Architectural RNAs for Membraneless Nuclear Body Formation

Yamazaki, Tomohiro; Nakagawa, Shinichi; Hirose, Tetsuro

doi:10.1101/sqb.2019.84.039404

Cited by 51 publications

(50 citation statements)

References 87 publications

(146 reference statements)

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“…NEAT1L increases expression of anti-inflammatory and growth factors including peroxisome proliferator activated receptor-γ (PPARG), Nuclear Factor Kappa B Subunit 1 (NFκB1), and brain-derived neurotrophic factor (BDNF), which are also targets of MeCP2-mediated repression ( Martinowich et al, 2003 ; Mann et al, 2010 ; Kishi et al, 2016 ). The short (3,735 nt, Neat1S ) and long (22,741 nt, Neat1L ) NEAT1 transcripts are ubiquitously expressed in mammalian cells, and the long isoform is required for the formation of massive ribonucleoprotein paraspeckles, which are heavily implicated in transcriptional regulation ( Yamazaki et al, 2020 ). Neat1 , Malat1 , and Evf2 are upregulated upon neuronal differentiation, similar to MeCP2 ( Olson et al, 2014 ; Roberts et al, 2014 ).…”

Section: Subsectionsmentioning

confidence: 99%

MeCP2: The Genetic Driver of Rett Syndrome Epigenetics

2021

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Mutations in methyl CpG binding protein 2 (MeCP2) are the major cause of Rett syndrome (RTT), a rare neurodevelopmental disorder with a notable period of developmental regression following apparently normal initial development. Such MeCP2 alterations often result in changes to DNA binding and chromatin clustering ability, and in the stability of this protein. Among other functions, MeCP2 binds to methylated genomic DNA, which represents an important epigenetic mark with broad physiological implications, including neuronal development. In this review, we will summarize the genetic foundations behind RTT, and the variable degrees of protein stability exhibited by MeCP2 and its mutated versions. Also, past and emerging relationships that MeCP2 has with mRNA splicing, miRNA processing, and other non-coding RNAs (ncRNA) will be explored, and we suggest that these molecules could be missing links in understanding the epigenetic consequences incurred from genetic ablation of this important chromatin modifier. Importantly, although MeCP2 is highly expressed in the brain, where it has been most extensively studied, the role of this protein and its alterations in other tissues cannot be ignored and will also be discussed. Finally, the additional complexity to RTT pathology introduced by structural and functional implications of the two MeCP2 isoforms (MeCP2-E1 and MeCP2-E2) will be described. Epigenetic therapeutics are gaining clinical popularity, yet treatment for Rett syndrome is more complicated than would be anticipated for a purely epigenetic disorder, which should be taken into account in future clinical contexts.

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Section: Subsectionsmentioning

confidence: 99%

MeCP2: The Genetic Driver of Rett Syndrome Epigenetics

2021

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“…NEAT1 serves as a scaffold for protein binding, seeding paraspeckle formation; SFPQ and its paralogue NONO bind NEAT1 to form a minimal ribonucleoprotein particle, which triggers polymerization of SFPQ (and presumably NONO). It is hypothesized that the low-complexity domains of SFPQ interact with additional proteins found in paraspeckles most of which also harbor low-complexity domains, inducing liquid–liquid separation to form paraspeckles [ 22 ]. While the precise functions of paraspeckles and the underlying mechanisms remain to be elucidated, it is generally accepted that they are involved in gene regulation in response to certain stress conditions, such as proteasomal inhibition and viral infection [ 23 ].…”

Section: The Rna-binding Protein Sfpqmentioning

confidence: 99%

The Emerging Role of the RNA-Binding Protein SFPQ in Neuronal Function and Neurodegeneration

Lim

James

Huang

et al. 2020

IJMS

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RNA-binding proteins (RBPs) are a class of proteins known for their diverse roles in RNA biogenesis, from regulating transcriptional processes in the nucleus to facilitating translation in the cytoplasm. With higher demand for RNA metabolism in the nervous system, RBP misregulation has been linked to a wide range of neurological and neurodegenerative diseases. One of the emerging RBPs implicated in neuronal function and neurodegeneration is splicing factor proline- and glutamine-rich (SFPQ). SFPQ is a ubiquitous and abundant RBP that plays multiple regulatory roles in the nucleus such as paraspeckle formation, DNA damage repair, and various transcriptional regulation processes. An increasing number of studies have demonstrated the nuclear and also cytoplasmic roles of SFPQ in neurons, particularly in post-transcriptional regulation and RNA granule formation. Not surprisingly, the misregulation of SFPQ has been linked to pathological features shown by other neurodegenerative disease-associated RBPs such as aberrant RNA splicing, cytoplasmic mislocalization, and aggregation. In this review, we discuss recent findings on the roles of SFPQ with a particular focus on those in neuronal development and homeostasis as well as its implications in neurodegenerative diseases.

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“…In addition, by physical interaction with DNA, lncRNAs regulate transcription by favoring or inhibiting transcription factor recruitment and RNA polymerase activity [37,38]. Meanwhile, by orchestrating protein and nucleic acid interaction, lncRNAs give shape to the nuclear bodies [39]. Matured lncRNAs, provided with 5 -capping, polyadenylation, and methylation of adenosine (N6-methyladenosine, m6A), are exported to the cytoplasm, where they control post-transcriptional gene regulation.…”

Section: Non-coding Rnas In Extracellular Vesiclesmentioning

confidence: 99%

Emerging Insights on the Biological Impact of Extracellular Vesicle-Associated ncRNAs in Multiple Myeloma

Raimondo

Urzì

Conigliaro

et al. 2020

ncRNA

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Increasing evidence indicates that extracellular vesicles (EVs) released from both tumor cells and the cells of the bone marrow microenvironment contribute to the pathobiology of multiple myeloma (MM). Recent studies on the mechanisms by which EVs exert their biological activity have indicated that the non-coding RNA (ncRNA) cargo is key in mediating their effect on MM development and progression. In this review, we will first discuss the role of EV-associated ncRNAs in different aspects of MM pathobiology, including proliferation, angiogenesis, bone disease development, and drug resistance. Finally, since ncRNAs carried by MM vesicles have also emerged as a promising tool for early diagnosis and therapy response prediction, we will report evidence of their potential use as clinical biomarkers.

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Architectural RNAs for Membraneless Nuclear Body Formation

Cited by 51 publications

References 87 publications

MeCP2: The Genetic Driver of Rett Syndrome Epigenetics

MeCP2: The Genetic Driver of Rett Syndrome Epigenetics

The Emerging Role of the RNA-Binding Protein SFPQ in Neuronal Function and Neurodegeneration

Emerging Insights on the Biological Impact of Extracellular Vesicle-Associated ncRNAs in Multiple Myeloma

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