MicroRNAs Establish Robustness and Adaptability of a Critical Gene Network to Regulate Progenitor Fate Decisions during Cortical Neurogenesis

Ghosh, Tanay; Aprea, Julieta; Nardelli, Jeannette; Engel, Hannes; Selinger, Christian; Mombereau, Cédric; Lemonnier, Thomas; Moutkine, Imane; Schwendimann, Leslie; Dori, Martina; Irinopoulou, Théano; Henrion‐Caude, Alexandra; Benecke, Arndt; Arnold, Sebastian J.; Gressèns, Pierre; Calegari, Federico; Groszer, Matthias

doi:10.1016/j.celrep.2014.05.029

Cited by 49 publications

(45 citation statements)

References 37 publications

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“…We refer the reader to excellent recent reviews for a detailed discussion of miRNA function in adult neurogenesis (Luikart et al, 2012;Schouten et al, 2012) and focus our discussion here on embryonic neurogenesis -a period during which many miRNAs are enriched. Indeed, the global monitoring of miRNA expression during neurogenesis in vivo has identified timespecific (Barca-Mayo and De Pietri Tonelli, 2014;Lv et al, 2014;Miska et al, 2004;Nielsen et al, 2009;Yao et al, 2012), spatially restricted (ventral midline/midbrain dopaminergic progenitor pool) (Anderegg et al, 2013) or cell type-specific (Paridaen and Huttner, 2014;Ghosh et al, 2014) miRNAs, suggesting that different sets of miRNAs might be involved in neuronal versus glial differentiation. This is supported by the finding that 116 miRNAs (out of 351) are differentially expressed in primary cultures enriched for neurons, astrocytes, oligodendrocytes and microglia (Jovicic et al, 2013).…”

Section: Cell Fate Determinationmentioning

confidence: 99%

“…Similar to the miR-9/TLX interaction ), TLX and miR-137 constitute a negative-feedback loop. Additional miRNAs such as miR-20a/20b and miR-23 also negatively regulate cyclin D1 levels via direct 3′UTR interaction (Ghosh et al, 2014), and increased cyclin D1 activity leads to elevated miR-23 and decreased miR-20a/b expression levels; importantly, the inhibition of each of these miRNAs interferes with proper neuronal differentiation (Ghosh et al, 2014). Finally, it has been shown that another miRNA, miR-15b, inhibits cyclin D1 expression by regulating the methylation status of the cyclin D1 promoter via suppression of Tet methylcytosine dioxygenase 3 (TET3) mRNA translation (Lv et al, 2014).…”

Section: Neurogenesismentioning

confidence: 99%

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MicroRNAs in neural development: from master regulators to fine-tuners

2017

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The proper formation and function of neuronal networks is required for cognition and behavior. Indeed, pathophysiological states that disrupt neuronal networks can lead to neurodevelopmental disorders such as autism, schizophrenia or intellectual disability. It is wellestablished that transcriptional programs play major roles in neural circuit development. However, in recent years, post-transcriptional control of gene expression has emerged as an additional, and probably equally important, regulatory layer. In particular, it has been shown that microRNAs (miRNAs), an abundant class of small regulatory RNAs, can regulate neuronal circuit development, maturation and function by controlling, for example, local mRNA translation. It is also becoming clear that miRNAs are frequently dysregulated in neurodevelopmental disorders, suggesting a role for miRNAs in the etiology and/or maintenance of neurological disease states. Here, we provide an overview of the most prominent regulatory miRNAs that control neural development, highlighting how they act as 'master regulators' or 'fine-tuners' of gene expression, depending on context, to influence processes such as cell fate determination, cell migration, neuronal polarization and synapse formation.

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Section: Cell Fate Determinationmentioning

confidence: 99%

Section: Neurogenesismentioning

confidence: 99%

MicroRNAs in neural development: from master regulators to fine-tuners

2017

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“…[3][4][5] A polycistronic miRNA cluster, miR-17~92, consisting of six mature miRNAs (miR-17, miR-18a, mIR-19a, miR-20a, miR-19-b1, and miR-92a-1), has been reported to play a fundamental role in development and remodeling. [6][7][8][9] Furthermore, members of miR-17-92 cluster are found to be commonly down-regulated in aging human cells. 10 We have found that ectopic expression of miR-17 retards tissue growth 11 and inhibits cell senescence.…”

