DEAD-box helicase DDX27 regulates 3′ end formation of ribosomal 47S RNA and stably associates with the PeBoW-complex

Kellner, Markus; Michaela, Rohrmoser; Forné, Ignasi; Voß, Kirsten; Burger, Kaspar; Mühl, Bastian; Anita, Gruber-Eber; Kremmer, Elisabeth; Imhof, Axel; Eick, Dirk

doi:10.1016/j.yexcr.2015.03.017

Cited by 32 publications

(34 citation statements)

References 42 publications

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“…This accumulation of early precursors and of precursors C suggests an early defect in the rRNA maturation process and indicative of delayed cleavages in the 5'ETS and 3'ETS. These results are in accordance with recent data showing that depletion of DDX27 in human cells leads to the release of an extended form of the 47S primary transcript [34]. In addition, our data reveal an accumulation of 41S pre-rRNAs and a concomitant decrease of 30S pre-rRNAs, which are indicative of an impaired cleavage at site 2 ( Fig 5C).…”

Section: Nucleolar Abnormalities and Rrna Maturation Defects In Ddx27supporting

confidence: 93%

RNA helicase, DDX27 regulates skeletal muscle growth and regeneration by modulation of translational processes

Bennett

O’Donohue

Gundry

et al. 2017

Preprint

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Gene expression in a tissue-specific context depends on the combined efforts of epigenetic, transcriptional and post-transcriptional processes that lead to the production of specific proteins that are important determinants of cellular identity. Ribosomes are a central component of the protein biosynthesis machinery in cells; however, their regulatory roles in the translational control of gene expression in skeletal muscle remain to be defined. In a genetic screen to identify critical regulators of myogenesis, we identified a DEAD-Box RNA helicase, DDX27, that is required for skeletal muscle growth and regeneration. We demonstrate that DDX27 regulates ribosomal RNA (rRNA) maturation, and thereby the ribosome biogenesis and the translation of specific transcripts during myogenesis. These findings provide insight into the translational regulation of gene expression in myogenesis and suggest novel functions for ribosomes in regulating gene expression in skeletal muscles. AUTHOR SUMMARYInherited skeletal muscle diseases are the most common form of genetic disorders with primary abnormalities in the structure and function of skeletal muscle resulting in the impaired locomotion in affected patients. A major hindrance to the development of effective therapies is a lack of understanding of biological processes that promote skeletal muscle growth. By performing a forward genetic screen in zebrafish we have identified mutation in a RNA helicase that leads to perturbations of ribosomal biogenesis pathway and impairs skeletal muscle growth and regeneration. Therefore, our studies have identified novel ribosome-based disease processes that may be therapeutic modulated to restore muscle function in skeletal muscle diseases.

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Section: Nucleolar Abnormalities and Rrna Maturation Defects In Ddx27supporting

confidence: 93%

RNA helicase, DDX27 regulates skeletal muscle growth and regeneration by modulation of translational processes

Bennett

O’Donohue

Gundry

et al. 2017

Preprint

View full text Add to dashboard Cite

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“…Moreover, Ddx27 (mammalian counterpart of Drs1) has been coprecipitated with Bop1 in cellular extracts (Kellner et al, 2015). Nevertheless, it has not been show in vitro, without any possible secondary factors such as rRNA, that the binding between Drs1 and Erb1 or Nop7 takes place.…”

Section: Erb1mentioning

confidence: 99%

“…It is not clear how 3'-ETS is trimmed to give rise to the final 3' end of 25S but it has been suggested that 3'-ETS and ITS1 processing occur concomitantly (Fernández-Pevida et al, 2015). A recent study in mammals has proposed that DDX27 helicase (Drs1 in yeast) is indispensable for the 3' end maturation of 27S rRNA (Kellner et al, 2015). In eukaryotes there are known two pathways involved in 5.8S formation.…”

Section: Lsu Rrna Processingmentioning

confidence: 99%

“…Interesting mechanism of action has been proposed for Rea1 thanks to the structural information obtained by cryo-electron microscopy combined with biochemical analysis. d) helicases: at least 10 RNA helicases participate in LSU maturation (Bernstein et al, 2006;Granneman et al, 2006;Kellner et al, 2015;Rodríguez-Galán et al, 2013). All of them, except one, belong to SF2 DExD/H-box family.…”

Section: Trans-acting Factorsmentioning

confidence: 99%

“…The most recent reports on Nop7 function have suggested that it could act as a co-factor of Drs1 helicase because, at least under certain conditions, it was found to form part of the same small sub-complexes, tightly related to Nop7 (Merl et al, 2010). Moreover, the human ortholog of Drs1, Ddx27 has been shown to interact with Pes1 in total cell extracts (Kellner et al, 2015).…”

Section: Nop7mentioning

confidence: 99%

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Structural, biophysical and functional characterization of Nop7-Erb1-Ytm1 complex and its implications in eukaryotic ribosome biogenesis

Wegrecki¹

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The PES1/FOXM1 heterodimer suppresses TCF21 and ERβ expression in ovarian endometriosis

Zhu,

Wu,

et al. 2023

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Transcription factor 21 (TCF21) and estrogen receptor beta (ERβ, encoded by ESR2) are highly expressed in endometriotic stromal cells (ESCs) and contribute to the pathogenesis of endometriosis. However, the exploration of TCF21 and ERβ expression regulation at the molecular level remains limited. Here, by using bioinformatics analysis and experimental verification, we identified PES1, also known as Pescadillo, as a negative regulator in the development of endometriosis that downregulates TCF21 and ERβ expression in ESCs. PES1 overexpression regulated critical biological processes involved in endometriosis development, such as invasion and apoptosis. A coimmunoprecipitation assay showed that PES1 could form a complex with Forkhead box M1 (FOXM1). Further analyses elucidated that siPES1 in ectopic lesions decreased the stability of FOXM1 protein and reduced the binding activities of FOXM1 to TCF21 and ESR2 promoters, thus weakening the transcriptional inhibition of TCF21 and ERβ by FOXM1. Moreover, in an endometriosis mouse model, overexpressing PES1 effectively reduced the growth of ectopic lesions and suppressed TCF21 and ERβ expression, which suggests a promising therapeutic strategy for endometriosis. Collectively, our results indicate that the loss of PES1 in ectopic lesions contributes to endometriosis progression by upregulating ERβ and TCF21 expression through heterodimer formation with FOXM1. Moreover, targeting PES1 could serve as a treatment method for endometriosis.

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DEAD-box helicase DDX27 regulates 3′ end formation of ribosomal 47S RNA and stably associates with the PeBoW-complex

Cited by 32 publications

References 42 publications

RNA helicase, DDX27 regulates skeletal muscle growth and regeneration by modulation of translational processes

RNA helicase, DDX27 regulates skeletal muscle growth and regeneration by modulation of translational processes

Structural, biophysical and functional characterization of Nop7-Erb1-Ytm1 complex and its implications in eukaryotic ribosome biogenesis

The PES1/FOXM1 heterodimer suppresses TCF21 and ERβ expression in ovarian endometriosis

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