<i>Myogenin</i>
            promoter‐associated lnc
            <scp>RNA</scp>
            <i>Myoparr</i>
            is essential for myogenic differentiation

Hitachi, Keisuke; Nakatani, Masashi; Takasaki, Akihiko; Ouchi, Yuya; Uezumi, Akiyoshi; Ageta, Hiroshi; Inagaki, Hidehito; Kurahashi, Hiroki; Tsuchida, Kunihiro

doi:10.15252/embr.201847468

Cited by 52 publications

(79 citation statements)

References 62 publications

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“…They found that, in denervated muscles, Myoparr knockdown prevents atrophy by activating the bone morphogenetic protein signaling and by increasing the expression of GDF5, a muscle atrophy inhibitor. The existence of a Myoparr human counterpart makes the lncRNA potentially eligible as therapeutic target for neurogenic atrophy (Hitachi et al, 2019b).…”

Section: Nuclear-enriched Lncrnasmentioning

confidence: 99%

Non-coding RNAs Shaping Muscle

Martone

Mariani

Desideri

et al. 2020

Front. Cell Dev. Biol.

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In 1957, Francis Crick speculated that RNA, beyond its protein-coding capacity, could have its own function. Decade after decade, this theory was dramatically boosted by the discovery of new classes of non-coding RNAs (ncRNAs), including long ncRNAs (lncRNAs) and circular RNAs (circRNAs), which play a fundamental role in the fine spatio-temporal control of multiple layers of gene expression. Recently, many of these molecules have been identified in a plethora of different tissues, and they have emerged to be more cell-type specific than protein-coding genes. These findings shed light on how ncRNAs are involved in the precise tuning of gene regulatory mechanisms governing tissues homeostasis. In this review, we discuss the recent findings on the mechanisms used by lncRNAs and circRNAs to sustain skeletal and cardiac muscle formation, paying particular attention to the technological developments that, over the last few years, have aided their genome-wide identification and study. Together with lncRNAs and circRNAs, the emerging contribution of Piwi-interacting RNAs and transfer RNA-derived fragments to myogenesis will be also discussed, with a glimpse on the impact of their dysregulation in muscle disorders, such as myopathies, muscle atrophy, and rhabdomyosarcoma degeneration.

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Section: Nuclear-enriched Lncrnasmentioning

confidence: 99%

Non-coding RNAs Shaping Muscle

Martone

Mariani

Desideri

et al. 2020

Front. Cell Dev. Biol.

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“…We previously identified an lncRNA, Myoparr, from the promoter region of the myogenin gene, which codes for a transcriptional factor that is indispensable for skeletal muscle differentiation [34]. Myoparr interacts with a transcriptional co-activator, DEAD (Asp-Glu-Ala-Asp) box polypeptide 17 (Ddx17), and is essential both for the specification of myoblasts into the differentiation lineage and for the myoblast cell cycle withdrawal.…”

Section: Introductionmentioning

confidence: 99%

Expression Levels of Long Non-Coding RNAs Change in Models of Altered Muscle Activity and Muscle Mass

Hitachi

Nakatani

Funasaki

et al. 2020

IJMS

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Skeletal muscle is a highly plastic organ that is necessary for homeostasis and health of the human body. The size of skeletal muscle changes in response to intrinsic and extrinsic stimuli. Although protein-coding RNAs including myostatin, NF-κβ, and insulin-like growth factor-1 (IGF-1), have pivotal roles in determining the skeletal muscle mass, the role of long non-coding RNAs (lncRNAs) in the regulation of skeletal muscle mass remains to be elucidated. Here, we performed expression profiling of nine skeletal muscle differentiation-related lncRNAs (DRR, DUM1, linc-MD1, linc-YY1, LncMyod, Neat1, Myoparr, Malat1, and SRA) and three genomic imprinting-related lncRNAs (Gtl2, H19, and IG-DMR) in mouse skeletal muscle. The expression levels of these lncRNAs were examined by quantitative RT-PCR in six skeletal muscle atrophy models (denervation, casting, tail suspension, dexamethasone-administration, cancer cachexia, and fasting) and two skeletal muscle hypertrophy models (mechanical overload and deficiency of the myostatin gene). Cluster analyses of these lncRNA expression levels were successfully used to categorize the muscle atrophy models into two sub-groups. In addition, the expression of Gtl2, IG-DMR, and DUM1 was altered along with changes in the skeletal muscle size. The overview of the expression levels of lncRNAs in multiple muscle atrophy and hypertrophy models provides a novel insight into the role of lncRNAs in determining the skeletal muscle mass.

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“…But since the exogenous pncRNA-D suppressed the proliferation of HeLa cells, there is a possibility that it could also work in trans. Several lncRNAs have been reported to work both in cis and in trans (57,58), but generally, individual lncRNA regulate different genes in cis or in trans. However, there is lncRNA such as ANRIL, which is able to reduce expression of neighboring gene (CDKN2B) both in cis and in trans (59).…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA pncRNA-D reduces cyclin D1 gene expression and arrests cell cycle through RNA m6A modification

Yoneda

Ueda

Uranishi

et al. 2020

Journal of Biological Chemistry

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pncRNA-D is an irradiation-induced 602-nt long noncoding RNA transcribed from the promoter region of the cyclin D1 (CCND1) gene. CCND1 expression is predicted to be inhibited through an interplay between pncRNA-D and RNA-binding protein TLS/FUS. Because the pncRNA-D–TLS interaction is essential for pncRNA-D–stimulated CCND1 inhibition, here we studied the possible role of RNA modification in this interaction in HeLa cells. We found that osmotic stress induces pncRNA-D by recruiting RNA polymerase II to its promoter. pncRNA-D was highly m6A-methylated in control cells, but osmotic stress reduced the methylation and also arginine methylation of TLS in the nucleus. Knockdown of the m6A modification enzyme methyltransferase-like 3 (METTL3) prolonged the half-life of pncRNA-D, and among the known m6A recognition proteins, YTH domain-containing 1 (YTHDC1) was responsible for binding m6A of pncRNA-D. Knockdown of METTL3 or YTHDC1 also enhanced the interaction of pncRNA-D with TLS, and results from RNA pulldown assays implicated YTHDC1 in the inhibitory effect on the TLS–pncRNA-D interaction. CRISPR/Cas9-mediated deletion of candidate m6A site decreased the m6A level in pncRNA-D and altered its interaction with the RNA-binding proteins. Of note, a reduction in the m6A modification arrested the cell cycle at the G0/G1 phase, and pncRNA-D knockdown partially reversed this arrest. Moreover, pncRNA-D induction in HeLa cells significantly suppressed cell growth. Collectively, these findings suggest that m6A modification of the long noncoding RNA pncRNA-D plays a role in the regulation of CCND1 gene expression and cell cycle progression.

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Myogenin promoter‐associated lnc RNA Myoparr is essential for myogenic differentiation

Cited by 52 publications

References 62 publications

Non-coding RNAs Shaping Muscle

Non-coding RNAs Shaping Muscle

Expression Levels of Long Non-Coding RNAs Change in Models of Altered Muscle Activity and Muscle Mass

Long noncoding RNA pncRNA-D reduces cyclin D1 gene expression and arrests cell cycle through RNA m6A modification

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