Feedback control by the human microRNA, let-7, regulates expression of the RNA sielncing enzyme, Dicer
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PROVIDER: PRJNA92605 | ENA |
REPOSITORIES: ENA
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Project description:let-7 regulates Dicer and HMGA2 expression and decrease the steady state levels of these genes Keywords: miRNA inhibition and overexpression
2009-06-30 | GSE2918 | GEO
Project description:Epigenetic mechanisms can be influenced by environmental cues and thus evoke phenotypic variation. This plasticity can be advantageous for adaption, but also detrimental if not under tight control. Although having attracted considerable interest, it remains largely unknown if and how environmental cues such as temperature trigger epigenetic alterations. Using fission yeast, we demonstrate that environmentally induced discontinuous phenotypic variation is buffered by a negative feedback loop that involves the RNase Dicer and the protein disaggregase Hsp104. In the absence of Hsp104, Dicer accumulates in cytoplasmic inclusions and heterochromatin becomes unstable at elevated temperatures, an epigenetic state that is inherited for many generations after the heat stress. Dicer instead averts the toxic aggregation of a prionogenic protein. Our results highlight the importance of feedback regulation in building epigenetic memory and uncover Hsp104 and Dicer as homeostatic controllers that buffer environmentally induced stochastic epigenetic variation and toxic aggregation of prionogenic proteins. Various strains grown at 30°C or 37°C
2015-04-23 | E-GEOD-60638 | biostudies-arrayexpress
Project description:Epigenetic mechanisms can be influenced by environmental cues and thus evoke phenotypic variation. This plasticity can be advantageous for adaption, but also detrimental if not under tight control. Although having attracted considerable interest, it remains largely unknown if and how environmental cues such as temperature trigger epigenetic alterations. Using fission yeast, we demonstrate that environmentally induced discontinuous phenotypic variation is buffered by a negative feedback loop that involves the RNase Dicer and the protein disaggregase Hsp104. In the absence of Hsp104, Dicer accumulates in cytoplasmic inclusions and heterochromatin becomes unstable at elevated temperatures, an epigenetic state that is inherited for many generations after the heat stress. Dicer instead averts the toxic aggregation of a prionogenic protein. Our results highlight the importance of feedback regulation in building epigenetic memory and uncover Hsp104 and Dicer as homeostatic controllers that buffer environmentally induced stochastic epigenetic variation and toxic aggregation of prionogenic proteins. wt_spb75 grown at 30°C or 37°C
2015-04-23 | E-GEOD-60429 | biostudies-arrayexpress
Project description:Epigenetic mechanisms can be influenced by environmental cues and thus evoke phenotypic variation. This plasticity can be advantageous for adaption, but also detrimental if not under tight control. Although having attracted considerable interest, it remains largely unknown if and how environmental cues such as temperature trigger epigenetic alterations. Using fission yeast, we demonstrate that environmentally induced discontinuous phenotypic variation is buffered by a negative feedback loop that involves the RNase Dicer and the protein disaggregase Hsp104. In the absence of Hsp104, Dicer accumulates in cytoplasmic inclusions and heterochromatin becomes unstable at elevated temperatures, an epigenetic state that is inherited for many generations after the heat stress. Dicer instead averts the toxic aggregation of a prionogenic protein. Our results highlight the importance of feedback regulation in building epigenetic memory and uncover Hsp104 and Dicer as homeostatic controllers that buffer environmentally induced stochastic epigenetic variation and toxic aggregation of prionogenic proteins.
2015-04-23 | GSE60429 | GEO
Project description:Epigenetic mechanisms can be influenced by environmental cues and thus evoke phenotypic variation. This plasticity can be advantageous for adaption, but also detrimental if not under tight control. Although having attracted considerable interest, it remains largely unknown if and how environmental cues such as temperature trigger epigenetic alterations. Using fission yeast, we demonstrate that environmentally induced discontinuous phenotypic variation is buffered by a negative feedback loop that involves the RNase Dicer and the protein disaggregase Hsp104. In the absence of Hsp104, Dicer accumulates in cytoplasmic inclusions and heterochromatin becomes unstable at elevated temperatures, an epigenetic state that is inherited for many generations after the heat stress. Dicer instead averts the toxic aggregation of a prionogenic protein. Our results highlight the importance of feedback regulation in building epigenetic memory and uncover Hsp104 and Dicer as homeostatic controllers that buffer environmentally induced stochastic epigenetic variation and toxic aggregation of prionogenic proteins.
