Erratum: A vlincRNA participates in senescence maintenance by relieving H2AZ-mediated repression at the INK4 locus

Lazorthes, Sandra; Vallot, Céline; Briois, Sébastien; Aguirrebengoa, Marion; Thuret, Jean‐Yves; Laurent, Georges St.; Rougeulle, Claire; Kapranov, Philipp; Mann, Carl; Trouche, Didier; Nicolas, Estelle

doi:10.1038/ncomms7918

Cited by 3 publications

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“…The images were all acquired with identical settings. either proliferating or driven into senescence (Lazorthes et al, 2015) or (D) BJ cells exposed to H 2 O 2 for the indicated times (Giannakakis et al, 2015). (E) Hypothetical model: an initial source of oxidative stress increases elongation and reduces degradation of pegeRNAs that will eventually contain sequences encoded by repeats originating from retrotransposons.…”

Section: Immunofluorescent Stainingmentioning

confidence: 99%

“…To date, the role of RNA in senescence has mostly been examined at the level of discrete long non-coding RNAs (lncRNAs) regulating expression or activity of proteins relevant for cellular senescence (Montes & Lund, 2016). For example, VAD, a "very lncRNA," partially antisense to the DDAH1 gene, inhibits the incorporation of the repressive histone variant H2A.Z at the promoter of the INK4 gene in senescent cells (Lazorthes et al, 2015). Inversely, SENEBLOC, a Myc-regulated lncRNA, interferes with senescence in part by regulating p53-mediated repression of the p21 gene (Xu et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

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Reduced RNA turnover as a driver of cellular senescence

et al. 2021

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Accumulation of senescent cells is an important contributor to chronic inflammation upon aging. The inflammatory phenotype of senescent cells was previously shown to be driven by cytoplasmic DNA. Here, we propose that cytoplasmic double-stranded RNA has a similar effect. We find that several cell types driven into senescence by different routes share an accumulation of long promoter RNAs and 3′ gene extensions rich in retrotransposon sequences. Accordingly, these cells display increased expression of genes involved in response to double stranded RNA of viral origin downstream of the interferon pathway. The RNA accumulation is associated with evidence of reduced RNA turnover, including in some cases, reduced expression of RNA exosome subunits. Reciprocally, depletion of RNA exosome subunit EXOSC3 accelerated expression of multiple senescence markers. A senescence-like RNA accumulation was also observed in cells exposed to oxidative stress, an important trigger of cellular senescence. Altogether, we propose that in a subset of senescent cells, repeat-containing transcripts stabilized by oxidative stress or reduced RNA exosome activity participate in driving and maintaining the permanent inflammatory state characterizing cellular senescence.

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Section: Immunofluorescent Stainingmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Reduced RNA turnover as a driver of cellular senescence

et al. 2021

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Shining the Light on Senescence Associated LncRNAs

Ghanam¹,

Xu²,

Ke³

et al. 2017

Aging and disease

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Cellular senescence can be described as a complex stress response that leads to irreversible cell cycle arrest. This process was originally described as an event that primary cells go through after many passages of cells during cell culture. More recently, cellular senescence is viewed as a programmed process by which the cell displays a senescence phenotype when exposed to a variety of stresses. Cellular senescence has been implicated in tumor suppression and aging such that senescence may contribute to both tumor progression and normal tissue repair. Here, we review different forms of cellular senescence, as well as current biomarkers used to identify senescent cells in vitro and in vivo. Additionally, we highlight the role of senescence-associated long noncoding RNAs (lncRNAs).

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The Histone Code of Senescence

Paluvai

Giorgio

Brancolini

2020

Cells

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Senescence is the end point of a complex cellular response that proceeds through a set of highly regulated steps. Initially, the permanent cell-cycle arrest that characterizes senescence is a pro-survival response to irreparable DNA damage. The maintenance of this prolonged condition requires the adaptation of the cells to an unfavorable, demanding and stressful microenvironment. This adaptation is orchestrated through a deep epigenetic resetting. A first wave of epigenetic changes builds a dam on irreparable DNA damage and sustains the pro-survival response and the cell-cycle arrest. Later on, a second wave of epigenetic modifications allows the genomic reorganization to sustain the transcription of pro-inflammatory genes. The balanced epigenetic dynamism of senescent cells influences physiological processes, such as differentiation, embryogenesis and aging, while its alteration leads to cancer, neurodegeneration and premature aging. Here we provide an overview of the most relevant histone modifications, which characterize senescence, aging and the activation of a prolonged DNA damage response.

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Erratum: A vlincRNA participates in senescence maintenance by relieving H2AZ-mediated repression at the INK4 locus

Cited by 3 publications

References 0 publications

Reduced RNA turnover as a driver of cellular senescence

Reduced RNA turnover as a driver of cellular senescence

Shining the Light on Senescence Associated LncRNAs

The Histone Code of Senescence

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