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4. Metabolic reprogramming during Candida albicans planktonic-biofilm transition is modulated by the transcription factors Zcf15 and Zcf26.

Author

Rai, Laxmi Shanker, Chauvel, Murielle, Sanchez, Hiram, van Wijlick, Lasse, Maufrais, Corinne, Cokelaer, Thomas, Sertour, Natacha, Legrand, Mélanie, Sanyal, Kaustuv, Andes, David R., Bachellier-Bassi, Sophie, and d'Enfert, Christophe

Subjects
*CANDIDA albicans, *METABOLIC reprogramming, *TRANSCRIPTION factors, *KREBS cycle, *ARTIFICIAL implants, *HUMAN microbiota
Abstract

Candida albicans is a commensal of the human microbiota that can form biofilms on implanted medical devices. These biofilms are tolerant to antifungals and to the host immune system. To identify novel genes modulating C. albicans biofilm formation, we performed a large-scale screen with 2,454 C. albicans doxycycline-dependent overexpression strains and identified 16 genes whose overexpression significantly hampered biofilm formation. Among those, overexpression of the ZCF15 and ZCF26 paralogs that encode transcription factors and have orthologs only in biofilm-forming species of the Candida clade, caused impaired biofilm formation both in vitro and in vivo. Interestingly, overexpression of ZCF15 impeded biofilm formation without any defect in hyphal growth. Transcript profiling, transcription factor binding, and phenotypic microarray analyses conducted upon overexpression of ZCF15 and ZCF26 demonstrated their role in reprogramming cellular metabolism by regulating central metabolism including glyoxylate and tricarboxylic acid cycle genes. Taken together, this study has identified a new set of biofilm regulators, including ZCF15 and ZCF26, that appear to control biofilm development through their specific role in metabolic remodeling. Fungal biofilms are complex communities that can form on surfaces of implanted medical devices. This study uses an overexpression screen to identify novel modulators of Candida albicans biofilm formation, revealing that the transcription factors ZCF15 and ZCF26 regulate metabolic reprogramming during the transition from planktonic to biofilm growth. [ABSTRACT FROM AUTHOR]

Published
2024
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5. Metabolic reprogramming duringCandida albicansplanktonic-biofilm transition is modulated by theZCF15andZCF26paralogs

Author

Rai, Laxmi Shanker, primary, Chauvel, Murielle, additional, Sanchez, Hiram, additional, van Wijlick, Lasse, additional, Maufrais, Corinne, additional, Cokelaer, Thomas, additional, Sertour, Natacha, additional, Legrand, Mélanie, additional, Andes, David R, additional, Bachellier-Bassi, Sophie, additional, and d’Enfert, Christophe, additional

Published
2023
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10. Ethylzingerone, a Novel Compound with Antifungal Activity

Author

Rossignol, Tristan, primary, Znaidi, Sadri, additional, Chauvel, Murielle, additional, Wesgate, Rebecca, additional, Decourty, Laurence, additional, Menard-Szczebara, Florence, additional, Cupferman, Sylvie, additional, Dalko-Sciba, Maria, additional, Barnes, Rosemary, additional, Maillard, Jean-Yves, additional, Saveanu, Cosmin, additional, and d’Enfert, Christophe, additional

Published
2021
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11. Identification and Characterization of Mediators of Fluconazole Tolerance in Candida albicans

Author

Delarze, Eric, primary, Brandt, Ludivine, additional, Trachsel, Emilie, additional, Patxot, Marion, additional, Pralong, Claire, additional, Maranzano, Fabio, additional, Chauvel, Murielle, additional, Legrand, Mélanie, additional, Znaidi, Sadri, additional, Bougnoux, Marie-Elisabeth, additional, d’Enfert, Christophe, additional, and Sanglard, Dominique, additional

Published
2020
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12. Modular Gene Over-expression Strategies for Candida albicans

Author

Cabral, Vitor, primary, Chauvel, Murielle, additional, Firon, Arnaud, additional, Legrand, Mélanie, additional, Nesseir, Audrey, additional, Bachellier-Bassi, Sophie, additional, Chaudhari, Yogesh, additional, Munro, Carol A., additional, and d’Enfert, Christophe, additional

Published
2012
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13. Overexpression approaches to advance understanding of Candida albicans.

