Short-term diet intervention alters the small non coding RNA (sncRNA) landscape of human sperm
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA670419 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12858025.fastq.gz | Fastqsanger.gz | |||
| SRR12858026.fastq.gz | Fastqsanger.gz | |||
| SRR12858027.fastq.gz | Fastqsanger.gz | |||
| SRR12858028.fastq.gz | Fastqsanger.gz | |||
| SRR12858029.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 34 |
Similar Datasets
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.
2021-10-31 | GSE159752 | GEO
Project description:Exhaustive catalogue of sncRNA content of bovine sperm cell
| PRJEB33940 | ENA
Project description:Microplastics (MPs) has been known for its toxicity on various organs and cells in humans, and its exposure leading to disease. Nevertheless, the toxic effects and underlying mechanisms on the profile of small non-coding RNAs (sncRNAs) in sperm, as well as their effects on embryo development, are not well understood. We recently developed the novel RNA sequencing (RNA-seq) technique, PANDORA-seq to overcome the limitations of traditional RNA sequencing. In this study, we elucidated the sncRNA changes using PANDORA-seq in mouse sperm after four weeks of oral gavage with MPs. We also examined the effects of sncRNAs on mouse embryonic stem cells (mESCs). MP exposure significantly altered sncRNA biogenesis-related genes in the testis and cauda epididymis, but not in the caput epididymis. PANDORA-seq revealed that a sncRNA landscape including transfer RNA-derived small RNAs (tsRNAs) and ribosomal RNA-derived small RNAs (rsRNAs) in the sperm was changed by MPs gavage. Interestingly, transfections of changed sncRNA, tsRNA-Glu-CTC and 5S ribosomal RNA (5S rRNA), in mESC changed pluripotency, inflammation, and cardiovascular development related genes. In conclusion, exposure to MPs may alter the sncRNA profile in sperm, which could affect embryonic development and increase the risk of inheritable diseases such as atherosclerosis and metabolic disorders.
2025-10-01 | GSE306011 | GEO
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 paternal effects. Here, we characterised the baseline sncRNA landscape of human sperm and the effect of a 6-week dietary intervention on their expression profile. This study involves sncRNAseq profiling, that was performed on a subset (n = 17) of the participants enrolled in the PREPARE trial: 9 from the control group and 8 from the intervention group. 5'tRFs, miRNAs and piRNAs were the most abundant sncRNA subtypes identified; their expression was associated with age, BMI, and sperm quality. Nutritional intervention with olive oil, 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. PREPARE Trial registration number: ISRCTN50956936, Trial registration date: 10/02/2014.
| S-EPMC11882820 | biostudies-literature
Project description:sncRNA from bovine sperm at different male tract localization
| PRJEB41989 | ENA
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
2021-10-07 | PXD022865 | Pride
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.
2021-10-04 | GSE162527 | GEO
Project description:Extracellular vesicles (EVs) are known to contain important cargo of biologically active and regulatory molecules including small non-coding RNA (sncRNA). EVs from cauda epididymis play crucial role in post-testicular maturation of sperm. We assessed levels of cauda epididymosomes sncRNAs following exposure to low dose anti-androgenic Di-n-butyl phthalate (DBP), Di(2-ethylhexyl) phthalate (DEHP), and their mixtures in mice.
2025-10-13 | GSE267272 | GEO
Project description:The discovery of RNAs (e.g. mRNAs, non-coding RNAs) in sperm has opened the possibility that sperm may function in delivering additional paternal information aside from solely providing the DNA1. Increasing evidence now suggests that sperm small non-coding RNAs (sncRNAs) can mediate intergenerational transmission of paternally acquired phenotypes, including mental stress2, 3 and metabolic disorders4-6. How sperm sncRNAs encode paternal information remains unclear, but the mechanism may involve RNA modifications. Here we show that deletion of a mouse tRNA methyltransferase, DNMT2, abolished sperm sncRNA-mediated transmission of high-fat diet (HFD)-induced metabolic disorders to offspring. Dnmt2 deletion prevented the elevation of RNA modifications (m5C, m2G) in sperm 30-40nt RNA fractions that are induced by HFD. Also, Dnmt2 deletion altered the sperm small RNA expression profile, including levels of tRNA-derived small RNAs (tsRNAs) and rRNA-derived small RNAs (rsRNA-28S), which might be essential in composing a sperm RNA ‘coding signature’ that is needed for paternal epigenetic memory. Finally, we show that Dnmt2-mediated m5C contributes to the secondary structure and biological properties of sncRNAs, implicating sperm RNA modifications as an additional layer of paternal hereditary information.
2018-03-06 | GSE97645 | GEO
Project description:Spermatozoa harbor a complex and environment sensitive pool of small non-coding RNAs (sncRNA)1, which influences offspring development and adult phenotypes1-7. Whether spermatozoa in the epididymis are directly susceptible to environmental cues is not fully understood8. We used two distinct paradigms of preconception acute high fat diet to dissect epididymal vs testicular contributions to the sperm sncRNA pool and offspring health. We show that epididymal spermatozoa, but not developing germ cells, are sensitive to the environment and identify mitochondrial tRNAs and their fragments (mt-tsRNA) as sperm-borne factors. In humans, mt-tsRNAs in spermatozoa correlate with BMI and paternal overweight at conception doubles offspring obesity risk and compromises metabolic health. Sperm sncRNA-seq of mice mutant for genes involved in mitochondrial function, and metabolic phenotyping of their wild-type offspring, suggest that alterations of mt-tsRNAs are downstream of mitochondrial dysfunction. Most importantly, single embryo transcriptomics of genetically hybrid two-cell embryos demonstrated sperm-to-oocyte transfer of mt-tRNAs at fertilisation and implied them in the control of early embryo transcription. Our study supports the importance of paternal health at conception for offspring metabolism, shows that mt-tRNAs are diet-induced and sperm-borne and demonstrates, for the first time in a physiological setting, father-to-offspring transfer of sperm mitochondrial RNAs at fertilization. This SuperSeries is composed of the SubSeries listed below.
2024-04-03 | GSE239815 | GEO