Myb-binding Protein 1a (Mybbp1a) Regulates Levels and Processing of Pre-ribosomal RNA

Hochstatter, Julia; Hölzel, Michael; Michaela, Rohrmoser; Schermelleh, Lothar; Leonhardt, Heinrich; Keough, Rebecca A.; Gonda, Thomas J.; Imhof, Axel; Eick, Dirk; Längst, Gernot; Németh, Attila

doi:10.1074/jbc.m111.303719

Cited by 38 publications

(35 citation statements)

References 70 publications

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“…MYBBP1A, a protein known to stabilize p53, was strongly enriched (Figures 5A–C) in the PURPL pulldowns (Ono et al, 2014, Kuroda et al, 2011, Kumazawa et al, 2015, Akaogi et al, 2013). MYBBP1A is a predominantly nucleolar protein that associates with RNA and directly binds to p53 in the nucleoplasm resulting in p53 activation and stabilization (Ono et al, 2014, Kuroda et al, 2011, Hochstatter et al, 2012, George et al, 2015). Given the known role of MYBBP1A in regulating p53, we selected MYBBP1A for further analysis.…”

Section: Resultsmentioning

confidence: 99%

Long Noncoding RNA PURPL Suppresses Basal p53 Levels and Promotes Tumorigenicity in Colorectal Cancer

et al. 2017

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SUMMARY Basal p53 levels are tightly suppressed under normal conditions. Disrupting this regulation results in elevated p53 levels to induce cell cycle arrest, apoptosis and tumor suppression. Here, we report the suppression of basal p53 levels by a nuclear, p53-regulated long noncoding RNA that we termed PURPL (p53 upregulated regulator of p53 levels). Targeted depletion of PURPL in colorectal cancer cells results in elevated basal p53 levels and induces growth defects in cell culture and in mouse xenografts. PURPL associates with MYBBP1A, a protein that binds to and stabilizes p53, and inhibits the formation of the p53-MYBBP1A complex. In the absence of PURPL, MYBBP1A interacts with and stabilizes p53. Silencing MYBBP1A significantly rescues basal p53 levels and proliferation in PURPL-deficient cells, suggesting that MYBBP1A mediates the effect of PURPL in regulating p53. These results reveal a p53-PURPL autoregulatory feedback loop and demonstrate a role for PURPL in maintaining basal p53 levels.

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Section: Resultsmentioning

confidence: 99%

Long Noncoding RNA PURPL Suppresses Basal p53 Levels and Promotes Tumorigenicity in Colorectal Cancer

et al. 2017

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“…We previously showed that newly replicated viral genomes are occupied by the chromatin‐organizing factor CTCF, (CCCTC‐binding factor) which is reported to interact with Mybbp1a . In addition, proteomic studies and biochemical analyses have identified several chromatin modulators as interactors of Mybbp1a . Taken together, this raises the possibility that Mybbp1a may be part of a chromatin‐remodeling complex, which controls viral chromatin assembly linked to genome organization and/or incorporation into progeny virions.…”

Section: Discussionmentioning

confidence: 98%

“…Mybbp1a is another regulator of nucleolar processes. Under physiological conditions, Mybbp1a is associated with epigenetic modulators to regulate ribosomal RNA transcription, an activity which is correlated with the rate of cellular proliferation, and deletion of the Mybbp1a gene results in embryonic death in mice . Mybbp1a was also shown to regulate the stability of the major tumor suppressor p53 upon nucleolar stress .…”

Section: Introductionmentioning

confidence: 99%

Tracking adenovirus genomes identifies morphologically distinct late DNA replication compartments

