ArticleMolecular microbiology2021
Mrr1 regulation of methylglyoxal catabolism and methylglyoxal-induced fluconazole resistance in Candida lusitaniae.
Article in Molecular microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- The emerging pathogen Candida auris: host interactions and disease drivers.Journal of biomedical science · 2026Review
- Article
- Effects of low intracellular glutathione and CbrA-CbrB-Crc signaling on methylglyoxal sensitivity inJournal of bacteriology · 2025Article
- Adaptation of Candida albicans to specific host environments by gain-of-function mutations in transcription factors.PLoS pathogens · 2024Review
- Drivers of diversification in fungal pathogen populations.PLoS pathogens · 2024Review
- From environmental adaptation to host survival: Attributes that mediate pathogenicity ofVirulence · 2022Article
- Candida parapsilosis Mdr1B and Cdr1B Are Drivers of Mrr1-Mediated Clinical Fluconazole Resistance.Antimicrobial agents and chemotherapy · 2022Article
- Transcriptional Response of Candida auris to the Mrr1 Inducers Methylglyoxal and Benomyl.mSphere · 2022Article
- Oxidative stress response pathways in fungi.Cellular and molecular life sciences : CMLS · 2022Review
- Article
- Balancing Positive and Negative Selection:mBio · 2021Article
- Fructose Induces Fluconazole Resistance inInternational journal of molecular sciences · 2021Article
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Authors and funding
3 authors.
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Abstract
Transcription factor Mrr1, best known for its regulation of Candida azole resistance genes such as MDR1, regulates other genes that are poorly characterized. Among the other Mrr1-regulated genes are putative methylglyoxal reductases. Methylglyoxal (MG) is a toxic metabolite that is elevated in diabetes, uremia, and sepsis, which are diseases that increase the risk for candidiasis, and MG serves as a regulatory signal in diverse organisms. Our studies in Clavispora lusitaniae, also known as Candida lusitaniae, showed that Mrr1 regulates expression of two paralogous MG reductases, MGD1 and MGD2, and that both participate in MG resistance and MG catabolism. Exogenous MG increased Mrr1-dependent expression of MGD1 and MGD2 as well as expression of MDR1, which encodes an efflux pump that exports fluconazole. MG improved growth in the presence of fluconazole and this was largely Mrr1-dependent with contributions from a secondary transcription factor, Cap1. Increased fluconazole resistance was also observed in mutants lacking Glo1, a Mrr1-independent MG catabolic enzyme. Isolates from other Candida species displayed heterogeneity in MG resistance and MG stimulation of azole resistance. We propose endogenous and host-derived MG can induce MDR1 and other Mrr1-regulated genes causing increased drug resistance, which may contribute to some instances of fungal treatment failure.
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