Ontology highlight
ABSTRACT:
PROVIDER: PRJNA252866 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genomic analysis of Fungal Pathogenesis
| PRJNA252863 | ENA
Project description:Genomic analysis of Fungal Pathogenesis
| PRJNA257495 | ENA
Project description:Genomic analysis of Fungal Pathogenesis
| PRJNA252862 | ENA
Project description:Genomic analysis of Fungal Pathogenesis
| PRJNA257493 | ENA
Project description:Genomic analysis of Fungal Pathogenesis
| PRJNA257494 | ENA
Project description:Fungal keratitis (FK) is a blinding eye disease with a high incidence in the world. At present, there is no effective treatment for this disease. At the same time, we found that animal organisms have inherent immune response mechanisms to fungal infections such as C-type lectin receptors (CLRs), which can identify fungal invaders and trigger signal transduction pathways and cellular responses to eliminate pathogens. However, previous studies mostly focused on single receptor factors, lacking a systematic analysis of the genetic factors underlying the pathogenesis of FK. Herein,we performed a transcriptomic study of FK in mice model using RNA sequencing to obtain the relevant gene expression profiles and screen the differentially expressed gene sets, signaling pathways and regulatory networks of key genetic factors in the pathogenesis of FK in mice. As a result, several marker genes of FK were identified such as Il1b and Wnt5a. Wnt signaling pathway, cGMP-PKG signaling pathway and Hippo signaling pathway were significantly enriched during fungal infection in mice cornea. In conclusion, our study may provide a novel insights into the pathogenesis of FK as well as more target sites for its drug treatment.
2021-04-24 | E-MTAB-7907 | biostudies-arrayexpress
Project description:Diversification of effector function, driven by a co-evolutionary arms race, enables pathogens to establish compatible interactions with their hosts. Structurally conserved plant pathogenesis-related PR-1 and PR-1-like (PR-1L) proteins are involved in plant defense and fungal virulence, respectively. It is unclear how fungal PR-1L counteracts plant defense. Here, we show that Ustilago maydis UmPR-1La and yeast ScPRY1 with conserved phenolic detoxification functions are Ser/Thr-rich region-mediated cell-surface localization proteins. However, UmPR-1La has gained additional specialized activity in eliciting hyphal-like formation, suggesting that U. maydis deploys UmPR-1La to sense phenolics and direct their growth in plants. U. maydis also hijacks plant cathepsin B-like 3 (CatB3) to release functional CAPE-like peptides after cleaving a conserved CNYD motif of UmPR-1La to subvert plant immunity for promoting fungal virulence. Surprisingly, CatB3 avoids cleavage of plant PR-1s, despite the presence of the same conserved CNYD motif. Our work highlights that UmPR-1La has acquired additional dual roles to suppress plant defense and sustain the infection process of fungal pathogens.
2024-03-22 | PXD041022 | JPOST Repository
Project description:MicroRNAs (miRNAs) are small, stable non-coding RNA molecules with regulatory function and marked tissue specificity that post-transcriptionally regulate gene expression, however their role in fungal keratitis remain unknown. Our purpose was to identify the miRNAs in human cornea from fungal keratitis patients and understand their key role in regulation of pathogenesis. Corneal samples from normal cadaver (n=3) and fungal keratitis (n=5) patients were pooled separately and total RNA was extracted. Deep sequencing was done using Illumina HiSeq1000 platform to identify miRNA profile. We identified seventy five differentially expressed miRNAs in fungal keratitis corneas. Select miRNAs were validated by real-time RT-PCR (Q-PCR). We predicted their role in regulating target genes in several pathways by combining miRNA target genes and pathway analysis, and mRNA expression of select target genes were further analysed by Q-PCR. MiR-21-5p, miR-223-3p, miR-146b-5p, miR-155-5p, miR-511-5p were found to be involved in inflammatory and immune responses, regulating Toll like receptor signaling pathways, which is of particular interest. MiR-451a with an increased expression in keratitis may have a role in wound healing by targeting Macrophage Migration Inhibitory Factor (MIF). Further, we highlighted that Neurotrophin signaling pathway may play a role in wound healing process. One novel miRNA was also detected in cornea. In conclusion, several miRNAs with high expression in fungal keratitis corneas point towards their role in regulation of pathogenesis. Further insights in understanding miRNAs role in wound healing and inflammation may help design new therapeutic strategies.
2016-07-28 | GSE64843 | GEO
Project description:Aim of this project is to identify biomarkers associated with fungal persistence in the host and genomic variability among strains isolated from different environments.
2016-04-30 | E-SYBR-8 | biostudies-arrayexpress
Project description:With the rise in immunocompromised individuals and patients with immune-related comorbidities such as COVID-19, the rate of fungal infections is growing. This increase, along with the current plateau in anti-fungal drug development, has made understanding the pathogenesis and dissemination of these organisms more pertinent than ever. The mouse model of fungal infection, while informative on a basic science level, has severe limitations in terms of translation to the human disease. Here we present data supporting the implementation of the human cerebral organoid model, which is generated from human embryonic stem cells and accurately recapitulates relevant brain cell types and structures, to study fungal infection and dissemination to the central nervous system (CNS). This approach provides direct insight into the relevant pathogenesis of specific fungal organisms in human tissues where in vivo models are impossible. With this model system we assessed the specific brain tropisms and cellular effects of fungal pathogens that are known to cross the blood brain barrier such as Cryptococcus neoformans. We determined the effects this fungal pathogen has on the overall gross morphology, cellular architecture, and cytokine release of these model organoids. Furthermore, we demonstrated that C. neoformans can penetrate and invade the organoid tissue and remain present throughout the course of infection. These results demonstrate the utility of this new model to the field and highlight the potential for this system to elucidate fungal pathogenesis to new therapeutic strategies to prevent and treat the terminal stages of fungal diseases such as cryptococcal meningitis.
2025-07-14 | GSE302166 | GEO