Maternally infection promotes offspring tissue-specific immune fitness [scRNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA667785 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12782814_1.fastq.gz | Fastqsanger.gz | |||
| SRR12782814_2.fastq.gz | Fastqsanger.gz | |||
| SRR12782815_1.fastq.gz | Fastqsanger.gz | |||
| SRR12782815_2.fastq.gz | Fastqsanger.gz | |||
| SRR12782816_1.fastq.gz | Fastqsanger.gz |
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Project description:Maternally infection promotes offspring tissue-specific immune fitness
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Project description:Mammals evolved in the face of pathogen exposure, the vast majority of these encounters resulting in asymptomatic or mild infections. How these constitutive exposures at specific developmental stages impact the host immune system for the long term remains poorly understood. Here we show that maternally restricted, mild infections, can have a permanent and tissue-specific impact on the offspring immunity. This imprinting is associated with a selective increase of Th17 cells within the gut, but not other compartment, and results from enhanced tonic responses to the microbiota. Mechanistically, we found that IL-6 produced by the mother during infection can directly act on fetus intestinal epithelial cells, leading to long-term alteration in chromatin and transcriptomic profiles in intestinal epithelial cells. As such at the adult stage, offspring display enhanced protective responses to oral infections. Together this work proposes that maternal infections can be coopted during fetal development as a mean to promote long-term tissue-specific immune fitness in offspring.
2021-09-24 | GSE159149 | GEO
Project description:Mammals evolved in the face of pathogen exposure, the vast majority of these encounters resulting in asymptomatic or mild infections. How these constitutive exposures at specific developmental stages impact the host immune system for the long term remains poorly understood. Here we show that maternally restricted, mild infections, can have a permanent and tissue-specific impact on the offspring immunity. This imprinting is associated with a selective increase of Th17 cells within the gut, but not other compartment, and results from enhanced tonic responses to the microbiota. Mechanistically, we found that IL-6 produced by the mother during infection can directly act on fetus intestinal epithelial cells, leading to long-term alteration in chromatin and transcriptomic profiles in intestinal epithelial cells. As such at the adult stage, offspring display enhanced protective responses to oral infections. Together this work proposes that maternal infections can be coopted during fetal development as a mean to promote long-term tissue-specific immune fitness in offspring.
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Project description:<p>The gut microbiota operates at the interface of host-environment interactions to influence human homeostasis and metabolic networks. Environmental factors that unbalance gut microbial ecosystems can therefore elicit physiological and disease-associated responses across somatic tissues. However, the systemic impact of the gut microbiome on the germline - and consequently on the F1 offspring it gives rise to - is unexplored. Here we show that the gut microbiota act as a key interface between paternal preconception environment and intergenerational health in mice. Perturbations to the gut microbiota of prospective fathers increase the probability of their offspring presenting with low birth weight, severe growth restriction and premature mortality. Transmission of disease risk occurs via the germline and is provoked by pervasive gut microbiome perturbations, including non-absorbable antibiotics or osmotic laxatives, but is rescued by restoring the paternal microbiota before conception. This effect is linked with a dynamic response to induced dysbiosis in the male reproductive system, including impaired leptin signalling, altered testicular metabolite profiles and remapped small RNA payloads in sperm. As a result, dysbiotic fathers trigger an elevated risk of in utero placental insufficiency, revealing a placental origin of mammalian intergenerational effects. Our study defines a regulatory ‘gut-germline axis’ in males, which is sensitive to environmental exposures and programs offspring fitness through impacting placental function.</p>
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Project description:Genetic imprinting is an epigenetic phenomenon that describes unequal expression of paternal and maternal alleles of a gene in sexually reproducing organisms including mammals and flowering plants. The function of imprinted genes was rarely reported. We report genome-wide analysis of gene expression, DNA methylation, and small RNAs in the rice endosperm and functional tests of five imprinted genes in seed development using CRISPR/Cas9 editing technology. We identified 162 maternally expressed genes(MEGs) and 95 paternally expressed genes (PEGs) in the rice endosperm, which were associated with miniature inverted-repeat transposable elements, imprinted differentially methylated loci, and some 21-22-siRNAs and lncRNAs. Remarkably, one-third of MEGs and nearly half of PEGs were associated with grain-yield quantitative trait loci and enriched in the endosperm-expressed genes. Disrupting two MEGs increased the amount of small starch granules and reduced grain size, weight, and embryo size, while mutating three PEGs reduced starch content and seed fertility. Our data support both MEGs and PEGs in rice are required for starch and nutrient accumulation, mediating offspring fitness and optimal seed size. This imprinting strategy provides potential means for improving grain yield of rice and other cereal crops.
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Project description:The piRNA pathway controls transposon expression in animal germ cells, thereby ensuring genome stability over generations. piRNAs are maternally deposited and required for proper transposon silencing in adult offspring. However, a long-standing question in the field is the precise function of maternally deposited piRNAs and its associated factors during embryogenesis. Here, we probe the spatio-temporal expression patterns of several piRNA pathway components during early stages of development. Amongst those, factors required for transcriptional gene silencing (TGS) showed ubiquitous abundance in somatic and pole cells throughout the first half of embryogenesis. We further analyzed the transcriptomes of various embryo stages and correlated these with the presence of selected chromatin marks. We found that a number of transposon families show bursts of transcription during early embryonic stages. Transposons heavily targeted by maternally deposited piRNAs accumulated repressive chromatin marks following their spike in expression. Furthermore, depletion of maternally deposited Piwi protein in early embryos resulted in increased expression of transposons targeted by inherited piRNAs and was accompanied by a strong loss of repressive chromatin marks at coding sequences. Overall, our data suggests a pivotal role for the piRNA pathway in transposon defence during Drosophila embryogenesis in somatic cells.
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