Author

Rai, Laxmi Shanker, van Wijlick, Lasse, Chauvel, Murielle, d'Enfert, Christophe, Legrand, Mélanie, and Bachellier‐Bassi, Sophie

Subjects
CANDIDA albicans, GENETIC overexpression, DRUG tolerance, GENE expression, GENE knockout, PHENOTYPES, CANDIDIASIS, BIOFILMS
Abstract

Candida albicans is an opportunistic fungal pathogen that is responsible for infections linked to high mortality. Loss‐of‐function approaches, taking advantage of gene knockouts or inducible down‐regulation, have been successfully used in this species in order to understand gene function. However, overexpression of a gene provides an alternative, powerful tool to elucidate gene function and identify novel phenotypes. Notably, overexpression can identify pathway components that might remain undetected using loss‐of‐function approaches. Several repressible or inducible promoters have been developed which allow to shut off or turn on the expression of a gene in C. albicans upon growth in the presence of a repressor or inducer. In this review, we summarize recent overexpression approaches used to study different aspects of C. albicans biology, including morphogenesis, biofilm formation, drug tolerance, and commensalism. [ABSTRACT FROM AUTHOR]

Published
2022
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15. Large-scale genome mining allows identification of neutral polymorphisms and novel resistance mutations in genes involved in Candida albicans resistance to azoles and echinocandins

Author

Sitterlé, Emilie, primary, Coste, Alix T, primary, Obadia, Thomas, primary, Maufrais, Corinne, primary, Chauvel, Murielle, primary, Sertour, Natacha, primary, Sanglard, Dominique, primary, Puel, Anne, primary, D’Enfert, Christophe, primary, and Bougnoux, Marie-Elisabeth, primary

Published
2020
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16. Generating genomic platforms to study Candida albicans pathogenesis

Author

Legrand, Mélanie, primary, Bachellier-Bassi, Sophie, additional, Lee, Keunsook K, additional, Chaudhari, Yogesh, additional, Tournu, Hélène, additional, Arbogast, Laurence, additional, Boyer, Hélène, additional, Chauvel, Murielle, additional, Cabral, Vitor, additional, Maufrais, Corinne, additional, Nesseir, Audrey, additional, Maslanka, Irena, additional, Permal, Emmanuelle, additional, Rossignol, Tristan, additional, Walker, Louise A, additional, Zeidler, Ute, additional, Znaidi, Sadri, additional, Schoeters, Floris, additional, Majgier, Charlotte, additional, Julien, Renaud A, additional, Ma, Laurence, additional, Tichit, Magali, additional, Bouchier, Christiane, additional, Van Dijck, Patrick, additional, Munro, Carol A, additional, and d’Enfert, Christophe, additional

Published
2018
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17. Generating genomic platforms to studyCandida albicanspathogenesis

Author

Legrand, Mélanie, primary, Bachellier-Bassi, Sophie, additional, Lee, Keunsook K., additional, Chaudhari, Yogesh, additional, Tournu, Hélène, additional, Arbogast, Laurence, additional, Boyer, Hélène, additional, Chauvel, Murielle, additional, Cabral, Vitor, additional, Maufrais, Corinne, additional, Nesseir, Audrey, additional, Maslanka, Irena, additional, Permal, Emmanuelle, additional, Rossignol, Tristan, additional, Walker, Louise A., additional, Zeidler, Ute, additional, Znaidi, Sadri, additional, Schoeters, Floris, additional, Majgier, Charlotte, additional, Julien, Renaud A., additional, Ma, Laurence, additional, Tichit, Magali, additional, Bouchier, Christiane, additional, Dijck, Patrick Van, additional, Munro, Carol A., additional, and d’Enfert, Christophe, additional

Published
2018
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18. Azole resistance in a Candida albicans mutant lacking the ABC transporter CDR6/ROA1 depends on TOR signaling

Author

Khandelwal, Nitesh Kumar, primary, Chauhan, Neeraj, additional, Sarkar, Parijat, additional, Esquivel, Brooke D., additional, Coccetti, Paola, additional, Singh, Ashutosh, additional, Coste, Alix T., additional, Gupta, Meghna, additional, Sanglard, Dominique, additional, White, Theodore C., additional, Chauvel, Murielle, additional, d’Enfert, Christophe, additional, Chattopadhyay, Amitabha, additional, Gaur, Naseem A., additional, Mondal, Alok Kumar, additional, and Prasad, Rajendra, additional

