Human Microbiome Samples
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA724050 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16023300_1.fastq.gz | Fastqsanger.gz | |||
| SRR16023300_2.fastq.gz | Fastqsanger.gz | |||
| SRR16023301_1.fastq.gz | Fastqsanger.gz | |||
| SRR16023301_2.fastq.gz | Fastqsanger.gz | |||
| SRR16023302_1.fastq.gz | Fastqsanger.gz |
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Project description:The microbiome has revealed itself as a key player in health and disease. To better understand its role, in addition to microbial diversity, it is important to understand species-specific activity and gene expression. While metatranscriptomics investigates mRNA abundance2, it does not inform about faster post-transcriptional regulation3. Although prokaryotic translation is a common target for antibiotics, a direct measurement of microbiome ribosome dynamics remains inaccessible. Here we demonstrate that, contrary to expectation, co-translational mRNA degradation is common in prokaryotes, and that in vivo ribosome protection generates widespread 3-nt periodicity in 5´P mRNA decay intermediates. Consequently, 5´P sequencing allows the study of codon and gene specific ribosome stalling in response to stress and drug treatment at single nucleotide resolution. We validate its wide applicability by investigating in vivo species-specific ribosome footprints of clinical and environmental microbiomes and show that amino acid-specific ribosome protection patterns can be used to phenotype microbiome perturbations. Furthermore, we show that multiple RNase activities collaborate to generate in vivo ribosome footprints and that co-translational degradation is phylogenetically conserved across prokaryotes. This strategy opens the way for the study of the metatranslatome, and allows to investigate fast species-specific post-transcriptional responses to environmental and chemical perturbations in unculturable microbial communities.
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Project description:Differences in male vs. female immune responses are well-documented and have significant clinical implications. While the immunomodulatory effects of sex hormones are well established, the contributions of sex chromosome complement (XX vs. XY) and gut microbiome diversity on immune sexual dimorphisms have only recently become appreciated. Here we investigate the individual and collaborative influences of sex chromosome complements and gut microbiome bacteria on humoral immune activation. Sham-operated and gonadectomized male and female Four Core Genotype (FCG) mice were immunized with heat-killed Streptococcus pneumoniae (HKSP). Humoral immune responses were assessed and X-linked immune-related gene expression was evaluated to explain the identified XX-dependent phenotypes. Ex vivo studies investigated the functional role of Kdm6a, an X-linked epigenetic regulatory gene of interest, in mitogenic B cell activation. We further evaluated whether gut microbiome communities, or their metabolites, differentially influence immune cell activation in a sex chromosome-dependent manner. Endogenous gut microbiomes were antibiotically depleted and reconstituted with select short-chain fatty acid (SCFA)-producing bacteria prior to HKSP immunization and immune responses assessed. XX mice exhibited higher HKSP-specific IgM-secreting B cells and plasma cell frequencies than XY mice, regardless of gonadal sex. Although Kdm6a was identified as an X-linked gene overexpressed in XX B cells, inhibition of its enzymatic activity did not affect mitogen-induced plasma cell differentiation or antibody production in a sex chromosome-dependent manner ex vivo. Enhanced humoral responses in XX vs. XY immunized FCG mice were eliminated after microbiome depletion, indicating that the microbiome contributes to the identified XX-dependent immune enhancement. Reconstituting microbiota-depleted mice with select SCFA-producing bacteria increased humoral responses in XX, but not XY, FCG mice. This XX-dependent enhancement appears to be independent of SCFA production in males, while female XX-dependent responses relied on SCFAs. FCG mice have been used to assess sex hormones and sex chromosome complements influences on various sexually dimorphic traits. The current study indicates that the gut microbiome impacts humoral responses in an XX-dependent manner, suggesting that the collaborative influence of gut bacteria and other sex-specific factors should be considered when interpreting data aimed at delineating the mechanisms that promote sexual dimorphisms.
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