mentioning

confidence: 99%

Reciprocal regulation of miRNAs and piRNAs in embryonic development

Yang

Xuan

et al. 2016

Cell Death Differ

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MicroRNAs (miRNAs) and piwi-interacting RNAs (piRNAs) are two classes of small noncoding RNAs, both of which play roles in regulating tissue development. It is unknown whether these distinct classes of noncoding RNAs can regulate one another. Here we show that ectopic expression of miR-17 inhibited mouse fertility and early embryonic development. Specifically, we found that the piRNA amplification loop was repressed by miR-17-5p, leading to increased levels of transposition mutagenesis. This occurred by suppressing the amplification loop of piRNAs with an identical 5′ sequence and by targeting Mili/Miwi2, an essential component of the piRNA amplification loop, and the DNA methyltransferase, Dnmt3a. We also found that increased levels of piRNAs could compete with miRNAs for target binding, resulting in increased expression of Dnmt3a and Mili. Increased Dnmt3a levels could in turn block miR-17-5p expression, while increased Mili expression could accelerate piRNA amplification and inhibit transposon generation, favoring embryonic development. We report for the first time the reciprocal regulation between miRNAs and piRNAs in mouse embryonic development. Cell Death and Differentiation (2016) 23, 1458-1470 doi:10.1038/cdd.2016; published online 18 March 2016A microRNA (miRNA) is a small non-coding RNA molecule of 18-24 nucleotides in length that are post-transcriptional regulators of gene expression. A miRNA has the capacity to affect the stability of hundreds of unique mRNAs 1 and may repress synthesis of hundreds of proteins by base-pairing with the targeting mRNAs. 2 The discovery of miRNAs in gene regulation has improved our understanding of posttranscriptional control of tissue development and aging. 3-5 A polycistronic miRNA cluster, miR-17~92, consisting of six mature miRNAs , and miR-92a-1), has been reported to play a fundamental role in development and remodeling. [6][7][8][9] Furthermore, members of miR-17-92 cluster are found to be commonly down-regulated in aging human cells. 10 We have found that ectopic expression of miR-17 retards tissue growth 11 and inhibits cell senescence. 12 Piwi-interacting RNA (piRNA) is the largest class of small non-coding RNAs expressed by animal cells. 13 piRNAs form complexes with piwi proteins, which function posttranscriptionally in silencing retrotransposons and other genetic elements in germ-line cells. 14 piRNA activity in gene regulation may lead to silencing of transposon expression, 15 as most piRNA sequences are antisense to transposon sequences. 16 The activity of piRNAs in transposon silencing appears to be the most important event during embryonic development. 17 To facilitate silencing transposons in the testes of mammals or in the germ cells of invertebrates, the piwi proteins play essential roles in interacting with piRNAs.These piwi proteins are members of Argonautes, proteins that are needed for gene silencing in miRNA action, including MIWI, MIWI2 and MILI. The sequences of piRNAs guide the piwi proteins to their transposon targets. 17 Decreased expressio...

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“…miRNAs negatively regulate gene expression by inhibiting protein translation or by causing mRNA degradation through partial or complete base-pairing with the 3' untranslated region (3'UTR) of the target mRNA. Dysregulation of miRNA expression has been reported in various human cancers (5,7). Therefore, exploring the mechanisms underlying the carcinogenic effects of these aberrant tumor miRNAs is critical for cancer diagnosis and therapy.…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies have revealed that microRNAs (miRNAs) regulate numerous cellular processes, including those associated with cancer (5). miRNAs are a class of small non-coding RNAs that range from 22-25 nucleotides in length (6).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-433 regulates apoptosis by targeting PDCD4 in human osteosarcoma cells

Sun

Wang

et al. 2017

Oncology Letters

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Abstract. Osteosarcoma is the most common aggressive sarcoma of the bone in children and adolescents. It is characterized by a high level of genetic instability and recurrent DNA deletions and amplifications. microRNAs (miRNAs) play a key role in cancer initiation, progression and metastasis; however, the potential role of miRNAs in osteosarcoma remains largely unknown. In the present study, miR-433 was shown to be overexpressed in osteosarcoma tissues compared with normal human osteoblasts. Transfection of miR-433 mimics into osteosarcoma cell lines significantly decreased apoptosis by targeting programmed cell death 4, a tumor suppressor that is involved in apoptosis. In contrast, inhibition of miR-433 enhanced apoptosis. Furthermore, in vivo miR-433 overexpression inhibited the apoptosis of tumor cells and increased tumor growth. The results of the present study suggested that miR-433 is a potential molecular target for osteosarcoma therapy.

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MicroRNAs Establish Robustness and Adaptability of a Critical Gene Network to Regulate Progenitor Fate Decisions during Cortical Neurogenesis

Cited by 49 publications

References 37 publications

MicroRNAs in neural development: from master regulators to fine-tuners

MicroRNAs in neural development: from master regulators to fine-tuners

Reciprocal regulation of miRNAs and piRNAs in embryonic development

MicroRNA-433 regulates apoptosis by targeting PDCD4 in human osteosarcoma cells

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