Crt10 directs the cullin-E3 ligase Rtt101 to nonfunctional 25S rRNA decay

Crt10 directs the cullin-E3 ligase Rtt101 to nonfunctional 25S rRNA decay
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Crt10 引导 cullin-E3 连接酶 Rtt101 进行非功能性 25S rRNA 衰变

DOI:
10.1016/j.bbrc.2014.12.072
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发表时间:
2015
期刊:
Biochem. Biophys. Res. Commu
影响因子:
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通讯作者:
Kitabatake M
Kitabatake M
中科院分区:
--
文献类型:
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作者:
Sakata T;Fujii K;Ohno M;Kitabatake M

文献摘要

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在真核细胞中,40S或60S亚基的非功能性突变核糖体RNA被选择性地降解(非功能性rRNA Decay,NRD)。我们先前报道,25S rRNA的NRD需要cullin-E3连接酶Rtt101及其相关因子Mms1,两者都参与DNA修复。虽然Mms22是E3复合体的一个辅助成分,它被认为可以指导E3复合体进行DNA修复,但目前还不清楚引导该复合体进行25S NRD的因素。我们在这里证明了另一个辅助成分Crt10是25S NRD所必需的,但不是DNA修复所必需的,这表明该辅助成分对E3复合体的功能有不同的规定。我们还鉴定了两个不同的含有Crt10的E3复合体,其中一个包含Paf1复合体,这是一个Pol-II结合复合体,调节胁迫相关基因的转录。我们的结果显示了伤害核酸的胁迫的多条途径的收敛,并为E3复合体的底物多样性提供了一个分子框架。
Nonfunctional mutant ribosomal RNAs in 40S or 60S subunits are selectively degraded in eukaryotic cells (nonfunctional rRNA decay, NRD). We previously reported that NRD of 25S rRNA required cullin-E3 ligase Rtt101 and its associating factor Mms1, both of which are involved in DNA repair. Although Mms22, an accessory component of the E3 complex, was suggested to direct the E3 complex to DNA repair, the factor that directs the complex to 25S NRD currently remains unknown. We herein demonstrated that another accessory component, Crt10 was required for 25S NRD, but not for DNA repair, suggesting that this accessory component specifies the function of the E3 complex differently. We also identified two distinct Crt10-containing E3 complexes, one of which contained the Paf1 complex, a Pol-II binding complex that modulates the transcription of stress-related genes. Our results showed the convergence of multiple pathways for stresses that harm nucleic acids and provided a molecular framework for the substrate diversity of the E3 complex.