulator, Cap1, induces the overexpression of MDR1 by recruiting Ada2, a subunit of the SAGA/ADA coactivator complex on MDR1 promoter, thereby leading to an activation of drug resistance genes. Cap1 and Mrr1, both bind to the MDR1 promoter, and cooperate to promote MDR1 upregulation in response to inducing chemicals.

    2. (2)

      Metal Stress

      1. (i)

        Iron depletion leads to downregulation of ERG11 gene, along with a parallel upregulation of ERG3 gene. The downregulation of ERG11 increases the membrane fluidity leading to a rise in passive drug diffusion, and hence increased drug susceptibility. The increase in Erg3 levels leads to accumulation of toxic sterols on the cell membrane resulting in cell death.

      2. (ii)

        Magnesium depletion influences drug resistance majorly toward echinocandins. Its deficiency influences mutations in the histidine kinase gene, NIK1, thereby blocks the activation of Hog1 in response to the drug, enhancing caspofungin activity.

      3. (iii)

        Calcium depletion either by chelating extracellular calcium with ethylene diamine tetra-acetic acid (EDTA) or the inhibition of calcium importers with benidipine and nifedipine, leading to enhanced azole activity against C. albicans.

    3. (3)

      Heat Stress

      1. (i)

        By binding to and chaperoning calcineurin, the thermal stress regulator, Hsp90, regulates calcineurin-dependent stress responses, thereby enabling the cell to survive the membrane stress induced by azoles. Several downstream effectors of calcineurin mediate cellular responses to azoles, including the transcription factor Crz1.

      2. (ii)

        Heat shock factor 1, Hsf1, has been observed to be crucial for the survival of C. albicans in the presence of various classes of drugs. The susceptibility shown toward certain classes of drugs was seen to be iron dependent.

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Authors and Affiliations

  1. Amity Institute of Integrative Science and Health and Amity Institute of Biotechnology, Amity University Haryana, Amity Education Valley, Gurgaon, Haryana, India

    Rajendra Prasad

  2. Rajiv Gandhi Institute of IT & Biotechnology, Bharati Vidyapeeth University, Pune, India

    Remya Nair

  3. School of Computational and Integrative Sciences, Jawaharlal Nehru University, New Delhi, India

    Atanu Banerjee

  4. Amity Institute of Biotechnology, Amity University Haryana, Gurgaon, India

    Remya Nair & Atanu Banerjee

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  1. Rajendra Prasad
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Correspondence to Rajendra Prasad .

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  1. Institute for Bioengineering and Biosciences (iBB) and Department of Bioengineering, Instituto Superior Técnico, Universidade de Lisboa, Lisboa, Portugal

    Isabel Sá-Correia

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Prasad, R., Nair, R., Banerjee, A. (2019). Emerging Mechanisms of Drug Resistance in Candida albicans. In: Sá-Correia, I. (eds) Yeasts in Biotechnology and Human Health. Progress in Molecular and Subcellular Biology, vol 58. Springer, Cham. https://doi.org/10.1007/978-3-030-13035-0_6

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