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Senescence-associated ribosome biogenesis defects contributes to cell cycle arrest through the Rb pathway.

Abstract：

:Cellular senescence is a tumour suppressor programme characterized by a stable cell cycle arrest. Here we report that cellular senescence triggered by a variety of stimuli leads to diminished ribosome biogenesis and the accumulation of both rRNA precursors and ribosomal proteins. These defects were associated with reduced expression of several ribosome biogenesis factors, the knockdown of which was also sufficient to induce senescence. Genetic analysis revealed that Rb but not p53 was required for the senescence response to altered ribosome biogenesis. Mechanistically, the ribosomal protein S14 (RPS14 or uS11) accumulates in the soluble non-ribosomal fraction of senescent cells, where it binds and inhibits CDK4 (cyclin-dependent kinase 4). Overexpression of RPS14 is sufficient to inhibit Rb phosphorylation, inducing cell cycle arrest and senescence. Here we describe a mechanism for maintaining the senescent cell cycle arrest that may be relevant for cancer therapy, as well as biomarkers to identify senescent cells.

journal_name

Nat Cell Biol

journal_title

Nature cell biology

authors

Lessard F,Igelmann S,Trahan C,Huot G,Saint-Germain E,Mignacca L,Del Toro N,Lopes-Paciencia S,Le Calvé B,Montero M,Deschênes-Simard X,Bury M,Moiseeva O,Rowell MC,Zorca CE,Zenklusen D,Brakier-Gingras L,Bourdeau V,Oeffin

doi

10.1038/s41556-018-0127-y

subject

Has Abstract

pub_date

2018-07-01 00:00:00

pages

789-799

issue

7

eissn

1465-7392

issn

1476-4679

pii

10.1038/s41556-018-0127-y

journal_volume

20

pub_type

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