Published
2018
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19. Selective BET bromodomain inhibition as an antifungal therapeutic strategy

Author

Mietton, Flore, primary, Ferri, Elena, additional, Champleboux, Morgane, additional, Zala, Ninon, additional, Maubon, Danièle, additional, Zhou, Yingsheng, additional, Harbut, Mike, additional, Spittler, Didier, additional, Garnaud, Cécile, additional, Courçon, Marie, additional, Chauvel, Murielle, additional, d’Enfert, Christophe, additional, Kashemirov, Boris A., additional, Hull, Mitchell, additional, Cornet, Muriel, additional, McKenna, Charles E., additional, Govin, Jérôme, additional, and Petosa, Carlo, additional

Published
2017
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20. Targeted Changes of the Cell Wall Proteome Influence Candida albicans Ability to Form Single- and Multi-strain Biofilms

Author

Cabral, Vitor, primary, Znaidi, Sadri, additional, Walker, Louise A., additional, Martin-Yken, Hélène, additional, Dague, Etienne, additional, Legrand, Mélanie, additional, Lee, Keunsook, additional, Chauvel, Murielle, additional, Firon, Arnaud, additional, Rossignol, Tristan, additional, Richard, Mathias L., additional, Munro, Carol A., additional, Bachellier-Bassi, Sophie, additional, and d'Enfert, Christophe, additional

Published
2014
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21. Systematic Phenotyping of a Large-Scale Candida glabrata Deletion Collection Reveals Novel Antifungal Tolerance Genes

Author

Schwarzmüller, Tobias, primary, Ma, Biao, additional, Hiller, Ekkehard, additional, Istel, Fabian, additional, Tscherner, Michael, additional, Brunke, Sascha, additional, Ames, Lauren, additional, Firon, Arnaud, additional, Green, Brian, additional, Cabral, Vitor, additional, Marcet-Houben, Marina, additional, Jacobsen, Ilse D., additional, Quintin, Jessica, additional, Seider, Katja, additional, Frohner, Ingrid, additional, Glaser, Walter, additional, Jungwirth, Helmut, additional, Bachellier-Bassi, Sophie, additional, Chauvel, Murielle, additional, Zeidler, Ute, additional, Ferrandon, Dominique, additional, Gabaldón, Toni, additional, Hube, Bernhard, additional, d'Enfert, Christophe, additional, Rupp, Steffen, additional, Cormack, Brendan, additional, Haynes, Ken, additional, and Kuchler, Karl, additional

Published
2014
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23. A Versatile Overexpression Strategy in the Pathogenic Yeast Candida albicans: Identification of Regulators of Morphogenesis and Fitness

Author

Chauvel, Murielle, primary, Nesseir, Audrey, additional, Cabral, Vitor, additional, Znaidi, Sadri, additional, Goyard, Sophie, additional, Bachellier-Bassi, Sophie, additional, Firon, Arnaud, additional, Legrand, Mélanie, additional, Diogo, Dorothée, additional, Naulleau, Claire, additional, Rossignol, Tristan, additional, and d’Enfert, Christophe, additional

Published
2012
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24. Comparative Transcript Profiling of Candida albicans and Candida dubliniensis Identifies SFL2 , a C. albicans Gene Required for Virulence in a Reconstituted Epithelial Infection Model

Author

Spiering, Martin J., primary, Moran, Gary P., additional, Chauvel, Murielle, additional, MacCallum, Donna M., additional, Higgins, Judy, additional, Hokamp, Karsten, additional, Yeomans, Tim, additional, d'Enfert, Christophe, additional, Coleman, David C., additional, and Sullivan, Derek J., additional

Published
2010
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25. The Yak1 Kinase Is Involved in the Initiation and Maintenance of Hyphal Growth inCandida albicans

Author

Goyard, Sophie, primary, Knechtle, Philipp, additional, Chauvel, Murielle, additional, Mallet, Adeline, additional, Prévost, Marie-Christine, additional, Proux, Caroline, additional, Coppée, Jean-Yves, additional, Schwarz, Patrick, additional, Dromer, Françoise, additional, Park, Hyunsook, additional, Filler, Scott G., additional, Janbon, Guilhem, additional, and d'Enfert, Christophe, additional

Published
2008
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27. Systematic Phenotyping of a Large-Scale Candida glabrata Deletion Collection Reveals Novel Antifungal Tolerance Genes.

