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      • Record: found
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      Long noncoding RNA TUG1 facilitates osteogenic differentiation of periodontal ligament stem cells via interacting with Lin28A

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          Abstract

          Periodontal ligament stem cells (PDLSCs) are mesenchymal stem cells derived from dental tissues with multidirectional differentiation potential and excellent self-renewing ability. Recently, long noncoding RNAs (lncRNAs) have been shown to play important roles in MSC osteogenic differentiation. In this study, we found that taurine upregulated gene 1 (TUG1), an evolutionarily conserved and widely present lncRNA was significantly upregulated in osteogenically induced PDLSCs compared to their undifferentiated counterparts. Further investigation demonstrated that the expression of TUG1 was positively correlated with the osteogenic differentiation of PDLSCs following the induction, as evidenced by the increase in cellular alkaline phosphatase (ALP) level, formation of calcium nodules, and the upregulation of several osteogenic-related gene markers such as ALP, osteocalcin (OCN), and runt-related transcription factor 2 (Runx2). Conversely, TUG1 knockdown was demonstrated to inhibit the potential of PDLSCs for osteogenic differentiation. Using bioinformatics analysis, we identified lin-28 homolog A (Lin28A) as a potential target of TUG1 during osteogenic differentiation of PDLSCs. Lin28A was found to be significantly downregulated in TUG1-repressed PDLSCs and contained multiple binding sites for lncRNA TUG1. Moreover, suppression of Lin28A was shown to be able to inhibit osteogenic differentiation and decreased the expression of several osteogenic genes. Taken together, these results could help researchers better understand the mechanism that governs the osteogenic differentiation of PDLSCs, and also serve as a stepping stone for the development of novel therapeutic strategies that can be used to regenerate dental tissues.

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          Selective blockade of microRNA processing by Lin28.

          S. Viswanathan, G Daley, R. I. Gregory (2008)
          MicroRNAs (miRNAs) play critical roles in development, and dysregulation of miRNA expression has been observed in human malignancies. Recent evidence suggests that the processing of several primary miRNA transcripts (pri-miRNAs) is blocked posttranscriptionally in embryonic stem cells, embryonal carcinoma cells, and primary tumors. Here we show that Lin28, a developmentally regulated RNA binding protein, selectively blocks the processing of pri-let-7 miRNAs in embryonic cells. Using in vitro and in vivo studies, we found that Lin28 is necessary and sufficient for blocking Microprocessor-mediated cleavage of pri-let-7 miRNAs. Our results identify Lin28 as a negative regulator of miRNA biogenesis and suggest that Lin28 may play a central role in blocking miRNA-mediated differentiation in stem cells and in certain cancers.
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            Functionality or transcriptional noise? Evidence for selection within long noncoding RNAs.

            Jasmina Ponjavic, Chris P. Ponting, Gerton Lunter (2007)
            Long transcripts that do not encode protein have only rarely been the subject of experimental scrutiny. Presumably, this is owing to the current lack of evidence of their functionality, thereby leaving an impression that, instead, they represent "transcriptional noise." Here, we describe an analysis of 3122 long and full-length, noncoding RNAs ("macroRNAs") from the mouse, and compare their sequences and their promoters with orthologous sequence from human and from rat. We considered three independent signatures of purifying selection related to substitutions, sequence insertions and deletions, and splicing. We find that the evolution of the set of noncoding RNAs is not consistent with neutralist explanations. Rather, our results indicate that purifying selection has acted on the macroRNAs' promoters, primary sequence, and consensus splice site motifs. Promoters have experienced the greatest elimination of nucleotide substitutions, insertions, and deletions. The proportion of conserved sequence (4.1%-5.5%) in these macroRNAs is comparable to the density of exons within protein-coding transcripts (5.2%). These macroRNAs, taken together, thus possess the imprint of purifying selection, thereby indicating their functionality. Our findings should now provide an incentive for the experimental investigation of these macroRNAs' functions.
            Article 0 comments Cited 283 times – based on 0 reviews     Review now
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              A quantitative analysis of CLIP methods for identifying binding sites of RNA-binding proteins.

              Shivendra Kishore, Lukasz Jaskiewicz, Lukas Burger … (2011)
              Cross-linking and immunoprecipitation (CLIP) is increasingly used to map transcriptome-wide binding sites of RNA-binding proteins. We developed a method for CLIP data analysis, and applied it to compare CLIP with photoactivatable ribonucleoside-enhanced CLIP (PAR-CLIP) and to uncover how differences in cross-linking and ribonuclease digestion affect the identified sites. We found only small differences in accuracies of these methods in identifying binding sites of HuR, which binds low-complexity sequences, and Argonaute 2, which has a complex binding specificity. We found that cross-link-induced mutations led to single-nucleotide resolution for both PAR-CLIP and CLIP. Our results confirm the expectation from original CLIP publications that RNA-binding proteins do not protect their binding sites sufficiently under the denaturing conditions used during the CLIP procedure, and we show that extensive digestion with sequence-specific RNases strongly biases the recovered binding sites. This bias can be substantially reduced by milder nuclease digestion conditions.
              Article 0 comments Cited 221 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Chunling Wang: +86 531 8838 2069 , wangchl@sdu.edu.cn
                Fulan Wei:
                ORCID: http://orcid.org/0000-0001-6827-8293
                +86 531 88382069 , weifl@sdu.edu.cn
                Journal
                Journal ID (nlm-ta): Cell Death Dis
                Journal ID (iso-abbrev): Cell Death Dis
                Title: Cell Death & Disease
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2041-4889
                Publication date (Electronic): 19 April 2018
                Publication date PMC-release: 19 April 2018
                Publication date Collection: May 2018
                Volume: 9
                Issue: 5
                Electronic Location Identifier: 455
                Affiliations
                [1 ]ISNI 0000 0004 1761 1174, GRID grid.27255.37, Department of Orthodontics, School of Stomatology, , Shandong University, ; Jinan, People’s Republic of China
                [2 ]ISNI 0000 0004 1761 1174, GRID grid.27255.37, Shandong Provincial Key Laboratory of Oral Tissue Regeneration, School of Stomatology, , Shandong University, ; Jinan, People’s Republic of China
                Author information
                http://orcid.org/0000-0003-0082-650X
                http://orcid.org/0000-0001-6827-8293
                Article
                Publisher ID: 484
                DOI: 10.1038/s41419-018-0484-2
                PMC ID: 5908786
                PubMed ID: 29674645
                SO-VID: f7b1e59f-dec5-4f93-a6a6-c17a6d3db3fd
                Copyright © © The Author(s) 2018
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 21 November 2017
                Date revision received : 25 January 2018
                Date accepted : 14 March 2018
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Cell biology
                Data availability:
                ScienceOpen disciplines: Cell biology

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