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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Hypothalamic reprogramming by sperm microRNA

ABSTRACT: Nine microRNAs (miRs) previously identified as increased in the sperm of stressed sires were microinjected into C57/Bl6:129S6/SvEvTac mouse single cell zygotes to examine the hypothesis that specific sperm miRs function postfertilization to alter offspring stress responsivity. Derived mice were exmined for hypothalamic-pituitary-adrenal axis stress response in adulthood, and the paraventricular nucleus of the hypothalamus was subsequently collected for gene expression analysis by next gen sequencing. Similar to what we reported previously in our paternal stress model, the majority of diffferenitally expressed genes in the PVN exhibited decreased expression, supporting that an increase of specific sperm miRs in the zygote can elicit long-term genetic reprogramming. Futher, marked changes in the expression of extracellular matrix and collagen gene sets suggested altered blood-brain barrier permeability with potential consequences for neuroendocrine function. mRNA profiling of paraventricular nucleus from adult male mice derived from zygote microinjection of nine miRs (multi-miR; miR-29, miR-30a, miR-30c, miR-32, miR-193-5p, miR-204, miR-375, miR-532-3p, miR-698) or PBS. Six biological replicates per group (12 total cDNA libraries) were multiplexed and sequenced on two identical HiSeq2000 lanes (Illumina).

ORGANISM(S): Mus musculus

SUBMITTER: Ali Rodgers

PROVIDER: E-GEOD-73574 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Hypothalamic reprogramming by sperm microRNA

Project description:Nine microRNAs (miRs) previously identified as increased in the sperm of stressed sires were microinjected into C57/Bl6:129S6/SvEvTac mouse single cell zygotes to examine the hypothesis that specific sperm miRs function postfertilization to alter offspring stress responsivity. Derived mice were exmined for hypothalamic-pituitary-adrenal axis stress response in adulthood, and the paraventricular nucleus of the hypothalamus was subsequently collected for gene expression analysis by next gen sequencing. Similar to what we reported previously in our paternal stress model, the majority of diffferenitally expressed genes in the PVN exhibited decreased expression, supporting that an increase of specific sperm miRs in the zygote can elicit long-term genetic reprogramming. Futher, marked changes in the expression of extracellular matrix and collagen gene sets suggested altered blood-brain barrier permeability with potential consequences for neuroendocrine function.

2016-01-01 | GSE73574 | GEO

Active and Passive Demethylation of Male and Female Pronuclear DNA in the Mammalian Zygote

Project description:The epigenomes of mammalian sperm and oocytes, characterized by gamete-specific 5-methylcytosine (5mC) patterns, are reprogrammed during early embryogenesis to establish full developmental potential. Previous studies have suggested that the paternal genome is actively demethylated in the zygote while the maternal genome undergoes subsequent passive demethylation via DNA replication during cleavage. Active demethylation is known to depend on 5mC oxidation by Tet dioxygenases and excision of oxidized bases by thymine DNA glycosylase (TDG). Here we show that both maternal and paternal genomes undergo widespread active and passive demethylation in zygotes before the first mitotic division. Passive demethylation was blocked by the replication inhibitor aphidicolin, and active demethylation was abrogated by deletion of Tet3 in both pronuclei. At actively demethylated loci, 5mCs were processed to unmodified cytosines. Surprisingly, the demethylation process was unaffected by the deletion of TDG from the zygote, suggesting the existence of other demethylation mechanisms downstream of Tet3-mediated oxidation. The dataset includes RRBS anlysis of 2 MII oocyte samples, 3 WT female pronuclei samples PN3-4 stage, 2 Tet3 KO female pronuclei samples and 2 Aphidicolin treated female pronuclei samples. Also as male counterpart, a Sperm sample, 2 WT male pronuclei samples PN3-4 stage, 2 Tet3 KO male pronuclei samples and 2 Aphidicolin treated male pronuclei samples were included.

