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The G3BP1-Family-USP10 Deubiquitinase Complex Rescues Ubiquitinated 40S Subunits of Ribosomes Stalled in Translation from Lysosomal Degradation.
Molecular Cell ( IF 14.5 ) Pub Date : 2020-01-20 , DOI: 10.1016/j.molcel.2019.12.024 Cindy Meyer 1 , Aitor Garzia 1 , Pavel Morozov 1 , Henrik Molina 2 , Thomas Tuschl 1
Molecular Cell ( IF 14.5 ) Pub Date : 2020-01-20 , DOI: 10.1016/j.molcel.2019.12.024 Cindy Meyer 1 , Aitor Garzia 1 , Pavel Morozov 1 , Henrik Molina 2 , Thomas Tuschl 1
Affiliation
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Ribosome-associated quality control (RQC) purges aberrant mRNAs and nascent polypeptides in a multi-step molecular process initiated by the E3 ligase ZNF598 through sensing of ribosomes collided at aberrant mRNAs and monoubiquitination of distinct small ribosomal subunit proteins. We show that G3BP1-family-USP10 complexes are required for deubiquitination of RPS2, RPS3, and RPS10 to rescue modified 40S subunits from programmed degradation. Knockout of USP10 or G3BP1 family proteins increased lysosomal ribosomal degradation and perturbed ribosomal subunit stoichiometry, both of which were rescued by a single K214R substitution of RPS3. While the majority of RPS2 and RPS3 monoubiquitination resulted from ZNF598-dependent sensing of ribosome collisions initiating RQC, another minor pathway contributed to their monoubiquitination. G3BP1 family proteins have long been considered RNA-binding proteins, however, our results identified 40S subunits and associated mRNAs as their predominant targets, a feature shared by stress granules to which G3BP1 family proteins localize under stress.
中文翻译：
G3BP1-家族-USP10去泛素酶复合物可拯救溶酶体降解导致翻译中停滞的核糖体泛素化的40S亚基。
核糖体相关质量控制（RQC）在E3连接酶ZNF598引发的多步分子过程中，通过感测核糖体在异常mRNAs上碰撞以及独特的小核糖体亚基蛋白的单泛素化，在多步分子过程中清除异常的mRNA和新生多肽。我们表明，G3BP1-家族-USP10复合物是RPS2，RPS3和RPS10的去泛素化所必需的，以从程序化的降解中拯救修饰的40S亚基。敲除USP10或G3BP1家族蛋白会增加溶酶体核糖体降解和扰动的核糖体亚基化学计量，这两者都是通过RPS3的单个K214R取代而得以挽救的。虽然大多数RPS2和RPS3单泛素化是由ZNF598依赖性的核糖体碰撞引发RQC引起的，但另一个次要途径是它们的单泛素化。
更新日期：2020-01-24
中文翻译：
G3BP1-家族-USP10去泛素酶复合物可拯救溶酶体降解导致翻译中停滞的核糖体泛素化的40S亚基。
核糖体相关质量控制（RQC）在E3连接酶ZNF598引发的多步分子过程中，通过感测核糖体在异常mRNAs上碰撞以及独特的小核糖体亚基蛋白的单泛素化，在多步分子过程中清除异常的mRNA和新生多肽。我们表明，G3BP1-家族-USP10复合物是RPS2，RPS3和RPS10的去泛素化所必需的，以从程序化的降解中拯救修饰的40S亚基。敲除USP10或G3BP1家族蛋白会增加溶酶体核糖体降解和扰动的核糖体亚基化学计量，这两者都是通过RPS3的单个K214R取代而得以挽救的。虽然大多数RPS2和RPS3单泛素化是由ZNF598依赖性的核糖体碰撞引发RQC引起的，但另一个次要途径是它们的单泛素化。
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