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 |
Similar Datasets
Project description:Novel pathogenic Mucorales identified using the silkworm infection model
| PRJNA752231 | ENA
Project description:Genomes of clinical isolates of Mucorales species
| PRJNA766449 | ENA
Project description:Mucormycosis, a rapidly progressive and often lethal fungal infection caused by Mucorales, has limited therapeutic options and incompletely understood pathogenesis. The epigenetic modification N6-methyladenine (6mA), symmetrically distributed on both DNA strands, is highly abundant in Mucorales, opposed to other fungal pathogens, and regulates multiple biological processes. In contrast, symmetric 6mA and its associated enzymatic machinery are largely absent in mammals, highlighting a striking evolutionary divergence that suggests potential pathogen-specific therapeutic vulnerabilities. Here, we develop a tetracycline-regulatable system in Rhizopus microsporus that enables repression of the essential methyltransferase Mta1 and consequent reduction of genomic 6mA levels. Induced depletion of 6mA profoundly attenuates fungal virulence in murine infection models, an effect associated with downregulation of key virulence determinants, including the mycotoxin mucoricin and the CotH3 invasin. Attenuated fungal pathogenicity was further accompanied by enhanced neutrophil swarming, resulting in efficient restriction of germinating fungi. Multi-organ transcriptomic analyses revealed that the host inflammatory immune response was reduced upon 6mA depletion. Together, our findings identify symmetric 6mA as a central regulator of Mucorales pathogenicity, representing a promising, fungus-specific therapeutic target for the treatment of mucormycosis.
2026-08-21 | GSE326497 | GEO
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.
2024-03-20 | GSE233894 | GEO
Project description:DNA N6-methylation orchestrates the pathogenicity of Mucorales fungi
| PRJNA1445789 | ENA
Project description:H3K4 methylation regulates development, DNA repair, and virulence in Mucorales
| PRJNA978531 | ENA