2014-09-11 | E-GEOD-56650 | biostudies-arrayexpress

T cell activation decreases microRNA-15a/16 levels as a mechanism to promote MEK1-ERK1/2-Elk1 signaling for optimal proliferative capacity

Project description:While microRNAs (miRs) have been extensively studied in the context of malignancy and tumor progression, their functions in regulating T cell activation are less clear. We found reduced levels of miR-15a/16 at 3-18 h post-T cell receptor (TCR) stimulation, suggesting a role in shaping T cell activation. An inducible miR15a/16 transgenic mouse model was developed to determine how elevating miR-15a/16 levels during early stages of activation would affect T cell proliferation and to identify TCR signaling pathways regulated by this miR pair. Doxycyclin (DOX) induced expression of miR-15a/16 from 0-18 h post-TCR stimulation decreased ex vivo proliferation as well as in vivo antigen-specific proliferation. Bioinformatic and proteomic approaches were combined to identify MEK1 as a target of miR-15a/16. MEK1 targeting by miR-15a/16 was confirmed using miR mimics that decreased MEK1 containing the 3’-UTR target nucleotide sequence (UGCUGCUA) but did not decrease MEK1 containing a mutated control sequence (AAAAAAAA). Phosphorylation of downstream signaling molecules ERK1/2 and Elk1 were decreased with DOX-induced miR-15a/16 expression. In addition to MEK1, ERK1 was subsequently found to be targeted by miR-15a/16, with DOX induced miR-15a/16 reducing total ERK1 levels in T cells. These findings show that TCR stimulation reduces miR-15a/16 levels at early stages of T cell activation to facilitate increased MEK1 and ERK1, and this promotes sustained MEK1-ERK1/2-Elk1 signaling required for optimal proliferation.

2022-04-04 | PXD030935 | Pride

Active Demethylation of Both Maternal and Paternal Genomes in Mouse Zygotes

Project description:The epigenomes of mammalian sperm and oocytes, characterized by gamete-specific 5-methylcytosine (5mC) patterns, are reprogrammed in early embryogenesis to establish full developmental potential. It is broadly accepted that the paternal genome is actively demethylated in the zygote while the maternal genome undergoes passive demethylation thanks to DNA replication over the subsequent cleavage divisions. Here we reveal that both maternal and paternal genomes undergo widespread active and passive demethylation in the pronuclear zygote before the first mitotic division. Whereas the passive demethylation requires DNA replication, the active demethylation relies on enzymatic oxidation of 5mC, as deletion of the DNA dioxygenase, Tet3, but not the inhibition of replication, blocks the active demethylation. At actively demethylated loci, 5mCs appear to be processed to unmodified cytosines in a manner independent of the DNA glycosylase TDG. These observations suggest the occurrence of genuine active demethylation in both parental genomes following fertilization. An extra supportive Tet3 knock-out female pronuclear sample related to experiment Series GSE56650.

2016-09-01 | E-GEOD-60777 | biostudies-arrayexpress

MonoMac6 (MM6) cells proteomics LC-MS/MS

Project description:MicroRNAs (miRs) are small non-coding RNAs, which control the expression of target genes by either translational repression or RNA degradation, known as canonical miR function. MiR-328 has a non-canonical function and can activate gene expression by antagonizing the activity of heterogeneous ribonuclear protein E2 (hnRNP E2). The global importance of such non-canonical miR function is not yet known. In order to achieve a better understanding of the non-canonical miR activity, a compartment specific tandem mass tag (TMT)-based proteomic analysis in differentiated MonoMac6 (MM6) cells was performed.

2019-11-27 | PXD013106 | Pride

The effect of miRNA overexpression on gene expression profile of MCF-7 cells

Project description:To identify microRNAs impacting estrogen receptor ERÎ± expression in breast cancer, we have screened ER-positive breast cancer cells with a library of pre-miRs, and systematically monitored the ERÎ± expression by protein lysate microarrays. There was a significant enrichment of the in silico predicted ERÎ± targeting microRNAs among the hits. The most potent pre-miRs miR-18a/b, miR-193b, miR-206, and miR-302c, were confirmed to directly target ERÎ± and to repress estrogen-responsive genes. The effect of miRNA overexpression on gene expression profile of MCF-7 cells was studied. Furthermore, miR-18a and miR-18b showed increased expression in ERÎ±-negative as compared to ERÎ±-positive clinical tumors. In summary, we present systematic and direct functional and correlative clinical evidence on microRNAs inhibiting ERÎ± signaling in breast cancer. MCF-7 cells (300Â 000 per well on 6-well plates) were transfected with an siRNA for ERÎ± or with Ambion pre-miRâ?¢ constructs for miR-18a, miR-193b, miR-206, miR-302c, or pre-miR negative control #1 (scrambled pre-miR) at 20 nM, and incubated for 24h.

2010-04-09 | E-GEOD-14847 | biostudies-arrayexpress

Cooperative target mRNA destabilization and translation inhibition by miR-58 microRNA family in C. elegans

Project description:Comparative proteomic study between C. elegans wild type, mir-58.1 single, mir-80; mir-58.1 double and mir-80; mir-58.1; mir-81-82 quadruple mutants.

