ArticleMicrobiology (Reading, England)2010
Overexpression of TUF1 restores respiratory growth and fluconazole sensitivity to a Cryptococcus neoformans vad1Delta mutant.
Article in Microbiology (Reading, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Emerging insights into pulmonary hypertension: the potential role of mitochondrial dysfunction and redox homeostasis.Molecular and cellular biochemistry · 2025Review
- Atypical changes in Candida albicans cells treated with the Venetin-1 complex from earthworm coelomic fluid.Scientific reports · 2023Article
- Silencing TUFM Inhibits Development of Monocrotaline-Induced Pulmonary Hypertension by Regulating Mitochondrial Autophagy via AMPK/mTOR Signal Pathway.Oxidative medicine and cellular longevity · 2022Article
- Down-regulation of TUFM impairs host cell interaction and virulence by Paracoccidioides brasiliensis.Scientific reports · 2019Article
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- Colony and Single Cell Level Analysis of the Heterogeneous Response ofFrontiers in cellular and infection microbiology · 2018Article
- A conserved mechanism of TOR-dependent RCK-mediated mRNA degradation regulates autophagy.Nature cell biology · 2015Article
- Mitochondria and fungal pathogenesis: drug tolerance, virulence, and potential for antifungal therapy.Eukaryotic cell · 2011Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The yeast-like fungus Cryptococcus neoformans favours respiration as a mechanism of energy production, and thus depends heavily on mitochondrial function. Previous studies of a C. neoformans vad1Delta mutant revealed reduced expression of the mitochondrial elongation factor TUF1 and defects in glycerol utilization, consistent with mitochondrial dysfunction. In this study, we found that in trans expression of TUF1 in the vad1Delta mutant suppressed the mitochondrial defects, including growth on respiration-dependent carbon sources and fluconazole resistance, associated with VAD1 deletion. Tetracycline, an inhibitor of mitochondrial translation, was found to confer resistance to fluconazole in the wild-type and vad1Delta mutant, whereas the fluconazole susceptibility of the TUF1-overexpressing strain was unaffected by tetracycline treatment. In the presence of fluconazole, the vad1Delta mutant exhibited increased activation of the global transcriptional regulator Sre1. TUF1 overexpression failed to alter cleavage of Sre1 in response to fluconazole in the vad1Delta mutant, suggesting that TUF1 repression in the vad1Delta mutant is distal to Sre1, or that it occurs through an independent pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.