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保守的 RNaseII 结构域蛋白在细胞质 mRNA 衰变中发挥作用,并抑制拟南芥去帽突变体的表型。

Conserved RNaseII domain protein functions in cytoplasmic mRNA decay and suppresses Arabidopsis decapping mutant phenotypes.

机构信息

Department of Biology, University of Utah, Salt Lake City, 84112-6517, USA.

出版信息

Proc Natl Acad Sci U S A. 2010 Sep 7;107(36):15981-5. doi: 10.1073/pnas.1007060107. Epub 2010 Aug 23.

Abstract

Both transcription and RNA decay are critical for normal gene regulation. Arabidopsis mutants with defects in VARICOSE (VCS), a decapping complex scaffold protein, lack mRNA decapping and 5'-to-3' decay. These mutants show either severe or suppressed phenotypes, depending on the Arabidopsis accession. Here, we show that the molecular basis for this variation is the SUPPRESSOR OF VARICOSE (SOV), a locus that encodes a conserved, cytoplasmically localized RRP44-like RNaseII-domain protein. In vivo RNA decay assays suggest that active forms of this protein carry out decay on mRNA substrates that overlap with those of the decapping complex. Members of this conserved gene family encode proteins lacking the PIN domain, suggesting that SOV is not a functional component of the RNA exosome.

摘要

转录和 RNA 衰变对于正常的基因调控都很关键。拟南芥中 VCS(一种去帽复合物支架蛋白)突变体表现出 mRNA 去帽和 5’到 3’衰变缺陷。这些突变体的表型要么很严重,要么受到抑制,这取决于拟南芥品系。在这里,我们发现造成这种差异的分子基础是 VCS 的抑制子 SOV,它编码一个保守的、定位于细胞质的 RRP44 样 RNaseII 结构域蛋白。体内 RNA 衰变实验表明,这种蛋白的活性形式在 mRNA 底物上发挥作用,与去帽复合物的作用重叠。这个保守基因家族的成员编码缺乏 PIN 结构域的蛋白,这表明 SOV 不是 RNA 外切体的功能性成分。

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