SncRNA origine
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB41989 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4991490.fastq.gz | Fastqsanger.gz | |||
| ERR4991500.fastq.gz | Fastqsanger.gz | |||
| ERR4991491.fastq.gz | Fastqsanger.gz | |||
| ERR4991492.fastq.gz | Fastqsanger.gz | |||
| ERR4991493.fastq.gz | Fastqsanger.gz |
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Project description:Offspring health outcomes are often linked with epigenetic alterations triggered by maternal nutrition and intrauterine environment. Strong experimental data also link paternal preconception nutrition with pathophysiology in the offspring, but the mechanism(s) routing effects of paternal exposures remain elusive. Animal experimental models have highlighted small non-coding RNAs (sncRNAs) as potential regulators of these effects. This study characterised the baseline sncRNA landscape of human sperm and the effect of a 6 week dietary intervention on their expression profile. 5’tRFs, miRNA and piRNAs were the most abundant sncRNA subtypes identified; their expression was associated with age, BMI and sperm quality. Nutritional intervention with vitamin D and omega-3 fatty acids altered expression of 3 tRFs, 15 miRNAs and 112 piRNAs, targeting genes involved in fatty acid metabolism and transposable elements in the sperm genome.
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Project description:Paternal exposure to a range of environmental and lifestyle factors elicits distinct changes to the sperm sncRNA profile; modifications that have significant post-fertilization consequences. Despite this knowledge, there remains limited mechanistic understanding of how paternal exposures effect the sperm sncRNA landscape. Here, we report the acute sensitivity of the sperm sncRNA profile to the potent reproductive toxicant, acrylamide. Further, we traced the differential accumulation of acrylamide responsive sncRNAs to coincide with sperm transit of the proximal (caput) segment of the epididymis, wherein acrylamide exposure altered the expression of several transcription factors implicated in the expression of acrylamide-sensitive sncRNAs. We also identified extracellular vesicles secreted from the caput epithelium in relaying altered sncRNA profiles to maturing spermatozoa, the implications of which manifest in the form of dysregulated gene expression during early embryonic development. These data provide a causative mechanistic link to account for how environmental insults can alter the sperm epigenome and compromise the transcriptomic profile of early embryos
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Project description:Analysis of sncRNA expression in 22 primary cSCC (10 from cSCCs that had evolved to histologically confirmed metastases, or MSCC, and 12 from a cSCC control group who had not developed any metastasis in a 5-year follow-up period). Unsupervised hierarchical clustering of the most variably expressed sncRNAs stratified the tumors into two groups, one formed mainly by NMSCC and the other formed exclusively by metastasizing cSCC, the latter displaying an overall sncRNA downregulation. Supervised clustering of MSCC vs. NMSCC identified the differential expression of 330 sncRNAs, most of them downregulated in the metastasizing group (248 sncRNAs; 75%). Functional and sequence-based classification of the probes in the array revealed alterations in the proportion of the snoRNAs represented in MSCCs when compared to their expression in NMSCCs.
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Project description:Paternal exposure to environmental stressors elicits distinct changes to the sperm sncRNA profile; modifications that have significant post-fertilization consequences. Despite this knowledge, there remains limited mechanistic understanding of how paternal exposures modify the sperm sncRNA landscape. Here, we report the acute sensitivity of the sperm sncRNA profile to the reproductive toxicant, acrylamide. Further, we traced the differential accumulation of acrylamide-responsive sncRNAs to coincide with sperm transit of the proximal (caput) segment of the epididymis, wherein acrylamide exposure altered the abundance of several transcription factors implicated in the expression of acrylamide-sensitive sncRNAs. We also identified extracellular vesicles secreted from the caput epithelium in relaying altered sncRNA profiles to maturing spermatozoa, and dysregulated gene expression during early embryonic development following fertilisation by acrylamide-exposed spermatozoa. These data provide mechanistic links to account for how environmental insults can alter the sperm epigenome and compromise the transcriptomic profile of early embryos.
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