Author

Schwarzmüller, Tobias, Ma, Biao, Hiller, Ekkehard, Istel, Fabian, Tscherner, Michael, Brunke, Sascha, Ames, Lauren, Firon, Arnaud, Green, Brian, Cabral, Vitor, Marcet-Houben, Marina, Jacobsen, Ilse D., Quintin, Jessica, Seider, Katja, Frohner, Ingrid, Glaser, Walter, Jungwirth, Helmut, Bachellier-Bassi, Sophie, Chauvel, Murielle, and Zeidler, Ute

Subjects
PATHOGENIC microorganisms, FUNGAL genes, CANDIDIASIS, AZOLES, ANTIFUNGAL agents, ECHINOCANDINS, THERAPEUTICS
Abstract

The opportunistic fungal pathogen Candida glabrata is a frequent cause of candidiasis, causing infections ranging from superficial to life-threatening disseminated disease. The inherent tolerance of C. glabrata to azole drugs makes this pathogen a serious clinical threat. To identify novel genes implicated in antifungal drug tolerance, we have constructed a large-scale C. glabrata deletion library consisting of 619 unique, individually bar-coded mutant strains, each lacking one specific gene, all together representing almost 12% of the genome. Functional analysis of this library in a series of phenotypic and fitness assays identified numerous genes required for growth of C. glabrata under normal or specific stress conditions, as well as a number of novel genes involved in tolerance to clinically important antifungal drugs such as azoles and echinocandins. We identified 38 deletion strains displaying strongly increased susceptibility to caspofungin, 28 of which encoding proteins that have not previously been linked to echinocandin tolerance. Our results demonstrate the potential of the C. glabrata mutant collection as a valuable resource in functional genomics studies of this important fungal pathogen of humans, and to facilitate the identification of putative novel antifungal drug target and virulence genes. [ABSTRACT FROM AUTHOR]

Published
2014
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29. A Comprehensive Functional Portrait of Two Heat Shock Factor-Type Transcriptional Regulators Involved in Candida albicans Morphogenesis and Virulence.

Author

Znaidi, Sadri, Nesseir, Audrey, Chauvel, Murielle, Rossignol, Tristan, and d'Enfert, Christophe

Subjects
CANDIDA albicans, MORPHOGENESIS, MICROBIAL virulence, HEAT shock proteins, PATHOGENIC microorganisms
Abstract

Sfl1p and Sfl2p are two homologous heat shock factor-type transcriptional regulators that antagonistically control morphogenesis in Candida albicans, while being required for full pathogenesis and virulence. To understand how Sfl1p and Sfl2p exert their function, we combined genome-wide location and expression analyses to reveal their transcriptional targets in vivo together with the associated changes of the C. albicans transcriptome. We show that Sfl1p and Sfl2p bind to the promoter of at least 113 common targets through divergent binding motifs and modulate directly the expression of key transcriptional regulators of C. albicans morphogenesis and/or virulence. Surprisingly, we found that Sfl2p additionally binds to the promoter of 75 specific targets, including a high proportion of hyphal-specific genes (HSGs; HWP1, HYR1, ECE1, others), revealing a direct link between Sfl2p and hyphal development. Data mining pointed to a regulatory network in which Sfl1p and Sfl2p act as both transcriptional activators and repressors. Sfl1p directly represses the expression of positive regulators of hyphal growth (BRG1, UME6, TEC1, SFL2), while upregulating both yeast form-associated genes (RME1, RHD1, YWP1) and repressors of morphogenesis (SSN6, NRG1). On the other hand, Sfl2p directly upregulates HSGs and activators of hyphal growth (UME6, TEC1), while downregulating yeast form-associated genes and repressors of morphogenesis (NRG1, RFG1, SFL1). Using genetic interaction analyses, we provide further evidences that Sfl1p and Sfl2p antagonistically control C. albicans morphogenesis through direct modulation of the expression of important regulators of hyphal growth. Bioinformatic analyses suggest that binding of Sfl1p and Sfl2p to their targets occurs with the co-binding of Efg1p and/or Ndt80p. We show, indeed, that Sfl1p and Sfl2p targets are bound by Efg1p and that both Sfl1p and Sfl2p associate in vivo with Efg1p. Taken together, our data suggest that Sfl1p and Sfl2p act as central “switch on/off” proteins to coordinate the regulation of C. albicans morphogenesis. [ABSTRACT FROM AUTHOR]

