| Literature DB >> 28673543 |
Antonio Gentilella1, Francisco D Morón-Duran2, Pedro Fuentes2, Guilherme Zweig-Rocha2, Ferran Riaño-Canalias2, Joffrey Pelletier2, Marta Ruiz2, Gemma Turón2, Julio Castaño3, Albert Tauler4, Clara Bueno5, Pablo Menéndez6, Sara C Kozma7, George Thomas8.
Abstract
Ribosomal protein (RP) expression in higher eukaryotes is regulated translationally through the 5′TOP sequence. This mechanism evolved to more rapidly produce RPs on demand in different tissues. Here we show that 40S ribosomes, in a complex with the mRNA binding protein LARP1, selectively stabilize 5′TOP mRNAs, with disruption of this complex leading to induction of the impaired ribosome biogenesis checkpoint (IRBC) and p53 stabilization. The importance of this mechanism is underscored in 5q− syndrome, a macrocytic anemia caused by a large monoallelic deletion, which we found to also encompass the LARP1 gene. Critically, depletion of LARP1 alone in human adult CD34+ bone marrow precursor cells leads to a reduction in 5′TOP mRNAs and the induction of p53. These studies identify a 40S ribosome function independent of those in translation that, with LARP1, mediates the autogenous control of 5′TOP mRNA stability, whose disruption is implicated in the pathophysiology of 5q− syndrome.Entities:
Keywords: 40S ribosomes; 5?TOP mRNAs; 5q(?) syndrome; impaired ribosome biogenesis checkpoint; p53 stabilization; polysome profiles; ribosomal proteins
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Year: 2017 PMID: 28673543 PMCID: PMC5553558 DOI: 10.1016/j.molcel.2017.06.005
Source DB: PubMed Journal: Mol Cell ISSN: 1097-2765 Impact factor: 17.970