Gentilella Antonio, Morón-Duran Francisco D, Fuentes Pedro, Zweig-Rocha Guilherme, Riaño-Canalias Ferran, Pelletier Joffrey, Ruiz Marta, Turón Gemma, Castaño Julio, Tauler Albert, Bueno Clara, Menéndez Pablo, Kozma Sara C, Thomas George
Metabolism and Cancer Group, Molecular Mechanisms And Experimental Therapy In Oncology Program, Bellvitge Biomedical Research Institute, IDIBELL, 08908 Barcelona, Spain; Department of Biochemistry and Physiology, Faculty of Pharmacy, Universitat de Barcelona, 08028 Barcelona, Spain.
Metabolism and Cancer Group, Molecular Mechanisms And Experimental Therapy In Oncology Program, Bellvitge Biomedical Research Institute, IDIBELL, 08908 Barcelona, Spain.
Mol Cell. 2017 Jul 6;67(1):55-70.e4. doi: 10.1016/j.molcel.2017.06.005. Epub 2017 Jun 29.
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.
高等真核生物中的核糖体蛋白(RP)表达通过5′TOP序列进行翻译调控。这种机制的进化是为了在不同组织中根据需求更快地产生核糖体蛋白。我们在此表明,与mRNA结合蛋白LARP1形成复合物的40S核糖体选择性地稳定5′TOP mRNA,该复合物的破坏会导致核糖体生物合成受损检查点(IRBC)的诱导和p53的稳定。这种机制的重要性在5q−综合征中得到强调,5q−综合征是一种由大片单等位基因缺失引起的大细胞性贫血,我们发现该缺失区域也包含LARP1基因。至关重要的是,在人类成年CD34+骨髓前体细胞中单独敲低LARP1会导致5′TOP mRNA减少并诱导p53。这些研究确定了一种独立于翻译过程的40S核糖体功能,该功能与LARP1一起介导5′TOP mRNA稳定性的自体控制,其破坏与5q−综合征的病理生理学有关。