Komatsu

Robinson

Hisaoka

et al. 2016

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In adenoviral virions, the genome is organized into a chromatin-like structure by viral basic core proteins. Consequently viral DNAs must be replicated, chromatinized and packed into progeny virions in infected cells. Although viral DNA replication centers can be visualized by virtue of viral and cellular factors, the spatiotemporal regulation of viral genomes during subsequent steps remains to be elucidated. In this study, we used imaging analyses to examine the fate of adenoviral genomes and to track newly replicated viral DNA as well as replication-related factors. We show de novo formation of a subnuclear domain, which we termed Virus-induced Post-Replication (ViPR) body, that emerges concomitantly with or immediately after disintegration of initial replication centers. Using a nucleoside analogue, we show that viral genomes continue being synthesized in morphologically distinct replication compartments at the periphery of ViPR bodies and are then transported inward. In addition, we identified a nucleolar protein Mybbp1a as a molecular marker for ViPR bodies, which specifically associated with viral core protein VII. In conclusion, our work demonstrates the formation of previously uncharacterized viral DNA replication compartments specific for late phases of infection that produce progeny viral genomes accumulating in ViPR bodies. 1 Like cellular chromatin, the resulting chromatin structure plays a critical role in genome functions, eg, as template for transcription or replication. 1 Additionally, viral genome/chromatin has to be remodeled from an 'intracellular' to an 'intravirion' form to be packed into viral particles before or during virion assembly and maturation. Despite these essential steps, for many DNA viruses, the timing, the mechanistic details and the subcellular environment where these transitions take place remain largely unknown. During the first few hours of infection, the chromatin structure of the viral genome changes. We have shown that cellular histones are deposited onto incoming viral genomes. 5 We also reported that newly replicated viral DNAs associate with cellular histones. 6 Our analyses on histone deposition are consistent with other independent biochemical studies. 7-10 The deposition of cellular

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“…MyBBP1A, a known RNA-binding protein, is associated with both the RNA polymerase I complex and the ribosome biogenesis machinery (46). Direct interactions between MyBBP1A and lincRNA-Cox2 were demonstrated by our RNA pull-down analysis.…”

Section: Discussionmentioning

confidence: 99%

LincRNA-Cox2 Promotes Late Inflammatory Gene Transcription in Macrophages through Modulating SWI/SNF-Mediated Chromatin Remodeling

Gong

Wang

et al. 2016

The Journal of Immunology

178

169

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LincRNAs are long non-coding transcripts (>200 nt) from the intergenic regions of annotated protein-coding genes. One of the most highly induced lincRNAs in macrophages upon TLR ligation is lincRNA-Cox2, which has recently been shown to mediate both the activation and repression of distinct classes of immune genes in innate immune cells. We report here that lincRNA-Cox2 located at chromosome 1 proximal to the prostaglandin-endoperoxide synthase 2 (Ptgs2/Cox2) gene is an early-primary inflammatory gene controlled by NF-κB signaling in murine macrophages. Functionally, lincRNA-Cox2 is required for the transcription of NF-κB-regulated late-primary inflammatory response genes stimulated by bacterial lipopolysaccharide. Specifically, lincRNA-Cox2 is assembled into the SWI/SNF (SWItch/Sucrose NonFermentable) complex in cells after lipopolysaccharide stimulation. This resulting lincRNA-Cox2/SWI/SNF complex can modulate the assembly of NF-κB subunits to the SWI/SNF complex, and ultimately, SWI/SNF-associated chromatin remodeling and transactivation of the late-primary inflammatory response genes in macrophages in response to microbial challenge. Therefore, our data indicate a new regulatory role of NF-κB-induced lincRNA-Cox2 to act as a co-activator of NF-κB for the transcription of late-primary response genes in innate immune cells through modulation of epigenetic chromatin remodeling.

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Myb-binding Protein 1a (Mybbp1a) Regulates Levels and Processing of Pre-ribosomal RNA

Cited by 38 publications

References 70 publications

Long Noncoding RNA PURPL Suppresses Basal p53 Levels and Promotes Tumorigenicity in Colorectal Cancer

Long Noncoding RNA PURPL Suppresses Basal p53 Levels and Promotes Tumorigenicity in Colorectal Cancer

Tracking adenovirus genomes identifies morphologically distinct late DNA replication compartments

LincRNA-Cox2 Promotes Late Inflammatory Gene Transcription in Macrophages through Modulating SWI/SNF-Mediated Chromatin Remodeling

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