2015-08-06 | PXD001998 | Pride

Transcription profiling of human 13q14-\- cell line expressing doxycylin-inducible miR-15a/16-1 and empty vector (EV)

Project description:Reexpression of microRNAs miR-15a/16-1 in a cell line deficient for these miRs (homozygous deletion of chromosomal region 13q14) results in the downregulation of certain mRNAs. Experiment Overall Design: A doxycyclin-inducible expression vector containing miR-15a/16-1 was transfected into CLL-I83E95 cells that are deficient for those miRs. miR-expression was induced by addition of doxycyclin to the medium, and cell were harvested 48 hours later. Labeled cRNA was hybridized to microarrays and gene expression data were compared to CLL-I83U95 stably transfected with an empty vector.

2009-12-05 | E-GEOD-18866 | biostudies-arrayexpress

ena-DATASET-VUMC-CCA-23-10-2015-09:58:10:052-218 - samples

Project description:MicroRNAs (miRs) have been recognized as promising biomarkers. It is unknown to what extent tumor-derived miRs are differentially expressed between primary colorectal cancers (pCRCs) and metastatic lesions, and to what extent the expression profiles of tumor tissue differ from the surrounding normal tissue. Next-generation sequencing (NGS) of 220 fresh-frozen samples, including paired primary and metastatic tumor tissue and non-tumorous tissue from 38 patients, revealed expression of 2245 known unique mature miRs and 515 novel candidate miRs. Unsupervised clustering of miR expression profiles of pCRC tissue with paired metastases did not separate the two entities, whereas unsupervised clustering of miR expression profiles of pCRC with normal colorectal mucosa demonstrated complete separation of the tumor samples from their paired normal mucosa. Two hundred and twenty-two miRs differentiated both pCRC and metastases from normal tissue samples (false discovery rate (FDR) <0.05). The highest expressed tumor-specific miRs were miR-21 and miR-92a, both previously described to be involved in CRC with potential as circulating biomarker for early detection. Only eight miRs, 0.5% of the analysed miR transcriptome, were differentially expressed between pCRC and the corresponding metastases (FDR <0.1), consisting of five known miRs (miR-320b, miR-320d, miR-3117, miR-1246 and miR-663b) and three novel candidate miRs (chr 1-2552-5p, chr 8-20656-5p and chr 10-25333-3p). These results indicate that previously unrecognized candidate miRs expressed in advanced CRC were identified using NGS. In addition, miR expression profiles of pCRC and metastatic lesions are highly comparable and may be of similar predictive value for prognosis or response to treatment in patients with advanced CRC.

| EGAD00001001644 | EGA

MiR expression profiles of paired primary colorectal cancerand metastases by next-generation sequencing

Project description:MicroRNAs (miRs) have been recognized as promising biomarkers. It is unknown to what extent tumor-derived miRs are differentially expressed between primary colorectal cancers (pCRCs) and metastatic lesions, and to what extent the expression profiles of tumor tissue differ from the surrounding normal tissue. Next-generation sequencing (NGS) of 220 fresh-frozen samples, including paired primary and metastatic tumor tissue and non-tumorous tissue from 38 patients, revealed expression of 2245 known unique mature miRs and 515 novel candidate miRs. Unsupervised clustering of miR expression profiles of pCRC tissue with paired metastases did not separate the two entities, whereas unsupervised clustering of miR expression profiles of pCRC with normal colorectal mucosa demonstrated complete separation of the tumor samples from their paired normal mucosa. Two hundred and twenty-two miRs differentiated both pCRC and metastases from normal tissue samples (false discovery rate (FDR) o0.05). The highest expressed tumor-specific miRs were miR-21 and miR-92a, both previously described to be involved in CRC with potential as circulating biomarker for early detection. Only eight miRs, 0.5% of the analysed miR transcriptome, were differentially expressed between pCRC and the corresponding metastases (FDR o0.1), consisting of five known miRs (miR-320b, miR-320d, miR-3117, miR-1246 and miR-663b) and three novel candidate miRs (chr 1-2552-5p, chr 8-20656-5p and chr 10-25333-3p). These results indicate that previously unrecognized candidate miRs expressed in advanced CRC were identified using NGS. In addition, miR expression profiles of pCRC and metastatic lesions are highly comparable and may be of similar predictive value for prognosis or response to treatment in patients with advanced CRC

| EGAS00001001127 | EGA

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