Imprinted maternally-expressed microRNAs in induced neurons
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ABSTRACT:
PROVIDER: PRJNA591126 | ENA |
REPOSITORIES: ENA
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Project description:Imprinted genes with parental-biased allelic expression are enriched in pathways regulating energy homeostasis. Here, we functionally characterize a large cluster of maternally-expressed microRNAs (miRNAs) to explore the molecular and cellular consequences of imprinted miRNA activity in neurons. Using an induced neuron (iN) culture system, we show maternally-expressed miRNAs from the miR-379/410 cluster direct the RNA induced silencing complex (RISC) to transcriptional and developmental regulators, including paternally-expressed transcripts. Maternal deletion of this imprinted miRNA cluster results in increased protein levels of several targets and up-regulation of a broader gene program regulating synaptic transmission and neuronal function. A subset of these transcriptional changes can be attributed to de-repression of Plagl1, a paternally-expressed transcriptional activator that regulates Igf2, a major factor in energy homeostasis. These data suggest non-coding RNAs actively engage as maternally-expressed miRNAs antagonize paternally-driven gene programs in neurons.
2019-11-23 | GSE140838 | GEO
Project description:Maternally expressed imprinted lncRNA and snoRNA are expressed in osteosarcoma and Ewing sarcoma
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Project description:Maternally expressed imprinted gene SDC modulates circadian period and hypocotyl length
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Project description: Not available
| S-EPMC7176019 | biostudies-literature
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.
2017-02-04 | GSE77710 | GEO
Project description:Adenylation of maternally inherited microRNAs by Wispy
| PRJNA262696 | ENA
Project description: Not available
| S-EPMC2582151 | biostudies-literature
Project description:Some flowering plant and vertebrate genes are expressed primarily or exclusively from either the maternal or paternal allele, a phenomenon called genomic imprinting. Flowering plant imprinted gene expression has been described primarily in endosperm, a terminal nutritive tissue consumed by the embryo during seed development or after germination. Imprinted expression in Arabidopsis thaliana endosperm is orchestrated by differences in cytosine DNA methylation between the paternal and maternal genomes, as well as by Polycomb group (PcG) proteins. Currently only eleven imprinted Arabidopsis genes are known. Here we use extensive sequencing of cDNA libraries to identify many new paternally and maternally imprinted genes in A. thaliana endosperm, including transcription factors, proteins involved in hormone signaling, and epigenetic regulators. The imprinted status of many maternally-expressed genes is not altered by mutations in the DNA-demethylating glycosylase DEMETER, the DNA methyltransferase MET1 or the core PcG protein FIE, indicating that these genes are regulated by novel mechanisms or deposited from maternal tissues. We did not find any imprinted genes in the embryo. Our results demonstrate that imprinted gene expression, particularly from the maternal genome, is an extensive, mechanistically complex phenomenon that likely affects multiple aspects of seed development. Epigenetics Examination of genomic imprinting in Arabidopsis endosperm
2011-03-10 | E-GEOD-24644 | biostudies-arrayexpress
Project description:Early development depends heavily on accurate control of maternally inherited mRNAs, and yet it remains unknown how maternal microRNAs (miRNAs) are regulated during maternal to zygotic transition (MZT). We here find that maternal miRNAs are highly adenylated at their 3' ends in mature oocytes and early embryos. Pervasive adenylation is observed in oocytes of fly, sea urchin and mouse, indicating that maternal miRNA adenylation may be widely conserved in animals. We identify Wispy as the enzyme responsible for miRNA adenylation in flies. Wispy is known to be expressed specifically in oocytes and early embryos and function as a noncanonical poly(A) polymerase. Knockout of wispy abrogates miRNA adenylation and induces miRNA accumulation in fly eggs whereas overexpression of Wispy increases adenylation and reduces miRNA levels in S2 cells. Adenylation occurs on both the 5p and 3p miRNAs, indicating that Wispy acts on miRNAs after Dicer processing. We further find that Wispy interacts with Ago1 through protein-protein interaction, which may allow the effective and selective adenylation of miRNAs. Thus, adenylation may contribute to the clearance of maternally deposited miRNAs during MZT. Our work provides the first mechanistic insights into the regulation of maternal miRNAs and illustrates the importance of RNA tailing in development. MiRNA expression and modification profile during early embryo development of fruit fly and zebra fish using high throughput sequencing
2014-10-01 | E-GEOD-61931 | biostudies-arrayexpress
Project description:The dysregulation of genes in neurodevelopmental disorders that lead to social and cognitive phenotypes is a complex, multilayered process involving both genetics and epigenetics. Parent-of-origin effects of deletion and duplication of the 15q11-q13 locus leading to Angelman, Prader-Willi, and Dup15q syndromes are due to imprinted genes, including UBE3A, which is maternally expressed exclusively in neurons. UBE3A encodes a ubiquitin E3 ligase protein with multiple downstream targets, including RING1B, which in turn monoubiquitinates histone variant H2A.Z. To understand the impact of neuronal UBE3A levels on epigenome-wide marks of DNA methylation, histone variant H2A.Z positioning, active H3K4me3 promoter marks, and gene expression, we took a multi-layered genomics approach. We performed an siRNA knockdown of UBE3A in two human neuroblastoma cell lines, including parental SH-SY5Y and the SH(15M) model of Dup15q. Genes differentially methylated across cells with differing UBE3A levels were enriched for functions in gene regulation, DNA binding, and brain morphology. Importantly, we found that altering UBE3A levels had a profound epigenetic effect on the methylation levels of up to half of known imprinted genes. Genes with differential H2A.Z peaks in SH(15M) compared to SH-SY5Y were enriched for ubiquitin and protease functions and associated with autism, hypoactivity, and energy expenditure. Together, these results support a genome-wide epigenetic consequence of altered UBE3A levels in neurons and suggest that UBE3A regulates an imprinted gene network involving DNA methylation patterning and H2A.Z deposition.
2017-09-26 | GSE103309 | GEO