2015-04-23 | GSE60638 | GEO
Project description:As the biogenesis of miRNAs depends on the cleavage by the RNase III enzyme Dicer, miR-18a may change the miRNA expression profiles by targeting dicer. We then performed the miRNA array assay to investigate the miRNA profiles change caused by miR-18a.
2012-03-01 | GSE32680 | GEO
Project description:DICER is an RNase III enzyme which plays a critical role in the microRNA mature process in the cytoplasm, but also is involved in other functions such as chromatin remodeling, epigenetic modification and DNA damage repair in the nucleus. The expression of DICER is almost decreased across the board in human cancers, which highlights that its expression is strictly controlled, however the underlying mechanisms still remain unknown. In this study, we find that deubiquitinase USP7 suppresses the expression of DICER at the protein level, which impacts DNA damage response (DDR) and cancer progression. MDM2, which is a well-known oncoprotein and also a substrate of USP7, is identified as a novel DICER ubiquitin E3 ligase, thus forming a new regulatory axis of USP7-MDM2-DICER. These findings may provide a new approach to the diagnosis, treatment and prognosis of malignant tumors.
2024-01-10 | GSE225307 | GEO
Project description:As the biogenesis of miRNAs depends on the cleavage by the RNase III enzyme Dicer, miR-18a may change the miRNA expression profiles by targeting dicer. We then performed the miRNA array assay to investigate the miRNA profiles change caused by miR-18a. Total RNA obtained from two pairs,one is the miR-18a overexpression cell line compared to the miRNAs (control), the other is the over-expression miR-18a cell line transfected Dicer plasmid.
2012-03-01 | E-GEOD-32680 | biostudies-arrayexpress
Project description:Dicer, also known as endoribonuclease Dicer or helicase with RNase motif, cleaves double-stranded RNA (dsRNA) and pre-microRNA (pre-miRNA) into short mature double-stranded RNA fragments called small interfering RNA and microRNA, respectively. MicroRNAs are potent post-transcriptional regulators in developmental switches, lineage commitment and gene expression regulation. To evaluate their post-transcriptional role in gene expression of Medullary thymic epithelial cells (mTECS) we knocked down Dicer transcript by means of siRNA transfection in a Mus musculus mTEC cell line (3.10 mTEC). The Agilent oligo microarrays were used to determine the large scale microRNA (miRNA) transcriptional profiles of control or Dicer-knockdown 3.10 mTECs.
2016-06-27 | E-MTAB-4627 | biostudies-arrayexpress
Project description:Tumor-associated macrophages (TAMs) have immunosuppressive capacity in mouse models of cancer. Here we show that the genetic deletion of the microRNA (miRNA)-processing enzyme DICER in TAMs broadly programs them to a CD11c+MRC1−/low M1-like immunostimulatory phenotype characterized by activated interferon-γ (IFN-γ)/STAT1/IRF signaling. M1-like TAM programming fostered the recruitment of cytotoxic T-cells (CTLs), including tumor-antigen-specific CTLs, inhibited tumor growth, and enhanced the efficacy of PD1 checkpoint blockade. Bioinformatics analysis of TAM transcriptomes identified a limited set of miRNAs putatively involved in TAM programming. Re-expression of Let-7 in Dicer-deficient TAMs was sufficient to partly rescue the M2-like (protumoral) TAM phenotype and abate tumor CTL infiltration. Targeted suppression of DICER activity in TAMs may, therefore, stimulate antitumor immunity and enhance the efficacy of cancer immunotherapy.
2016-06-13 | GSE76356 | GEO