ArticleScientific reports2019
Down-regulation of TUFM impairs host cell interaction and virulence by Paracoccidioides brasiliensis.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- TUFM: a central regulator in mitochondrial quality control and beyond.Cell death discovery · 2026Review
- Review
- Role of paracoccin onVirulence · 2023Article
- On the relationship between Pathogenic Potential and Infective Inoculum.PLoS pathogens · 2022Article
- Silencing TUFM Inhibits Development of Monocrotaline-Induced Pulmonary Hypertension by Regulating Mitochondrial Autophagy via AMPK/mTOR Signal Pathway.Oxidative medicine and cellular longevity · 2022Article
- Drk1, a Dimorphism Histidine Kinase, Contributes to Morphology, Virulence, and Stress Adaptation inJournal of fungi (Basel, Switzerland) · 2021Article
- Updates inJournal of fungi (Basel, Switzerland) · 2021Review
- One Century of Study: What We Learned aboutJournal of fungi (Basel, Switzerland) · 2021Review
- Mitochondrial Protein Translation: Emerging Roles and Clinical Significance in Disease.Frontiers in cell and developmental biology · 2021Review
- Molecular characterization of siderophore biosynthesis inIMA fungus · 2020Article
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Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genus Paracoccidioides consist of dimorphic fungi geographically limited to the subtropical regions of Latin America, which are responsible for causing deep systemic mycosis in humans. However, the molecular mechanisms by which Paracoccidioides spp. causes the disease remain poorly understood. Paracoccidioides spp. harbor genes that encode proteins involved in host cell interaction and mitochondrial function, which together are required for pathogenicity and mediate virulence. Previously, we identified TufM (previously known as EF-Tu) in Paracoccidioides brasiliensis (PbTufM) and suggested that it may be involved in the pathogenicity of this fungus. In this study, we examined the effects of downregulating PbTUFM using a silenced strain with a 55% reduction in PbTUFM expression obtained by antisense-RNA (aRNA) technology. Silencing PbTUFM yielded phenotypic differences, such as altered translation elongation, respiratory defects, increased sensitivity of yeast cells to reactive oxygen stress, survival after macrophage phagocytosis, and reduced interaction with pneumocytes. These results were associated with reduced virulence in Galleria mellonella and murine infection models, emphasizing the importance of PbTufM in the full virulence of P. brasiliensis and its potential as a target for antifungal agents against paracoccidioidomycosis.
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