Ontology highlight
ABSTRACT:
PROVIDER: PRJNA909945 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22572852_1.fastq.gz | Fastqsanger.gz | |||
| SRR22572852_2.fastq.gz | Fastqsanger.gz | |||
| SRR22572853_1.fastq.gz | Fastqsanger.gz | |||
| SRR22572853_2.fastq.gz | Fastqsanger.gz | |||
| SRR22572854_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 84 |
Similar Datasets
Project description:Ciboria carunculoides is a major fungal pathogen that infect of mulberry fruit causing popcorn disease leading extensive damage and productivity loss. In spite of such a major impact, mulberry fruit response to C. carunculoides infection is yet to be witnessed. We carried out a transcriptomic study to get insights into the molecular mechanisms and dynamics of the mulberry fruit response to the C. carunculoides infection using RNA-seq analysis with Illumina HiSeq 2000.
2021-03-01 | GSE111319 | GEO
Project description:Bacterial wilt, caused by the soil-borne bacterium Ralstonia solanacearum, is a lethal disease of mulberry, but the molecular mechanisms of the host resistance responses to R. solanacearum remain unclear. In order to better understand molecular resistance mechanisms to R. solanacearum in mulberry, we set out to define the changes in gene expression of resistance and susceptible mulberry cultivars after inoculation with R. solanacearum. Susceptible cultivar YSD10, resistance cultivar KQ10 and YS283 were inoculation with R. solanacearum, mulberry root samples were collected at 1 dpi and non-treated control in all cultivars. Then we performed RNA-Seq analyses on all mulberry root samples using Illumina HiSeq 2000.
2019-06-13 | GSE60030 | GEO
Project description:<p><strong>Background</strong></p><p>Antibiotic treatment has a well-established detrimental effect on the gut bacterial composition, but effects on the fungal community are less clear. Bacteria in the lumen of the gastrointestinal tract may limit fungal colonization and invasion. Antibiotic drugs targeting bacteria are therefore seen as an important risk factor for fungal infections and induced allergies. However, antibiotic effects on gut bacterial-fungal interactions, including disruption and resilience of fungal community compositions, were not investigated in humans. We analysed stool samples collected from 14 healthy human participants over three months following a 6-day antibiotic administration. We integrated data from shotgun metagenomics, metatranscriptomics, metabolomics, and fungal ITS2 sequencing. </p><p><strong>Results</strong></p><p>While the bacterial community recovered mostly over three months post treatment, the fungal community was shifted from mutualism at baseline to competition. Half of the bacterial-fungal interactions present before drug intervention had disappeared three months later. During treatment, fungal abundances were associated with the expression of bacterial genes with functions for cell growth and repair. By extending the metagenomic species approach, we revealed bacterial strains inhibiting the opportunistic fungal pathogen Candida albicans. We demonstrate in vitro how C. albicans pathogenicity and host cell damage might be controlled naturally in the human gut by bacterial metabolites such as propionate or 5-dodecenoate.</p><p><strong>Conclusions</strong></p><p>We demonstrate that antibacterial drugs have long-term influence on the human gut mycobiome. While bacterial communities recovered mostly 30-days post antibacterial treatment, the fungal community was shifted from mutualism towards competition.</p><p><br></p><p><strong>Linked data:</strong></p><p>Metagenomics has been submitted to NCBI SRA repository as projects PRJNA573821, PRJNA573905 and PRJNA579284.</p>
2020-09-28 | MTBLS1846 | MetaboLights
Project description:The rate, timing, and mode of species dispersal is recognized as a key driver of the structure and function of communities of macroorganisms, and may be one ecological process that determines the diversity of microbiomes. Many previous studies have quantified the modes and mechanisms of bacterial motility using monocultures of a few model bacterial species. But most microbes live in multispecies microbial communities, where direct interactions between microbes may inhibit or facilitate dispersal through a number of physical (e.g., hydrodynamic) and biological (e.g., chemotaxis) mechanisms, which remain largely unexplored. Using cheese rinds as a model microbiome, we demonstrate that physical networks created by filamentous fungi can impact the extent of small-scale bacterial dispersal and can shape the composition of microbiomes. From the cheese rind of Saint Nectaire, we serendipitously observed the bacterium Serratia proteamaculans actively spreads on networks formed by the fungus Mucor. By experimentally recreating these pairwise interactions in the lab, we show that Serratia spreads on actively growing and previously established fungal networks. The extent of symbiotic dispersal is dependent on the fungal network: diffuse and fast-growing Mucor networks provide the greatest dispersal facilitation of the Serratia species, while dense and slow-growing Penicillium networks provide limited dispersal facilitation. Fungal-mediated dispersal occurs in closely related Serratia species isolated from other environments, suggesting that this bacterial-fungal interaction is widespread in nature. Both RNA-seq and transposon mutagenesis point to specific molecular mechanisms that play key roles in this bacterial-fungal interaction, including chitin utilization and flagellin biosynthesis. By manipulating the presence and type of fungal networks in multispecies communities, we provide the first evidence that fungal networks shape the composition of bacterial communities, with Mucor networks shifting experimental bacterial communities to complete dominance by motile Proteobacteria. Collectively, our work demonstrates that these strong biophysical interactions between bacterial and fungi can have community-level consequences and may be operating in many other microbiomes.
2017-08-02 | GSE85095 | GEO