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Effect of glucose availability on microRNA expression and Ago2 occupancy.

ABSTRACT: For cells to grow and proliferate both a growth signal and available nutrients are required. Several lines of evidence suggest that there is recriprocal regulation of nutrients by growth signals and growth signals by nutrients. Since microRNAs are regulated by growth signals, we sought to determine if microRNAs could also be regulated by nutrient availability. We found that several microRNAs change expression following glucose starvation and that their Ago2 occupancy remains constant.

ORGANISM(S): Mus musculus

PROVIDER: GSE41921 | GEO | 2012/12/17

SECONDARY ACCESSION(S): PRJNA178569

REPOSITORIES: GEO

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Effect of glucose availability on microRNA expression and Ago2 occupancy.

Project description:For cells to grow and proliferate both a growth signal and available nutrients are required. Several lines of evidence suggest that there is recriprocal regulation of nutrients by growth signals and growth signals by nutrients. Since microRNAs are regulated by growth signals, we sought to determine if microRNAs could also be regulated by nutrient availability. We found that several microRNAs change expression following glucose starvation and that their Ago2 occupancy remains constant. Immortalized Bax/Bak double-knockout mouse embryonic fibroblasts were deprived of glucose for 5 days and then re-fed glucose for 2 days. Cells were collected at the beginning of the starvation period (d0), following five days of glucose deprivation (d5), and following two days of glucose re-feed (d7). Total RNA was isolated from half of the collected cells using Trizol and the remaining cells were used to perform Ago2 immunoprecipitation followed by isolation of bound RNA.

2012-12-17 | E-GEOD-41921 | biostudies-arrayexpress

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Project description:Ago2 binds mature microRNAs (miRNAs) to regulate gene expression. A mutant Ago2 is constructed to render it unable to bind miRNAs and inhibit mRNA translation.

2013-03-01 | GSE37941 | GEO

microRNA binding by wildtype Ago2 and mutant Ago2 in human cells

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Ago2-CLASH reveals a wide repertoire of small RNA mediated regulation [RNA-Seq]

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Precipitation of mRNAs by Ago2 and phosphorylation mutants

Project description:Argonaute (Ago) proteins associate with microRNAs (miRNAs), which guide them to complementary target mRNAs resulting in gene silencing. RNA coimmunoprecipitations (RIP) were performed with Ago2 and Ago2 mutants. The precipitated mRNAs were analyzed using one Affymetrix microarrays to compare the mRNA preciptation rates of mutants vs Ago2 wild type.

2017-06-22 | GSE92698 | GEO

miRNA* loading on Ago2

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mRNAs associated with Ago2: Ago2, Ago2+miR-1, Ago2+miR-124, mock transfected

Project description:As a core RISC component, Ago2 associates with miRNAs and target mRNAs. To identify these mRNAs, we ran lysate from HEK293T cells over a FLAG resin from 2 conditions: +FLAG-Ago2, +mock transfection. To identify mRNAs associated with specific miRNAs, we ran lysate from HEK293T cells over a FLAG resin from 2 conditions: +FLAG-Ago2 & miR-1, and +FLAG-Ago2 & miR-124. Set of arrays that are part of repeated experiments Compound Based Treatment: mock transfected Keywords: Biological Replicate

2008-04-08 | GSE11079 | GEO

miRNA* loading on Ago2

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Ago2 protects against diabetic cardiomyopathy via activating mitochondrial gene translation II

Project description:Diabetes is associated with cardiovascular complications. microRNAs translocate into subcellular organelles to modify genes involved in diabetic cardiomyopathy. However, functional properties of subcellular Ago2, a core microRNA, remain elusive. We elucidated the function and mechanism of subcellular localized Ago2 on mouse models for diabetes mellitus and diabetic cardiomyopathy. Ago2 decreased in cardiomyocyte mitochondria in both models. Overexpression of mitochondrial Ago2 attenuated diabetes-induced cardiac dysfunction. Ago2 recruited TUFM, a mitochondria translation elongation factor, to activate translation of electron transport chain (ETC) subunits and decrease reactive oxygen species. Malonylation, a post-translational modification of Ago2, reduced the importing of Ago2 into mitochondria in diabetic cardiomyopathy. Ago2 malonylation was regulated by a cytoplasmic-localized short isoform of SIRT3 through a previously unknown demalonylase function. Our results reveal that the SIRT3–Ago2–CYTB axis links glucotoxicity to cardiac ETC imbalance, providing new mechanistic insights and the basis to develop mitochondria targeting therapies for diabetic cardiomyopathy.

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