snOPY: a small nucleolar RNA orthological gene database

Yoshihama, Maki; Nakao, Akihiro; Kenmochi, Naoya

doi:10.1186/1756-0500-6-426

Cited by 100 publications

(118 citation statements)

References 18 publications

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“…We therefore postulated that the proliferative arrest induced by dyskerin depletion resulted from reduced availability of snoRNAs, and consequently ribosomal stress. We therefore quantified the abundance of three H/ACA snoRNAs, SNORA16, SNORA42, and SNORA75 (U23), which are involved in rRNA processing in human cancer cells, in siRNA-transfected NB69 cells (29,30). qRT-PCR analyses confirmed that the level of each of these snoRNAs was substantially less in dyskerin-depleted cells than in control siRNA-transfected cells (Fig.…”

Section: Downregulation Of Dyskerin Depletes H/aca Snornas and Causesmentioning

confidence: 84%

MYC-Driven Neuroblastomas Are Addicted to a Telomerase-Independent Function of Dyskerin

et al. 2016

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The RNA-binding protein dyskerin, encoded by the DKC1 gene, functions as a core component of the telomerase holoenzyme as well as ribonuclear protein complexes involved in RNA processing and ribosome biogenesis. The diverse roles of dyskerin across many facets of RNA biology implicate its potential contribution to malignancy. In this study, we examined the expression and function of dyskerin in neuroblastoma. We show that DKC1 mRNA levels were elevated relative to normal cells across a panel of 15 neuroblastoma cell lines, where both N-Myc and c-Myc directly targeted the DKC1 promoter. Upregulation of MYCN was shown to dramatically increase DKC1 expression. In two independent neuroblastoma patient cohorts, high DKC1 expression correlated strongly with poor event-free and overall survival (P < 0.0001), independently of established prognostic factors. RNAi-mediated depletion of dyskerin inhibited neuroblastoma cell proliferation, including cells immortalized via the telomerase-independent ALT mechanism. Furthermore, dyskerin attenuation impaired anchorage-independent proliferation and tumor growth. Overexpression of the telomerase RNA component, hTR, demonstrated that this proliferative impairment was not a consequence of telomerase suppression. Instead, ribosomal stress, evidenced by depletion of small nucleolar RNAs and nuclear dispersal of ribosomal proteins, was the likely cause of the proliferative impairment in dyskerindepleted cells. Accordingly, dyskerin suppression caused p53-dependent G 1 cell-cycle arrest in p53 wild-type cells, and a p53-independent pathway impaired proliferation in cells with p53 dysfunction. Together, our findings highlight dyskerin as a new therapeutic target in neuroblastoma with crucial telomerase-independent functions and broader implications for the spectrum of malignancies driven by MYC family oncogenes. Cancer Res; 76(12); 3604-17. Ó2016 AACR.

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Section: Downregulation Of Dyskerin Depletes H/aca Snornas and Causesmentioning

confidence: 84%

MYC-Driven Neuroblastomas Are Addicted to a Telomerase-Independent Function of Dyskerin

et al. 2016

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“…In addition to the well-characterized ribosomal RNAs and transfer RNAs, several other broad classes have been defined, including microRNAs (miRNA), long noncoding RNAs (lncRNA), and small nuclear and nucleolar RNAs (snRNA and snoRNA) Yoshihama et al 2013;Kozomara and Griffiths-Jones 2014). These classes are still being continuously added to and enlarged by newly discovered molecules.…”

Section: Introductionmentioning

confidence: 99%

The yeast noncoding RNA interaction network

Panni

Prakash

Bateman

et al. 2017

RNA

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This article describes the creation of the first expert manually curated noncoding RNA interaction networks for S. cerevisiae. The RNA-RNA and RNA-protein interaction networks have been carefully extracted from the experimental literature and made available through the IntAct database (www.ebi.ac.uk/intact). We provide an initial network analysis and compare their properties to the much larger protein-protein interaction network. We find that the proteins that bind to ncRNAs in the network contain only a small proportion of classical RNA binding domains. We also see an enrichment of WD40 domains suggesting their direct involvement in ncRNA interactions. We discuss the challenges in collecting noncoding RNA interaction data and the opportunities for worldwide collaboration to fill the unmet need for this data.

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“…Within our dataset, we found snoRNA-rRNA hybrids for all of the 43 C/D box snoRNAs reported to methylate yeast rRNA in the snOPY database ( Yoshihama et al , 2013). For 42 of these snoRNAs (all except snR65), hybrids were present in the dataset that overlapped each of the reported methylation sites in rRNA associated with the relevant snoRNA ( Figure 2).…”

Section: Resultsmentioning

confidence: 90%

Mapping targets for small nucleolar RNAs in yeast

Dudnakova¹,

Dunn-Davies²,

Peters³

et al. 2018

Wellcome Open Res

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Background: Recent analyses implicate changes in the expression of the box C/D class of small nucleolar RNAs (snoRNAs) in several human diseases. Methods: Here we report the identification of potential novel RNA targets for box C/D snoRNAs in budding yeast, using the approach of UV crosslinking and sequencing of hybrids (CLASH) with the snoRNP proteins Nop1, Nop56 and Nop58. We also developed a bioinformatics approach to filter snoRNA-target interactions for bona fide methylation guide interactions. Results: We recovered 241,420 hybrids, out of which 190,597 were classed as reproducible, high energy hybrids. As expected, the majority of snoRNA interactions were with the ribosomal RNAs (rRNAs). Following filtering, 117,047 reproducible hybrids included 51 of the 55 reported rRNA methylation sites. The majority of interactions at methylation sites were predicted to guide methylation. However, competing, potentially regulatory, binding was also identified. In marked contrast, following CLASH performed with the RNA helicase Mtr4 only 7% of snoRNA-rRNA interactions recovered were predicted to guide methylation. We propose that Mtr4 functions in dissociating inappropriate snoRNA-target interactions. Numerous snoRNA-snoRNA interactions were recovered, indicating potential cross regulation. The snoRNAs snR4 and snR45 were recently implicated in site-directed rRNA acetylation, and hybrids were identified adjacent to the acetylation sites. We also identified 1,368 reproducible snoRNA-mRNA interactions, representing 448 sites of interaction involving 39 snoRNAs and 382 mRNAs. Depletion of the snoRNAs U3, U14 or snR4 each altered the levels of numerous mRNAs. Targets identified by CLASH were over-represented among these species, but causality has yet to be established. Conclusions: Systematic mapping of snoRNA-target binding provides a catalogue of high-confidence binding sites and indicates numerous potential regulatory interactions.

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snOPY: a small nucleolar RNA orthological gene database

Cited by 100 publications

References 18 publications

MYC-Driven Neuroblastomas Are Addicted to a Telomerase-Independent Function of Dyskerin

MYC-Driven Neuroblastomas Are Addicted to a Telomerase-Independent Function of Dyskerin

The yeast noncoding RNA interaction network

Mapping targets for small nucleolar RNAs in yeast

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