Mucorales
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB17581 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| DRR531249_subreads.fastq.gz | Fastqsanger.gz | |||
| DRR531250_subreads.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 3 of 3 |
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Project description:Mucorales are basal fungi that opportunistically cause a fatal infection known as mucormycosis (black fungus disease), which poses a significant threat to human health due to its high mortality rate and its recent association with SARS-CoV-2 infections. On the other hand, histone methylation is a regulatory mechanism with pleiotropic effects, including the virulence of several pathogenic organisms. However, the role of epigenetic changes at the histone level never has been studied in Mucorales. Here, we dissected the functional role of Set1, a histone methyltransferase that catalyzes the methylation of H3K4, which is associated with the activation of gene transcription and virulence. A comparative analysis of the Mucor lusitanicus genome (previously known as Mucor circinelloides f. lusitanicus) identified only one homolog of Set1 from Candida albicans and Saccharomyces cerevisiae that contains the typical SET domain. Knockout strains in the gene set1 lacked H3K4 monomethylation, dimethylation, and trimethylation enzymatic activities. These strains also showed a significant reduction in vegetative growth and sporulation. Additionally, set1 null strains were more sensitive to SDS, EMS, and UV light, indicating severe impairment in the repair process of the cell wall and DNA lesions and a correlation between Set1 and these processes. During pathogen-host interactions, strains lacking the set1 gene exhibited shortened polar growth within the phagosome and attenuated virulence both in vitro and in vivo. Our findings suggest that the histone methyltransferase Set1 coordinates several cell processes related to the pathogenesis of M. lusitanicus and may be an important target for future therapeutic strategies against mucormycosis.
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Project description:H3K4 methylation regulates development, DNA repair, and virulence in Mucorales
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Project description:Mucormycosis, caused by Mucoralean fungi, is among the most lethal fungal diseases, and a deeper understanding of its pathogenesis is urgently needed. In this study, we examined the early stages of fungal interaction with host macrophages using Mucor lusitanicus and Rhizopus microsporus as model organisms. Transcriptomic profiling of virulent (WT) and an RNAi-deficient strain (r3b2Δ) of M. lusitanicus strains during phagocytosis uncovered thousands of differentially expressed genes (DEGs), highlighting early metabolic activation as a key survival strategy inside the phagosome. Enriched pathways included amino acid transport, nucleotide metabolism, and translation, reflecting an adaptive fungal response to nutrient deprivation and host immune stress. Integrative analyses of mRNA and sRNA profiles also revealed a critical role of the RNAi pathways in modulating gene expression during infection. Building on these observations, we identified four chromatin- and transcription-related candidate virulence genes—brca1, box, hist1, and hda10—which were strongly upregulated during phagocytosis and regulated by RNAi. Functional validation through gene deletion in M. lusitanicus and disruption in R. microsporus revealed that while loss of these genes in M. lusitanicus did not significantly affect virulence, R. microsporus mutants for brca1, hist1, and hda10 showed attenuated virulence in a murine model. Our findings suggest that although M. lusitanicus remains a valuable tool for genetic manipulation, species-specific differences must be considered when studying virulence. The study also underscores the importance of using multiple Mucorales models to uncover conserved and divergent strategies employed by pathogenic fungi. These insights contribute to a broader understanding of fungal adaptation, immune evasion, and the identification of novel targets for antifungal intervention.
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