Regulation of a TrkB Alternative Transcript by microRNAs

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Abstract

Background/Aims: Tropomyosin-related kinase B receptor (TrkB)-mediated signaling is vital for neuronal differentiation, survival, plasticity, and cognition. In this study, the focus was placed on TrkB-Shc, a neuron-specific transcript, to determine if microRNAs (miRNAs) play a role in TrkB-Shc regulation. Methods: A combination of bioinformatics and molecular gene expression analysis techniques was used to assess the effect of miR-409-3p and miR-216b on TrkB-Shc expression. Results: miR-409-3p and miR-216b were found to regulate the TrkB-Shc 3′UTR through the identified putative binding sites. When the effect of the miRNAs on TrkB was assessed using SHSY5Y neuronal cells, differential effects were observed between mRNA and protein expression. Conclusion: This study highlights the importance of miRNA-mediated regulation in TrkB signaling.

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Most cited references 24

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Comprehensive modeling of microRNA targets predicts functional non-conserved and non-canonical sites

Doron Betel, Anjali Koppal, Phaedra Agius … (2010)

mirSVR is a new machine learning method for ranking microRNA target sites by a down-regulation score. The algorithm trains a regression model on sequence and contextual features extracted from miRanda-predicted target sites. In a large-scale evaluation, miRanda-mirSVR is competitive with other target prediction methods in identifying target genes and predicting the extent of their downregulation at the mRNA or protein levels. Importantly, the method identifies a significant number of experimentally determined non-canonical and non-conserved sites.

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Control of translation and mRNA degradation by miRNAs and siRNAs.

Marco Valencia-Sanchez, Jidong Liu, Gregory Hannon … (2006)

The control of translation and mRNA degradation is an important part of the regulation of gene expression. It is now clear that small RNA molecules are common and effective modulators of gene expression in many eukaryotic cells. These small RNAs that control gene expression can be either endogenous or exogenous micro RNAs (miRNAs) and short interfering RNAs (siRNAs) and can affect mRNA degradation and translation, as well as chromatin structure, thereby having impacts on transcription rates. In this review, we discuss possible mechanisms by which miRNAs control translation and mRNA degradation. An emerging theme is that miRNAs, and siRNAs to some extent, target mRNAs to the general eukaryotic machinery for mRNA degradation and translation control.

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miR-24 Inhibits cell proliferation by targeting E2F2, MYC, and other cell-cycle genes via binding to "seedless" 3'UTR microRNA recognition elements.

Ashish Lal, Francisco Navarro, Christopher Maher … (2009)

miR-24, upregulated during terminal differentiation of multiple lineages, inhibits cell-cycle progression. Antagonizing miR-24 restores postmitotic cell proliferation and enhances fibroblast proliferation, whereas overexpressing miR-24 increases the G1 compartment. The 248 mRNAs downregulated upon miR-24 overexpression are highly enriched for DNA repair and cell-cycle regulatory genes that form a direct interaction network with prominent nodes at genes that enhance (MYC, E2F2, CCNB1, and CDC2) or inhibit (p27Kip1 and VHL) cell-cycle progression. miR-24 directly regulates MYC and E2F2 and some genes that they transactivate. Enhanced proliferation from antagonizing miR-24 is abrogated by knocking down E2F2, but not MYC, and cell proliferation, inhibited by miR-24 overexpression, is rescued by miR-24-insensitive E2F2. Therefore, E2F2 is a critical miR-24 target. The E2F2 3'UTR lacks a predicted miR-24 recognition element. In fact, miR-24 regulates expression of E2F2, MYC, AURKB, CCNA2, CDC2, CDK4, and FEN1 by recognizing seedless but highly complementary sequences.

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Author and article information

Journal

Journal ID (publisher-id): DEE

Journal ID (pmc): DEE

Journal ID (doi): 10.1159/issn.1664-5464

Title: Dementia and Geriatric Cognitive Disorders Extra

Publisher: S. Karger AG

ISSN (Electronic): 1664-5464

Publication date Subscription-year: 2014

Publication date Collection: September – December 2014

Publication date (Electronic): 11 September 2014

Volume: 4

Issue: 3

Pages: 364-374

Affiliations

Illawarra Health and Medical Research Institute and School of Biological Sciences, University of Wollongong, Wollongong, N.S.W., Australia

Author notes

*Dr. Jenny Wong, School of Biological Sciences, University of Wollongong, Northfields Avenue, Wollongong, NSW 2522 (Australia), E-Mail jennywong245@gmail.com

Article

Publisher ID: 365917 Pmcid ID: PMC4202609 Other ID: Dement Geriatr Cogn Disord Extra 2014;4:364-374

DOI: 10.1159/000365917

PMC ID: PMC4202609

PubMed ID: 25337079

SO-VID: 783e8f2d-7088-460a-9eaa-a911b4530ea5

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Open Access License: This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) ( http://www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

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Regulation of a TrkB Alternative Transcript by microRNAs

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Karger: Neurology and Neuroscience

Most cited references 24

Comprehensive modeling of microRNA targets predicts functional non-conserved and non-canonical sites

Control of translation and mRNA degradation by miRNAs and siRNAs.

miR-24 Inhibits cell proliferation by targeting E2F2, MYC, and other cell-cycle genes via binding to "seedless" 3'UTR microRNA recognition elements.

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