Published
2013
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30. The Yak1 Kinase Is Involved in the Initiation and Maintenance of Hyphal Growth in Candida albicans

Author

Goyard, Sophie, Knechtle, Philipp, Chauvel, Murielle, Mallet, Adeline, Prévost, Marie-Christine, Proux, Caroline, Coppée, Jean-Yves, Schwarz, Patrick, Dromer, Françoise, Park, Hyunsook, Filler, Scott G., Janbon, Guilhem, and d'Enfert, Christophe

Abstract

Members of the dual-specificity tyrosine-phosphorylated and regulated kinase (DYRK) family perform a variety of functions in eukaryotes. We used gene disruption, targeted pharmacologic inhibition, and genome-wide transcriptional profiling to dissect the function of the Yak1 DYRK in the human fungal pathogen Candida albicans. C. albicansstrains with mutant yak1alleles showed defects in the yeast-to-hypha transition and in maintaining hyphal growth. They also could not form biofilms. Despite their in vitro filamentation defect, C. albicans yak1Δ/yak1Δ mutants remained virulent in animal models of systemic and oropharyngeal candidiasis. Transcriptional profiling showed that Yak1 was necessary for the up-regulation of only a subset of hypha-induced genes. Although downstream targets of the Tec1 and Bcr1 transcription factors were down-regulated in the yak1Δ/yak1Δ mutant, TEC1and BCR1were not. Furthermore, 63% of Yak1-dependent, hypha-specific genes have been reported to be negatively regulated by the transcriptional repressor Tup1 and inactivation of TUP1in the yak1Δ/yak1Δ mutant restored filamentation, suggesting that Yak1 may function upstream of Tup1 in governing hyphal emergence and maintenance.

Published
2008
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31. Vancomycin-Dependent Enterococcus faecalisClinical Isolates and Revertant Mutants

Author

Van Bambeke, Françoise, Chauvel, Murielle, Reynolds, Peter E., Fraimow, Henry S., and Courvalin, Patrice

Abstract

ABSTRACTThree vancomycin-dependent clinical isolates of Enterococcus faecalisof the VanB type were studied by determining (i) the sequence of the ddlgene encoding the hostd-Ala:d-Ala ligase and thevanSB-vanRBgenes specifying the two-component regulatory system that activates transcription of the vanBoperon, (ii) the level of expression of resistance genes by using dd-dipeptidase activity as a reporter, and (iii) the proportions of the peptidoglycan precursors synthesized. Each strain had a mutation in ddlleading to an amino acid substitution (D295 to V; T316 to I) or deletion (DAK251-253 to E) at invariant positions ind-Ala:d-Ala,d-Ala:d-Lac, andd-Ala:d-Ser ligases. These mutations resulted in impaired host d-Ala:d-Ala ligases since only precursors terminating in d-Ala-d-Lac were synthesized under vancomycin-inducing conditions. Two types of vancomycin-independent revertants of one isolate were obtained in vitro after growth in the absence of vancomycin: (i) vancomycin-resistant, teicoplanin-susceptible mutants had a 6-bp insertion in the hostddlgene, causing the E251-to-EYK change that restoredd-Ala:d-Ala ligase activity, (ii) constitutive vancomycin-resistant, teicoplanin-resistant mutants had substitutions (S232 to F or E247 to K) in the vicinity of the autophosphorylation site of the VanSBsensor and produced exclusively precursors ending in d-Ala-d-Lac. Vancomycin- and teicoplanin-dependent mutants obtained by growth in the presence of teicoplanin had an 18-bp deletion in VanSB, affecting residues 402 to 407 and overlapping the G2 ATP binding domain. The rapid emergence of vancomycin-independent revertants in vitro suggests that interruption of vancomycin therapy may not be sufficient to cure patients infected with vancomycin-dependent enterococci.

Published
1999
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