The Nuclear Ribonucleoprotein SmD1 Interplays with Splicing, RNA Quality Control, and Posttranscriptional Gene Silencing in Arabidopsis
The Nuclear Ribonucleoprotein SmD1 Interplays with Splicing, RNA Quality Control, and Posttranscriptional Gene Silencing in Arabidopsis
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DOI：
10.1105/tpc.15.01045
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发表时间：
2016-02-01
期刊：
影响因子：
11.6
通讯作者：
Vaucheret, Herve
中科院分区：
文献类型：
--
作者：
Elvira-Matelot, Emilie;Bardou, Florian;Vaucheret, Herve
RNA质量控制（RQC）基于异常RNA的非典型结构消除异常RNA，而转录后基因沉默（PTGS）通过短干扰RNA （sirna）的序列特异性作用消除异常RNA和功能RNA。拟南芥突变体smd1b在PTGS缺陷的遗传筛选中被鉴定出来，揭示了SmD1 （Smith （Sm）复合体的一个组成部分）参与PTGS。smd1a和smd1b单突变体是活的，但smd1a和smd1b双突变体是胚胎致死性的，这表明SmD1的功能是必不可少的。SmD1b存在于核核和核质斑点中，与剪接相关因子SR34共定位。与此一致的是，smd1b突变体在某些内源性mrna上表现出内含子保留。SmD1可以与沉默转基因转录的rna结合，但不能与非沉默转基因转录的rna结合，这表明SmD1在PTGS中起直接作用。然而，RQC因子UPFRAMESHIFT3、EXORIBONUCLEASE2 （XRN2）、XRN3和XRN4的突变恢复了smd1b中的PTGS，这表明SmD1对PTGS不是必需的，而是促进了PTGS。此外，smd1b mtr4双突变体具有胚胎致死性，这表明SmD1对于mRNA TRANSPORT regulator4依赖性RQC至关重要。这些结果表明SmD1与剪接、RQC和PTGS相互作用。我们认为SmD1通过保护转基因衍生的异常rna免受核内RQC的降解，从而促进PTGS，允许足够数量的siRNA进入细胞质小体来激活PTGS。
RNA quality control (RQC) eliminates aberrant RNAs based on their atypical structure, whereas posttranscriptional gene silencing (PTGS) eliminates both aberrant and functional RNAs through the sequence-specific action of short interfering RNAs (siRNAs). The Arabidopsis thaliana mutant smd1b was identified in a genetic screen for PTGS deficiency, revealing the involvement of SmD1, a component of the Smith (Sm) complex, in PTGS. The smd1a and smd1b single mutants are viable, but the smd1a smd1b double mutant is embryo-lethal, indicating that SmD1 function is essential. SmD1b resides in nucleoli and nucleoplasmic speckles, colocalizing with the splicing-related factor SR34. Consistent with this, the smd1b mutant exhibits intron retention at certain endogenous mRNAs. SmD1 binds to RNAs transcribed from silenced transgenes but not nonsilenced ones, indicating a direct role in PTGS. Yet, mutations in the RQC factors UPFRAMESHIFT3, EXORIBONUCLEASE2 (XRN2), XRN3, and XRN4 restore PTGS in smd1b, indicating that SmD1 is not essential for but rather facilitates PTGS. Moreover, the smd1b mtr4 double mutant is embryo-lethal, suggesting that SmD1 is essential for mRNA TRANSPORT REGULATOR4-dependent RQC. These results indicate that SmD1 interplays with splicing, RQC, and PTGS. We propose that SmD1 facilitates PTGS by protecting transgene-derived aberrant RNAs from degradation by RQC in the nucleus, allowing sufficient amounts to enter cytoplasmic siRNA bodies to activate PTGS.