LncRNA Dum interacts with Dnmts to regulate Dppa2 expression during myogenic differentiation and muscle regeneration

Wang, Lijun; Zhao, Yu; Bao, Xichen; Xihua, Zhu; Kwok, Yvonne Ka-yin; Sun, Kun; Chen, Xiaona; Huang, Yong-Heng; Jauch, Ralf; Esteban, Miguel A.; Sun, Hao; Wang, Huating

doi:10.1038/cr.2015.21

Cited by 230 publications

(194 citation statements)

References 40 publications

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“…As well as our findings, Sun et al have found that lncRNA HOXA11-AS stimulates cell proliferation and metastasis of GC via scaffolding the chromatin modification factors PRC2, LSD1 and DNMT1 [32]. Wang et al have found that lncRNA Dum inhibits Dppa2, its adjacent gene, in cis by recruiting DNMT1, DNMT3A and DNMT3B [33]. In accordance, we found that increased expression of Linc00441 could enhance the methylation rate in the promoter region of RB1, which could be reversed by DNMTs antagonist 5-aza-2'-deoxycytidine ( Figure 5D).…”

Section: Discussionsupporting

confidence: 89%

Linc00441 interacts with DNMT1 to regulate RB1 gene methylation and expression in gastric cancer

Zhou

Shi

et al. 2018

Oncotarget

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Section: Discussionsupporting

confidence: 89%

Linc00441 interacts with DNMT1 to regulate RB1 gene methylation and expression in gastric cancer

Zhou

Shi

et al. 2018

Oncotarget

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“…More reports clearly demonstrate that bona fide single-exonic lncRNAs are as functional as multi-exonic ones; therefore, the common practice of omitting single-exonic transcripts to simplify the identification pipeline may lead to an incomplete catalogue of lincRNAs. Despite the rapidly increasing number of lincRNAs functionally investigated so far, research of lincRNA in myogenesis is still at its infancy with a handful being characterized to date 11,[38][39][40] . Our study provides a comprehensive characterization of Linc-YY1 functionally and mechanistically.…”

Section: Discussionmentioning

confidence: 99%

Linc-YY1 promotes myogenic differentiation and muscle regeneration through an interaction with the transcription factor YY1

et al. 2015

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Little is known how lincRNAs are involved in skeletal myogenesis. Here we describe the discovery of Linc-YY1 from the promoter of the transcription factor (TF) Yin Yang 1 (YY1) gene. We demonstrate that Linc-YY1 is dynamically regulated during myogenesis in vitro and in vivo. Gain or loss of function of Linc-YY1 in C2C12 myoblasts or muscle satellite cells alters myogenic differentiation and in injured muscles has an impact on the course of regeneration. Linc-YY1 interacts with YY1 through its middle domain, to evict YY1/Polycomb repressive complex (PRC2) from target promoters, thus activating the gene expression in trans. In addition, Linc-YY1 also regulates PRC2-independent function of YY1. Finally, we identify a human Linc-YY1 orthologue with conserved function and show that many human and mouse TF genes are associated with lincRNAs that may modulate their activity. Altogether, we show that Linc-YY1 regulates skeletal myogenesis and uncover a previously unappreciated mechanism of gene regulation by lincRNA.

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“…For example, the lncRNA HOTAIR colocalises with polycomb repressive complex (PRC) 2 components and directs PRC2-mediated transcriptional silencing at the HOXD locus [44]. In fact, lncRNAs have been shown to interact with not only PRC2 but also ATP-dependent chromatin remodellers [45], H3K4 HMTs [46], and DNMTs [47,48].…”

Section: Non-coding Rnasmentioning

confidence: 99%

Resetting the epigenome for heart regeneration.

Quaife-Ryan

Sim

Porrello

et al. 2016

Seminars in Cell & Developmental Biology

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In contrast to adults, recent evidence suggests that neonatal mice are able to regenerate following cardiac injury. This regenerative capacity is reliant on robust induction of cardiomyocyte proliferation, which is required for faithful regeneration of the heart following injury. However, cardiac regenerative potential is lost as cardiomyocytes mature and permanently withdraw from the cell cycle shortly after birth. Recently, a handful of factors responsible for the regenerative disparity between the adult and neonatal heart have been identified, but the proliferative response of adult cardiomyoctes following modulation of these factors rarely reaches neonatal levels. The inefficient re-induction of proliferation in adult cardiomyocytes may be due to the epigenetic landscape, which drastically changes during cardiac development and maturation. In this review, we provide an overview of the role of epigenetic modifiers in developmental processes related to cardiac regeneration. We propose an epigentic framework for heart regeneration whereby adult cardiomyocyte identity requires resetting to a neonatal-like state to facilitate cell cycle re-entry and regeneration following cardiac injury.

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LncRNA Dum interacts with Dnmts to regulate Dppa2 expression during myogenic differentiation and muscle regeneration

Cited by 230 publications

References 40 publications

Linc00441 interacts with DNMT1 to regulate RB1 gene methylation and expression in gastric cancer

Linc00441 interacts with DNMT1 to regulate RB1 gene methylation and expression in gastric cancer

Linc-YY1 promotes myogenic differentiation and muscle regeneration through an interaction with the transcription factor YY1

Resetting the epigenome for heart regeneration.

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